FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Whitmarsh, I Davis, AM Skinner, D Bailey, DB AF Whitmarsh, Ian Davis, Arlene M. Skinner, Debra Bailey, Donald B., Jr. TI A place for genetic uncertainty: Parents valuing an unknown in the meaning of disease SO SOCIAL SCIENCE & MEDICINE LA English DT Article DE USA; uncertainty; sex chromosome anomaly; fragile X syndrome; Klinefelter syndrome; turner syndrome; genetic diagnosis ID FRAGILE-X-SYNDROME; TURNER-SYNDROME; DIAGNOSTIC UNCERTAINTY; HEALTH-PROFESSIONALS; KLINEFELTER-SYNDROME; FAMILY EXPERIENCES; DOWN-SYNDROME; CHILDREN; AUTISM; PERCEPTIONS AB Klinefelter, Turner, and fragile X syndromes are conditions defined by a genetic or chromosomal variant. The timing of diagnosis, tests employed, specialists involved, symptoms evident, and prognoses available vary considerably within and across these syndromes, but all three share in common a diagnosis verified through a molecular or cytogenetic test. The genetic or chromosomal variant identified designates a syndrome, even when symptoms associated with the particular syndrome are absent. This article analyzes interviews conducted with parents and grandparents of children with these syndromes from across the USA to explore how they interpret a confirmed genetic diagnosis that is associated with a range of possible symptoms that may never be exhibited. Parents' responses indicate that they see the genetic aspects of the syndrome as stable, permanent, and authoritative. But they allow, and even embrace, uncertainty about the condition by focusing on variation between diagnosed siblings, the individuality of their diagnosed child, his or her accomplishments, and other positive aspects that go beyond the genetic diagnosis. Some families counter the genetic diagnosis by arguing that in the absence of symptoms, the syndrome does not exist. They use their own expertise to question the perceived certainty of the genetic diagnosis and to employ the diagnosis strategically. These multiple and often conflicting evaluations of the diagnostic label reveal the rich ways families make meaning of the authority attributed to genetic diagnosis. (C) 2007 Elsevier Ltd. All rights reserved. C1 Univ N Carolina, Chapel Hill, NC 27515 USA. RTI Int, Chapel Hill, NC USA. RP Whitmarsh, I (reprint author), Univ N Carolina, Chapel Hill, NC 27515 USA. 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Sci. Med. PD SEP PY 2007 VL 65 IS 6 BP 1082 EP 1093 DI 10.1016/j.socscimed.2007.04.034 PG 12 WC Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Public, Environmental & Occupational Health; Biomedical Social Sciences GA 211QL UT WOS:000249538300003 PM 17561324 ER PT J AU Blair, KSC Umbreit, J Dunlap, G Jung, G AF Blair, Kwang-Sun Cho Umbreit, John Dunlap, Glen Jung, Gilsoon TI Promoting inclusion and peer participation through assessment-based intervention SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID FUNCTIONAL BEHAVIORAL-ASSESSMENT; YOUNG-CHILDREN; SCHOOL SETTINGS; DISORDERS; SUPPORT; PREFERENCE; ATTENTION; STUDENTS; OUTCOMES; AUTISM AB In the current investigation, the processes of functional assessment and functionbased intervention were used to resolve the severe challenging behaviors of a boy with autism and mental retardation in an inclusive kindergarten in South Korea. 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PD FAL PY 2007 VL 27 IS 3 BP 134 EP 147 PG 14 WC Education, Special SC Education & Educational Research GA 238FM UT WOS:000251432700003 ER PT J AU Kohler, FW Greteman, C Raschke, D Highnam, C AF Kohler, Frank W. Greteman, Cindy Raschke, Donna Highnam, Clifford TI Using a buddy skills package to increase the social interactions between a preschooler with Autism and her peers SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID COMMUNICATION-SKILLS; YOUNG-CHILDREN; INTERVENTION; BEHAVIOR; DISABILITIES AB The purpose of this study was to examine the impact of a buddy skills package on the social interactions between a preschooler with autism and her peers. Following baseline, the children participated in 8 sessions of training that focused on the strategies of Play, Stay, and Talk. An intervention consisting of teacher feedback, praise, and picture cards was then implemented to support peers' overtures to their classmate with autism. 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TI Volumetric brain changes in females with fragile X-associated tremor/ataxia syndrome (FXTAS) SO NEUROLOGY LA English DT Article ID FMR1 MESSENGER-RNA; INTRANUCLEAR INCLUSIONS; PREMUTATION CARRIERS; INTENTION TREMOR; FULL-MUTATION; PRE-MUTATION; ALLELES; MALES; POPULATION; CEREBELLAR AB Background: Fragile X-associated tremor/ ataxia syndrome (FXTAS) is a late-onset neurodegenerative disorder occurring in male and rare female carriers of a premutation expansion (55 to 200 CGG repeats) of the fragile X mental retardation 1 (FMR1) gene. Methods: Volumetric MRI studies, clinical staging, cognitive testing, and molecular analysis were conducted in 15 female premutation carriers affected by FXTAS (age 59.5 +/- 10.3 years), 20 unaffected female carriers (43.3 +/- 11.2 years), 11 genetically normal female controls (51.0 +/- 10.3 years), 36 affected male carriers (65.0 +/- 5.6 years), 25 unaffected male carriers (53.5 +/- 12.5 years), and 39 male controls (58.0 +/- 15.0 years). Female and male carriers with FXTAS were matched on duration of disease. Results: We found less pronounced reductions of cerebellar volume and a lower incidence of involvement (symmetric high T2 signal) of the middle cerebellar peduncles (MCP sign) in females affected by FXTAS (13%) compared with affected males (58%). We found reduced brain volumes and increased white matter disease associated with the presence of FXTAS in females compared with female controls. We also observed significant associations between reduced cerebellar volume and both increased severity of FXTAS symptoms and increased length of the CGG repeat expansion in male premutation carriers, but not in females. Conclusions: Females affected by fragile X-associated tremor/ataxia syndrome (FXTAS) demonstrated milder brain changes than affected males, although they showed a similar pattern of radiologic findings consistent with brain atrophy and white matter disease. FXTAS should be considered (by ordering fragile X DNA testing) in females who present with late-onset ataxia, action tremor, or neuropathy, particularly in those with a family history of mental retardation, autism, or premature ovarian failure. C1 Univ Calif Davis, Med Ctr, MIND Inst, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Pediat, Div Biostat, Sacramento, CA 95817 USA. Univ Colorado, Dept Med, Denver, CO USA. Univ Colorado, Hlth Sci Ctr, Denver, CO USA. RP Hagerman, RJ (reprint author), Univ Calif Davis, Med Ctr, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. 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S. Hefter, Rebecca L. Cherkasova, Mariya V. Manoach, Dara S. TI Investigations of face expertise in the social developmental disorders SO NEUROLOGY LA English DT Article ID AUTISM SPECTRUM DISORDER; ASPERGER-SYNDROME; VISUAL AGNOSIA; OBJECT RECOGNITION; PROCESSING DEFICIT; COVERT RECOGNITION; REVISED VERSION; INVERTED FACES; PROSOPAGNOSIA; PERCEPTION AB Background: Patients with social developmental disorders (SDD), also known as autism spectrum disorders, may have impaired recognition of facial identity or facial expressions. Objective: Our goal was to determine whether SDDs were characterized by loss of a perceptual mechanism responsible for face expertise, as current theories suggest that such a loss should be selective for upright faces, disproportionately affect the perception of facial configuration, and possibly be more severe in the eye region. Method: We tested a group of 24 adult patients with SDD with an oddity paradigm that required them to detect changes in facial configuration or feature color, in either the eyes or the mouth, in both upright and inverted faces. Results: One group of subjects with SDD with normal famous face recognition had only a mild reduction in accuracy and a normal pattern of inversion effects. A second group of subjects with SDD with impaired famous face recognition had a severe reduction of accuracy. This deficit was not limited to upright faces. It affected the perception of feature configuration and feature color to a similar degree and both eye and mouth changes were discriminated poorly in upright faces. Conclusion: The impaired face recognition that is present in a subset of patients with social developmental disorders is accompanied by impaired face perception, and this impairment is not exclusive to upright faces, facial configuration, or the eye region. 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TI Autism and fertility drugs SO CHEMICAL & ENGINEERING NEWS LA English DT Letter NR 0 TC 0 Z9 0 PU AMER CHEMICAL SOC PI WASHINGTON PA 1155 16TH ST, NW, WASHINGTON, DC 20036 USA SN 0009-2347 J9 CHEM ENG NEWS JI Chem. Eng. News PD AUG 27 PY 2007 VL 85 IS 35 BP 6 EP 7 PG 2 WC Chemistry, Multidisciplinary; Engineering, Chemical SC Chemistry; Engineering GA 206NT UT WOS:000249190900008 ER PT J AU Tash, S AF Tash, Steve TI Inheriting autism SO NEW SCIENTIST LA English DT Letter NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD AUG 25 PY 2007 VL 195 IS 2618 BP 23 EP 23 DI 10.1016/S0262-4079(07)62139-3 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 205ZH UT WOS:000249153200022 ER PT J AU [Anonymous] AF [Anonymous] TI Inheriting autism SO NEW SCIENTIST LA English DT Letter NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD AUG 25 PY 2007 VL 195 IS 2618 BP 23 EP 23 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 205ZH UT WOS:000249153200023 ER PT J AU Singh, SK Yamashita, A Gouaux, E AF Singh, Satinder K. Yamashita, Atsuko Gouaux, Eric TI Antidepressant binding site in a bacterial homologue of neurotransmitter transporters SO NATURE LA English DT Article ID CYSTEINE-SCANNING MUTAGENESIS; HUMAN SEROTONIN TRANSPORTERS; NOREPINEPHRINE TRANSPORTER; INHIBITION; COTRANSPORTER; MUTATIONS; RECEPTORS; MECHANISM; DRUGS; MODEL AB Sodium-coupled transporters are ubiquitous pumps that harness pre-existing sodium gradients to catalyse the thermodynamically unfavourable uptake of essential nutrients, neurotransmitters and inorganic ions across the lipid bilayer(1). Dysfunction of these integral membrane proteins has been implicated in glucose/galactose malabsorption(2), congenital hypothyroidism(3), Bartter's syndrome(4), epilepsy(5), depression(6), autism(7) and obsessive-compulsive disorder(8). Sodium-coupled transporters are blocked by a number of therapeutically important compounds, including diuretics(9), anticonvulsants(10) and antidepressants(11), many of which have also become indispensable tools in biochemical experiments designed to probe antagonist binding sites and to elucidate transport mechanisms. Steady-state kinetic data have revealed that both competitive(12,13) and noncompetitive(14,15) modes of inhibition exist. Antagonist dissociation experiments on the serotonin transporter (SERT) have also unveiled the existence of a low-affinity allosteric site that slows the dissociation of inhibitors from a separate high-affinity site(16). Despite these strides, atomic-level insights into inhibitor action have remained elusive. Here we screen a panel of molecules for their ability to inhibit LeuT, a prokaryotic homologue of mammalian neurotransmitter sodium symporters, and show that the tricyclic antidepressant (TCA) clomipramine noncompetitively inhibits substrate uptake. Cocrystal structures show that clomipramine, along with two other TCAs, binds in an extracellular-facing vestibule about 11 angstrom above the substrate and two sodium ions, apparently stabilizing the extracellular gate in a closed conformation. Off-rate assays establish that clomipramine reduces the rate at which leucine dissociates from LeuT and reinforce our contention that this TCA inhibits LeuT by slowing substrate release. Our results represent a molecular view into noncompetitive inhibition of a sodium-coupled transporter and define principles for the rational design of new inhibitors. C1 Oregon Hlth & Sci Univ, Vollum Inst, Portland, OR 97239 USA. Oregon Hlth & Sci Univ, Howard Hughes Med Inst, Portland, OR 97239 USA. 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TI Increased cerebral oxygen consumption in Eker rats and effects of N-methyl-D-aspartate blockade: Implications for autism SO JOURNAL OF NEUROSCIENCE RESEARCH LA English DT Article DE autism spectrum disorder; excitatory amino acids; cerebral blood flow; cerebral O-2 consumption; rats ID TUBEROUS SCLEROSIS; GLUTAMATE-RECEPTOR-6 GENE; SPECTRUM DISORDERS; BLOOD-FLOW; NMDA; ASSOCIATION; RECEPTORS; GLUCOSE; METABOLISM; CHILDREN AB Because there is a strong correlation between tuberous sclerosis and autism, we used a tuberous sclerosis model (Eker rat) to test the hypothesis that these animals would have an altered regional cerebral O-2 consumption that might be associated with autism. We also examined whether the altered cerebral O-2 consumption was related to changes in the importance of N-methyl-D-aspartate (NMDA) receptors. Young (4 weeks) male control Long Evans (N = 14) and Eker (N = 14) rats (70-100 g) were divided into control and CGS-19755 (10 mg/kg, competitive NMDA antagonist)-treated animals. Cerebral regional blood flow (C-14-iodoantipyrine) and O-2 consumption (cryomicrospectrophotometry) were determined in isoflurane-anesthetized rats. NMDA receptor protein levels were determined by Western immunoblotting. We found significantly increased basal 02 consumption in the cortex (6.2 +/- 0.6 ml O-2/min/100 g Eker vs. 4.7 +/- 0.4 Long Evans), hippocampus, cerebellum, and pons. Regional cerebral blood flow was also elevated in Eker rats at baseline, but cerebral O-2 extraction was similar. CGS-19755 significantly lowered O-2 consumption in the cortex (2.8 +/- 0.3), hippocampus, and pons of the Long Evans rats but had no effect on cortex (5.8 +/- 0.8) or other regions of the Eker rats. Cerebral blood flow followed a similar pattern. NMDA receptor protein levels (NR1 subunit) were similar between groups. In conclusion, Eker rats had significantly elevated cerebral O-2 consumption and blood flow, but this was not related to NMDA receptor activation. In fact, the importance of NMDA receptors in the control of basal cerebral O-2 consumption was reduced. This might have important implications in the treatment of autism. (C) 2007 Wiley-Liss, Inc. C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Physiol & Biophys, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Anesthesia, Piscataway, NJ 08854 USA. RP Weiss, HR (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Physiol & Biophys, 675 Hoes Lane W, Piscataway, NJ 08854 USA. 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Mueller, Ralph-Axel Courchesne, Eric TI N-acetyl aspartate in autism spectrum disorders: Regional effects and relationship to fMRI activation SO BRAIN RESEARCH LA English DT Article DE autism; fMRI; magnetic resonance spectroscopy; verbal fluency; cerebellum; frontal lobe; NAA ID MAGNETIC-RESONANCE SPECTROSCOPY; DEVELOPMENTAL CEREBELLAR ABNORMALITY; COGNITIVE-AFFECTIVE SYNDROME; VERBAL FLUENCY; FRONTAL-CORTEX; CHILDHOOD AUTISM; INFANTILE-AUTISM; HEAD CIRCUMFERENCE; LANGUAGE DISORDER; BRAIN-METABOLITES AB Rapid progress in our understanding of macrostructural abnormalities in autism spectrum disorders (ASD) has occurred in recent years. However, the relationship between the integrity of neural tissue and neural function has not been previously investigated. Single-voxel proton magnetic resonance spectroscopy and functional magnetic resonance imaging of an executive functioning task was obtained in 13 high functioning adolescents and adults with ASD and 13 age-matched controls. The ASD group showed significant reductions in N-acetyl aspartate (NAA) in all brain regions combined and a specific reduction in left frontal cortex compared to controls. Regression analyses revealed a significant group interaction effect between frontal and cerebellar NAA. In addition, a significant positive semi-partial correlation between left frontal lobe NAA and frontal lobe functional activation was found in the ASD group. These findings suggest that widespread neuronal dysfunction is present in high functioning individuals with ASD. Hypothesized developmental links between frontal and cerebellar vermis neural abnormalities were supported, in that impaired neuronal functioning in the vermis was associated with impaired neuronal functioning in the frontal lobes in the ASD group. Furthermore, this study provided the first direct evidence of the relationship between abnormal functional activation in prefrontal cortex and neuronal dysfunction in ASD. (c) 2007 Elsevier B.V. All rights reserved. C1 Univ Washington, Dept Radiol, Seattle, WA 98195 USA. Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. VA San Diego Healthcare Syst, San Diego, CA 92161 USA. George Washington Univ, Sch Med, Washington, DC 20037 USA. Univ Calif San Diego, Dept Cognit Sci, La Jolla, CA 92093 USA. San Diego State Univ, Dept Psychol, San Diego, CA 92120 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Childrens Hosp Res Ctr, San Diego, CA 92123 USA. RP Kleinhans, NM (reprint author), Univ Washington, Dept Radiol, Box 357115, Seattle, WA 98195 USA. 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PD AUG 8 PY 2007 VL 1162 BP 85 EP 97 DI 10.1016/j.brainres.2007.04.081 PG 13 WC Neurosciences SC Neurosciences & Neurology GA 202BS UT WOS:000248877100010 PM 17612510 ER PT J AU Fortier, ME Luheshi, GN Boksa, P AF Fortier, Marie-Eve Luheshi, Giamal N. Boksa, Patricia TI Effects of prenatal infection on prepulse inhibition in the rat depend on the nature of the infectious agent and the stage of pregnancy SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE maternal infection; prepulse inhibition; schizophrenia; neurodevelopment; lipopolysaccharide; poly I : C; turpentine; startle ID NEURODEVELOPMENTAL ANIMAL-MODEL; DISRUPTED LATENT INHIBITION; PITUITARY-ADRENAL AXIS; ADULT SCHIZOPHRENIA; IMMUNE CHALLENGE; BACTERIAL-ENDOTOXIN; MATERNAL EXPOSURE; DOPAMINERGIC HYPERFUNCTION; TYROSINE-HYDROXYLASE; FEVER AB Maternal infection during pregnancy is a risk factor for some psychiatric illnesses of neurodevelopmental origin such as schizophrenia and autism. In experimental animals, behavioral and neuropathological outcomes relevant to schizophrenia have been observed in offspring of infected dams. However, the type of infectious agent used and gestational age at time of administration have varied. The objective of the present study was to compare the effects of prenatal challenge with different immune agents given at different time windows during gestation on behavioral outcomes in offspring. For this, pregnant rats were administered bacterial endotoxin (lipopolysaccharide, LPS), the viral mimic polyinosinic: polycytidylic acid (poly I:C), or turpentine, an inducer of local inflammation, at doses known to produce fever, at three different stages in pregnancy: embryonic day (E) 10-11, E 15-16 and E 18-19. Prepulse inhibition of acoustic startle (PPI) was later measured in male adult offspring. PPI was significantly decreased in offspring after prenatal LPS treatment at E15-16 and E18-19. Intramuscular injection of pregnant dams with turpentine at E15-16 also decreased PPI in adult offspring. Maternal poly l:C administration had no significant effect on PPI in offspring. In contrast to prenatal LPS exposure, acute LPS administration to naive adult males had no effect on PPI. Thus, prenatal exposure both to a systemic immunogen and to local inflammation at brief periods during later pregnancy produced lasting deficits in PPI in rat offspring. These findings support the idea that maternal infection during critical windows of pregnancy could contribute to sensorimotor gating deficits in schizophrenia. (c) 2007 Elsevier B.V. All rights reserved. C1 McGill Univ, Douglas Hosp, Res Ctr, Dept Psychiat,Neurosci Div, Verdun, PQ H4H 1R3, Canada. RP Boksa, P (reprint author), McGill Univ, Douglas Hosp, Res Ctr, Dept Psychiat,Neurosci Div, 6875 LaSalle Blvd, Verdun, PQ H4H 1R3, Canada. 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Both of these mechanisms for ensuring good health in children may be compromised by contact with mercury (Hg). Maternal exposure to environmental Hg during pregnancy can predispose nursing children to neurodevelopmental disorders. Despite the World Health Organization assurance that thimerosalpreserved vaccines are safe to use in infants, the United States, the European Union, and dozens of other countries have eliminated thimerosal as a vaccine preservative and stopped the immunization of children with such vaccines. Because of the increase in environmental pollution and the need to produce cheap and safe vaccines, there is a need to address the uncertainty of vaccine-ethylmercury risk of toxicity and Hg exposure during breastfeeding. C1 Univ Brasilia, Fac Hlth Sci, BR-70919970 Brasilia, DF, Brazil. RP Dorea, JG (reprint author), Univ Brasilia, Fac Hlth Sci, BR-70919970 Brasilia, DF, Brazil. 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J. Perinatol. PD AUG PY 2007 VL 24 IS 7 BP 387 EP 400 DI 10.1055/s-2007-982074 PG 14 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA 199IK UT WOS:000248689200001 PM 17564957 ER PT J AU Dettmer, K Hanna, D Whetstone, P Hansen, R Hammock, BD AF Dettmer, K. Hanna, D. Whetstone, P. Hansen, R. Hammock, B. D. TI Autism and urinary exogenous neuropeptides: development of an on-line SPE-HPLC-tandem mass spectrometry method to test the opioid excess theory SO ANALYTICAL AND BIOANALYTICAL CHEMISTRY LA English DT Article DE autism; neuropeptides; beta-casomorphin; gliadinomorphin; opioid peptide excess theory; on-line SPE-HPLC-MS/MS ID SPECTRUM DISORDER; CHILDREN; PEPTIDES AB Autism is a complex neurodevelopmental disorder with unknown etiology. One hypothesis regarding etiology in autism is the "opioid peptide excess" theory that postulates that excessive amounts of exogenous opioid-like peptides derived from dietary proteins are detectable in urine and that these compounds may be pathophysiologically important in autism. A selective LC-MS/MS method was developed to analyze gliadinomorphin, beta-casomorphin, deltorphin 1, and deltorphin 2 in urine. The method is based on on-line SPE extraction of the neuropeptides from urine, column switching, and subsequent HPLC analysis. A limit of detection of 0.25 ng/mL was achieved for all analytes. Analyte recovery rates from urine ranged between 78% and 94%, with relative standard deviations of 0.2-6.8%. The method was used to screen 69 urine samples from children with and without autism spectrum disorders for the occurrence of neuropeptides. The target neuropeptides were not detected above the detection limit in either sample set. C1 Univ Regensburg, Inst Funct Genom, D-93053 Regensburg, Germany. Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA. Univ Calif Davis, Sch Med, MIND Inst, Dept Pediat, Sacramento, CA 95817 USA. RP Dettmer, K (reprint author), Univ Regensburg, Inst Funct Genom, Josef Engert Str 9, D-93053 Regensburg, Germany. 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Bioanal. Chem. PD AUG PY 2007 VL 388 IS 8 BP 1643 EP 1651 DI 10.1007/s00216-007-1301-4 PG 9 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 194WA UT WOS:000248373300012 PM 17520243 ER PT J AU Uhlhaas, PJ Singer, W AF Uhlhaas, Peter. J. Singer, Wolf TI What do disturbances in neural synchrony tell us about autism? SO BIOLOGICAL PSYCHIATRY LA English DT Editorial Material ID SPECTRUM DISORDERS; SCHIZOPHRENIA C1 Max Planck Inst Brain Res, Dept Neurophysiol, Frankfurt, Germany. Goethe Univ Frankfurt, Dept Psychiat, Lab Neurophysiol & Neuroimaging, D-6000 Frankfurt, Germany. Max Planck Inst Brain Res, Dept Neurophysiol, D-60496 Frankfurt, Germany. Goethe Univ Frankfurt, Inst Adv Studies, D-6000 Frankfurt, Germany. RP Uhlhaas, PJ (reprint author), Max Planck Inst Brain Res, Dept Neurophysiol, Frankfurt, Germany. 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Psychiatry PD AUG 1 PY 2007 VL 62 IS 3 BP 190 EP 191 DI 10.1016/j.biopsych.2007.05.023 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 192NF UT WOS:000248208100001 PM 17631116 ER PT J AU Wilson, TW Rojas, DC Reite, ML Teale, PD Rogers, SJ AF Wilson, Tony W. Rojas, Donald C. Reite, Martin L. Teale, Peter D. Rogers, Sally J. TI Children and adolescents with autism exhibit reduced MEG steady-state gamma responses SO BIOLOGICAL PSYCHIATRY LA English DT Article DE ASD; auditory; autism; connectivity; gamma; MEG ID MODULATION FOLLOWING RESPONSE; AGED HUMAN-SUBJECTS; ASPERGER-SYNDROME; ENHANCED DISCRIMINATION; MINICOLUMNAR PATHOLOGY; CENTRAL COHERENCE; NEURAL SYNCHRONY; PLANUM TEMPORALE; SCHIZOPHRENIA; ADULTS AB Background: Recent neuroimaging studies of autism have indicated reduced functional connectivity during both cognitive tasks and rest. These data suggest long-range connectivity may be compromised in this disorder, and current neurological theories of autism contend disrupted inter-regional interactions may be an underlying mechanism explaining behavioral symptomatology. However, it is unclear whether deficient neuronal communication is attributable to fewer long-range tracts or more of a local deficit in neural circuitry.This study examines the integrity of local circuitry by focusing on gamma band activity in auditory cortices of children and adolescents with autism. Methods: Ten children and adolescents with autism and 10 matched controls participated. Both groups listened to 500 ms duration monaural click trains with a 25 ms inter-click interval, as magnetoencephalography was acquired from the contralateral hemisphere. To estimate 40 Hz spectral power density,we performed time-frequency decomposition of the single-trial magnetic steady-state response data using complex demodulation. Results: Children and adolescents with autism exhibited significantly reduced left hemispheric 40 Hz power from 200-500 ms post-stimulus onset. In contrast, no significant between group differences were observed for right hemispheric cortices. Conclusions: The production and/or maintenance of left hemispheric gamma oscillations appeared abnormal in participants with autism. We interpret these data as indicating that in autism, particular brain regions may be unable to generate the high-frequency activity likely necessary for binding and other forms of inter-regional interactions. These findings augment connectivity theories of autism with novel evidence that aberrations in local circuitry could underlie putative deficiencies in long-range neural communication. C1 Univ Colorado, Hlth Sci Ctr, Neuromagnet Imaging Ctr, Denver, CO USA. Univ Calif Davis, MIND Inst, Dept Psychiat & Behav Sci, Davis, CA 95616 USA. RP Wilson, TW (reprint author), Univ Colorado, Hlth Sci Ctr, 4200 E 9th Ave, Denver, CO 80262 USA. 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Psychiatry PD AUG 1 PY 2007 VL 62 IS 3 BP 192 EP 197 DI 10.1016/j.biopsych.2007.07.002 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 192NF UT WOS:000248208100002 PM 16950225 ER PT J AU Kana, RK Keller, TA Minshew, NJ Just, MA AF Kana, Rajesh K. Keller, Timothy A. Minshew, Nancy J. Just, Marcel Adam TI Inhibitory control in high-functioning autism: Decreased activation and underconnectivity in inhibition networks SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; factor analysis; fMRI; functional connectivity; inhibitory control; response inhibition; underconnectivity ID ANTERIOR CINGULATE CORTEX; EVENT-RELATED FMRI; WORKING-MEMORY; RESPONSE-INHIBITION; EXECUTIVE FUNCTIONS; SPECTRUM DISORDERS; PREFRONTAL CORTEX; ERROR-DETECTION; SENTENCE COMPREHENSION; SHIFTING ATTENTION AB Background: Inhibiting prepotent responses is critical to optimal cognitive and behavioral function across many domains. Several behavioral studies have investigated response inhibition in autism, and the findings varied according to the components involved in inhibition. There has been only one published functional magnetic resonance imaging (fMRI) study so far on inhibition in autism, which found greater activation in participants with autism than control participants. Methods: This study investigated the neural basis of response inhibition in 12 high-functioning adults with autism and 12 age- and intelligence quotient (IQ)-matched control participants during a simple response inhibition task and an inhibition task involving working memory. Results: In both inhibition tasks, the participants with autism showed less brain activation than control participants in areas often found to be active in response inhibition tasks, namely the anterior cingulate cortex. In the more demanding inhibition condition, involving working memory, the participants with autism showed more activation than control participants in the premotor areas. In addition to the activation differences, the participants with autism showed lower levels of synchronization between the inhibition network (anterior cingulate gyrus, middle cingulate gyrus, and insula) and the right middle and inferior frontal and right inferior parietal regions. Conclusions: The results indicate that the inhibition circuitry in the autism group is activated atypically and is less synchronized, leaving inhibition to be accomplished by strategic control rather than automatically. At the behavioral level, there was no difference between the groups. C1 Carnegie Mellon Univ, Ctr Cognit Brain Imaging, Dept Psychol, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, Ctr Cognit Brain Imaging, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA. Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA. RP Just, MA (reprint author), Carnegie Mellon Univ, Ctr Cognit Brain Imaging, Dept Psychol, Pittsburgh, PA 15213 USA. 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Psychiatry PD AUG 1 PY 2007 VL 62 IS 3 BP 198 EP 206 DI 10.1016/j.biopsych.2006.08.004 PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 192NF UT WOS:000248208100003 PM 17137558 ER PT J AU Deeley, Q Daly, EM Surguladze, S Page, L Toal, F Robertson, D Curran, S Giampietro, V Seal, M Brammer, MJ Andrew, C Murphy, K Phillips, ML Murphy, DGM AF Deeley, Quinton Daly, Eileen M. Surguladze, Simon Page, Lisa Toal, Fiona Robertson, Dene Curran, Sarah Giampietro, Vincent Seal, Marc Brammer, Michael J. Andrew, Christopher Murphy, Kieran Phillips, Mary L. Murphy, Declan G. M. TI An event related functional magnetic resonance imaging study of facial emotion processing in asperger syndrome SO BIOLOGICAL PSYCHIATRY LA English DT Article DE Asperger syndrome; autism; emotion; facial expression; functional MRI; fusiform gyrus ID FUSIFORM FACE AREA; PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; GENERIC BRAIN ACTIVATION; CEREBRAL-BLOOD-FLOW; HUMAN AMYGDALA; AUTISTIC-CHILDREN; SPECTRUM DISORDER; SOCIAL-BEHAVIOR; EXPRESSIONS AB Background: People with Asperger syndrome (AS) have life-long deficits in social behavior. The biological basis of this is unknown, but most likely includes impaired processing of facial emotion. Human social communication involves processing different facial emotions, and at different intensities. However nobody has examined brain function in people with AS when implicitly (unconsciously) processing four primary emotions at varying emotional intensities. Methods: We used event-related functional magnetic resonance imaging (MRI) to examine neural responses when people with AS and controls implicitly processed neutral expressions, and mild (25%) and intense (100%) expressions of fear, disgust, happiness, and sadness. We included 18 right-handed adults; 9 with AS and 9 healthy controls who did not differ significantly in IQ. Results: Both groups significantly activated 'face perception' areas when viewing neutral faces, including fusiform and extrastriate cortices. Further, both groups had significantly increased activation of fusiform and other extrastriate regions to increasing intensities of fear and happiness. However, people with AS generally showed fusiform and extrastriate hyporesponsiveness compared to controls across emotion types and intensities. Conclusions: Fusiform and extrastriate cortices are activated by facial expressions of four primary emotions in people with AS, but generally to a lesser degree than controls. 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C. van Engeland, Herman TI Caudate nucleus is enlarged in high-functioning medication-naive subjects with autism SO BIOLOGICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Internatoional Meeting for Autism Research CY JUN 01-03, 2006 CL Montreal, CANADA DE autism; basal ganglia; high-functioning; magnetic resonance imaging; medication-naive; repetitive and stereotyped behavior ID OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA VOLUMES; PERVASIVE DEVELOPMENTAL DISORDERS; REPETITIVE BEHAVIORS; SCHIZOPHRENIC-PATIENTS; CHILDREN; BRAIN; MRI; CLOZAPINE; SYMPTOMS AB Background: Autism is defined by three symptom clusters, including repetitive and stereotyped behavior. Previous studies have implicated basal ganglia in these behaviors. Earlier studies investigating basal ganglia in autism have included subjects on neuroleptics known to affect basal ganglia volumes. Therefore, we investigated these structures in medication-naive subjects with autism. Methods: Volumetric magnetic resonance measures of caudate, putamen, and nucleus accumbens were compared in two independent samples of medication-naive, high-functioning subjects with autism or Asperger syndrome: 1) 21 affected children and adolescents and 21 matched control subjects; and 2) 21 affected adolescents and young adults and 21 matched control subjects. Results: Caudate nucleus was enlarged in both samples. This result remained significant after correction for total brain volume. Conclusions: These results implicate caudate nucleus in autism, as an enlargement of this structure was disproportional to an increase in total brain volume in two independent samples of medication-naive subjects with autism. C1 Univ Med Ctr Utrecht, Rudolf Magnus Inst Neurosci, Dept Child & Adolescent Psychiat, Utrecht, Netherlands. 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Sekine, Yoshimoto Suda, Shiro Sugihara, Genichi Matsuzaki, Hideo Sugiyama, Toshiro Kawai, Masayoshi Minabe, Yoshio Takei, Nori Mori, Norio TI Decreased serum levels of epidermal growth factor in adult subjects with high-functioning autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; developmental disorders; ELISA; epidermal growth factor; growth factors; human blood ID SPECTRUM DISORDERS; NEONATAL BLOOD; FACTOR-ALPHA; BRAIN; CHILDREN; NEUROTROPHINS; NEUROPEPTIDES; ACTIVATION; RESPONSES; RECEPTOR AB Background: The neurobiological basis for autism remains poorly understood. Given the role of growth factors in brain development, we hypothesized that epidermal growth factor (EGF) may play a role in the pathophysiology of autism. In this study, we examined whether serum levels of EGF are altered in adult subjects with high-functioning autism. Methods: We measured serum levels of EGF in the 17 male subjects with high-functioning autism and 18 age-matched healthy male subjects. Results: The serum levels of EGF in the subjects with high-functioning autism (72.4 +/- 102.8 pg/mL [mean +/- SD]) were significantly lower (Mann-Whitney U = 22.0, p <.001) than those of normal control subjects (322.3 +/- 122.0 pg/mL [mean +/- SD]). However, there were no correlations between serum EGF levels and clinical variables in the subjects with autism. Conclusions: This study suggests that decreased levels of EGF might be implicated in the pathophysiology of high-functioning autism. C1 Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, Chiba 260, Japan. Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 43131, Japan. Chukyo Univ, Fac Sociol, Toyota, Aichi, Japan. Aichi Childrens Hlth & Med Ctr, Obu, Aichi, Japan. RP Hashimoto, K (reprint author), Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, 1-8-1 Inohana, Chiba 260, Japan. 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Psychiatry PD AUG 1 PY 2007 VL 62 IS 3 BP 267 EP 269 DI 10.1016/j.biopsych.2006.08.001 PG 3 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 192NF UT WOS:000248208100012 PM 17123472 ER PT J AU Murias, M Webb, SJ Greenson, J Dawson, G AF Murias, Michael Webb, Sara J. Greenson, Jessica Dawson, Geraldine TI Resting state cortical connectivity reflected in EEG coherence in individuals with autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE developmental neuropathology; frontal lobe; functional connectivity; neural synchrony; oscillations ID HIGH-FUNCTIONING AUTISM; ABNORMALITIES; DISORDER AB Background: Theoretical conceptions of autism spectrum disorder (ASD) and experimental studies of cerebral blood flow suggest abnormalities in connections among distributed neural systems in ASD. Methods: Functional connectivity was assessed with electroencepha log ra phic coherence between pairs of electrodes in a high-density electrode array in narrow frequency bands among 18 adults with ASD and 18 control adults in an eyes closed resting state. Results: In the theta (3-6 Hz) frequency range, locally elevated coherence was evident for the ASD group, especially within left hemisphere frontal and temporal regions. In the lower alpha range (8-10 Hz), globally reduced coherence was evident for the ASD group within frontal regions and between frontal and all other scalp regions. The ASD group exhibited significantly greater relative power between 3 and 6 Hz and 13-17 Hz and significantly less relative power between 9 and 10 Hz. Conclusions: Robust patterns of over- and under-connectivity are apparent at distinct spatial and temporal scales in ASD subjects in the eyes closed resting state. C1 Univ Washington, Autism Ctr, Seattle, WA 98195 USA. RP Murias, M (reprint author), Univ Washington, Autism Ctr, UW,Box 357920, Seattle, WA 98195 USA. 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Gidley TI Increased motor cortex white matter volume predicts motor impairment in autism SO BRAIN LA English DT Article DE autism; white matter; imaging; motor; central coherence ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEVELOPMENTAL LANGUAGE DISORDER; DEFICIT HYPERACTIVITY DISORDER; SPECTRUM DISORDERS; CRITERION VALIDITY; CHILDREN; RELIABILITY; ABNORMALITIES; INDIVIDUALS; ADOLESCENTS AB Careful consideration of motor impairments, such as those documented in autism, can afford valuable insights into the neurological basis of developmental disorders. Motor signs are highly quantifiable and reproducible and can serve as markers for deficits in parallel systems important for socialization and communication. Correlations of motor signs with anatomic MRI (aMRI) measures therefore offer an important means of investigating brain abnormalities contributing to autism. Prior aMRI studies have revealed increased cerebral volume in young children with autism, particularly in 'outer zone' radiate white matter; however functional correlates of these findings have not been reported. In this study, we examined whether radiate white matter within the primary motor cortex would predict impaired motor performance in children with autism. Subjects included children ages 8-12 years: 20 with autism, 36 typically developing (TD) controls and 20 clinical controls with attention-deficit/hyperactivity disorder (ADHD). Regional tissue volumes were measured using an automated tissue classification algorithm followed by a semi-automated parcellation method. Motor performance was assessed using the Physical and Neurologic Examination of Subtle Signs (PANESS), with higher scores indicating poorer performance. Independent linear regression analyses revealed that for TD controls there was a significant negative correlation between total PANESS score and primary motor cortex white matter volume in both the right and left hemispheres, such that increased white matter volume predicted improved motor skill. In contrast, children with autism showed a robust positive correlation between total PANESS score and left hemisphere primary motor and premotor white matter volumes, such that increased white matter volume predicted poorer motor skill. No significant correlations were found for ADHD. Multivariate regression analyses revealed that the correlation between PANESS score and left motor cortex white matter volume in children with autism significantly differed from those in both ADHD and TD children. The correlation in ADHD did not significantly differ from that in TD children. The findings for the first time demonstrate an association between increasing radiate white matter volume and functional impairment in children with autism, in this case basic motor skill impairment. The observed association, which appears specific to autism, may be representative of global patterns of brain abnormality that not only contribute to motor dysfunction in autism, but also deficits in socialization and communication that define the disorder. C1 Kennedy Krieger Inst, Baltimore, MD 21205 USA. Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA. Johns Hopkins Sch Med, Dept Psychiat, Baltimore, MD USA. RP Mostofsky, SH (reprint author), Kennedy Krieger Inst, 707 N Broadway, Baltimore, MD 21205 USA. 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Dawson, G. Webb, S. Murias, M. TI EEG mu rhythm and imitation impairments in individuals with autism spectrum disorder SO BRAIN AND COGNITION LA English DT Article DE autism; imitation; EEG; mu rhythm; mirror neurons ID HIGH-RESOLUTION EEG; MIRROR NEURON DYSFUNCTION; DEVELOPMENTAL DISORDERS; FUNCTIONAL-SIGNIFICANCE; CHILDHOOD AUTISM; MOTOR IMITATION; ALPHA-RHYTHM; CHILDREN; MOVEMENT; PERCEPTION AB Imitation ability has consistently been shown to be impaired in individuals with autism. A dysfunctional execution/observation matching system has been proposed to account for this impairment. The EEG mu rhythm is believed to reflect an underlying execution/observation matching system. This study investigated evidence of differential mu rhythm attenuation during the observation, execution, and imitation of movements and examined its relation to behaviorally assessed imitation abilities. Fourteen high-functioning adults with autism spectrum disorder (ASD) and 15 IQ- and age-matched typical adults participated. On the behavioral imitation task, adults with ASD demonstrated significantly poorer performance compared to typical adults in all domains of imitation ability. On the EEG task, both groups demonstrated significant attenuation of the mu rhythm when executing an action. However, when observing movement, the individuals with ASD showed significantly reduced attenuation of the mu wave. Behaviorally assessed imitation skills were correlated with degree of mu wave attenuation during observation of movement. These findings suggest that there is execution/observation matching system dysfunction in individuals with autism and that this matching system is related to degree of impairment in imitation abilities. (C) 2007 Elsevier Inc. All rights reserved. C1 Univ Washington, Ctr Dev & Disabil, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Univ Washington, UW Autism Ctr, Seattle, WA 98195 USA. Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. RP Bernier, R (reprint author), Univ Washington, Ctr Dev & Disabil, Box 357920, Seattle, WA 98195 USA. 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PD AUG PY 2007 VL 64 IS 3 BP 228 EP 237 DI 10.1016/j.bandc.2007.03.004 PG 10 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 197LI UT WOS:000248556500004 PM 17451856 ER PT J AU Neeley, ES Bigler, ED Krasny, L Ozonoff, S McMahon, W Lainhart, JE AF Neeley, E. Shannon Bigler, Erin D. Krasny, Lori Ozonoff, Sally McMahon, William Lainhart, Janet E. TI Quantitative temporal lobe differences: Autism distinguished from controls using classification and regression tree analysis SO BRAIN & DEVELOPMENT LA English DT Article DE autism; temporal lobe; CART analysis; MRI ID HEAD CIRCUMFERENCE; BRAIN OVERGROWTH; SOCIAL-BEHAVIOR; MATTER VOLUME; ABNORMALITIES; CONNECTIVITY; INDIVIDUALS; DISSECTION; DISORDERS; DYSLEXIA AB The temporal lobe is thought to be abnormal in autism, yet standard volumetric analyses are often unrevealing when age, sex, IQ, and head size are controlled. Quantification of temporal lobe structures were obtained in male subjects with autism and controls, where subjects with head circumference (HC) defined macrocephaly were excluded, so that volume differences were not just related to the higher prevalence of macrocephaly in autism. Various statistical methods were applied to the analysis including a classification and regression tree (CART) method, a non-parametric technique that helps define patterns of relationships that may be meaningful in distinguishing temporal lobe differences between subjects with autism and age and IQ matched controls. Subjects with autism were also compared to a separate control group with reading disorder (RD), with the prediction that the temporal lobe morphometric analysis of the reading disorder controls would be more similar to that of the autism group. The CART method yielded a high specificity in classifying autism subjects from controls based on the relationship between the volume of the left fusiform gyrus (LFG) gray and white matter, the right temporal stem (RTS) and the right inferior temporal gyrus gray matter (RITG-GM). Reading disordered individuals were more similar to subjects with autism. Simple size differences did not distinguish the groups. These findings demonstrate different relationships within temporal lobe structures that distinguish subjects with autism from controls. Results are discussed in terms of pathological connectivity within the temporal lobe as it relates to autism. (c) 2006 Elsevier B.V. All rights reserved. C1 Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA. Brigham Young Univ, Dept Neurosci, Provo, UT 84602 USA. Brigham Young Univ, Dept Stat, Provo, UT 84602 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT 84112 USA. Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. 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PD AUG PY 2007 VL 29 IS 7 BP 389 EP 399 DI 10.1016/j.braindev.2006.11.006 PG 11 WC Clinical Neurology SC Neurosciences & Neurology GA 179OZ UT WOS:000247300800001 PM 17204387 ER PT J AU Kondo, A Saito, Y Floricel, F Maegaki, Y Ohno, K AF Kondo, Akiko Saito, Yoshiaki Floricel, Florin Maegaki, Yoshihiro Ohno, Kousaku TI Congenital ocular motor apraxia: Clinical and neuroradiological findings, and long-term intellectual prognosis SO BRAIN & DEVELOPMENT LA English DT Article DE congenital ocular motor apraxia; saccade initiation; cerebellar vermis; tectum ID CEREBELLAR VERMIS; JUVENILE NEPHRONOPHTHISIS; JOUBERT-SYNDROME; SACCADE FAILURE; CHILDREN; INITIATION; ABNORMALITIES; DYSGENESIS; HYPOPLASIA; AUTISM AB The severity of intellectual sequelae and prognosis varies in patients with congenital ocular motor apraxia (COMA). Here, we explored this phenomenon with regard to the accompanying oculornotor signs and gross motor development, as well as the subtentorial structure defects. Ten patients diagnosed with COMA (M:F = 4:6, 4-37 years old) were reviewed. Four individuals who gained the ability to walk at 2 years or earlier showed normal intellect and social skills. Those who walked later often showed accompanying intellectual (5/6) and speech (6/6) disabilities. In this latter group, atypical oculornotor signs for COMA (presence of nystagmus, mild limitation of vertical gaze, slower head thrust, and marked improvement of lateral saccade during early childhood) were often noted (4/6). Minor anomalies of fingers and toes were also common in this group. Neuromiaging was conduced in nine patients (pneumoencepharography 1; computed tomography: 8, magnetic resonance imaging: 2). Dilatation of the fourth ventricle, mainly at the level of the midbrain or upper pons (n = 7), and hypoplastic cerebellar verinis (n = 6) were commonly observed in both the early- and late-walking groups. 'Molar tooth' signs (n = 3) were exclusively noted in the late-walking group, and often accompanied by atypical oculomotor signs (3/3) and intellectual disabilities (2/3). Vermian hypoplasia and dilatation of the fourth ventricle at the upper brainstem level in COMA patients, with or without intellectual disabilities, suggested that the cardinal lesion for OMA may exist in these areas. The presence of a subset of 'atypical' COMA patients may suggest that COMA with subtle infratentorial abnormality represents a heterogeneous disease category, showing similar oculomotor disturbance. This review indicated that clinical and neuroradiological inspection might be valuable for prediction of long-term intellectual prognosis in COMA patients. (c) 2007 Elsevier B.V. All rights reserved. C1 Tottori Univ, Fac Med, Inst Neurol Sci, Div Child Neurol, Yonago, Tottori 6808504, Japan. RP Kondo, A (reprint author), Tottori Univ, Fac Med, Inst Neurol Sci, Div Child Neurol, 36-1 Nishi Cho, Yonago, Tottori 6808504, Japan. 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PD AUG PY 2007 VL 29 IS 7 BP 431 EP 438 DI 10.1016/j.braindev.2007.01.002 PG 8 WC Clinical Neurology SC Neurosciences & Neurology GA 179OZ UT WOS:000247300800007 PM 17336010 ER PT J AU Mills, JL Hediger, ML Molloy, CA Chrousos, GP Manning-Courtney, P Yu, KF Brasington, M England, LJ AF Mills, James L. Hediger, Mary L. Molloy, Cynthia A. Chrousos, George P. Manning-Courtney, Patricia Yu, Kai F. Brasington, Mark England, Lucinda J. TI Elevated levels of growth-related hormones in autism and autism spectrum disorder SO CLINICAL ENDOCRINOLOGY LA English DT Article ID BINDING-PROTEIN; CHILDREN; ADOLESCENTS; ADRENARCHE; ANDROGENS; DISEASE; WEIGHT; HEIGHT; LIFE AB Objective Children with autism are known to have larger head circumferences; whether they are above average in height and weight is less clear. Moreover, little is known about growth-related hormone levels in children with autism. We investigated whether children with autism were taller and heavier, and whether they had higher levels of growth-related hormones than control children did. Design A case-control study design was employed. Patients Boys with autism spectrum disorder (ASD) or autism (n = 71) and age-matched control boys (n = 59) were evaluated at Cincinnati Children's Hospital. Measurements Height, weight and head circumference were measured. Blood samples were assayed for IGF-1 and 2, IGFBP-3, growth hormone binding protein (GHBP) and for dehydroepiandrosterone (DHEA) and DHEA sulphate (DHEAS). Results Subjects with autism/ASD had significantly (P = 0.03) greater head circumferences (mean z-score 1.24, SD 1.35) than controls (mean z-score 0.78, SD 0.93). Subjects with autism also had significantly (P = 0.01) greater weights (mean z-score 0.91, SD 1.13) than controls (mean z-score 0.41, SD 1.11). Height did not differ significantly between groups (P = 0.65); subjects with autism/ASD had significantly (P = 0.003) higher body mass indices (BMI) (mean z-score 0.85, SD 1.19) than controls (mean z-score 0.24, SD 1.17). Levels of IGF-1, IGF-2, IGFBP-3 and GHBP in the group with autism/ASD were all significantly higher (all P <= 0.0001) than in controls. Conclusions Children with autism/ASD had significantly higher levels of many growth-related hormones: IGF-1, IGF-2, IGFBP-3 and GHBP. These findings could help explain the significantly larger head circumferences and higher weights and BMIs seen in these subjects. Future studies should examine the potential role of growth-related hormones in the pathophysiology of autism. C1 NICHHD, NIH, DHHS, Div Epidemiol Stat & Prevent Res, Bethesda, MD 20892 USA. Univ Cincinnati, Coll Med, Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45221 USA. Univ Cincinnati, Coll Med, Dept Pediat, Cincinnati, OH 45221 USA. NICHHD, NIH, DHHS, Reprod Biol & Med Branch, Bethesda, MD 20892 USA. Ctr Dis Control & Prevent, DHHS, Div Reprod Hlth, Atlanta, GA USA. RP Mills, JL (reprint author), NICHD, DESPR, NIH, Room 7B03,6100 Bldg, Bethesda, MD 20892 USA. 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Endocrinol. PD AUG PY 2007 VL 67 IS 2 BP 230 EP 237 DI 10.1111/j.1365-2265.2007.02868.x PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 197BH UT WOS:000248527600012 PM 17547689 ER PT J AU Stroganova, TA Nygren, G Tsetlin, MM Posikera, IN Gillberg, C Elam, M Orekhova, EV AF Stroganova, Tatiana A. Nygren, Gudrun Tsetlin, Marina M. Posikera, Irina N. Gillberg, Christopher Elam, Mikael Orekhova, Elena V. TI Abnormal EEG lateralization in boys with autism SO CLINICAL NEUROPHYSIOLOGY LA English DT Article DE autism; children; EEG; lateralization; temporal lobes; Mu rhythm ID CHILDHOOD AUTISM; INFANTILE-AUTISM; SEROTONIN SYNTHESIS; SPECTRUM DISORDERS; HEAD CIRCUMFERENCE; ASPERGER-SYNDROME; HAND PREFERENCE; FOCAL ATTENTION; BRAIN ACTIVITY; CHILDREN AB Objective: Functional brain abnormalities associated with autism in 3-8-year-old boys were studied with EEG recorded under controlled experimental condition of sustained visual attention and behavioral stillness. Methods: EEG was recorded in two independent samples of boys with autism (BWA) from Moscow (N = 21) and Gothenburg (N = 23) and a corresponding number of age-matched typically developing boys (TDB). EEG spectral power (SP) and SP interhemispheric asymmetry within delta, theta and alpha bands were analyzed. Results: BWA comprised a non-homogeneous group in relation to theta and alpha SP. When four outliers were excluded the only between-group difference in absolute SP was a higher amount of prefrontal delta in BWA. BWA of both samples demonstrated atypical leftward broadband EEG asymmetry with a maximum effect over the mid-temporal regions. Concurrently, the nor-Mal leftward asymmetry of mu rhythm was absent in BWA. Conclusions: The abnormal broadband EEG asymmetry in autism may point to a diminished capacity of right temporal cortex to generate EEG rhythms. The concurrent lack of normal leftward asymmetry of mu rhythm suggests that abnormalities in EEG lateralization in autism may be regionally/functionally specific. Significance: The data provide evidence for abnormal functional brain lateralization in autism. (c) 2007 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. C1 [Elam, Mikael; Orekhova, Elena V.] Sahlgrens Univ Hosp, Dept Clin Neurophysiol, S-41345 Gothenburg, Sweden. [Stroganova, Tatiana A.; Tsetlin, Marina M.; Posikera, Irina N.] Moscow Univ Physiol & Educ, Moscow 103051, Russia. [Stroganova, Tatiana A.; Posikera, Irina N.] Russian Acad Educ, Inst Psychol, Moscow 125009, Russia. [Nygren, Gudrun; Gillberg, Christopher] Sahlgrens Univ Hosp, Dept Child & Adolescent Psychiat, S-41345 Gothenburg, Sweden. RP Orekhova, EV (reprint author), Sahlgrens Univ Hosp, Dept Clin Neurophysiol, S-41345 Gothenburg, Sweden. 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However, the literature is highly inconsistent. One possible explanation for these discrepancies is differences in intelligence. Children with ASD and below average intelligence may be hypothesised to show additional or different neural abnormalities. This possibility was explored using structural magnetic resonance imaging (MRI) and event-related potentials (ERP). Two groups of children with ASD were studied, those with average or above average intelligence (high ASD group) and those with below average intelligence (low ASD group). The structural MRI data were analysed using voxel-based morphometry (VBM). Using the family-wise error threshold, results showed bilateral abnormality common to the two ASD groups in the cerebellum, fusiform gyrus and frontal cortex. 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Melyn published an electroencephalographic study on autistic children and found 46% with seizures and also a relatively high prevalence of 20% with epileptiform discharges but without any clinical seizures (Clin EEG Neurosci 2005;36:15-20). Because the discharges have always been viewed as focal events and the clinical seizures as requiring spread, the conclusion from these data was that children with autism may have a deficiency of corticocortical fibers. Since that time many MRI and functional MRI studies have been published confirming that one of the first findings in this devastating condition is underconnectivity. Specific findings are the thinning of the corpus callosum and the reduced connectivity, especially with the frontal areas and also the fusiform face area. Other studies involving positron emission tomography scans, magnetoencephalography, and perception have added to the evidence of underconnectivity. One final point is the initial overgrowth of white matter in the first 2 years of life in autistic children, followed later by arrested growth, resulting in aberrant connectivity; myelination of white matter will likely be significant in the etiology of autism. (c) 2007 Elsevier Inc. All rights reserved. C1 Univ Illinois, Med Ctr Chicago, Dept Neurol, Chicago, IL 60612 USA. RP Hughes, JR (reprint author), Univ Illinois, Med Ctr Chicago, Dept Neurol, 912 S Wood St, Chicago, IL 60612 USA. 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PD AUG PY 2007 VL 11 IS 1 BP 20 EP 24 DI 10.1016/j.yebeh.2007.03.010 PG 5 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA 199EZ UT WOS:000248680300004 PM 17531541 ER PT J AU Jha, P Sheth, D Ghaziuddin, M AF Jha, P. Sheth, D. Ghaziuddin, M. TI Autism spectrum disorder and Klinefelter syndrome SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; chromosomes; klinefelter syndrome ID X-CHROMOSOME; CHILDREN; REGION AB Background Autism is a severe handicapping disorder of early childhood characterized by a distinct pattern of social and communication impairment with rigid ritualistic interests. In about 10-25% of cases, it is associated with known medical conditions. Population-based studies of autism have found that Klinefelter's syndrome (KS), a common chromosome abnormality, is sometimes associated with autism. 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Child Adolesc. Psych. PD AUG PY 2007 VL 16 IS 5 BP 305 EP 308 DI 10.1007/s00787-007-0601-8 PG 4 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 207ZD UT WOS:000249288700004 PM 17401614 ER PT J AU Duarte, S Duarte, A Monteiro, JP Ventosa, L Lourenco, L Fonseca, MJ Breia, P AF Duarte, S. Duarte, A. Monteiro, J. P. Ventosa, L. Lourenco, L. Fonseca, M. J. Breia, P. TI Epilepsy and epileptiform abnormalities in a population of children with autism spectrum disorders SO EUROPEAN JOURNAL OF NEUROLOGY LA English DT Meeting Abstract CT 11th Congress of the European-Federation-of-Neurological-Societies CY AUG 25-28, 2007 CL Brussels, BELGIUM SP European Federat Neurol Soc C1 [Duarte, S.; Breia, P.] Dept Neurol, Almada, Portugal. [Duarte, A.; Monteiro, J. P.; Ventosa, L.; Lourenco, L.; Fonseca, M. J.] Hosp Garcia Orta, Neuropediat & Dev Unit, Almada, Portugal. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1351-5101 J9 EUR J NEUROL JI Eur. J. Neurol. PD AUG PY 2007 VL 14 SU 1 BP 248 EP 248 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 225LL UT WOS:000250519300813 ER PT J AU Myers, SM AF Myers, Scott M. TI The status of pharmacotherapy For autism spectrum disorders SO EXPERT OPINION ON PHARMACOTHERAPY LA English DT Review DE autism; medication; pervasive developmental disorders; psychopharmacology ID PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN-REUPTAKE INHIBITORS; PLACEBO-CONTROLLED CROSSOVER; SELF-INJURIOUS-BEHAVIOR; FRAGILE-X-SYNDROME; OPEN-LABEL TRIAL; OUTPATIENT SCHIZOPHRENIC CHILDREN; DEFICIT HYPERACTIVITY DISORDER; LONG-TERM TREATMENT; DOUBLE-BLIND AB The use of pharmacologic agents as a component of treatment for children and adults with autism spectrum disorders is common and a substantial body of literature describing controlled and open-label clinical trials now exists to guide clinical practice. Empiric evidence of efficacy of risperidone, methylphenidate and some selective serotonin re-uptake inhibitors for maladaptive behaviors commonly associated with autism spectrum disorders has increased substantially in recent years. Preliminary controlled trials of valproate, atomoxetine, alpha-2 adrenergic agonists and olanzapine are promising. in addition to traditional psychotropic medications, investigators have examined the potential role of a variety of agents with glutamatergic or cholinergic mechanisms, and the results warrant further investigation. Although psychotropic medications are effective in treating some important associated behaviors, evidence of significant impact on the core features of autism spectrum disorders is very limited. C1 Geisinger Med Clin, Jefferson Med Coll, Danville, PA 17822 USA. RP Myers, SM (reprint author), Geisinger Med Clin, Jefferson Med Coll, 100 N Acad Ave, Danville, PA 17822 USA. 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TI Deep brain stimulation in the treatment of psychiatric disorders SO FORTSCHRITTE DER NEUROLOGIE PSYCHIATRIE LA German DT Review DE deep brain stimulation; psychiatric disorders; Tourette syndrome; obsessive compulsive disorder; major depression ID OBSESSIVE-COMPULSIVE-DISORDER; SUBTHALAMIC NUCLEUS STIMULATION; HIGH-FREQUENCY STIMULATION; ANTERIOR CAPSULAR STIMULATION; CHRONIC BILATERAL STIMULATION; LA-TOURETTE-SYNDROME; PARKINSONS-DISEASE; MAJOR DEPRESSION; COGNITIVE FUNCTION; GLOBUS-PALLIDUS AB As a well and long-established approach in the treatment of selected movement disorders, deep brain stimulation (DBS) is also increasingly considered a potential treatment method in the case of mental disorders. Only recently, a number of highly promising case reports and case series have been published, in which impressive therapeutic outcomes under application of DBS in otherwise treatment-resistant psychiatric illnesses are reported. The current article aims to provide a detailed synopsis of the DBS approach and more specifically its application to mental disorders. By means of a systematic literature search, all relevant treatment studies published to date and focusing on obsessive compulsive disorder, Tourette syndrome, major depression, anxiety disorder and autism were incorporated and evaluated with respect to the scientific evidence presented. C1 Klinikum Univ Koln, Klin Psychiat & Psychotherapie, D-50924 Cologne, Germany. Klinikum Univ Koln, Klin Stereotaxie & Funkt Neurochirurg, D-50924 Cologne, Germany. RP Kuhn, J (reprint author), Klinikum Univ Koln, Klin Psychiat & Psychotherapie, Kerpener Str 62, D-50924 Cologne, Germany. 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Mouse models of these syndromes harboring an similar to 2 Mb chromosome engineered deletion and duplication, respectively, displayed abnormal locomotor activity and/or learning deficits. To determine the contribution of RAI1 in the neurobehavioral traits in SMS, we performed a battery of behavioral tests on Rail mutant mice and the Df(11)17-1/+ mice that have a small deletion of similar to 590 kb. The mice with the small deletion were hypoactive like the large deletion mice and they also showed learning deficits. The Rai1+/- mice exhibited normal locomotor activity. However, they had an abnormal electroencephalogram with overt seizure observed in a subset of mice. The few surviving Rai1 -/- mice displayed more severe neurobehavioral abnormalities including hind limb clasping, overt seizures, motor impairment and context- and tone-dependant learning deficits. X-gal staining of the Rai1 +/- mice suggests that Rail is predominantly expressed in neurons of the hippocampus and the cerebellum. Our results suggest that Rail is a critical gene in the central nervous system functioning in a dosage sensitive manner and that the neurobehavioral phenotype is modified by regulator(s) in the similar to 590 kb genomic interval, wherein the major modifier affecting the craniofacial penetrance resides. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA. Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA. Texas Childrens Hosp, Houston, TX 77030 USA. RP Lupski, JR (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Room 604B,1 Bayor Plaza, Houston, TX 77030 USA. 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Mol. Genet. PD AUG 1 PY 2007 VL 16 IS 15 BP 1802 EP 1813 DI 10.1093/hmg/ddm128 PG 12 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 211BZ UT WOS:000249500600003 PM 17517686 ER PT J AU Orsmond, GI Lin, LY Seltzer, MM AF Orsmond, Gael I. Lin, Ling-Yi Seltzer, Marsha Mailick TI Mothers of adolescents and adults with autism: Parenting multiple children with disabilities SO INTELLECTUAL AND DEVELOPMENTAL DISABILITIES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; COPING STRATEGIES; MENTAL-RETARDATION; FAMILY HISTORY; SPECTRUM DISORDERS; BEHAVIOR PROBLEMS; AGING MOTHERS; SIBLINGS; STRESS; ADJUSTMENT AB We examined types of disabilities in siblings from a large sample of families of adolescents and adults with autism spectrum disorders (ASD) and the impact of another child with a disability on maternal and family well-being. The most frequent disabilities in siblings were attention and hyperactivity (4.6%) and autism spectrum (2.4%) disorders and psychiatric (2.1%) and learning (2.0%) disabilities. Mothers parenting another child with a disability (in addition to the child with ASD) had higher levels of depressive symptoms and anxiety and lower family adaptability and cohesion compared with mothers whose only child with a disability had ASD (matched on child age and family size). Findings are discussed with respect to understanding the needs of such families, including service provision. C1 Sargent Coll Hlth & Rehabil Sci, Dept Occupat Therapy & Rehabil Counseling, Boston, MA 02215 USA. Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. RP Orsmond, GI (reprint author), Sargent Coll Hlth & Rehabil Sci, Dept Occupat Therapy & Rehabil Counseling, 635 Commonwealth Ave, Boston, MA 02215 USA. 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Dev. Disabil. PD AUG PY 2007 VL 45 IS 4 BP 257 EP 270 DI 10.1352/1934-9556(2007)45[257:MOAAAW]2.0.CO;2 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 200KX UT WOS:000248763400003 PM 17627373 ER PT J AU Yang, SH AF Yang, Sanghwa TI Gene amplifications at chromosome 7 of the human gastric cancer genome SO INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE LA English DT Article DE gastric cancer; array comparative genomic hybridization; chromosome 7 ID DNA COPY-NUMBER; CDNA MICROARRAY; HIGH-RESOLUTION; GROWTH-FACTOR; HYBRIDIZATION; ADENOCARCINOMAS; CARCINOMAS; ABERRATIONS; PROGRESSION; ESOPHAGEAL AB Genetic aberrations at chromosome 7 are known to be related with diverse human diseases, including cancer and autism. In a number of cancer research areas involving gastric cancer, several comparative genomic hybridization studies employing metaphase chromosome or BAC clone micro-arrays have repeatedly identified human chromosome 7 as containing 'regions of changes' related with cancer progression. cDNA microarray-based comparative genomic hybridization can be used to directly identify individual target genes undergoing copy number variations. Copy number change analysis for 17,000 genes on a microarray format was performed with tumor and normal gastric tissues from 30 patients. A group of 90 genes undergoing copy number increases (gene amplification) at the p11 similar to p22 or q21 similar to q36 region of chromosome 7 is reported. The list of genes includes wingless-type MMTV integration site family member 2 (WNT2). a proto-oncogene and acyloxyacyl hydrolase (AOAH) that was amplified in > 80% of the tested cases. The amplified genes are those functioning in the biological processes such as signal transduction pathways, cell proliferation, metabolism, transport, inflammatory response and protein folding or proteolysis. Also found in the list are genes that are targets for drug development, such as maltase-glucoamylase (MGAM), cyclin-dependent kinase 5 (CDK5), neuropeptide Y (NPY) and dopa decarboxylase (DDC). The current dataset can be used as one of the resources in understanding genetic aberrations of chromosome 7 in human gastric cancer. C1 Yonsei Univ, Coll Med, Canc Metastasis Res Ctr, Seoul 120752, South Korea. RP Yang, SH (reprint author), Yonsei Univ, Coll Med, Canc Metastasis Res Ctr, 134 Shinchon Dong, Seoul 120752, South Korea. 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PD AUG PY 2007 VL 88 BP 825 EP 842 DI 10.1516/ijpa.2007.825 PN 4 PG 18 WC Psychology, Psychoanalysis SC Psychology GA 202VY UT WOS:000248933400001 PM 17681895 ER PT J AU Sofronoff, K Attwood, T Hinton, S Levin, I AF Sofronoff, Kate Attwood, Tony Hinton, Sharon Levin, Irina TI A randomized controlled trial of a cognitive behavioural intervention for anger management in children diagnosed with Asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; anger management; cognitive behaviour therapy ID EXECUTIVE FUNCTIONS; DISORDER; AUTISM; STUDENTS; THERAPY AB The purpose of the study described was to evaluate the effectiveness of a cognitive behavioural intervention for anger management with children diagnosed with Asperger syndrome. Forty-five children and their parents were randomly assigned to either intervention or wait-list control conditions. Children in the intervention participated in six 2-h weekly sessions while parents participated in a larger parent group. Parent reports indicated a significant decrease in episodes of anger following intervention and a significant increase in their own confidence in managing anger in their child. Qualitative information gathered from parents and teachers indicated some generalization of strategies learned in the clinic setting to both home and school settings. Limitations of the study and suggestions for future research are also discussed. C1 Univ Queensland, Sch Psychol, Brisbane, Qld, Australia. Asperger Syndrome Clin, Brisbane, Qld, Australia. Washington Univ, St Louis, MO USA. RP Sofronoff, K (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld, Australia. 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V., 2003, GOOD AUTISM PRACTICE, V4, P2 NR 32 TC 51 Z9 52 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1203 EP 1214 DI 10.1007/s10803-006-0262-3 PG 12 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000001 PM 17082978 ER PT J AU Stanley, GC Konstantareas, MM AF Stanley, Gillian C. Konstantareas, M. Mary TI Symbolic play in children with Autism Spectrum Disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism Spectrum Disorder; symbolic play; functional play; predictors of play ID LANGUAGE-DEVELOPMENT; PRETEND PLAY; SKILLS; CHILDHOOD; BEHAVIOR; SCALE; LOWE AB The relationship between symbolic play and other domains, such as degree of autistic symptomatology, nonverbal cognitive ability, receptive language, expressive language, and social development, was investigated. The assessment files of 101 children with Autism Spectrum Disorder were studied. Nonverbal cognitive ability and expressive language were both significantly and uniquely related to symbolic play, although receptive language was not. Autistic symptomatology ceased to be significantly related to symbolic play when controlling for two or more other variables. Social development was related to symbolic play in those children with high nonverbal cognitive ability but not those with low nonverbal cognitive ability. The diagnostic and treatment implications of these results are discussed. C1 Univ Guelph, Dept Psychol, Guelph, ON N1G 2W1, Canada. RP Stanley, GC (reprint author), Univ Guelph, Dept Psychol, Guelph, ON N1G 2W1, Canada. EM gstanley@uoguelph.ca CR ALPERN GD, 1980, DEVELOPMENTAL PROFIL American Psychiatric Association, 2000, DIAGN STAT MAN MENT ARTHUR G, 1980, INSTRUCTION MANUAL A BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 Bayley N, 1993, BAYLEY SCALES INFANT Boutot EA, 2005, EDUC TRAIN DEV DISAB, V40, P285 Costello A. J., 1976, MANUAL SYMBOLIC PLAY Dawson G, 1998, CHILD DEV, V69, P1276, DOI 10.2307/1132265 Dunn L. M., 1981, MANUAL PEABODY PICTU El'Konin D. B., 1999, J RUSSIAN E EUROPEAN, V37, P31, DOI 10.2753/RPO1061-0405370631 Fein G. G., 1979, NEW DIR CHILD ADOLES, V6, P1 FEIN GG, 1981, CHILD DEV, V52, P1095, DOI 10.1111/j.1467-8624.1981.tb03157.x Fekonja U, 2005, STUD PSYCHOL, V47, P103 FOLGER KM, 1978, J SPEECH HEAR RES, V21, P519 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Frith U., 2003, AUTISM EXPLAINING EN Goncu A., 2002, BLACKWELL HDB CHILDH, P418 GOULD J, 1986, J AUTISM DEV DISORD, V16, P199, DOI 10.1007/BF01531730 Hobson R. P., 1989, DEV PSYCHOPATHOL, V1, P197, DOI 10.1017/S0954579400000390 HOBSON RP, 1990, PSYCHOL REV, V97, P114, DOI 10.1037/0033-295X.97.1.114 JARROLD C, 1993, J AUTISM DEV DISORD, V23, P281, DOI 10.1007/BF01046221 Kanner L, 1943, NERV CHILD, V2, P217 Konstantareas MM, 1999, J AUTISM DEV DISORD, V29, P275, DOI 10.1023/A:1022155201662 KONSTANTAREAS MM, 1988, J AUTISM DEV DISORD, V18, P647, DOI 10.1007/BF02211882 KONSTANTAREAS MM, 1987, J AUTISM DEV DISORD, V17, P585, DOI 10.1007/BF01486973 LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 Lord C., 1999, AUTISM DIAGNOSTIC OB MUNDY P, 1987, J AUTISM DEV DISORD, V17, P349, DOI 10.1007/BF01487065 Musatti T, 1998, CAH PSYCHOL COGN, V17, P155 Piaget J, 1962, PLAY DREAMS IMITATIO POWER TJ, 1989, J AUTISM DEV DISORD, V19, P97, DOI 10.1007/BF02212721 Reynell J., 1985, REYNELL DEV LANGUAGE Reynell J., 1977, REYNELL DEV LANGUAGE RIGUET CB, 1981, J AUTISM DEV DISORD, V11, P439 RUSSELL CL, 1981, CAN J BEHAV SCI, V13, P95, DOI 10.1037/h0081157 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SHAH A, 1985, J AUTISM DEV DISORD, V15, P195, DOI 10.1007/BF01531605 SIGMAN M, 1984, DEV PSYCHOL, V20, P293, DOI 10.1037/0012-1649.20.2.293 Spencer PE, 1996, CHILD DEV, V67, P867, DOI 10.1111/j.1467-8624.1996.tb01769.x STAHMER AC, 1995, J AUTISM DEV DISORD, V25, P123, DOI 10.1007/BF02178500 UDWIN O, 1982, CHILD CARE HLTH DEV, V8, P361, DOI 10.1111/j.1365-2214.1982.tb00296.x UNGERER JA, 1984, CHILD DEV, V55, P1448, DOI 10.2307/1130014 UZGIRIS IC, 1976, ASSESSMENT INFANCY A VONDRA J, 1991, PLAY DIAGNOSIS ASSES, P13 Wechsler D, 1974, WECHSLER INTELLIGENC Wechsler D., 2002, WPPSI 3 ADM SCORING WHYTE J, 1989, IRISH J PSYCHOL, V10, P317 WING L, 1977, J CHILD PSYCHOL PSYC, V18, P167, DOI 10.1111/j.1469-7610.1977.tb00426.x NR 48 TC 13 Z9 14 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1215 EP 1223 DI 10.1007/s10803-006-0263-2 PG 9 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000002 PM 17082977 ER PT J AU Klein-Tasman, BP Risi, S Lord, CE AF Klein-Tasman, Bonita P. Risi, Susan Lord, Catherine E. TI Effect of language and task demands on the diagnostic effectiveness of the autism diagnostic observation schedule: The impact of module choice SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT 4th International Meeting for Autism Research CY MAY 06-07, 2005 CL Boston, MA DE ADOS; autism; PDD-NOS; diagnosis; task demands; clinical judgment ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDREN AB The ADOS characterizes socio-communicative deficits in autism spectrum disorders (ASD). In this study the effect of module choice on ADOS classification was examined. For 74 participants (52 autism, 22 PDD-NOS), Module 1 and Module 2 were administered in a single session. Fifty-one participants maintained ADOS classification, with 17 more impaired on M2 and 6 more impaired on M1. For 64 participants (25 autism, 39 PDD-NOS), Module 2 and Module 3 were administered. Thirty-nine participants maintained classification, with 24 more impaired on M3 and 1 more impaired on M2. As expected, more impairment was indicated when a module with more language and task demands was administered. Clinical judgment of the most appropriate module for administration was found to be important. C1 Univ Wisconsin, Milwaukee, WI 53201 USA. Univ Michigan, Ann Arbor, MI 48109 USA. RP Klein-Tasman, BP (reprint author), Univ Wisconsin, Milwaukee, WI 53201 USA. EM bklein@uwm.edu CR DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x KOBAYASHI R, 1992, J AUTISM DEV DISORD, V22, P395, DOI 10.1007/BF01048242 LECOUTEUR A, 2003, AUTISM DIAGNOSTIC IN Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 MESIBOV GB, 1994, STRUCTURED TEACHING Sparrow S, 1984, VINELAND ADAPTIVE BE Tanguay PE, 2004, J AM ACAD CHILD PSY, V43, P181, DOI 10.1097/01.chi.0000101698.15837.7b Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 Walker DR, 2004, J AM ACAD CHILD PSY, V43, P172, DOI 10.1097/01.chi.0000101375.03068.db NR 14 TC 5 Z9 5 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1224 EP 1234 DI 10.1007/s10803-006-0266-z PG 11 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000003 PM 17149669 ER PT J AU Barbaro, J Dissanayake, C AF Barbaro, Josephine Dissanayake, Cheryl TI A comparative study of the use and understanding of self-presentational display rules in children with high functioning autism and Asperger's disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high-functioning autism; Asperger's disorder; self-presentational display rules; emotion ID EXPRESSIVE BEHAVIOR; KNOWLEDGE; MIND; DISTINCTION; PERCEPTION; EMOTION AB The use and understanding of self-presentational display rules (SPDRs) was investigated in 21 children with high-functioning autism (HFA), 18 children with Asperger's disorder (AspD) and 20 typically developing (TD) children (all male, aged 4- to 11-years, matched on mental age). Their behaviour was coded during a deception scenario to assess use of SPDRs; understanding of SPDRs was assessed via three real/apparent emotion-understanding vignettes. The children with HFA and AspD used less effective SPDRs than the TD children, but there were no group differences in understanding SPDRs. The children with HFA and AspD did not differ on their use or understanding of SPDRs, and the results are discussed in relation to the similarities and differences between these diagnostic conditions. C1 La Trobe Univ, Sch Psychol Sci, Melbourne, Vic 3086, Australia. RP Dissanayake, C (reprint author), La Trobe Univ, Sch Psychol Sci, Melbourne, Vic 3086, Australia. EM c.dissanayake@latrobe.edu.au CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Banerjee R, 1999, BRIT J DEV PSYCHOL, V17, P111, DOI 10.1348/026151099165186 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x CAPPS L, 1993, J CONSULT CLIN PSYCH, V61, P475, DOI 10.1037/0022-006X.61.3.475 Dennis M, 2000, AUTISM, V4, P370, DOI DOI 10.1177/1362361300004004003 Dissanayake C., 2003, INDIVIDUAL DIFFERENC, P213 DISSANAYAKE C, 2004, AUSTRALIAN J EARLY C, V29, P48 Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 Ekman P., 1969, SEMIOTICA, V1, P49 Ekman P., 1972, EMOTION HUMAN FACE G Frith U, 2004, J CHILD PSYCHOL PSYC, V45, P672, DOI 10.1111/j.1469-7610.2004.00262.x Garner PW, 1996, CHILD DEV, V67, P1406, DOI 10.2307/1131708 Gilchrist A, 2001, J CHILD PSYCHOL PSYC, V42, P227, DOI 10.1017/S0021963001006631 GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 GNEPP J, 1986, DEV PSYCHOL, V22, P103, DOI 10.1037/0012-1649.22.1.103 Gresham F. M., 1990, SOCIAL SKILLS RATING HARRIS PL, 1986, CHILD DEV, V57, P895, DOI 10.1111/j.1467-8624.1986.tb00253.x Harris PL, 1989, CHILDREN EMOTION DEV HOBSON RP, 1986, J CHILD PSYCHOL PSYC, V27, P321, DOI 10.1111/j.1469-7610.1986.tb01836.x HOBSON RP, 1986, J CHILD PSYCHOL PSYC, V19, P329 Hosie JA, 2000, J CHILD PSYCHOL PSYC, V41, P389, DOI 10.1111/1469-7610.00623 Howlin P, 2003, J AUTISM DEV DISORD, V33, P3, DOI 10.1023/A:1022270118899 Iwanaga R, 2000, J AUTISM DEV DISORD, V30, P169, DOI 10.1023/A:1005467807937 Klin A., 2000, ASPERGER SYNDROME LOVELAND KA, 1995, DEV PSYCHOPATHOL, V7, P409 Macintosh Kathleen, 2006, Autism, V10, P199, DOI 10.1177/1362361306062026 MACINTOSH K, IN PRESS J AUTISM DE Macintosh KE, 2004, J CHILD PSYCHOL PSYC, V45, P421, DOI 10.1111/j.1469-7610.2004.00234.x Martin P, 1986, MEASURING BEHAV INTR Matsumoto D, 2005, EMOTION, V5, P23, DOI 10.1037/1528-3542.5.1.23 Mayes SD, 2001, J ABNORM CHILD PSYCH, V29, P263, DOI 10.1023/A:1010337916636 Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x PERNER J, 1985, J EXPT CHILD PSYCHOL, V39, P347 REISSLAND N, 1991, BRIT J DEV PSYCHOL, V9, P431 SAARNI C, 1979, DEV PSYCHOL, V15, P424, DOI 10.1037//0012-1649.15.4.424 SAARNI C, 1984, CHILD DEV, V55, P1504, DOI 10.2307/1130020 Saarni C., 1993, HDB EMOTIONS, P435 SHROUT PE, 1979, PSYCHOL BULL, V86, P420, DOI 10.1037//0033-2909.86.2.420 SIGMAN M, 1995, LEARNING COGNITION A, P159 Sigman M., 1997, CHILDREN AUTISM Thorndike RL, 1986, STANFORD BINET INTEL World Health Organisation, 1993, INT CLASSIFICATION D YIRMIYA N, 1989, J CHILD PSYCHOL PSYC, V30, P725, DOI 10.1111/j.1469-7610.1989.tb00785.x Zaalberg R, 2004, COGNITION EMOTION, V18, P183, DOI 10.1080/02699930341000040 Ziatas K, 1998, J CHILD PSYCHOL PSYC, V39, P755, DOI 10.1017/S0021963098002510 NR 48 TC 16 Z9 16 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1235 EP 1246 DI 10.1007/s10803-006-0267-y PG 12 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000004 PM 17086441 ER PT J AU Renty, J Roeyers, H AF Renty, Jo Roeyers, Herbert TI Individual and marital adaptation in men with autism spectrum disorder and their spouses: The role of social support and coping strategies SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism spectrum disorder; double ABCX model; social support; coping; adaptation ID DOUBLE ABCX MODEL; FUNCTIONING AUTISM; ASPERGER-SYNDROME; PARENTAL STRESS; FAMILY STRESS; CHILDREN; MOTHERS; DISABILITIES; ADJUSTMENT; QUALITY AB The aim of the present study was to examine the predictive value of social support and coping for individual and marital adaptation in adult men with autism spectrum disorder (ASD) and their spouses, based on the double ABCX model of adaptation. Twenty-one couples participated in the study and completed measures of stressor severity, social support, coping, individual and marital adaptation. Bivariate analyses showed that each of the model components was related to adaptation in men and women. Hierarchical regression analyses revealed that, after controlling for relevant demographics and stressor severity, informal support was a strong, and unique predictor of adaptation in both spouses (explained variance: 27-89%). Coping did not add to the prediction of adaptation. Clinical implications and limitations are discussed. C1 Univ Ghent, Dept Expt Clin & Hlth Psychol, Res Grp Dev Disorders, B-9000 Ghent, Belgium. RP Roeyers, H (reprint author), Univ Ghent, Dept Expt Clin & Hlth Psychol, Res Grp Dev Disorders, Henri Dunantlaan 2, B-9000 Ghent, Belgium. EM Herbert.Roeyers@Ugent.be CR Arrindell W. A., 1986, SCL 90 HANDLEIDING B Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Barrera M, 1981, SOCIAL NETWORKS SOCI, P69 BARRERA M, 1981, AM J COMMUN PSYCHOL, V9, P435, DOI 10.1007/BF00918174 BRISTOL MM, 1987, J AUTISM DEV DISORD, V17, P469, DOI 10.1007/BF01486964 Bristol M. M., 1984, EFFECTS AUTISM FAMIL, P289 BRISTOL MM, 1988, DEV PSYCHOL, V24, P441, DOI 10.1037/0012-1649.24.3.441 Bromley J, 2004, AUTISM, V8, P409, DOI 10.1177/1362361304047224 BUNDY MB, 1996, DISS ABSTR INT, V56, P7090 Cohen J., 2003, APPL MULTIPLE REGRES COHEN S, 1983, J APPL SOC PSYCHOL, V13, P99, DOI 10.1111/j.1559-1816.1983.tb02325.x COYNE JC, 1991, ANNU REV PSYCHOL, V42, P401, DOI 10.1146/annurev.psych.42.1.401 Cutrona C. 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Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1247 EP 1255 DI 10.1007/s10803-006-0268-x PG 9 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000005 PM 17080274 ER PT J AU Constantino, JN Yang, D Gray, TL Gross, MM Abbacchi, AM Smith, SC Kohn, CE Kuhl, PK AF Constantino, John N. Yang, Dan Gray, Teddi L. Gross, Maggie M. Abbacchi, Anna M. Smith, Sarah C. Kohn, Catherine E. Kuhl, Patricia K. TI Clarifying the associations between language and social development in autism: A study of non-native phoneme recognition SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; language; social responsiveness scale; auditory discrimination; speech perception; information processing; phonemic awareness ID CHILDREN; SPEECH; PERCEPTION; TRAITS; IMPAIRMENT; SOUNDS AB Autism spectrum disorders (ASDs) are characterized by correlated deficiencies in social and language development. This study explored a fundamental aspect of auditory information processing (AIP) that is dependent on social experience and critical to early language development: the ability to compartmentalize close-sounding speech sounds into singular phonemes. We examined this ability by assessing whether close-sounding non-native language phonemes were more likely to be perceived as disparate sounds by school-aged children with high-functioning ASD (n = 27), than by unaffected control subjects (n = 35). No significant group differences were observed. Although earlier in autistic development there may exist qualitative deficits in this specific aspect of AIP, they are not an enduring characteristic of verbal school-aged children with ASD. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Univ Washington, Seattle, WA 98195 USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, 660 S Euclid Ave,Campus Box 8134, St Louis, MO 63110 USA. EM constantino@wustl.edu CR Alcantara JI, 2004, J CHILD PSYCHOL PSYC, V45, P1107, DOI 10.1111/j.1469-7610.2004.t01-1-00303.x Bishop DVM, 2004, AM J MED GENET B, V128B, P54, DOI 10.1002/ajmg.b.30039 Boddaert N, 2004, AM J PSYCHIAT, V161, P2117, DOI 10.1176/appi.ajp.161.11.2117 Cardoso FH, 2005, J DEMOCR, V16, P5, DOI 10.1353/jod.2005.0020 Ceponiene R, 2003, P NATL ACAD SCI USA, V100, P5567, DOI 10.1073/pnas.0835631100 Constantino JN, 2004, J CHILD PSYCHOL PSYC, V45, P719, DOI 10.1111/j.1469-7610.2004.00266.x Constantino JN, 2003, J AUTISM DEV DISORD, V33, P427, DOI 10.1023/A:1025014929212 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Constantino JN, 2005, SOCIAL RESPONSIVENES Gervais H, 2004, NAT NEUROSCI, V7, P801, DOI 10.1038/nn1291 Iverson P, 1996, J ACOUST SOC AM, V99, P1130, DOI 10.1121/1.415234 Just MA, 2004, BRAIN, V127, P1811, DOI 10.1093/brain/awh199 Kasai K, 2005, CLIN NEUROPHYSIOL, V116, P1655, DOI 10.1016/j.clinph.2005.03.007 KEMNER C, 1995, BIOL PSYCHIAT, V38, P150, DOI 10.1016/0006-3223(94)00247-Z Kjelgaard MM, 2001, LANG COGNITIVE PROC, V16, P287 Kuhl PK, 2005, DEVELOPMENTAL SCI, V8, pF1, DOI 10.1111/j.1467-7687.2004.00384.x Kuhl PK, 2000, P NATL ACAD SCI USA, V97, P11850, DOI 10.1073/pnas.97.22.11850 Kuhl PK, 2003, P NATL ACAD SCI USA, V100, P9096, DOI 10.1073/pnas.1532872100 Lopez B, 2003, J CHILD PSYCHOL PSYC, V44, P285, DOI 10.1111/1469-7610.00121 Lord C., 1997, HDB AUTISM PERVASIVE, P195 Senechal M, 2004, J EXP CHILD PSYCHOL, V89, P242, DOI 10.1016/j.jecp.2004.07.005 Spiker D, 2002, AM J MED GENET, V114, P129, DOI 10.1002/ajmg.10188 NR 22 TC 7 Z9 7 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1256 EP 1263 DI 10.1007/s10803-006-0269-9 PG 8 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000006 PM 17080273 ER PT J AU Kern, P Wolery, M Aldridge, D AF Kern, Petra Wolery, Mark Aldridge, David TI Use of songs to promote independence in morning greeting routines for young children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE music therapy; child care program; inclusion; autism; transitioning; collaborative consultation ID TRANSITIONS; BEHAVIORS AB This study evaluated the effects of individually composed songs on the independent behaviors of two young children with autism during the morning greeting/entry routine into their inclusive classrooms. A music therapist composed a song for each child related to the steps of the morning greeting routine and taught the children's teachers to sing the songs during the routine. The effects were evaluated using a single subject withdrawal design. The results indicate that the songs, with modifications for one child, assisted the children in entering the classroom, greeting the teacher and/or peers and engaging in play. For one child, the number of peers who greeted him was also measured, and increased when the song was used. C1 Univ Windsor, Sch Mus, Windsor, ON N9B 3P4, Canada. Univ N Carolina, Frank Porter Graham Child Dev Inst, Chapel Hill, NC USA. Vanderbilt Univ, George Peabody Coll Teachers, Dept Special Educ, Nashville, TN 37203 USA. Univ Witten Herdecke, Chair Qualitat Res Med, Witten, Germany. RP Kern, P (reprint author), Univ Windsor, Sch Mus, 401 Sunset Ave, Windsor, ON N9B 3P4, Canada. 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TI Validity of the social communication questionnaire in assessing risk of autism in preschool children with developmental problems SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism spectrum disorder; screening; sensitivity; specificity; questionnaire ID SPECTRUM DISORDERS; DIAGNOSTIC UNCERTAINTIES; INTERVENTION; INSTRUMENT; CHECKLIST AB This study estimates the sensitivity and specificity of the social communication questionnaire (SCQ) for autistic spectrum disorders in preschool children at high risk for developmental problems referred to a tertiary centre and compares the predictions of the SCQ and the referrer. The SCQ was completed by 81 parents prior to multidisciplinary assessment and compared with the final diagnosis. The sensitivity and specificity were 93% and 58% for children aged 2-6, and 100 and 62% for children aged 3-5 years, with a cut-off score of 11. The SCQ performed better than referrers. Low-specificity means the SCQ is not suitable as a diagnostic tool but will assist clinicians and tertiary services in selecting children with developmental problems who require autism-specific assessment. C1 Univ Sydney, Childrens Hosp Westmead, Sydney, NSW 2145, Australia. RP Allen, CW (reprint author), Univ Sydney, Childrens Hosp Westmead, Locked Bag 4001, Sydney, NSW 2145, Australia. EM wendya@chw.edu.au RI Williams, Katrina/B-6828-2015 OI Williams, Katrina/0000-0002-1686-4458 CR American Psychiatric Association. 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Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1272 EP 1278 DI 10.1007/s10803-006-0279-7 PG 7 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000008 PM 17080270 ER PT J AU Minassian, A Paulus, M Lincoln, A Perry, W AF Minassian, Arpi Paulus, Martin Lincoln, Alan Perry, William TI Adults with autism show increased sensitivity to outcomes at low error rates during decision-making SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; decision-making; perseveration; executive functioning; reinforcement; cognition ID CARD SORTING TEST; PREFRONTAL CORTEX; SCHIZOPHRENIC-PATIENTS; ANTERIOR CINGULATE; DISORDER; BEHAVIOR; DYSFUNCTION; ACTIVATION; SEQUENCES; PARIETAL AB Decision-making is an important function that can be quantified using a two-choice prediction task. Individuals with Autistic Disorder (AD) often show highly restricted and repetitive behavior that may interfere with adaptive decision-making. 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Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1279 EP 1288 DI 10.1007/s10803-006-0278-8 PG 10 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000009 PM 17080271 ER PT J AU Brenner, LA Turner, KC Muller, RA AF Brenner, Laurie A. Turner, Katherine C. Mueller, Ralph-Axel TI Eye movement and visual search: Are there elementary abnormalities in autism? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE autism; eye movement; visual search; joint attention; language ID POSTERIOR PARIETAL CORTEX; SACCADE TARGET SELECTION; EVENT-RELATED FMRI; INFERIOR PREFRONTAL CORTEX; HIGH-FUNCTIONING AUTISM; SUPERIOR COLLICULUS; SPATIAL ATTENTION; SPECTRUM DISORDER; DEVELOPMENTAL DISORDERS; NEURAL MECHANISMS AB Although atypical eye gaze is commonly observed in autism, little is known about underlying oculomotor abnormalities. Our review of visual search and oculomotor systems in the healthy brain suggests that relevant networks may be partially impaired in autism, given regional abnormalities known from neuroimaging. However, direct oculomotor evidence for autism remains limited. This gap is critical since oculomotor abnormalities might play a causal role in functions known to be impaired in autism, such as imitation and joint attention. We integrate our oculomotor review into a developmental approach to language impairment related to nonverbal prerequisites. Oculomotor abnormalities may play a role as a sensorimotor defect at the root of impairments in later developing functional systems, ultimately resulting in sociocommunicative deficits. C1 San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, San Diego, CA 92120 USA. Univ Calif San Diego, Dept Cognit Sci, La Jolla, CA 92093 USA. 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Videotapes of conversational interviews with 47 autism, 47 SLI, and 21 DS parents were scored blind to group membership. Autism and SLI parents had significantly lower communication abilities than DS parents. Fifteen percent of the autism and SLI parents showed severe deficits. Our results suggest that impaired communication is part of the broader autism phenotype and a broader SLI phenotype, especially among male family members. C1 Tufts Univ, New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC USA. Univ Iowa, Dept Speech Pathol, Iowa City, IA USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Inst Living, Dept Psychiat, Hartford, CT 06106 USA. New York Acad Med, Ctr Urban Epidemiol Studies, New York, NY USA. RP Ruser, TF (reprint author), Tufts Univ, New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. 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Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1323 EP 1336 DI 10.1007/s10803-006-0274-z PG 14 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000012 PM 17180460 ER PT J AU Harnum, M Duffy, J Ferguson, DA AF Harnum, Marsha Duffy, Jim Ferguson, Duncan A. TI Adults' versus children's perceptions of a child with autism or attention deficit hyperactivity disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE public perception; attention deficit hyperactivity disorder (ADHD); autism; children ID DEFICIT/HYPERACTIVITY DISORDER; PEER; ADHD; GIRLS; BOYS AB The present study examined public perceptions toward children with autism or with attention deficit hyperactivity disorder (ADHD). A convenience sample was used consisting of 30 children (7-12-year-olds) and 30 adults. Participants read a stereotyped scenario featuring either a child with autism, a child with ADHD, or a normal child. Child participants were significantly more likely than adults to (a) express dislike/avoidance toward a child described with either stereotypic autistic or ADHD behaviors, and (b) perceive the child with ADHD as unlike themselves. However, child participants and adults were equally likely to see the autistic child as unlike themselves. Reasons for the different perceptions of children and adults may include differences in perceived threat and in categorization. C1 Mem Univ Newfoundland, Sir Wilfred Grenfell Coll, Dept Psychol, Corner Brook, NF A2H 6P9, Canada. RP Duffy, J (reprint author), Mem Univ Newfoundland, Sir Wilfred Grenfell Coll, Dept Psychol, Corner Brook, NF A2H 6P9, Canada. 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PD AUG PY 2007 VL 37 IS 7 BP 1337 EP 1343 DI 10.1007/s10803-006-0273-0 PG 7 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000013 PM 17080272 ER PT J AU Stahmer, AC AF Stahmer, Aubyn C. TI The basic structure of community early intervention programs for children with autism: Provider descriptions SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; early intervention; usual care; evidence-based practices ID YOUNG-CHILDREN; DISORDERS; SYSTEM AB Autism researchers have identified a set of common effective practice elements for early intervention (EI) (e.g., intensive programming). The current study examined the reported about use of common elements of effective interventions in community El settings. Eighty El providers reported about their programs. The majority of participants reported using common effective elements, however, the depth and quality of the use of these elements was highly variable. 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TI Beyond perception: Musical representation and on-line processing in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; music cognition; local and global processing ID CENTRAL COHERENCE; EXPECTANCY; LANGUAGE; PITCH; ABILITIES; CONTEXT; SAVANT; CHORDS; INDIVIDUALS; CHILDREN AB Whilst findings from experimental studies suggest that perceptual mechanisms underpinning musical cognition are preserved or enhanced in autism, little is known about how higher-level, structural aspects of music are processed. Twenty participants with autism, together with age and intelligence matched controls, completed a musical priming task in which global and local musical contexts were manipulated. The results from the study revealed no between-group differences and showed that both global and local musical contexts influenced participants' congruity judgements. 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Sigurdardottir, Solveig Smari, Jakob TI Follow-up of children diagnosed with pervasive developmental disorders: Stability and change during the preschool years SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pervasive developmental disorders; ICD-10; preschool; stability; change ID AUTISM SPECTRUM DISORDERS; INTENSIVE BEHAVIORAL TREATMENT; EARLY SCHOOL-AGE; YOUNG-CHILDREN; EARLY INTERVENTION; ADAPTIVE-BEHAVIOR; COGNITIVE ASSESSMENT; INFANT DEVELOPMENT; CHILDHOOD AUTISM; BAYLEY SCALES AB Forty-one children with pervasive developmental disorders (PDDs) receiving eclectic services were assessed twice during their preschool years. Measures were compared over time for the whole group and for diagnostic subgroups: Childhood autism (CA group) and Other PDDs group. The mean intelligence quotient/developmental quotient (IQ/ DQ) of the whole group was stable (P = 0.209) and scores on the Childhood Autism Rating Scale (CARS) decreased (P = 0.001). At time 2, the CA group was more impaired than the other PDDs group: autistic symptoms were more severe (P = 0.01), adaptive behavior scores were lower (P = 0.014), and a trend for lower IQ/DQs (P = 0.06). Children in this study seemed to fare better than reported in previous follow-up studies on children with autism. C1 State Diagnost & Counselling Ctr, Div Autism & Commun Disorders, IS-200 Kopavogur, Iceland. Univ Iceland, Dept Social Sci, Reykjavik, Iceland. Reykjavik Hlth Care Serv, Ctr Child Hlth Serv, Reykjavik, Iceland. Reykjavik Hlth Care Serv, Iceland Ctr Social Res & Anal, Reykjavik, Iceland. RP Jonsdottir, SL (reprint author), State Diagnost & Counselling Ctr, Div Autism & Commun Disorders, Digranesvegur 5, IS-200 Kopavogur, Iceland. 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Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1361 EP 1374 DI 10.1007/s10803-006-0282-z PG 14 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000016 PM 17146706 ER PT J AU de Villiers, J Fine, J Ginsberg, G Vaccarella, L Szatmari, P AF de Villiers, Jessica Fine, Jonathan Ginsberg, Gary Vaccarella, Liezanne Szatmari, Peter TI Brief report: A scale for rating conversational impairment in autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE ASD; Asperger syndrome; pragmatic difficulties; linguistic analysis; conversation ID CHILDREN AB There are few well-standardized measures of conversational breakdown in Autism Spectrum Disorders (ASD). The study's objective was to develop a scale for measuring pragmatic impairments in conversations of individuals with ASD. We analyzed 46 semi-structured conversations of children and adolescents with high-functioning ASD using a functional linguistic paradigm. Five constructs were developed that assessed difficulties related to the pragmatics of conversation: atypical intonation; semantic drift; terseness; pedantic speech; perseveration. The scale shows good inter-rater reliability and variation in the scales is not simply a reflection of IQ or language competence. This tool represents a way of characterizing language use in ASD and is an initial step towards developing a tool to evaluate change in degree of social impairments in conversation. C1 McMaster Univ, Dept Psychiat & Behav Neurosci, McMaster Childrens Hosp, Hamilton, ON L8N 3Z5, Canada. Univ British Columbia, Dept English, Voncouver, BC V8N 1Z4, Canada. Bar Ilan Univ, Dept English, Ramat Gan, Israel. Hebrew Univ Jerusalem, Sch Publ Hlth, Jerusalem, Israel. Hebrew Univ Jerusalem, Minist Hlth, Jerusalem, Israel. RP Szatmari, P (reprint author), McMaster Univ, Dept Psychiat & Behav Neurosci, McMaster Childrens Hosp, Patterson Bldg,Chedoke Site,1200 Main St, Hamilton, ON L8N 3Z5, Canada. EM szatmar@mcmaster.ca CR ADAMS C, 1989, BRIT J DISORD COMMUN, V24, P211 Baron-Cohen S, 1993, UNDERSTANDING OTHER Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 Frith U., 1989, AUTISM EXPLAINING EN Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 GREGORY M, 1985, COMMUNICATION LINGUI, V2 Grice H. P., 1975, SPEECH ACTS, P41 Hadwin J, 1997, J AUTISM DEV DISORD, V27, P519, DOI 10.1023/A:1025826009731 Halliday M. A., 1994, INTRO FUNCTIONAL GRA, V3rd LEVINE MN, 1986, MANUAL LEITER INT PE MacWhinney B., 1995, CHILDES PROJECT TOOL McCarthy D, 1972, MANUAL MCCARTHY SCAL Newcomer P., 1988, TEST LANGUAGE DEV Szatmari P, 2000, AM J PSYCHIAT, V157, P1980, DOI 10.1176/appi.ajp.157.12.1980 THORNDIKE RL, 1986, STANDFORDBINET INTEL NR 15 TC 8 Z9 9 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1375 EP 1380 DI 10.1007/s10803-006-0264-1 PG 6 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000017 PM 17082976 ER PT J AU Carmody, DP Moreno, R Mars, AE Seshadri, K Lambert, GH Lewis, M AF Carmody, Dennis P. Moreno, Rosanne Mars, Audrey E. Seshadri, Kapila Lambert, George H. Lewis, Michael TI Brief report: Brain activation to social words in a sedated child with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; fMRI; self-awareness ID WORKING-MEMORY; FMRI; PROPOFOL AB A functional magnetic resonance imaging (fMRI) study was performed on a 4-year-old girl with autism. While sedated, she listened to three utterances (numbers, hello, her own first name) played through headphones. Based on analyses of the fMRI data, the amount of total brain activation varied with the content of the utterance. The greatest volume of overall activation was in response to numbers, followed by the word 'hello', with the least activation to her name. Frontal cortex activation was greatest in response to her name, with less activation for numbers, and the least for the word 'hello.' These findings indicate that fMRI can identify and quantify the brain regions that are activated in response to words in children with autism under sedation. C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Inst Study Child Dev, New Brunswick, NJ 08903 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pediat, Div Child Neurol & Neurodev Disabil, New Brunswick, NJ 08903 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pediat,Ctr Childhood Neurotoxicol & Exposure, Pediat Clin Res Ctr,Div Pediat Pharmacol & Toxico, New Brunswick, NJ 08903 USA. RP Carmody, DP (reprint author), Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Inst Study Child Dev, 97 Paterson St, New Brunswick, NJ 08903 USA. EM carmoddp@umdnj.edu CR Allen G, 2003, AM J PSYCHIAT, V160, P262, DOI 10.1176/appi.ajp.160.2.262 Altman NR, 2001, RADIOLOGY, V221, P56, DOI 10.1148/radiol.2211010074 American Psychological Association, 2002, AM PSYCHOL, V57, P1060, DOI DOI 10.1037/0003-066X.57.12.1060 Beery K., 1997, BEERY BUKTENICA DEV Carmody DP, 2006, BRAIN RES, V1116, P153, DOI 10.1016/j.brainres.2006.07.121 Cox RW, 1996, COMPUT BIOMED RES, V29, P162, DOI 10.1006/cbmr.1996.0014 Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 Elliot C. 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Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1381 EP 1385 DI 10.1007/s10803-006-0270-3 PG 5 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000018 PM 17136453 ER PT J AU Hubert, B Wicker, B Moore, DG Monfardini, E Duverger, H Da Fonseca, D Deruelle, C AF Hubert, B. Wicker, B. Moore, D. G. Monfardini, E. Duverger, H. Da Fonseca, D. Deruelle, C. TI Brief report: Recognition of emotional and non-emotional biological motion in individuals with autistic spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE biological motion; emotion; autism ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; VISUAL-PERCEPTION; LIGHT DISPLAYS; POINT-LIGHT; CHILDREN; ADOLESCENTS; EXPRESSIONS; ADULTS AB This study aimed to explore the perception of different components of biological movement in individuals with autism and Asperger syndrome. The ability to recognize a person's actions, subjective states, emotions, and objects conveyed by moving point-light displays was assessed in 19 participants with autism and 19 comparable typical control participants. Results showed that the participants with autism were as able as controls to name point-light displays of non-human objects and human actions. In contrast, they were significantly poorer at labeling emotional displays, suggesting that they are specifically impaired in attending to emotional states. Most studies have highlighted an emotional deficit in facial expression perception; our results extend this hypothesized deficit to the perception and interpretation of whole-body biological movements. C1 Mediterranean Inst Cognit Neurosci, CNRS, UMR 6193, F-13402 Marseille 20, France. Univ E London, Sch Psychol, London E15 4LZ, England. RP Deruelle, C (reprint author), Mediterranean Inst Cognit Neurosci, CNRS, UMR 6193, 31 Chemin Joseph Aiguie, F-13402 Marseille 20, France. EM deruelle@incm.cnrs-mrs.fr CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Atkinson AP, 2004, PERCEPTION, V33, P717, DOI 10.1068/p5096 BARONCOHEN S, 1986, BRIT J DEV PSYCHOL, V4, P113 Blake R, 2003, PSYCHOL SCI, V14, P151, DOI 10.1111/1467-9280.01434 Castelli F, 2002, BRAIN, V125, P1839, DOI 10.1093/brain/awf189 Celani G, 1999, J AUTISM DEV DISORD, V29, P57, DOI 10.1023/A:1025970600181 Clarke TJ, 2005, PERCEPTION, V34, P1171, DOI 10.1068/p5203 Dakin S, 2005, NEURON, V48, P497, DOI 10.1016/j.neuron.2005.10.018 DERUELLE C, IN PRESS INT J PSYCH Deruelle C, 2004, J AUTISM DEV DISORD, V34, P199, DOI 10.1023/B:JADD.0000022610.09668.4c Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 Fecteau S, 2003, AUTISM, V7, P255, DOI 10.1177/1362361303007003003 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 GROSS TF, 2005, J AUTISM DEV DISORDE Grossman ED, 2005, VISION RES, V45, P2847, DOI 10.1016/j.visres.2005.05.027 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x Hobson R. Peter, 1993, AUTISM DEV MIND HOBSON RP, 1988, PSYCHOL MED, V18, P911 HOBSON RP, 1989, AM J MENT RETARD, V93, P434 HUBERT B, IN PRESS AUTISM Jellema T, 2000, BRAIN COGNITION, V44, P280, DOI 10.1006/brcg.2000.1231 JOHANSSO.G, 1973, PERCEPT PSYCHOPHYS, V14, P201, DOI 10.3758/BF03212378 Lawson J, 2004, J AUTISM DEV DISORD, V34, P301, DOI 10.1023/B:JADD.0000029552.42724.1b Lawson J, 2003, J THEOR SOC BEHAV, V33, P189, DOI 10.1111/1468-5914.00213 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Moore DG, 1997, BRIT J DEV PSYCHOL, V15, P401 MOORE DG, 1994, THESIS U COLLEGE LON Mottron L, 2003, J CHILD PSYCHOL PSYC, V44, P904, DOI 10.1111/1469-7610.00174 Pelphrey K, 2004, MENT RETARD DEV D R, V10, P259, DOI 10.1002/mrdd Pollick FE, 2003, PERCEPTION, V32, P813, DOI 10.1068/p3319 Rondan C., 2004, J COGN BEHAV PSYCHOT, V4, P149 Rondan C., 2005, CURRENT PSYCHOL COGN, V23, P198 Wechsler D., 1996, MANUAL INTELLIGENCE Wechsler D, 1981, WECHSLER ADULT INTEL NR 34 TC 73 Z9 74 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1386 EP 1392 DI 10.1007/s10803-006-0275-y PG 7 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000019 PM 17160459 ER PT J AU Lowenthal, R Paula, CS Schwartzman, JS Brunoni, D Mercadante, MT AF Lowenthal, Rosane Paula, Cristiane S. Schwartzman, Jose S. Brunoni, Decio Mercadante, Marcos Tomanik TI Prevalence of pervasive developmental disorder in Down's syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter DE Down syndrome; autism; pervasive developmental disorder; prevalence AB The frequencies of pervasive developmental disorder (PDD) in Down's syndrome (DS) have been reported from 1% to 11%. However, it is not clear if the frequency of this co-occurrence is higher or lower than in other mental retardations. We study a large sample of DS population, finding a PDD frequency of 15.6%, with 5.58% of autism (eight males and two females) and 10.05% of PDD non autism (nine males and nine females. The meaning of this frequency is discussed. C1 Univ Prebiteriana Mackenzie, BR-01302907 Sao Paulo, Brazil. RP Mercadante, MT (reprint author), Univ Prebiteriana Mackenzie, Rua Consolacao 896,Sala 62, BR-01302907 Sao Paulo, Brazil. EM mt.mercadante@uol.com.br CR Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Capone GT, 2005, AM J MED GENET A, V134A, P373, DOI 10.1002/ajmg.a.30622 Fombonne E., 2006, PEDIATRICS, V118, P139 Kent L, 1999, DEV MED CHILD NEUROL, V41, P153, DOI 10.1017/S001216229900033X LUND J, 1988, ACTA PSYCHIAT SCAND, V78, P369, DOI 10.1111/j.1600-0447.1988.tb06350.x NR 5 TC 32 Z9 33 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1394 EP 1395 DI 10.1007/s10803-007-0374-4 PG 2 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000020 PM 17410415 ER PT J AU Snyder, A AF Snyder, Allan TI Comment on priming skills of autistic twins and Yamaguchi (2006) letter to the editor: "Questionable aspects of oliver sacks' (1985) report", journal of autism and developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID FRONTOTEMPORAL DEMENTIA; SAVANT C1 Australian Natl Univ, Univ Sydney, Ctr Mind, Sydney, NSW, Australia. RP Snyder, A (reprint author), Australian Natl Univ, Univ Sydney, Ctr Mind, Sydney, NSW, Australia. EM allan@centreforthemind.com CR HOWE MJA, 1989, FRAGMENTS GENIUS Miller BL, 1998, NEUROLOGY, V51, P978 Miller BL, 2000, BRIT J PSYCHIAT, V176, P458, DOI 10.1192/bjp.176.5.458 OCONNOR N, 1989, BRIT J DISORD COMMUN, V24, P1 SACK O, 1985, MAN MISTOOK WIFE HAT Snyder A, 2006, PERCEPTION, V35, P837, DOI 10.1068/p5539 Snyder Allan, 2004, Journal of Integrative Neuroscience, V3, P31, DOI 10.1142/S0219635204000361 Snyder Allan W, 2003, J Integr Neurosci, V2, P149, DOI 10.1142/S0219635203000287 Snyder AW, 1999, P ROY SOC B-BIOL SCI, V266, P587 TREFERT DA, 2000, EXTRAORDINARY PEOPLE YAMAGUCHI M, 2006, J AUTISM DEV DISORDE Young RL, 2004, NEUROCASE, V10, P215, DOI 10.1080/13554790490495140 NR 12 TC 0 Z9 0 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1398 EP 1399 DI 10.1007/s10803-006-0301-0 PG 2 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000022 ER PT J AU Yamaguchi, M AF Yamaguchi, Makoto TI Response to Snyder's "Comments on priming skills of autistic twins and Yamaguchi (2006) letter to the editor: 'Questionable aspects of oliver sacks' (1985) report,'" journal of autism and developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter C1 Univ Tokyo, Tokyo, Japan. RP Yamaguchi, M (reprint author), Univ Tokyo, Tokyo, Japan. EM myamag@mail.ecc.u-tokyo.ac.jp CR Dehaene S, 2001, MIND LANG, V16, P89, DOI 10.1111/1468-0017.00159 Dehaene S., 1997, NUMBER SENSE Horwitz W. A., 1969, AM J PSYCHIAT, V126, P160 HORWITZ WA, 1965, AM J PSYCHIAT, V121, P1075 Snyder A, 2006, PERCEPTION, V35, P837, DOI 10.1068/p5539 Snyder AW, 1999, P ROY SOC B-BIOL SCI, V266, P587 Treffert D. A., 1989, EXTRAORDINARY PEOPLE NR 7 TC 0 Z9 0 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2007 VL 37 IS 7 BP 1401 EP 1401 DI 10.1007/s10803-007-0397-x PG 1 WC Psychology, Developmental SC Psychology GA 200IB UT WOS:000248756000023 ER PT J AU Herguner, S Mukaddes, NM AF Herguner, Sabri Mukaddes, Nahit Motavalli TI Risperidone-induced enuresis in two children with autistic disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID INDUCED NOCTURNAL ENURESIS; INDUCED URINARY-INCONTINENCE; DESMOPRESSIN; SSRI AB Introduction: Risperidone appears to be effective in treating behavioral problems in children with autistic disorder. Although increased appetite, weight gain, and sedation are among the most common side effects, risperidone-induced enuresis is rarely reported. Method: We will present two cases with risperidone-induced enuresis, and discuss our findings in the context of current literature. Results: Two children aged 11 and 10 years, diagnosed with autism and mental retardation, have developed new-onset diurnal and nocturnal enuresis respectively on their first and second weeks of risperidone monotherapy (1.5 and 1 mg/day). They did not experience sedation, and their medical history and workup were unremarkable. As enuresis did not resolve spontaneously, we decided to substitute risperidone with olanzapine. Enuresis ceased rapidly after discontinuation of risperidone with no emergence when patients were treated with olanzapine 5 mg/day for a period of 6 months and 1 year, respectively. Discussion: Although the pathophysiology of antipsychotic-induced enuresis remains unclear, a number of mechanisms including alpha(1)-adrenergic blockade, dopamine blockade, and antimuscarinic effects has been proposed. Olanzapine has lower alpha(1)-adrenergic and dopaminergic blockade properties, thus changing risperidone to olanzapine may be an alternative modality in risperidone-induced enuresis when antipsychotic treatment is crucial. Clinicians should be more vigilant about screening for this side effect, especially in younger population with developmental disabilities. C1 Istanbul Univ, Fac Med, Dept Child & Adolescent Psychiat, Istanbul, Turkey. RP Herguner, S (reprint author), Istanbul Univ, Fac Med, Dept Child & Adolescent Psychiat, Istanbul, Turkey. 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Child Adolesc. Psychopharmacol. PD AUG PY 2007 VL 17 IS 4 BP 527 EP 530 DI 10.1089/cap.2007.0056 PG 4 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 210SB UT WOS:000249474800011 PM 17822346 ER PT J AU Luyster, R Lopez, K Lord, C AF Luyster, Rhiannon Lopez, Kristina Lord, Catherine TI Characterizing communicative development in children referred for Autism Spectrum Disorders using the MacArthur-Bates Communicative Development Inventory (CDI) SO JOURNAL OF CHILD LANGUAGE LA English DT Article ID DIAGNOSTIC OBSERVATION SCHEDULE; PRESCHOOL-CHILDREN; LANGUAGE-DEVELOPMENT; JOINT ATTENTION; VOCABULARY; INFANTS; RECOGNITION; COMPETENCE; ABILITY; SKILLS AB Characterizing early communicative development in children with Autism Spectrum Disorders (ASD) is valuable for understanding profiles of ability in this population. The current investigation was modeled on Charman, Drew, Baird & Baird (2003b). Analyses explored parent report of early vocabulary, non-verbal communication, functional object use and play skills on the MacArthur-Bates Communicative Development Inventory (CDI) in 93 children with ASD, 31 children with developmental delay (DD) and 29 typically developing children. Results were generally consistent with those of Charman and colleagues (2003b), suggesting that skills improve with increasing non-verbal mental age and chronological age but that most children with ASD are delayed in receptive and expressive vocabulary and non-verbal communication, functional object use and play skills. Vocabulary profiles in the ASD sample were similar to those in the comparison samples, as was the developmental pattern of gesture and vocabulary mastery. However, when compared to published norms, children with ASD may show less of a discrepancy between their receptive and expressive vocabulary. C1 Univ Michigan, Austin & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. Calif State Univ Northridge, Northridge, CA 91330 USA. RP Luyster, R (reprint author), Univ Michigan, Austin & Commun Disorders Ctr, 1111 E Catherine St, Ann Arbor, MI 48109 USA. EM rluyster@umich.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARTAK L, 1975, BRIT J PSYCHIAT, V126, P127, DOI 10.1192/bjp.126.2.127 BATES E, 1994, J CHILD LANG, V21, P85 Bayley N, 1993, BAYLEY SCALES INFANT Blalock H. M., 1960, SOCIAL STAT Bornstein MH, 1998, J CHILD LANG, V25, P367, DOI 10.1017/S0305000998003456 Carpenter M., 1998, MONOGR SOC RES CHILD, V63, P1, DOI DOI 10.2307/1166214 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Charman T, 2003, J CHILD LANG, V30, P213, DOI 10.1017/S0305000902005482 Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 Charman T, 1998, INF MENTAL HLTH J, V19, P260, DOI 10.1002/(SICI)1097-0355(199822)19:2<260::AID-IMHJ12>3.0.CO;2-W Charman T, 2004, J AUTISM DEV DISORD, V34, P59, DOI 10.1023/B:JADD.0000018075.77941.60 Charman T, 2003, INT J LANG COMM DIS, V38, P265, DOI 10.1080/136820310000104830 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Elliott C. 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Peter, 1989, AUTISM NATURE DIAGNO, P22 Klin A, 2005, J AUTISM DEV DISORD, V35, P221, DOI 10.1007/s10803-005-2001-6 LECOUTEUR A, 2003, AUTISM DIAGNOSTIC IN Lord C, 2006, ARCH GEN PSYCHIAT, V63, P694, DOI 10.1001/archpsyc.63.6.694 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C, 2004, J CHILD PSYCHOL PSYC, V45, P936, DOI 10.1111/j.1469-7610.2004.t01-1-00287.x LUYSTER R, J SPEECH LANGUAGE HE Mullen E, 1995, MULLEN SCALES EARLY MUNDY P, 1990, J AUTISM DEV DISORD, V20, P115, DOI 10.1007/BF02206861 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Roberts JE, 1999, CHILD DEV, V70, P92, DOI 10.1111/1467-8624.00008 Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 Sigman M, 2005, J AUTISM DEV DISORD, V35, P15, DOI 10.1007/s10803-004-1027-5 Stone WL, 1997, J AUTISM DEV DISORD, V27, P677, DOI 10.1023/A:1025854816091 Stone WL, 2001, AUTISM, V5, P341, DOI 10.1177/1362361301005004002 TAGERFLUSBERG H, 1990, J AUTISM DEV DISORD, V20, P1, DOI 10.1007/BF02206853 Tager-Flusberg H., 2005, HDB AUTISM PERVASIVE, V1, P335 Tager-Flusberg H, 2003, PHILOS T ROY SOC B, V358, P303, DOI 10.1098/rstb.2002.1198 TAYLOR A, 1998, STAT ANAL MED DATA N, P127 Verbeke G, 2000, LINEAR MIXED MODELS Volterra V., 1990, GESTURE LANGUAGE HEA Wetherby AM, 2004, J AUTISM DEV DISORD, V34, P473, DOI 10.1007/s10803-004-2544-y *WHO, 1992, ICD CLASS MENT BEHAV Wilkinson KM, 1998, MENT RETARD DEV D R, V4, P73, DOI 10.1002/(SICI)1098-2779(1998)4:2<73::AID-MRDD3>3.0.CO;2-Y WILLIAMS TI, 1993, J AUTISM DEV DISORD, V23, P185, DOI 10.1007/BF01066427 Zwaigenbaum L, 2005, INT J DEV NEUROSCI, V23, P143, DOI 10.1016/j.ijdevneu.2004.05.001 NR 46 TC 44 Z9 44 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0305-0009 J9 J CHILD LANG JI J. Child Lang. PD AUG PY 2007 VL 34 IS 3 BP 623 EP 654 DI 10.1017/S0305000907008094 PG 32 WC Psychology, Developmental; Linguistics; Psychology, Experimental SC Psychology; Linguistics GA 200MJ UT WOS:000248767200008 PM 17822142 ER PT J AU Chez, MG AF Chez, Michael G. TI Treating autism pharmacologically - Response SO JOURNAL OF CHILD NEUROLOGY LA English DT Letter ID SPECTRUM DISORDERS; CHILDREN; DONEPEZIL CR Chez MG, 2004, ANN NEUROL S, V56, P109 Chez MG, 2003, J PEDIAT NEUROL, V1, P83 Chez MG, 2000, ANN NEUROL, V48, P541 Chez MG, 2004, J CHILD NEUROL, V19, P165 Hardan AY, 2002, J CHILD ADOL PSYCHOP, V12, P237, DOI 10.1089/104454602760386923 Hertzman M, 2003, INT J PSYCHIAT MED, V33, P395, DOI 10.2190/JE5Q-1NFT-FL40-7PMW Perry EK, 2001, AM J PSYCHIAT, V158, P1058, DOI 10.1176/appi.ajp.158.7.1058 NR 7 TC 1 Z9 1 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD AUG PY 2007 VL 22 IS 8 BP 1054 EP 1055 DI 10.1177/0883073807305858 PG 2 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 206LF UT WOS:000249184200017 ER PT J AU Niederhofer, H AF Niederhofer, Helmut TI Treating autism pharmacologically: Also tacrine might improve symptomatology in some cases SO JOURNAL OF CHILD NEUROLOGY LA English DT Letter C1 Gen Hosp Bolzano, Bolzano, Italy. RP Niederhofer, H (reprint author), Gen Hosp Bolzano, Bolzano, Italy. CR AMAN MG, 1985, AM J MENT DEF, V89, P485 Chez MG, 2004, J CHILD NEUROL, V19, P165 Hertzman M, 2003, INT J PSYCHIAT MED, V33, P395, DOI 10.2190/JE5Q-1NFT-FL40-7PMW NR 3 TC 4 Z9 4 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD AUG PY 2007 VL 22 IS 8 BP 1054 EP 1054 DI 10.1177/0883073807305857 PG 1 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 206LF UT WOS:000249184200016 PM 17761662 ER PT J AU Turner, LM Stone, WL AF Turner, Lauren M. Stone, Wendy L. TI Variability in outcome for children with an ASD diagnosis at age 2 SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; early identification; diagnosis; diagnostic stability; longitudinal studies; infancy; pervasive developmental disorder. ID AUTISM SPECTRUM DISORDERS; JOINT ATTENTION; FOLLOW-UP; TIME; COMMUNICATION; DEFICITS AB Background: Few studies have examined the variability in outcomes of children diagnosed with autism spectrum disorder (ASD) at age 2. Research is needed to understand the children whose symptoms - or diagnoses - change over time. The objectives of this study were to examine the behavioral and diagnostic outcomes of a carefully defined sample of 2-year-old children with ASD, and to identify child and environmental factors that contribute to variability in outcomes at age 4. Methods: Forty-eight children diagnosed with autism or pervasive developmental disorder not otherwise specified (PDDNOS) at age 2 were followed to age 4. Diagnostic measures included the Autism Diagnostic Observation Schedule - Generic (ADOS-G) and clinical diagnosis at ages 2 and 4, and the ADI-R at age 4. Results: Diagnostic stability for an ASD diagnosis (autism or PDDNOS) was 63%, and for an autism diagnosis was 68%. Children who failed to meet diagnostic criteria for ASD at follow-up were more likely to: 1) be 30 months or younger at initial evaluation; 2) have milder symptoms of autism, particularly in the social domain; and 3) have higher cognitive scores at age 2. No differences between children with stable and unstable diagnoses were found for amount of intervention services received. Among the children with unstable diagnoses, all but one continued to have developmental disorders, most commonly in the area of language. Conclusions: The stability of ASD was lower in the present study than has been reported previously, a finding largely attributable to children who were diagnosed at 30 months or younger. Implications for clinical practice are discussed. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. Vanderbilt Univ, Kennedy Ctr, Nashville, TN 37420 USA. RP Turner, LM (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, CB 3367, Chapel Hill, NC 27599 USA. EM lauren_turner@med.unc.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Charman T, 2005, J CHILD PSYCHOL PSYC, V46, P500, DOI 10.1111/j.1469-7610.2004.00377.x Charman T, 2003, PHILOS T ROY SOC B, V358, P315, DOI 10.1098/rstb.2002.1199 Charvin G, 2002, SINGLE MOL, V3, P43, DOI 10.1002/1438-5171(200204)3:1<43::AID-SIMO43>3.3.CO;2-J Chawarska K, 2005, HDB AUTISM PERVASIVE, P223 CHAWARSKA K, J CHILD PSYCHOL PSYC Constantino JN, 2004, J CHILD PSYCHOL PSYC, V45, P719, DOI 10.1111/j.1469-7610.2004.00266.x Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 Eaves LC, 2004, J AUTISM DEV DISORD, V34, P367, DOI 10.1023/B:JADD.0000037414.33270.a8 Fein D, 2005, J AUTISM DEV DISORD, V35, P525, DOI 10.1007/s10803-005-5066-3 Hedrick D. L., 1984, SEQUENCED INVENTORY Huttenlocher Peter R., 1994, P137 Kelley E, 2006, J AUTISM DEV DISORD, V36, P807, DOI 10.1007/s10803-006-0111-4 Lord C., 2000, AUTISM SPECTRUM DISO, P11 Lord C, 2006, ARCH GEN PSYCHIAT, V63, P694, DOI 10.1001/archpsyc.63.6.694 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x Moore V, 2003, AUTISM, V7, P47, DOI 10.1177/1362361303007001018 Mullen E, 1995, MULLEN SCALES EARLY Mundy P, 1997, J AUTISM DEV DISORD, V27, P653, DOI 10.1023/A:1025802832021 Nelson C. A., 2000, HDB EARLY CHILDHOOD, P204 Schopler E., 1988, CHILDHOOD AUTISM RAT Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 Turner L, 2006, AUTISM, V10, P257, DOI DOI 10.1177/1362361306063296 Ventola PE, 2006, J AUTISM DEV DISORD, V36, P839, DOI 10.1007/s10803-006-0128-8 Volkmar F, 2005, ANNU REV PSYCHOL, V56, P315, DOI 10.1146/annurev.psych.56.091103.070159 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 Zimmerman I.L., 1992, PRESCHOOL LANGUAGE S NR 30 TC 74 Z9 75 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD AUG PY 2007 VL 48 IS 8 BP 793 EP 802 DI 10.1111/j.1469-7610.2007.01744.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 201PY UT WOS:000248846300007 PM 17683451 ER PT J AU Magiati, I Charman, T Howlin, P AF Magiati, Iliana Charman, Tony Howlin, Patricia TI A two-year prospective follow-up study of community-based early intensive behavioural intervention and specialist nursery provision for children with autism spectrum disorders SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism spectrum disorders (ASD); early intensive behavioural intervention (EIBI); autism-specific nursery provision; outcome ID PERVASIVE DEVELOPMENTAL DISORDER; YOUNG-CHILDREN; PREDICTORS; SCHOOL; BENEFITS; PROGRESS; AGE AB Background: This prospective study compared outcome for pre-school children with autism spectrum disorders (ASD) receiving autism-specific nursery provision or home-based Early Intensive Behavioural Interventions (EIBI) in a community setting. Methods: Forty-four 23- to 53-month-old children with ASD participated (28 in EIBI home-based programmes; 16 in autism-specific nurseries). Cognitive, language, play, adaptive behaviour skills and severity of autism were assessed at intake and 2 years later. Results: Both groups showed improvements in age equivalent scores but standard scores changed little over time. At follow-up, there were no significant group differences in cognitive ability, language, play or severity of autism. The only difference approaching significance (p =.06), in favour of the EIBI group, was for Vineland Daily Living Skills standard scores. However, there were large individual differences in progress, with intake IQ and language level best predicting overall progress. Conclusions: Home-based EIBI, as implemented in the community, and autism-specific nursery provision produced comparable outcomes after two years of intervention. C1 Kings Coll London, Dept Psychol, Inst Psychiat, London SE5 8AF, England. UCL Inst Child Hlth, London, England. RP Howlin, P (reprint author), Kings Coll London, Dept Psychol, Inst Psychiat, De Crespigny Pk, London SE5 8AF, England. EM Patricia.Howlin@iop.kcl.ac.uk; Iliana.Magiati@islingtonpct.nhs.uk RI Howlin, Patricia/A-7622-2011; Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR Bayley N, 1993, BAYLEY SCALES INFANT Bibby Peter, 2002, Research in Developmental Disabilities, V23, P81, DOI 10.1016/S0891-4222(02)00095-1 Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 BONDY A. S., 1994, PECS PICTURE EXCHANG Boyd RD, 2001, AUTISM, V5, P430, DOI 10.1177/1362361301005004007 Charman T, 2004, AUTISM, V8, P89, DOI 10.1177/1362361304040641 Cohen H, 2006, J DEV BEHAV PEDIATR, V27, P145, DOI DOI 10.1097/00004703-200604002-00013 Dunn L. M., 1997, BRIT PICTURE VOCABUL, V2nd Eikeseth S, 2002, BEHAV MODIF, V26, P49, DOI 10.1177/0145445502026001004 Gabriels RL, 2001, AUTISM, V5, P407, DOI 10.1177/1362361301005004006 GARDNER MF, 1990, EXPRESSIVE ONE WORD GROVE N, 1990, MAKATON VOCABULARY U Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 Howard JS, 2005, RES DEV DISABIL, V26, P359, DOI 10.1016/j.ridd.2004.09.005 Howlin P., 2002, OUTCOMES NEURODEVELO, P136, DOI 10.1017/CBO9780511543876.007 Jacobson J, 1998, BEHAV INTERVENT, V13, P201, DOI DOI 10.1002/(SICI)1099-078X Lewis V., 1997, TEST PRETEND PLAY Lord C, 2005, J AUTISM DEV DISORD, V35, P695, DOI 10.1007/s10803-005-0017-6 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LORD C, 1989, J CHILD PSYCHOL PSYC, V30, P575, DOI 10.1111/j.1469-7610.1989.tb00269.x LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 LOVAAS O. I., 2002, TEACHING INDIVIDUALS LOWE M, 1988, SUMBOLIC PLAY TEST 2 LUISELLI JK, 2000, AUTISM, V4, P427 Magiati I, 2001, AUTISM, V5, P399, DOI 10.1177/1362361301005004005 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 *NAS, 2001, APPR AUT EAS US GUID *NIASA, 2003, NAT AUT PLAN CHILD N *OFF NAT STAT, 2000, NAT STAT SOC EC CLAS Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 Panerai S, 2002, J INTELL DISABIL RES, V46, P318, DOI 10.1046/j.1365-2788.2002.00388.x Sallows GO, 2005, AM J MENT RETARD, V110, P417, DOI 10.1352/0895-8017(2005)110[417:IBTFCW]2.0.CO;2 Schopler E., 1997, HDB AUTISM PERVASIVE, P767 Shea V, 2004, AUTISM, V8, P349, DOI 10.1177/1362361304047223 Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 Smith T, 2000, AM J MENT RETARD, V105, P269, DOI 10.1352/0895-8017(2000)105<0269:RTOIEI>2.0.CO;2 Smith T, 1997, AM J MENT RETARD, V102, P238, DOI 10.1352/0895-8017(1997)102<0238:IBTFPW>2.0.CO;2 Smith T, 2000, RES DEV DISABIL, V21, P297, DOI 10.1016/S0891-4222(00)00043-3 Sparrow S, 1984, VINELAND ADAPTIVE BE Stutsman R., 1948, MERRILL PALMER SCALE Sundberg ML, 2001, BEHAV MODIF, V25, P698, DOI 10.1177/0145445501255003 Weiss MJ, 1999, BEHAV INTERVENT, V14, P3, DOI 10.1002/(SICI)1099-078X(199901/03)14:1<3::AID-BIN25>3.0.CO;2-F WESCHLER D, 1990, WESCHLER PRESCHOOL P Yoder P, 2004, MENT RETARD DEV D R, V10, P162, DOI 10.1002/mrdd.20013 NR 44 TC 77 Z9 78 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD AUG PY 2007 VL 48 IS 8 BP 803 EP 812 DI 10.1111/j.1469-7610.2007.01756.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 201PY UT WOS:000248846300008 PM 17683452 ER PT J AU Smith, EG Bennetto, L AF Smith, Elizabeth G. Bennetto, Loisa TI Audiovisual speech integration and lipreading in autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE speech reception threshold; speech in noise; audiovisual speech integration; autism ID PHONETIC INFORMATION; PERCEPTION; CHILDREN; NOISE; INFANTS; BRAIN; VOICE; LIPS; IDENTIFICATION; COMPREHENSION AB Background: During speech perception, the ability to integrate auditory and visual information causes speech to sound louder and be more intelligible, and leads to quicker processing. This integration is important in early language development, and also continues to affect speech comprehension throughout the lifespan. Previous research shows that individuals with autism have difficulty integrating information, especially across multiple sensory domains. Methods: In the present study, audiovisual speech integration was investigated in 18 adolescents with high-functioning autism and 19 well-matched adolescents with typical development using a speech in noise paradigm. Speech reception thresholds were calculated for auditory only and audiovisual matched speech, and lipreading ability was measured. Results: Compared to individuals with typical development, individuals with autism showed less benefit from the addition of visual information in audiovisual speech perception. We also found that individuals with autism were significantly worse than those in the comparison group at lipreading. Hierarchical regression demonstrated that group differences in the audiovisual condition, while influenced by auditory perception and especially by lipreading, were also attributable to a unique factor, which may reflect a specific deficit in audiovisual integration. Conclusions: Combined deficits in audiovisual speech integration and lipreading in individuals with autism are likely to contribute to ongoing difficulties in speech comprehension, and may also be related to delays in early language development. C1 Univ Rochester, Dept Clin & Social Sci Psychol, Rochester, NY 14627 USA. RP Bennetto, L (reprint author), Univ Rochester, Dept Clin & Social Sci Psychol, Box 270266, Rochester, NY 14627 USA. 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Child Psychol. Psychiatry PD AUG PY 2007 VL 48 IS 8 BP 813 EP 821 DI 10.1111/j.1469-7610.2007.01766.x PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 201PY UT WOS:000248846300009 PM 17683453 ER PT J AU Whitehouse, AJO Barry, JG Bishop, DVM AF Whitehouse, Andrew J. O. Barry, Johanna G. Bishop, Dorothy V. M. TI The broader language phenotype of autism: a comparison with specific language impairment SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism spectrum disorder; specific language impairment; broad phenotype; genetics ID SPECTRUM; CHILDREN; DISORDER; DEFICITS; TWIN; PREVALENCE; SIBLINGS AB Background: Some individuals with autism spectrum disorders (ASD) experience linguistic difficulties similar to those found in individuals with specific language impairment (SLI). Whether these behaviours are indicative of a common underlying genetic cause or a superficial similarity is unclear. Methods: Standardised language assessments were administered to three participant groups: parents of children with ASD (Par-A), parents of children with specific language/literacy impairment (Par-L) and parents of typically developing children (Par-T) (n = 30, in each group). Additionally, the Autism-Spcctrum Quotient (AQ) was used to assess autism-like tendencies, in particular, social language use. Results: The Par-A group performed better than the Par-L group (and identical to the Par-T group) on all language tests. Conversely, the Par-A group was characterised by higher levels of pragmatic difficulties than the other two groups, as measured by the communication subscale of the AQ. Conclusions: No evidence was found for a shared phenotype in parents of children with ASD and SLI. A model is presented describing the relation between SLI and ASD. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. 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Child Psychol. Psychiatry PD AUG PY 2007 VL 48 IS 8 BP 822 EP 830 DI 10.1111/j.1469-7610.2007.01765.x PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 201PY UT WOS:000248846300010 PM 17683454 ER PT J AU Correll, CU AF Correll, Christoph U. TI Clinical psychopharmacology of pediatric mood stabilizer and antipsychotic treatment, part 1: Challenges and developments SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Editorial Material ID CHILDHOOD-ONSET SCHIZOPHRENIA; DOUBLE-BLIND; BIPOLAR DISORDER; CONTROLLED-TRIALS; ADOLESCENT MANIA; CHILDREN; RISPERIDONE; DIVALPROEX; LITHIUM; AUTISM C1 Zucker Hillside Hosp, Glen Oaks, NY 11004 USA. Albert Einstein Coll Med, Bronx, NY 10467 USA. RP Correll, CU (reprint author), Zucker Hillside Hosp, Glen Oaks, NY 11004 USA. 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Clin. Psychiatry PD AUG PY 2007 VL 68 IS 8 BP 1301 EP 1302 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 207PB UT WOS:000249261900019 PM 17854257 ER PT J AU Anderson, DK Lord, C Risi, S Shulman, C Welch, K DiLavore, PS Thurm, A Pickles, A AF Anderson, Deborah K. Lord, Catherine Risi, Susan Shulman, Cory Welch, Kathleen DiLavore, Pamela S. Thurm, Audrey Pickles, Andrew TI Patterns of growth in verbal abilities among children with autism spectrum disorder SO JOURNAL OF CONSULTING AND CLINICAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT 4th International Meeting for Autism Research CY MAY 06-07, 2005 CL Boston, MA DE autism; PDD; growth trajectories; verbal age equivalent; verbal skills ID DIAGNOSTIC OBSERVATION SCHEDULE; PERVASIVE DEVELOPMENTAL DISORDER; RECEPTIVE LANGUAGE DISORDER; EARLY ADULT LIFE; JOINT ATTENTION; FOLLOW-UP; EARLY INTERVENTION; COMMUNICATION; AGE; PRESCHOOL AB Verbal skills were assessed at approximately ages 2, 3, 5, and 9 years for 206 children with a clinical diagnosis of autism (n = 98), pervasive developmental disorders-not otherwise specified (PDD-NOS; n = 58), or nonspectrum developmental disabilities (n = 50). Growth curve analyses were used to analyze verbal skills trajectories over time. Nonverbal IQ and joint attention emerged as strong positive predictors of verbal outcome. The gap between the autism and other. 2 groups widened with time as the latter improved at a higher rate. However, there was considerable variability within diagnostic groups. Children with autism most at risk for more serious language impairments later in life can be identified with considerable accuracy at a very young age, while improvement can range from minimal to dramatic. C1 Univ Michigan, Autism & Communicat Disorders Ctr, Ann Arbor, MI 48109 USA. Univ N Carolina, TEAACH Div, Chapel Hill, NC USA. Hebrew Univ Jerusalem, Sch Social Work & Social Welfare, Jerusalem, Israel. NIMH, Pediat & Dev Branch, Bethesda, MD 20892 USA. Univ Michigan, Ctr Stat Consultat & Res, Ann Arbor, MI 48109 USA. Univ Manchester, Sch Med, Oxford, England. RP Anderson, DK (reprint author), Univ Michigan, Autism & Communicat Disorders Ctr, 1111 E Catherine St, Ann Arbor, MI 48109 USA. 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Consult. Clin. Psychol. PD AUG PY 2007 VL 75 IS 4 BP 594 EP 604 DI 10.1037/0022-006X.75.4.594 PG 11 WC Psychology, Clinical SC Psychology GA 196ZR UT WOS:000248522700008 PM 17663613 ER PT J AU Bridgemohan, C AF Bridgemohan, Carolyn TI A parent's guide to Asperger syndrome & high-functioning autism: How to meet the challenges and help your child thrive SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review C1 Childrens Hosp, Boston, MA 02115 USA. RP Bridgemohan, C (reprint author), Childrens Hosp, 300 Longwood Ave, Boston, MA 02115 USA. CR Ozonoff S, 2002, PARENTS GUIDE ASPERG NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD AUG PY 2007 VL 28 IS 4 BP 301 EP 301 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 202RL UT WOS:000248920700006 ER PT J AU Rickards, AL Walstab, JE Wright-Rossi, RA Simpson, J Reddihough, DS AF Rickards, Anne L. Walstab, Janet E. Wright-Rossi, Roslyn A. Simpson, Jacquie Reddihough, Dinah S. TI A randomized, controlled trial of a home-based intervention program for children with autism and developmental delay SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE developmental disorders; autism spectrum disorder; home-based; early intervention; randomized control trial ID YOUNG-CHILDREN; BEHAVIORAL TREATMENT; PRESCHOOL-CHILDREN; EFFICACY RESEARCH; FAMILIES; INFANTS; COMMUNICATION; QUESTIONNAIRE; DISORDERS; PARENTS AB Objective: This study aimed to (1) investigate whether provision of a home-based program in addition to a center-based program improves development in young children with disabilities and coping abilities of their families and (2) describe the characteristics of children and families who benefit most from the intervention. Methods: Fifty-nine children, aged 3-5 years, with no cerebral palsy, participated in the study. Half of the group was randomized to receive an additional program in their homes. A special education teacher provided 40 visits over 12 months working with the families to help generalize skills to the home environment and assist with their concerns. All children were assessed before and after the intervention, and families completed questionnaires assessing family stress, support, and empowerment on both occasions. Differences in change over time and between the intervention and control group were analyzed by repeated measures and the association between characteristics of children and families with improved outcome by multivariate analysis of variance. Results: Change in cognitive development and behavior (in the centers) over time favored the children who received the extra intervention (p = .007 and p = .007, respectively). The groups did not differ on any of the family measures of change. Multivariate analysis of variance revealed more improvement for children in the intervention group from higher than lower stressed families. Conclusions: Results suggest the need for daily reinforcement of skills learned at the center-based program and the importance of involving families, especially those with few resources and relatively high stress. C1 Royal Childrens Hosp, Dept Child Dev & Rehabil, Parkville, Vic 3052, Australia. Royal Childrens Hosp, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia. Univ Melbourne, Dept Paediat, Parkville, Vic 3052, Australia. RP Rickards, AL (reprint author), Royal Childrens Hosp, Dept Child Dev & Rehabil, Flemington Rd, Parkville, Vic 3052, Australia. 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Dev. Behav. Pediatr. PD AUG PY 2007 VL 28 IS 4 BP 308 EP 316 DI 10.1097/DBP.0b013e318032792e PG 9 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 202RL UT WOS:000248920700008 PM 17700083 ER PT J AU Keen, D Brannigan, KL Cuskelly, M AF Keen, Deb Brannigan, Karen L. Cuskelly, Monica TI Toilet training for children with autism: The effects of video modeling SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; toilet training; video modeling ID PERVASIVE DEVELOPMENTAL DISORDER; RETARDED CHILDREN; SKILLS; SELF; AGE AB This study assessed the effectiveness of an animated toilet training video for teaching daytime urinary control to five young boys with autism across several settings. A between and across groups multiple baseline design was used following a 2-week baseline-monitoring period. Children in the treatment condition received video modeling plus operant conditioning strategies, whereas children in the control condition received only operant conditioning strategies. Frequency of in-toilet urinations was found to be greater for children who watched the toileting video than for children who did not. Gains were maintained for three participants at a 6-week follow-up with generalization to a new setting for two participants. Results indicate that, for young children with autism who are resistant to toilet training, acquisition of urinary control may be facilitated by use of an animated toileting video in conjunction with operant conditioning strategies. C1 Griffith Univ, Griffith Inst Educ Res, Sch Educ & Profess Studies, Brisbane, Qld 4111, Australia. Univ Queensland, Sch Educ, Brisbane, Qld 4072, Australia. RP Keen, D (reprint author), Griffith Univ, Griffith Inst Educ Res, Sch Educ & Profess Studies, Mt Gravatt Campus, Brisbane, Qld 4111, Australia. 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PD AUG PY 2007 VL 19 IS 4 BP 291 EP 303 DI 10.1007/s10882-007-9044-x PG 13 WC Rehabilitation SC Rehabilitation GA 200IH UT WOS:000248756600001 ER PT J AU Brasic, JR Holland, JA AF Brasic, James Robert Holland, Julie A. TI A qualitative and quantitative review of obstetric complications and autistic disorder SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article; Proceedings Paper CT 3rd Annual Psychiatry Research Day CY SEP 21, 2005 CL New York, NY DE case-control study; infant low birth weight; labor complications; pervasive child developmental disorders; pregnancy complications ID DIAGNOSTIC OBSERVATION SCHEDULE; MINOR PHYSICAL ANOMALIES; FETAL VALPROATE SYNDROME; PERVASIVE DEVELOPMENTAL DISORDER; PARENTAL PSYCHIATRIC HISTORY; INFANTILE-AUTISM; PERINATAL FACTORS; CHILDHOOD SCHIZOPHRENIA; REDUCED OPTIMALITY; ASPERGER-SYNDROME AB To investigate the possible association of obstetric complications and autistic disorder, we performed a review of case-control studies of any obstetric complication in autistic disorder. If the odds ratio = {(Number of cases with autistic disorder with any obstetric complication)/(Number of cases with autistic disorder without any obstetric complication)}/{(Number of controls without autistic disorder with any obstetric complication)/(Number of controls without autistic disorder without any obstetric complication)} <1, then there are more complications in controls; =1, then complications are equal in cases and controls; and >1, then there are more complications in cases. Most publications do not provide the raw data to calculate the odds ratio. Many calculated odds ratios support the hypothesis that cases with autism have more obstetric complications. Further investigation is warranted to clarify the relationships between obstetric complications and autism and related conditions in the general population worldwide. C1 Johns Hopkins Univ, Sch Med, Johns Hopkins Outpatient Ctr, Dept Radiol & Radiol Sci, Baltimore, MD 21287 USA. 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Dev. Phys. Disabil. PD AUG PY 2007 VL 19 IS 4 BP 337 EP 364 DI 10.1007/s10882-007-9054-8 PG 28 WC Rehabilitation SC Rehabilitation GA 200IH UT WOS:000248756600004 ER PT J AU Edlich, RF Son, DM Olson, BM Greene, JA Gubler, KD Winters, KL Kelley, AR Britt, LD Long, WB AF Edlich, Richard F. Son, Dana M. Olson, Brianna M. Greene, Jill Amanda Gubler, K. Dean Winters, Kathryne L. Kelley, Angela R. Britt, L. D. Long, William B. TI Update on the national vaccine injury compensation program SO JOURNAL OF EMERGENCY MEDICINE LA English DT Article DE vaccine injury compensation program; thimerosal ID AUTISM; THIMEROSAL; POPULATION; PREVALENCE; MERCURY AB The National Childhood Vaccine Injury Act of 1986, as amended, established the Vaccine Injury Compensation Program (VICP). The VICP went into effect on October 1, 1988 and is a Federal "no-fault" system designed to compensate individuals, or families of individuals, who have been injured by covered vaccines. From 1988 until July 2006, a total of 2531 non-autism/thimerosal and 5030 autism/thimerosal claims were made to the VICP. The compensation paid for the non-autism/thimerosal claims from 1988 until 2006 was $902,519,103.37 for 2542 awards. There was no compensation for any of the autism/thimerosal claims. On the basis of the deaths and extensive suffering to patients and families from the adverse reactions to vaccines, all physicians must provide detailed information in the Vaccine Information Statement to the patient or the parent or legal guardian of the child about the potential dangers of vaccines as well as the VICP. (C) 2007 Elsevier Inc. C1 Univ Virginia Hlth Syst, Charlottesville, VA USA. Legacy Emanuel Hosp LLP, Portland, OR USA. Eastern Virginia Med Sch, Dept Gen Surg, Norfolk, VA 23501 USA. Washington State Univ, Vancouver, WA USA. RP Edlich, RF (reprint author), 22500 NE 128th Circle, Brush Prairie, WA 98606 USA. 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Emerg. Med. PD AUG PY 2007 VL 33 IS 2 BP 199 EP 211 DI 10.1016/j.jemermed.2007.01.001 PG 13 WC Emergency Medicine SC Emergency Medicine GA 202HJ UT WOS:000248892300022 PM 17692778 ER PT J AU Pernon, E Pry, R Baghdadli, A AF Pernon, E. Pry, R. Baghdadli, A. TI Autism: tactile perception and emotion SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE addiction; attraction; autism; emotion; perception ID CHILDREN; RESPONSIVENESS AB Background For many years, and especially since Waynbaum and Wallon, psychology and psychopathology have dealt with cognitive perception, but have had little to do with the affective qualities of perception. Our aim was to study the influence of the sensory environment on people with autism. Method Several experiments were carried out using different forms of tactile stimulation (passive and active subjects). Results Our data showed specific responses in children with autism and intellectual disability. These children displayed a strong (positive) valence to the stimulation provided. Conclusion They were very attracted to the stimulation and were excited by it. C1 Ctr Hosp Univ, Ctr Ressources Autisme, F-34000 Montpellier, France. Univ Montpellier 3, F-34032 Montpellier, France. RP Pernon, E (reprint author), Ctr Hosp Univ, Ctr Ressources Autisme, 295 Ave Doyen Gaston Giraud, F-34000 Montpellier, France. EM e-pernonhu@montpellier.fr CR Ayres A. J., 1972, SENSORY INTEGRATION BARANEK GT, 1994, J AUTISM DEV DISORD, V24, P457, DOI 10.1007/BF02172128 Blakemore SJ, 2006, BRAIN COGNITION, V61, P5, DOI 10.1016/j.bandc.2005.12.013 BOISJOLY L, 2001, PRISME, V34, P92 Ekman P., 1978, FACIAL ACTION CODING FEYEREISEN P, 1987, PSYCHOL GESTE, P259 GRANDIN T, 1997, MA VIE DAUTISTE HATWELL Y, 1986, TOUCHER LESPACE LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Mottron L, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P131 MOTTRON L, 2001, B SCIENTIFIQUE LARAP, V8, P7 Nader R, 2004, CLIN J PAIN, V20, P88, DOI 10.1097/00002508-200403000-00005 ONeill M, 1997, J AUTISM DEV DISORD, V27, P283, DOI 10.1023/A:1025850431170 ORNITZ EM, 1968, ARCH GEN PSYCHIAT, V18, P76 PRY R, 2000, ENFANCE, V2, P149 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SOUSSIGNAN R, 1995, CHEM SENSES, V20, P47, DOI 10.1093/chemse/20.1.47 Sparrow S, 1984, VINELAND ADAPTIVE BE TURRO R, 1920, J PSYCHOL, V17, P769 WALLON H, 1984, LENFANT TURBULENT Waynbaum I., 1907, J PSYCHOL NORMALE PA, V4, P289 WHO, 1993, ICD 10 CLASS MENT BE Williams D., 1992, SI ME TOUCHE JE NEXI WILLIAMS D, 1996, QUELQU QUELQUE PART YIRMIYA N, 1989, J CHILD PSYCHOL PSYC, V30, P725, DOI 10.1111/j.1469-7610.1989.tb00785.x NR 26 TC 7 Z9 7 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD AUG PY 2007 VL 51 BP 580 EP 587 DI 10.1111/j.1365-2788.2006.00931.x PN 8 PG 8 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 183YG UT WOS:000247607700002 PM 17598871 ER PT J AU Schwichtenberg, A Poehlmann, J AF Schwichtenberg, A. Poehlmann, J. TI Applied behaviour analysis: does intervention intensity relate to family stressors and maternal well-being? SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE applied behaviour analysis; autism; depression; family; intensity ID PERVASIVE DEVELOPMENTAL DISORDERS; INTELLECTUAL DISABILITY; SYNDROME SPECIFICITY; PRESCHOOL-CHILDREN; AUTISM; SCALE; IMPACT; PREVALENCE; CHECKLIST AB Background Interventions based on applied behaviour analysis (ABA) are commonly recommended for children with an autism spectrum disorder (ASD); however, few studies address how this intervention model impacts families. The intense requirements that ABA programmes place on children and families are often cited as a critique of the programme, although little evidence is available to support this claim. Using Pearlin's (1999) stress process model, this study assessed: (I) whether mothers of children participating in a home-based ABA programme reported elevated depressive symptoms; and (2) whether ABA intensity related to unmet family needs and maternal feelings of depression, personal strain and mastery. Method Forty-one mothers of children diagnosed with an ASD participated in this study by completing questionnaires about their child's ASD behaviours, unmet family needs, and maternal feelings of depression, personal strain and mastery. Additionally, mothers provided information about their child's intervention programme and their own level of involvement in the programme. At the time of data collection, all families had been running a home-based ABA programme for at least 6 months. Results Single-sample t-tests and multiple regression analyses were used to test the proposed hypotheses. Mothers of children participating in a home-based ABA programme reported more depressive symptoms than mothers of children with other developmental disabilities. Comparisons revealed comparable depressive symptoms between the mothers of the present sample and those in other ASD samples. When considering weekly ABA intensity, mothers reported fewer depressive symptoms when their child was older and when their child participated in more ABA therapy hours. Conversely, mothers who were more involved in their child's ABA programme reported more personal strain. Conclusions The findings of this study supported the hypothesis that families participating in ABA experienced elevated depressive symptoms, much like any family raising a child with an ASD, suggesting a potential area for family-level intervention. Additionally, ABA intensity related to maternal depression and personal strain, and therefore deserves continued attention. Future studies should attempt to replicate these findings with a larger and more representative sample and seek to identify mechanisms through which ABA intensity may influence maternal and family well-being. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. RP Schwichtenberg, A (reprint author), Univ Wisconsin, Waisman Ctr, 1500 Highland Ave,Room 544, Madison, WI 53705 USA. EM ajschwichten@wisc.edu CR Abbeduto L, 2004, AM J MENT RETARD, V109, P237, DOI 10.1352/0895-8017(2004)109<237:PWACIM>2.0.CO;2 BAILEY DB, 1988, J SPEC EDUC, V22, P117 Bailey DB, 1999, MENT RETARD DEV D R, V5, P11, DOI 10.1002/(SICI)1098-2779(1999)5:1<11::AID-MRDD2>3.0.CO;2-U BAKER BL, 1991, AM J MENT RETARD, V96, P127 BILDT A, 2003, J AUTISM DEV DISORD, V33, P595 Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 Blacher J, 2006, J INTELL DISABIL RES, V50, P184, DOI 10.1111/j.1365-2788.2005.00768.x Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 CRAIG T, 1978, AM J PSYCHIAT, V137, P1036 Eaves RC, 2000, PSYCHOL SCHOOLS, V37, P311, DOI 10.1002/1520-6807(200007)37:4<323::AID-PITS2>3.0.CO;2-S Eisenhower AS, 2005, J INTELL DISABIL RES, V49, P657, DOI 10.1111/j.1365-2788.2005.00699.x Fombonne E, 2003, JAMA-J AM MED ASSOC, V289, P87, DOI 10.1001/jama.289.1.87 Guralnick M. J., 2000, FOCUS AUTISM OTHER D, V15, p[Early, 68], DOI DOI 10.1177/108835760001500202 Hastings RP, 2001, J AUTISM DEV DISORD, V31, P327, DOI 10.1023/A:1010799320795 JESSOP DJ, 1985, SOC SCI MED, V20, P993, DOI 10.1016/0277-9536(85)90255-2 Katz R, 1995, HDB DEPRESSION, P61 Koegel RL, 1996, J AUTISM DEV DISORD, V26, P347, DOI 10.1007/BF02172479 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x LOVAAS I, 1997, PREVENTION TREATMENT MAURICE C, 1996, BEHAV INTERVENTION Y Newsom C., 1998, TREATMENT CHILDHOOD, P416 Olsson MB, 2002, J INTELL DISABIL RES, V46, P548, DOI 10.1046/j.1365-2788.2002.00414.x Pearlin LI, 1999, HDB SOCIOLOGY MENTAL, P395, DOI 10.1007/0-387-36223-1_19 RADLOFF L S, 1977, Applied Psychological Measurement, V1, P385, DOI 10.1177/014662167700100306 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 Skorikov VB, 2003, EDUC PSYCHOL MEAS, V63, P319, DOI 10.1177/0013164402251035 STEIN REK, 1980, MED CARE, V18, P465, DOI 10.1097/00005650-198004000-00010 Stein REK, 2003, J DEV BEHAV PEDIATR, V24, P9 TURNBULL AP, 1982, MENT RETARD, V20, P115 NR 29 TC 11 Z9 13 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD AUG PY 2007 VL 51 BP 598 EP 605 DI 10.1111/j.1365-2788.2006.00940.x PN 8 PG 8 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 183YG UT WOS:000247607700004 PM 17598873 ER PT J AU Kwon, S Kim, J Choe, BH Ko, C Park, S AF Kwon, Soonhak Kim, Jungm Choe, Byung-Ho Ko, Cheolwoo Park, Sungpa TI Electrophysiologic assessment of central auditory processing by auditory brainstem responses in children with autism spectrum disorders SO JOURNAL OF KOREAN MEDICAL SCIENCE LA English DT Article DE autism spectrum disorder (ASD); central auditory processing; auditory Brainstem responses (ABR) ID EVOKED-RESPONSE; LANGUAGE; RISK; EEG AB In addition to aberrant features in the speech, children with Autism Spectrum Disorder (ASD) may present unusual responses to sensory stimuli, especially to auditory stimuli. We investigated the auditory ability of children with ASD by using Auditory Brainstem Responses (ABR) as they can directly judge both hearing status and the integrity of auditory brainstem pathways. One hundred twenty-one children (71: ASD; M 58/F 13, mean age; 41.8 months, 50: control group; M 41/F 9, mean age; 38 months) were included in the study. As compared with the values in the control group, the latency of wave V, wave IN, and wave III-V inter-peak latencies were significantly prolonged (p<0.05) in the ASD group. The findings indicate that children with ASD have a dysfunction or immaturity of the central auditory nervous system. We suggest any children with prolonged Ill-V inter-peak latencies, especially high functioning children should be further evaluated for central auditory processing to set up a more appropriate treatment plan. C1 Kyungpook Natl Univ Hosp, Dept Pediat, Taegu 700721, South Korea. Kyungpook Natl Univ, Sch Med, Dept Pediat, Taegu, South Korea. Kyungpook Natl Univ, Sch Med, Dept Neurol, Taegu, South Korea. RP Kwon, S (reprint author), Kyungpook Natl Univ Hosp, Dept Pediat, 50-2 Samdeok, Taegu 700721, South Korea. EM shkwon@knu.ac.kr CR Bauman ML, 2003, NOVART FDN SYMP, V251, P112 Cardy JEO, 2004, NEUROREPORT, V15, P1867 Charman T, 2004, J AUTISM DEV DISORD, V34, P59, DOI 10.1023/B:JADD.0000018075.77941.60 Chermak GD, 2002, OTOLARYNG CLIN N AM, V35, P733, DOI 10.1016/S0030-6665(02)00056-7 Courchesne E, 1997, CURR OPIN NEUROBIOL, V7, P269, DOI 10.1016/S0959-4388(97)80016-5 Coutinho MB, 2002, INT J PEDIATR OTORHI, V66, P81, DOI 10.1016/S0165-5876(02)00211-2 FERRE JM, 1986, EAR HEARING, V7, P336, DOI 10.1097/00003446-198610000-00009 Gopal KV, 1999, SCAND AUDIOL, V28, P77, DOI 10.1080/010503999424798 Gopal KV, 1999, SCAND AUDIOL, V28, P85, DOI 10.1080/010503999424806 Hashimoto Toshiaki, 2005, No To Hattatsu, V37, P124 HAYASHI M, 1989, Tokai Journal of Experimental and Clinical Medicine, V14, P339 Ho PT, 1999, LARYNGOSCOPE, V109, P129, DOI 10.1097/00005537-199901000-00025 Hughes JR, 2005, CLIN EEG NEUROSCI, V36, P15 JERGER S, 1987, EAR HEARING, V8, P78, DOI 10.1097/00003446-198704000-00004 Lewis V, 2003, AUTISM, V7, P391, DOI 10.1177/1362361303007004005 Martineau J, 2004, NEUROSCI LETT, V367, P298, DOI 10.1016/j.neulet.2004.06.018 Maziade M, 2000, ARCH GEN PSYCHIAT, V57, P1077, DOI 10.1001/archpsyc.57.11.1077 Palmen SJMC, 2004, BRAIN, V127, P2572, DOI 10.1093/brain/awh287 Rapin I, 2003, BRAIN DEV-JPN, V25, P166, DOI 10.1016/S0387-7604(02)00191-2 RAZ N, 1987, NEUROPSYCHOBIOLOGY, V18, P105, DOI 10.1159/000118401 Tillery KL, 2000, J SPEECH LANG HEAR R, V43, P893 Volden J, 2004, INT J LANG COMM DIS, V39, P171, DOI 10.1080/13682820410001663252 WONG V, 1991, J AUTISM DEV DISORD, V21, P329, DOI 10.1007/BF02207329 NR 23 TC 19 Z9 20 PU KOREAN ACAD MEDICAL SCIENCES PI SEOUL PA 302 75 DONG DU ICHON, DONG YONGSAN KU, SEOUL 140 031, SOUTH KOREA SN 1011-8934 J9 J KOREAN MED SCI JI J. Korean Med. Sci. PD AUG PY 2007 VL 22 IS 4 BP 656 EP 659 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 206IY UT WOS:000249178300012 PM 17728505 ER PT J AU Yurov, YB Vorsanova, SG Iourov, IY Demidova, IA Beresheva, AK Kravetz, VS Monakhov, VV Kolotii, AD Voinova-Ulas, VY Gorbachevskaya, NL AF Yurov, Y. B. Vorsanova, S. G. Iourov, I. Y. Demidova, I. A. Beresheva, A. K. Kravetz, V. S. Monakhov, V. V. Kolotii, A. D. Voinova-Ulas, V. Y. Gorbachevskaya, N. L. TI Unexplained autism is frequently associated with low-level mosaic aneuploidy SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID SOMATIC MOSAICISM; CHROMOSOMAL REARRANGEMENTS; SPECTRUM DISORDERS; INTERPHASE FISH; HUMAN BRAIN; IDENTIFICATION; CONSEQUENCES; INDIVIDUALS; MECHANISMS; CELLS AB Background: Autism is a common childhood neurodevelopmental disorder with a possible genetic background. About 5 10% of autism cases are associated with chromosomal abnormalities or monogenic disorders. However, the role of subtle genomic imbalances in autism has not been delineated. This study aimed to investigate a hypothesis suggesting autism to be associated with subtle genomic imbalances presenting as low-level chromosomal mosaicism. Methods: We surveyed stochastic ( background) aneuploidy in children with/without autism by interphase three-colour fluorescence in situ hybridisation. The rate of chromosome loss and gain involving six arbitrarily selected autosomes and the sex chromosomes was assessed in the peripheral blood cells of 60 unaffected children and 120 children with autism. Results: Of 120 analysed boys with autism, 4 ( 3.3%) with rare structural chromosomal abnormalities ( 46, XY, t( 1; 6)( q42.1; q27); 46, XY, inv( 2)( p11q13); 46, XY, der( 6), ins( 6; 1) ( q21; p13.3p22,1) pat; and 46, XY, r( 22)( p11q13)) were excluded from further molecular cytogenetic analysis. Studying,420 000 cells in 60 controls and 116 children with idiopathic autism, we determined the mean frequency of stochastic aneuploidy in control and autism: ( 1) autosome loss 0.58% ( 95% CI 0.42 to 0.75%) and 0.60% ( 95% CI 0.37 to 0.83%), respectively, p = 0.83; ( 2) autosome gain 0.15% ( 95% CI 0.09 to 0.21%) and 0.22% ( 95% CI 0.14 to 0.30%), respectively, p = 0.39; and ( 3) chromosome X gain 1.11% ( 95% CI 0.90 to 1.31%) and 1.01% ( 95% CI 0.85 to 1.17%), respectively, p = 0.30. A frequency of mosaic aneuploidy greater the background level was found in 19 ( 16%) of 116 children with idiopathic autism, whereas outlier values were not found in controls ( p = 0.0019). Conclusions: Our findings identify low-level aneuploidy as a new genetic risk factor for autism. Therefore, molecular cytogenetic analysis of somatic mosaicism is warranted in children with unexplained autism. C1 Russian Acad Med Sci, Lab Cytogenet, Natl Res Ctr Mental Hlth, Moscow 119152, Russia. Inst Pediat & Pediat Surg, Moscow, Russia. RP Yurov, YB (reprint author), Russian Acad Med Sci, Lab Cytogenet, Natl Res Ctr Mental Hlth, Moscow 119152, Russia. EM y_yurov@yahoo.com CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Balliff BC, 2006, AM J MED GENET A, V140A, P2757, DOI 10.1002/ajmg.a.31539 Battaglia A, 2006, AM J MED GENET C, V142C, P8, DOI 10.1002/ajmg.c.30077 Castermans D, 2004, AUTISM, V8, P141, DOI 10.1177/1362361304042719 de Vries BBA, 2003, J MED GENET, V40, P385, DOI 10.1136/jmg.40.6.385 Gottlieb B, 2001, TRENDS GENET, V17, P79, DOI 10.1016/S0168-9525(00)02178-8 Iourov IY, 2006, INT REV CYTOL, V249, P143, DOI 10.1016/S0074-7696(06)49003-3 Iourov IY, 2006, CURR GENOMICS, V7, P435, DOI 10.2174/138920206779116756 Iourov IY, 2006, CHROMOSOME RES, V14, P223, DOI 10.1007/s10577-006-1037-6 Jacquemont ML, 2006, J MED GENET, V43, P843, DOI 10.1136/jmg.2006.043166 Knight SJL, 1999, LANCET, V354, P1676, DOI 10.1016/S0140-6736(99)03070-6 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Muotri AR, 2006, NATURE, V441, P903 Volkmar FR, 2003, LANCET, V362, P1133, DOI 10.1016/S0140-6736(03)14471-6 Vorsanova SG, 2005, J HISTOCHEM CYTOCHEM, V53, P375, DOI 10.1369/jhc.4A6424.2005 Vorstman JAS, 2006, MOL PSYCHIATR, V11, P18, DOI 10.1038/sj.mp.4001757 Wassink AMJ, 2007, EUR J CLIN INVEST, V37, P8, DOI 10.1111/j.1365-2362.2007.01755.x Xu Jie, 2004, Current Genomics, V5, P347, DOI 10.2174/1389202043349246 Youssoufian H, 2002, NAT REV GENET, V3, P748, DOI 10.1038/nrg906 Yurov YB, 2005, J HISTOCHEM CYTOCHEM, V53, P385, DOI 10.1369/jhc.4A6430.2005 YUROV YB, 2002, EARLY PRENATAL DIAGN Yurov YB, 1996, HUM GENET, V97, P390 NR 22 TC 45 Z9 48 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0022-2593 J9 J MED GENET JI J. Med. Genet. PD AUG PY 2007 VL 44 IS 8 BP 521 EP 525 DI 10.1136/jmg.2007.049312 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 196NJ UT WOS:000248489000007 PM 17483303 ER PT J AU Peppe, S McCann, J Gibbon, F O'Hare, A Rutherford, M AF Peppe, Susan McCann, Joanne Gibbon, Fiona O'Hare, Anne Rutherford, Marion TI Receptive and expressive prosodic ability in children with high-functioning autism SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE high-functioning autism; prosody; intonation; language; assessment ID SPECTRUM DISORDERS; ASPERGER-SYNDROME; INTONATION; PERCEPTION; ADULTS; IMPAIRMENTS; DURATION; STRESS; SPEECH; MIND AB Purpose: This study aimed to identify the nature and extent of receptive and expressive prosodic deficits in children with high-functioning autism (HFA).,, Method: Thirty-one children with HFA, 72 typically developing controls matched on verbal mental age, and 33 adults with normal speech completed the prosody assessment procedure, Profiling Elements of Prosodic Systems in Children. Results: Children with HFA performed significantly less well than controls on 11 of 12 prosody tasks (p < .005). Receptive prosodic skills showed a strong correlation (p < .01)with verbal mental age in both groups, and to a lesser extent with expressive prosodic skills. Receptive prosodic scores also correlated with expressive prosody scores, particularly in grammatical prosodic functions. Prosodic development in the HFA group appeared to be delayed in many aspects of prosody and deviant in some. Adults showed near-ceiling scores in all tasks. Conclusions: The study demonstrates that receptive and expressive prosodic skills are closely associated in HFA. Receptive prosodic skills would be an appropriate focus for clinical intervention, and further investigation of prosody and the relationship between prosody and social skills is warranted. C1 Queen Margaret Univ, Edinburgh EH12 8TS, Midlothian, Scotland. Royal Hosp Sick Children, Edinburgh EH9 1LF, Midlothian, Scotland. Univ Edinburgh, Edinburgh, Midlothian, Scotland. RP Peppe, S (reprint author), Queen Margaret Univ, Edinburgh EH12 8TS, Midlothian, Scotland. EM speppe@qmu.ac.uk RI Gibbon, Fiona/J-8255-2013 CR American Psychiatric Association, 1994, DIAGN STAT MAN MET D Baltaxe C. A. M., 1985, COMMUNICATION PROBLE, P95, DOI 10.1007/978-1-4757-4806-2_7 BALTAXE CAM, 1987, J AUTISM DEV DISORD, V17, P255, DOI 10.1007/BF01495060 Banse R, 1996, J PERS SOC PSYCHOL, V70, P614, DOI 10.1037/0022-3514.70.3.614 Baron-Cohen S., 2004, MIND READING INTERAC Butcher Andrew, 1981, ASPECTS SPEECH PAUSE Cruttenden Alan, 1997, INTONATION, V2nd Crystal D., 1969, PROSODIC SYSTEMS INT Cutler A., 1983, PROSODY MODELS MEASU, P79 CUTLER A, 1987, J CHILD LANG, V14, P145 DILALLA DL, 1994, J AUTISM DEV DISORD, V24, P115, DOI 10.1007/BF02172092 Dunn L. M., 1997, BRIT PICTURE VOCABUL, V2nd Fay W. H., 1980, EMERGING LANGUAGE AU FINE J, 1991, J CHILD PSYCHOL PSYC, V32, P771, DOI 10.1111/j.1469-7610.1991.tb01901.x Fosnot S. 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L., 1998, SPEECH VARIABILITY E Paul R, 2005, J AUTISM DEV DISORD, V35, P205, DOI 10.1007/s10803-005-1999-9 Peppe S, 2003, CLIN LINGUIST PHONET, V17, P345, DOI 10.1080/0269920031000079994 Roachs P., 2000, ENGLISH PHONETICS PH Rutherford MD, 2002, J AUTISM DEV DISORD, V32, P189, DOI 10.1023/A:1015497629971 SCOTT DR, 1982, J ACOUST SOC AM, V71, P996, DOI 10.1121/1.387581 Shriberg LD, 2001, J SPEECH LANG HEAR R, V44, P1097, DOI 10.1044/1092-4388(2001/087) Stackhouse J., 1997, CHILDRENS SPEECH LIT Staunton R., 1994, 1 LANGUAGE, V14, P241, DOI 10.1177/014272379401404216 Tarplee C., 1996, PROSODY CONVERSATION, P406, DOI 10.1017/CBO9780511597862.012 THURBER C, 1993, J AUTISM DEV DISORD, V23, P309, DOI 10.1007/BF01046222 Wells B, 2004, J CHILD LANG, V31, P749, DOI 10.1017/S030500090400652X Wells B, 2003, J SPEECH LANG HEAR R, V46, P5, DOI 10.1044/1092-4388(2003/001) WHO, 1993, ICD 10 CLASS MENT BE Williams JHG, 2001, NEUROSCI BIOBEHAV R, V25, P287, DOI 10.1016/S0149-7634(01)00014-8 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 40 TC 77 Z9 77 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 1092-4388 J9 J SPEECH LANG HEAR R JI J. Speech Lang. Hear. Res. PD AUG PY 2007 VL 50 IS 4 BP 1015 EP 1028 DI 10.1044/1092-4388(2007/071) PG 14 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 200AQ UT WOS:000248736700016 PM 17675602 ER PT J AU Nadel, S Poss, JE AF Nadel, Stephen Poss, Jane E. TI Early detection of autism spectrum disorders: Screening between 12 and 24 months of age SO JOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS LA English DT Article DE autism; autism spectrum disorder; early intervention ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; MODIFIED CHECKLIST; DIAGNOSIS; PHENOTYPE; LIFE; TODDLERS; FAMILIES; CHAT; HOME AB Purpose: The purpose of this article is to present nurse practitioners (NPs) with information on screening for autism spectrum disorders (ASDs) in children between 12 and 24 months of age. Recommendations are also provided for appropriate referrals and initiation of early intervention (EI). Data sources: Review of published literature about ASD. Conclusions: Children with ASD exhibit impaired social interaction, verbal and nonverbal communication deficits, and repetitive, restricted, and stereotyped patterns of behavior or interests. Studies show that these children benefit from beginning intensive El as soon as possible. Implications for practice: Early detection enables children with suspected ASD to be evaluated by specialists and entered into treatment programs at the earliest possible opportunity. Because of the importance of early diagnosis of ASD, it is critical that NPs use established screening instruments to maximize time and increase the reliability of the assessment. C1 Univ Texas, Sch Nursing, El Paso, TX 79912 USA. Boston Univ, Sch Educ, Boston, MA 02215 USA. RP Poss, JE (reprint author), Univ Texas, Sch Nursing, 1101 N Campbell St, El Paso, TX 79912 USA. EM jeposs@utep.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Belmonte MK, 2004, MOL PSYCHIATR, V9, P646, DOI 10.1038/sj.mp.4001499 BOCK KA, 2005, S COND DAN 2005 SPRI, P75 Boyd B. A., 2002, FOCUS AUTISM OTHER D, V17, P208, DOI DOI 10.1177/10883576020170040301 *CDCP, 2006, AUT INF CTR Centers for Disease Control and Prevention, 2007, MMWR-MORBID MORTAL W, V56, P1 Coin R. 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PD AUG PY 2007 VL 19 IS 8 BP 408 EP 417 DI 10.1111/j.1745-7599.2007.00244.x PG 10 WC Health Care Sciences & Services; Nursing SC Health Care Sciences & Services; Nursing GA 197XR UT WOS:000248591000004 PM 17655570 ER PT J AU Safford, E AF Safford, Elizabeth TI Self-help skills for people with autism: A systematic teaching approach SO LIBRARY JOURNAL LA English DT Book Review C1 Nevins Memorial Lib, Methuen, MA 01844 USA. RP Safford, E (reprint author), Nevins Memorial Lib, Methuen, MA 01844 USA. CR ANDERSON SR, 2007, SELFHELP SKILLS PEO NR 1 TC 0 Z9 0 PU REED BUSINESS INFORMATION PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD AUG PY 2007 VL 132 IS 13 BP 111 EP 111 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 200XZ UT WOS:000248797400305 ER PT J AU Teuscher, C Triesch, J AF Teuscher, Christof Triesch, Jochen TI To each his own: The caregiver's role in a computational model of gaze following SO NEUROCOMPUTING LA English DT Article; Proceedings Paper CT 3rd International Conference on Development and Learning (ICDL 2004) CY OCT 20-22, 2004 CL La Jolla, CA DE gaze following; shared attention; temporal difference learning; reinforcement learning; computational model ID JOINT ATTENTION; AUTISM; LANGUAGE; INFANT; CHILDREN; ROBOT AB We investigate a computational model of the emergence of gaze following that is based on a generic basic set of mechanisms. Whereas much attention has been focused so far on the study of the infant's behavior, we systematically analyze the caregiver and show that he plays a crucial role in the development of gaze following in our model, especially for infant models with simulated developmental disorders such as autism and Williams syndrome. We first create two reference infant parameter sets and test their behavior with a simple standard caregiver. Based on these findings we then propose new caregiver models and evaluate them oil normally developing infants and on infants with simulated developmental disorders. Further, we investigate if and how a pair of infants (with and without simulated developmental disorders) might learn gaze following from scratch, without a mature caregiver. The findings of this paper suggest the pivotal role the caregiver plays for the infant in developing gaze following, that his predictability is the most important criterion, and that different infant models require particular caregivers for gaze following to emerge optimally. Our simulations are consistent with Leekam's finding, that autistics can learn to follow gaze through a contingent presentation of rewarding visual stimuli, but that a lack of motivation may impede learning. (C) 2007 Elsevier B.V. All rights reserved. C1 Los Alamos Natl Lab, Adv Comp Lab, Los Alamos, NM 87545 USA. Univ Frankfurt, Frankfurt Inst Adv Studies, D-60438 Frankfurt, Germany. Univ Calif San Diego, Dept Cognit Sci, La Jolla, CA 92093 USA. RP Teuscher, C (reprint author), Los Alamos Natl Lab, Adv Comp Lab, CCS-1,MS-B287, Los Alamos, NM 87545 USA. 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TI EEG evidence for mirror neuron activity during the observation of human and robot actions: Toward an analysis of the human qualities of interactive robots SO NEUROCOMPUTING LA English DT Article; Proceedings Paper CT 3rd International Conference on Development and Learning (ICDL 2004) CY OCT 20-22, 2004 CL La Jolla, CA DE mirror neuron; humanoid; anthropomorphic; robot; volition; action observation; social interaction ID AUTISM SPECTRUM DISORDERS; BIOLOGICAL MOTION; MU-RHYTHMS; MOTOR FACILITATION; PREMOTOR CORTEX; PERCEPTION; RECOGNITION; MECHANISMS; IMITATION; ACTIVATION AB The current study investigated the properties of stimuli that lead to the activation of the human mirror neuron system, with an emphasis on those that are critically relevant for the perception of humanoid robots. Results suggest that robot actions, even those without objects, may activate the human mirror neuron system. Additionally, both volitional and nonvolitional human actions also appear to activate the mirror neuron system to relatively the same degree. Results front the current studies leave open the opportunity to use mirror neuron activation as a 'Turing test' for the development of truly humanoid robots. (C) 2007 Elsevier B.V. All rights reserved. C1 Univ Calif San Diego, Dept Psychol, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Cognit Sci, La Jolla, CA 92093 USA. Univ Calif San Diego, Ctr Brain & Cognit, La Jolla, CA 92093 USA. RP Oberman, LM (reprint author), Univ Calif San Diego, Dept Psychol, La Jolla, CA 92093 USA. 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TI Sex differences in the relationship between cortisol levels and the Empathy and Systemizing Quotients in humans SO NEUROENDOCRINOLOGY LETTERS LA English DT Article DE extreme male brain theory; empathy; systemizing; cortisol; autism; stress ID HIGH-FUNCTIONING AUTISM; SALIVARY CORTISOL; ASPERGER-SYNDROME; ACTH LEVELS; ADULTS; ELEVATION; STRESS; TESTOSTERONE; NEURONS; MEMORY AB OBJECTIVE: Little is known regarding the relationship between cortisol (a stress hormone) levels and psychological cognitive styles. Baron-Cohen proposed two fundamental cognitive styles, which are measured by the Empathy Quotient (EQ) and the Systemizng Quotient (SQ). Previous studies have examined the influences of prenatal testosterone exposure on EQ and SQ scores. This study aimed to examine the relationships between morning cortisol levels and EQ and SQ scores, and the 'brain types' which were determined by two quotients in both sexes. These relationships are potentially important in the developmental psychopathology of autism and neuroeconomics of empathy. METHODS: We assessed morning cortisol levels with LC/MS (liquid chromatography-mass spectrometry) and ESQ in healthy male and female university students. CONCLUSIONS: Results indicate clear sex differences between brain types: i.e. Etype males and S-type females (participants with atypical cognitive styles) have significantly higher cortisol levels than S-type males and E-type females (participants ftl with typical cognitive styles). Implications for the role of sex in social adaptation of autistic patients are discussed. C1 Univ Tokyo, Grad Sch Arts & Sci, Dept Cognit & Behav Sci, Meguro Ku, Tokyo 1538902, Japan. Tamagawa Univ, Grad Sch Engn, Brain Sci Inst, Tokyo, Japan. Chiba Univ, Fac Letters, Dept Psychol, Chiba, Japan. Tohoku Univ, Sch Med, Dept Biol Psychiat, Sendai, Miyagi 980, Japan. RP Takahashi, T (reprint author), Univ Tokyo, Grad Sch Arts & Sci, Dept Cognit & Behav Sci, Meguro Ku, 3-8-1,Komaba, Tokyo 1538902, Japan. 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Lett. PD AUG PY 2007 VL 28 IS 4 BP 445 EP 448 PG 4 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 222JI UT WOS:000250291900018 PM 17693971 ER PT J AU Croonenberghs, J Wauters, A Deboutte, D Verkerk, R Scharpe, S Maes, M AF Croonenberghs, Jan Wauters, Annick Deboutte, Dirk Verkerk, Robert Scharpe, Simon Maes, Michael TI Centrat serotonergic hypofunction in autism: results of the 5-hydroxy-tryptophan challenge test SO NEUROENDOCRINOLOGY LETTERS LA English DT Article DE autism; serotonin; cortisol; prolactin; L-5-hydroxy-tryptophan ID PITUITARY-ADRENAL AXIS; 5-HYDROXYINDOLEACETIC ACID; PROLACTIN RESPONSES; HOMOVANILLIC-ACID; DISORDER; CHILDREN; FENFLURAMINE; CORTISOL; ADULTS; PRETREATMENT AB Some studies have suggested that disorders in the central serotonergic function may play a role in the pathophysiology of autistic disorder. In order to assess the central l actin serotonergic turnover in autism, this study examines the cortisol and pro responses to administration of L-5-hydroxy-tryptophan (5-HTP), the direct precursor of 5-HT in 18 male, post-pubertal, Caucasian autistic patients (age 13-19 y.; I.Q.> 55) and 22 matched healthy volunteers. Serum cortisol and prolactin were determined 45 and 30 minutes before administration of 5-HTP (4mg/kg in non enteric-coated tablets) or an identical placebo in a single blind order and, thereafter, every 30 minutes over a 3-hour period. The 5-HTP-induced increases in serum cortisol were significantly lower in autistic patients than in controls, whereas there were no significant differences in 5-HTP-induced prolactin responses between both study groups. In baseline conditions, no significant differences were found in serum cortisol and prolactin between autistic and normal children. 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PD AUG PY 2007 VL 28 IS 4 BP 449 EP 455 PG 7 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 222JI UT WOS:000250291900019 PM 17693983 ER PT J AU Bonati, MT Russo, S Finelli, P Valsecchi, MR Cogliati, F Cavalleri, F Roberts, W Elia, M Larizza, L AF Bonati, Maria Teresa Russo, Silvia Finelli, Palma Valsecchi, Maria Rosa Cogliati, Francesca Cavalleri, Florinda Roberts, Wendy Elia, Maurizio Larizza, Lidia TI Evaluation of autism traits in Angelman syndrome: a resource to unfold autism genes SO NEUROGENETICS LA English DT Article DE Angelman syndrome and autism; AS genetic subtypes; chromosome 15; ADOS and ADI-R ID INTERSTITIAL DUPLICATIONS; LINKAGE-DISEQUILIBRIUM; UNIPARENTAL DISOMY; MECP2 DEFICIENCY; PRADER-WILLI; DISORDER; UBE3A; PHENOTYPE; EXPRESSION; 15Q11-Q13 AB Linkage and cytogenetics studies have found the Angelman syndrome (AS) chromosomal region to be of relevance to autism disorder (AD) or autism spectrum disorder (ASD). Autism is considered part of the behavioural phenotype in AS based on formal autism assessments (autism diagnostic interview-revised [ADI-R] and autism diagnostic observation schedule [ADOS]), which have mainly addressed the deleted AS group. We explored 23 AS patients including all genetic subtypes and made a co-morbid diagnosis of AD/ASD in 14/23 (61%), which does not include 4 cases classified within the broader autism spectrum disorder (bASD). Deletions accounted for the main fraction (35%), ubiquitin-protein ligase E3A (UBE3A) mutation represented 13%, imprinting defects and uniparental disomy 9 and 4%, respectively. UBE3A mutations due to lack of the homologous to the E6-associated protein carboxyl terminus domain (n=3) were associated with the ASD, while more distal mutations (n=3) seem to escape from a co-morbid diagnosis of autism/autism spectrum. Differences in severity of autistic features were seen across subtypes of AS, with some behavioural features being unique to AS and some representing all forms of developmental disability. Autism signs (poor/lack of eye contact, showing, spontaneous initiation of joint attention, social quality of overtures [ADOS algorithm items for Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV)/International Statistical Classification of Diseases and Related Health Problems-10 (ICD-10) autism diagnosis belonging to the reciprocal social interaction domain]) discriminating all the co-morbid AS categories from non-autistic AS belonged to the social interaction domain. Impairments in the communication domain (gestures, pointing, use of another's body, frequency of vocalisation towards others [ADOS algorithm items for DSM-IV/ICD-10 autism diagnosis belonging to the communication domain]) justified classification of co-morbid AD/ASD vs the classification of less affected bASD. 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Ekstein, Perla M. Hendler, Talma Tarrasch, Ricardo Even, Ariela Levy, Yonata Sira, Liat Ben TI Accelerated maturation of white matter in young children with autism: A high b value DWI study SO NEUROIMAGE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DIFFUSION-TENSOR; HUMAN BRAIN; MINICOLUMNAR PATHOLOGY; LANGUAGE DISORDER; MRI; AGE; SPECTRUM; INFANCY; VOLUME AB The goal of this work was to study white matter maturation in young children with autism following previous reports of increased cerebral volume during early development, as well as arguments for abnormal neural growth patterns and regulation at this critical developmental period. We applied diffusion tensor imaging (DTI) and high b value diffusion-weighted imaging (DWI) to young children diagnosed with autism and to a typically developing (TD) control group. Fractional anisotropy (FA), probability and displacement were measured in overall analysis as well as in regions of interest (ROI). Individual data points of children with autism were compared to the developmental curves obtained from typically developing children. Increased restriction, reflected in significantly increased FA and probability along with reduced displacement values, was detected in overall analysis as well as in several brain regions. Increased restriction, suggesting an early and accelerated abnormal maturation of white matter, was more dominant in the left hemisphere and was mainly detected in the frontal lobe. No changes were detected in the occipital lobes. These results support previous claims of abnormal brain overgrowth in young children with autism and are in contrast to the decreased restricted diffusion reported in previous studies in adolescent with autism. (c) 2007 Elsevier Inc. All rights reserved. C1 Tel Aviv Sourasky Med Ctr, Wohl Inst Adv Imaging, Funct Brain Mapping Unit, IL-64239 Tel Aviv, Israel. Tel Aviv Univ, Lester & Sally Etin Fac Humanities, IL-69978 Tel Aviv, Israel. Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel. Tel Aviv Sourasky Med C4tr, Dept Anesthesia & Crit Care, Tel Aviv, Israel. Tel Aviv Univ, Dept Psychol, IL-69978 Tel Aviv, Israel. Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. Hebrew Univ Jerusalem, Hadassah Med Sch, IL-91010 Jerusalem, Israel. RP Bashat, DB (reprint author), Tel Aviv Sourasky Med Ctr, Wohl Inst Adv Imaging, Funct Brain Mapping Unit, 6 Weizamnn St, IL-64239 Tel Aviv, Israel. 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Annu. PD AUG PY 2007 VL 36 IS 8 BP 497 EP + PG 7 WC Pediatrics SC Pediatrics GA 198MX UT WOS:000248633300011 PM 17849608 ER PT J AU McGrew, S Malow, BA Henderson, L Wang, L Song, Y Stone, WL AF McGrew, Susan Malow, Beth A. Henderson, Lynnette Wang, Lily Song, Yanna Stone, Wendy L. TI Developmental and Behavioral questionnaire for autism spectrum disorders SO PEDIATRIC NEUROLOGY LA English DT Article ID PARENTS CONCERNS; CLINICAL-TRIALS; CHILDREN; PATTERNS; PSYCHOPHARMACOLOGY AB The validity of the Parental Concerns Questionnaire, a brief screening checklist assessing the presence and severity of 13 developmental and behavioral concerns expressed by parents of children with autism spectrum disorders, was determined in 53 children ages 4 to 10 years with a clinical diagnosis of autism spectrum disorder and 48 age-matched typically developing controls. Parents completed the Parental Concerns Questionnaire, the Child Behavior Checklist, the Child Sleep Habits Questionnaire, and either the Repetitive Behavior Scale or the Compulsive Behavior Checklist. A clinical examiner administered the Peabody Picture Vocabulary Test and the Autism Diagnostic Observation Scale. The Parental Concerns Questionnaire demonstrated high internal consistency in the autism spectrum disorder subgroup. Reliability and stability over time were demonstrated. Analyses showed variability in item responses for each child indicating that parents were not globally answering all items as concerns. Comparison of Parental Concerns Questionnaire item scores to scores for similar multiquestion domains on standardized parent-rated and clinician-administered assessment tools demonstrated external validity with other parent-rated and clinician-rated instruments. The Parental Concerns Questionnaire is a reliable screening instrument to assess parentally reported developmental and behavioral symptoms in children with autism spectrum disorders. (c) 2007 by Elsevier Inc. All rights reserved. C1 Vanderbilt Univ, Med Ctr, Ctr Child Dev, Sch Med, Dept Pediat, Nashville, TN 37203 USA. Vanderbilt Univ, Sch Med, Kennedy Ctr, Nashville, TN 37212 USA. Vanderbilt Univ, Sch Med, Dept Neurol, Nashville, TN 37212 USA. Vanderbilt Univ, Sch Med, Dept Biostat, Nashville, TN 37212 USA. RP McGrew, S (reprint author), Vanderbilt Univ, Med Ctr, Ctr Child Dev, Sch Med, Dept Pediat, 3401 W End Ave,Suite 460 W, Nashville, TN 37203 USA. 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PD AUG PY 2007 VL 49 IS 4 BP 513 EP 515 DI 10.1111/j.1442-200X.2007.02411.x PG 3 WC Pediatrics SC Pediatrics GA 181LX UT WOS:000247439300018 PM 17587278 ER PT J AU Focquaert, F Steven, MS Wolford, GL Colden, A Gazzaniga, MS AF Focquaert, Farah Steven, Megan S. Wolford, George L. Colden, Albina Gazzaniga, Michael S. TI Empathizing and systemizing cognitive traits in the sciences and humanities SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE empathizing; systemizing; cognition; gender differences; autism spectrum disorders; sciences; humanities ID SEX-DIFFERENCES; FUNCTIONING AUTISM; ASPERGER-SYNDROME; BRAIN; ADOLESCENTS; ABILITIES; QUOTIENT; ADULTS AB For several decades, cognitive research on personality and individual differences has focused on psychological traits other than general intelligence. Here we present data on empathizing and systemizing cognitive traits in science and humanities students. In view of existing data on autistic traits in scientists, we hypothesized that the science students would show higher systemizing than empathizing and that the humanities students would show the opposite pattern. Our findings suggest that individuals in the sciences possess a cognitive style that is more systemizing-driven than empathizing-driven, whereas individuals in humanities possess a cognitive style that is much more empathizing-driven than systemizing-driven. Both type of major and gender independently and highly significantly contribute to this effect. Within the sciences, the systemizing pattern is especially pronounced in engineering and physics. Men and women have been found previously to differ in their systemizing-empathizing cognitive style, with men being stronger in systemizing and women being stronger in empathizing. We find the same gender differences within each type of major. (c) 2007 Elsevier Ltd. All rights reserved. C1 Univ Ghent, Dept Philosophy & Moral Sci, B-9000 Ghent, Belgium. Dartmouth Coll, Ctr Cognit Neurosci, Hanover, NH 03755 USA. Dartmouth Coll, Psychiat & Brain Sci Dept, Hanover, NH 03755 USA. Univ Calif Santa Barbara, Sage Ctr Study Mind, Santa Barbara, CA 93106 USA. RP Focquaert, F (reprint author), Univ Ghent, Dept Philosophy & Moral Sci, Blandijnberg 2, B-9000 Ghent, Belgium. 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Individ. Differ. PD AUG PY 2007 VL 43 IS 3 BP 619 EP 625 DI 10.1016/j.paid.2007.01.004 PG 7 WC Psychology, Social SC Psychology GA 186VJ UT WOS:000247806200018 ER PT J AU Suwan, J Phunyamanee, C Kham-duang, N Kanjanarat, P AF Suwan, Jutamas Phunyamanee, Chondan Kham-duang, Nujaree Kanjanarat, Penkarn TI Costs of childhood autism in Thailand SO PHARMACOEPIDEMIOLOGY AND DRUG SAFETY LA English DT Meeting Abstract C1 Chiang Mai Univ, Fac Pharm, Chiang Mai 50000, Thailand. Minist Publ Hlth, Dept Mental Hlth, Rahanagarindra Inst Child Dev, Chiang Mai, Thailand. NR 0 TC 0 Z9 0 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 1053-8569 J9 PHARMACOEPIDEM DR S JI Pharmacoepidemiol. Drug Saf. PD AUG PY 2007 VL 16 SU 2 BP S246 EP S246 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 201GT UT WOS:000248820200516 ER PT J AU Alos, FJ Lora, MD AF Alos, Francisco J. del Mar Lora, M. TI Contextual control in teaching numbers to a child with intellectual disability SO PSICOTHEMA LA Spanish DT Article ID ARBITRARILY APPLICABLE RELATIONS; EMERGENT STIMULUS RELATIONS; CONDITIONAL DISCRIMINATIONS; EQUIVALENCE-RELATIONS; TRANSFORMATION; ACCORDANCE; AUTISM AB Contextual control in teaching numbers to a child with intellectual disability The aim of this work was to teach the discrimination of "equal" and "different" in numbers. The experiment was carried out a seven-year-old child with intellectual disability. The problem was analysed from the contextual control perspective. The learning procedure consisted of explicitly teaching a second-order conditional discrimination, and transfer to a novel second-order conditional discrimination was tested. In this study, the boy learned that, in presence of X1 (equal), he had to select the comparison B1 (the number one), given the sample A1 (the word one) and B2 (the number two), given A2 (the word two). He also he learned that, in the presence of X2 (different), he had to select the comparison B2 (the number two), given the sample A1 (the word one) and B1 (the number one), given A2 (the word two). We subsequently presented the contextual stimuli with two new numbers: three and four. The results showed the occurrence of learning transfer without explicit training in the new numbers. C1 Univ Cordoba, Fac Ciencias Educ, E-14071 Cordoba, Spain. RP Alos, FJ (reprint author), Univ Cordoba, Fac Ciencias Educ, E-14071 Cordoba, Spain. 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DEL RIO, 4-1 B, 33001 OVIEDO, SPAIN SN 0214-9915 J9 PSICOTHEMA JI Psicothema PD AUG PY 2007 VL 19 IS 3 BP 435 EP 439 PG 5 WC Psychology, Multidisciplinary SC Psychology GA 188EF UT WOS:000247901200012 PM 17617982 ER PT J AU Ashley-Koch, AE Jaworski, J Ma, DQ Mei, H Ritchie, MD Skaar, DA Delong, GR Worley, G Abramson, RK Wright, HH Cuccaro, ML Gilbert, JR Martin, ER Pericak-Vance, MA AF Ashley-Koch, Allison E. Jaworski, James Ma, De Qiong Mei, Hao Ritchie, Marylyn D. Skaar, David A. Delong, G. Robert Worley, Gordon Abramson, Ruth K. Wright, Harry H. Cuccaro, Michael L. Gilbert, John R. Martin, Eden R. Pericak-Vance, Margaret A. TI Investigation of potential gene-gene interactions between APOE and RELN contributing to autism risk SO PSYCHIATRIC GENETICS LA English DT Article DE APOE; autism; genetic susceptibility; human; RELN protein; statistical data analysis ID PEDIGREE DISEQUILIBRIUM TEST; REELIN GENE; SUSCEPTIBILITY GENES; VULNERABILITY FACTOR; GENOMEWIDE SCREEN; INFANTILE-AUTISM; GENOMIC SCREEN; LINKAGE; ASSOCIATION; DISORDER AB Background Several candidate gene studies support RELN as susceptibility gene for autism. Given the complex inheritance pattern of autism, it is expected that gene-gene interactions will exist. A logical starting point for examining potential gene-gene interactions is to evaluate the joint effects of genes involved in a common biological pathway. RELN shares a common biological pathway with APOE, and Persico et al have observed transmission distortion of the APOE-2 allele in autism families. Objective We evaluated RELN and APOE for joint effects in autism susceptibility. Methods A total of 470 Caucasian autism families were analyzed (265 multiplex; 168 trios with no family history; 37 positive family history but only one sampled affected). These families were genotyped for 11 RELN polymorphisms, including the 5' untranslated region repeat previously associated with autism, as well as for the APOE functional allele. We evaluated single locus allelic and genotypic association with the pedigree disequilibrium test and geno-PDT, respectively. Multilocus effects were evaluated using the extended version of the multifactorial dimensionality reduction method. Results For the single locus analyses, there was no evidence for an effect of APOE in our data set. Evidence for association with RELN (rs2073559; trio subset P = 0.07 PDT; P = 0.001 geno-PDT; overall geno-PDT P = 0.05), however, was found. For multilocus geno-PDT analysis, the joint genotype of APOE and RELN rs2073559 was highly significant (trio subset global P = 0.0001), probably driven by the RELN single locus effect. Using the extended version of the multifactorial dimensionality reduction method to detect multilocus effects, there were no statistically significant associations for any of the n-locus combinations involving RELN or APOE in the overall or multiplex subset. In the trio subset 1-locus and 2-locus models selected only markers in RELN as best models for predicting autism case Conclusion Thus, we conclude that there is no main effect of APOE in our autism data set, nor is there any evidence for a joint effect of APOE with RELN. RELN, however, remains a good candidate for autism susceptibility. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. Vanderbilt Univ, Vanderbilt Ctr Human Genet Res, Nashville, TN USA. WS Hall Psychiat Inst, Columbia, SC USA. RP Ashley-Koch, AE (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Box 3400,2007 Snyderman Genom Sci Bldg,595 LaSall, Durham, NC 27710 USA. 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Genet. PD AUG PY 2007 VL 17 IS 4 BP 221 EP 226 DI 10.1097/YPG.0b013e32809c2f75 PG 6 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 193TN UT WOS:000248297700003 PM 17621165 ER PT J AU Moriguchi, Y Ohnishi, T Mori, T Matsuda, H Komaki, G AF Moriguchi, Yoshiya Ohnishi, Takashi Mori, Takeyuki Matsuda, Hiroshi Komaki, Gen TI Changes of brain activity in the neural substrates for theory of mind during childhood and adolescence SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE autism; functional magnetic resonance imaging; medial prefrontal cortex; normal development; theory of mind ID MEDIAL PREFRONTAL CORTEX; SOCIAL COGNITION; CORTICAL DEVELOPMENT; 2ND-ORDER BELIEFS; ASPERGER-SYNDROME; MENTAL STATES; FRONTAL-LOBE; SELF; FMRI; PERCEPTION AB Theory of mind (ToM) refers to the ability to attribute independent mental states, such as beliefs, preferences and desires, to the self and others. Neuroimaging studies of normal adults have consistently demonstrated the importance of particular brain regions for ToM, the superior temporal sulcus (STS), temporal pole (TP) and the medial prefrontal cortex (MPFC). However, there are little data showing how ToM develops during childhood and adolescence. Such data are important for understanding the development of social functioning and its disorders. The authors used functional magnetic resonance imaging to study age-related changes in brain activity associated with ToM during childhood and early adolescence (9-16 years). Normally developed children and adolescents demonstrated significant activation in the bilateral STS, the TP adjacent to the amygdala (TP/Amy) and the MPFC. Furthermore, the authors found a positive correlation between age and the degree of activation in the dorsal part of the MPFC; in contrast, a negative correlation was found for the ventral part of the MPFC. The authors also found a positive correlation between the Z coordinate of the peak activation in the MPFC and age. The data indicated that activity in the MPFC associated with ToM shifted from the ventral to the dorsal part of the MPFC during late childhood and adolescence. No age-related changes were found in the STS and the TP/Amy regions. The authors consider that the age-related brain activity observed in the present study may be associated with the maturation of the prefrontal cortex and the associated development of cognitive functions. C1 Natl Ctr Neurol & Psychiat, Natl Ctr Hosp Mental Nervous & Muscular Disorders, Dept Radiol, Kodaira, Tokyo 1878551, Japan. Natl Ctr Neurol & Psychiat, NIMH, Dept Psychosomat Res, Kodaira, Tokyo, Japan. Saitama Med Sch Hosp, Dept Nucl Med, Iruma, Saitama, Japan. Natl Cardiovasc Ctr, Res Inst, Dept Investigat Radiol, Osaka, Japan. Natl Ctr Neurol & Psychiat, Natl Inst Neurosci, Dept Mental Disorder Res, Kodaira, Tokyo, Japan. RP Ohnishi, T (reprint author), Natl Ctr Neurol & Psychiat, Natl Ctr Hosp Mental Nervous & Muscular Disorders, Dept Radiol, 4-1-1 Ogawa Higashi Cho, Kodaira, Tokyo 1878551, Japan. 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Neurosci. PD AUG PY 2007 VL 61 IS 4 BP 355 EP 363 DI 10.1111/j.1440-1819.2007.01687.x PG 9 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 183YX UT WOS:000247609400003 PM 17610659 ER PT J AU Takeda, T Kasai, K Kato, N AF Takeda, Toshinobu Kasai, Kiyoto Kato, Nobumasa TI Moral judgment in high-functioning pervasive developmental disorders SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE autism; moral; pervasive developmental disorder; reasoning; socialization ID AUTISTIC-CHILD AB Individuals with pervasive developmental disorder (PDD) are characterized by deficits in socialization. To date, moral judgment, which may have a considerable influence on socialization, has not been fully investigated in high-functioning PDD (HFPDD), particularly from a viewpoint of practical adjustment with peers. Human External Action and its internal Reasoning Type (HEART), a standardized test for evaluating moral judgment in school children developed in Japan, was used to compare various aspects of moral judgment between 23 students with HFPDD (6-14 years old) and 23 students with typical development matched for age, intelligence, and socioeconomic status. Students with HFPDD scored significantly lower on Internal Moral Reasoning than control students. As for the level of Internal Moral Reasoning, while both groups reached a conventional (third) level in almost all items, fewer students with HFPDD achieved an autonomous (fourth) level and more students with HFPDD remained at a heteronomous (second) level than did control students. In the HFPDD group there were significant positive correlations between some items of Internal Moral Reasoning and verbal ability-related items of Wechsler Intelligence Scale for Children-III. 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Law, Kiely Law, Paul Qiu, Shanping Lord, Catherine Sebat, Jonathan Ye, Kenny Wigler, Michael TI A unified genetic theory for sporadic and inherited autism SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE human genetics; neurodevelopmental disorders; population genetics ID FRAGILE-X-SYNDROME; GENOMEWIDE SCREEN; CHROMOSOMAL REARRANGEMENTS; SUSCEPTIBILITY LOCI; SPECTRUM DISORDERS; IDENTIFICATION; LINKAGE; REGION; DNA AB Autism is among the most clearly genetically determined of all cognitive-developmental disorders, with males affected more often than females. We have analyzed autism risk in multiplex families from the Autism Genetic Resource Exchange (AGRE) and find strong evidence for dominant transmission to male offspring. By incorporating generally accepted rates of autism and sibling recurrence, we find good fit for a simple genetic model in which most families fall into two types: a small minority for whom the risk of autism in male offspring is near 50%, and the vast majority for whom male offspring have a low risk. We propose an explanation that links these two types of families: sporadic autism in the low-risk families is mainly caused by spontaneous mutation with high penetrance in males and relatively poor penetrance in females; and high-risk families are from those offspring, most often females, who carry a new causative mutation but are unaffected and in turn transmit the mutation in dominant fashion to their offspring. C1 Cold Spring Harbor Lab, Cold Spring Harbor, NY 11724 USA. Austim Genet Resource Exchange, Los Angeles, CA 90036 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA. Kennedy Krieger Inst, Dept Med Informat, Interact Austim Network, Baltimore, MD 21205 USA. Univ Michigan, Austim & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. Albert Einstein Coll Med, Dept Epidemiol & Populat Hlth, Bronx, NY 10461 USA. RP Ye, K (reprint author), Cold Spring Harbor Lab, 1 Bungtown Rd,POB 100, Cold Spring Harbor, NY 11724 USA. 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PD JUL 26 PY 2007 VL 357 IS 4 BP 392 EP 400 PG 9 WC Medicine, General & Internal SC General & Internal Medicine GA 193OL UT WOS:000248283500013 PM 17652655 ER PT J AU Hayden, BY Parikh, PC Deaner, RO Platt, ML AF Hayden, Benjamin Y. Parikh, Purak C. Deaner, Robert O. Platt, Michael L. TI Economic principles motivating social attention in humans SO PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES LA English DT Article DE attractiveness; neuroeconomics; temporal discounting; social neuroscience ID FACIAL ATTRACTIVENESS; BEHAVIORAL ECONOMICS; REWARDS; REINFORCERS; STIMULI; SYSTEMS; BEAUTY; AUTISM; BRAIN; FACES AB We know little about the processes by which we evaluate the opportunity to look at another person. We propose that behavioural economics provides a powerful approach to understanding this basic aspect of social attention. We hypothesized that the decision process culminating in attention to another person follows the same economic principles that govern choices about rewards such as food, drinks and money. Specifically, such rewards are discounted as a function of time, are tradable for other rewards, and reinforce work. Behavioural and neurobiological evidence suggests that looking at other people can also be described as rewarding, but to what extent these economic principles apply to social orienting remains unknown. Here, we show that the opportunity to view pictures of the opposite sex is discounted by delay to viewing, substitutes for money and reinforces work. The reward value of photos of the opposite sex varied with physical attractiveness and was greater in men, suggesting differential utility of acquiring visual information about the opposite sex in men and women. 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TI Genome-wide expression profiling of lymphoblastoid cell lines distinguishes different forms of autism and reveals shared pathways SO HUMAN MOLECULAR GENETICS LA English DT Article ID FRAGILE-X-SYNDROME; GENETIC RESOURCE EXCHANGE; QUANTITATIVE TRAIT LOCUS; BIPOLAR DISORDER; MENTAL-RETARDATION; SPECTRUM DISORDER; MESSENGER-RNAS; MOLECULAR CHARACTERIZATION; DEVELOPMENTAL DISORDERS; 15Q11-Q13 DUPLICATIONS AB Autism is a heterogeneous condition that is likely to result from the combined effects of multiple genetic factors interacting with environmental factors. Given its complexity, the study of autism associated with Mendelian single gene disorders or known chromosomal etiologies provides an important perspective. We used microarray analysis to compare the mRNA expression profile in lymphoblastoid cells from males with autism due to a fragile X mutation (FMR1-FM), or a 15q11-q13 duplication (dup(15q)), and non-autistic controls. Gene expression profiles clearly distinguished autism from controls and separated individuals with autism based on their genetic etiology. We identified 68 genes that were dysregulated in common between autism with FMR1-FM and dup(15q). We also identified a potential molecular link between FMR1-FM and dup(15q), the cytoplasmic FMR1 interacting protein 1 (CYFIP1), which was up-regulated in dup(15q) patients. We were able to confirm this link in vitro by showing common regulation of two other dysregulated genes, JAKMIP1 and GPR155, downstream of FMR1 or CYFIP1. We also confirmed the reduction of the Jakmip1 protein in Fmr1 knock-out mice, demonstrating in vivo relevance. Finally, we showed independent confirmation of roles for JAKMIP1 and GPR155 in autism spectrum disorders (ASDs) by showing their differential expression in male sib pairs discordant for idiopathic ASD. 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PD JUL 15 PY 2007 VL 16 IS 14 BP 1682 EP 1698 DI 10.1093/hmg/ddm116 PG 17 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 196LP UT WOS:000248483500004 PM 17519220 ER PT J AU Garber, K AF Garber, Ken TI Neuroscience - Autism's cause may reside in abnormalities at the synapse SO SCIENCE LA English DT News Item CR 2005, SCIENCE 0624, P1856 NR 1 TC 55 Z9 57 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD JUL 13 PY 2007 VL 317 IS 5835 BP 190 EP 191 DI 10.1126/science.317.5835.190 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 189DC UT WOS:000247968600011 PM 17626859 ER PT J AU Rzhetsky, A Wajngurt, D Park, N Zheng, T AF Rzhetsky, Andrey Wajngurt, David Park, Naeun Zheng, Tian TI Probing genetic overlap among complex human phenotypes SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE autism; bipolar disorder; harmful genetic polymorphisms; schizophrenia; shared genes ID BIPOLAR DISORDER; AUTISM; SCHIZOPHRENIA; SPECTRUM AB Geneticists and epidemiologists often observe that certain hereditary disorders cooccur in individual patients significantly more (or significantly less) frequently than expected, suggesting there is a genetic variation that predisposes its bearer to multiple disorders, or that protects against some disorders while predisposing to others. We suggest that, by using a large number of phenotypic observations about multiple disorders and an appropriate statistical model, we can infer genetic overlaps between phenotypes. Our proof-of-concept analysis of 1.5 million patient records and 161 disorders indicates that disease phenotypes form a highly connected network of strong pairwise correlations. Our modeling approach, under appropriate assumptions, allows us to estimate from these correlations the size of putative genetic overlaps. For example, we suggest that autism, bipolar disorder, and schizophrenia share significant genetic overlaps. Our disease network hypothesis can be immediately exploited in the design of genetic mapping approaches that involve joint linkage or association analyses of multiple seemingly disparate phenotypes. C1 Columbia Univ, Ctr Computat Biol & Bioinformat & Joint Ctr SB, Dept Biomed Informat, New York, NY 10032 USA. Columbia Univ, Columbia Genome Ctr, New York, NY 10032 USA. 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PD JUL 10 PY 2007 VL 104 IS 28 BP 11694 EP 11699 DI 10.1073/pnas.0704820104 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 190MQ UT WOS:000248063400034 PM 17609372 ER PT J AU Szatmari, P Maziade, M Zwaigenbaum, L Merette, C Roy, MA Joober, R Palmour, R AF Szatmari, Peter Maziade, Michel Zwaigenbaum, Lonnie Merette, Chantal Roy, Marc-Andre Joober, Ridha Palmour, Roberta TI Informative phenotypes for genetic studies of psychiatric disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE endophenotype; genetics; autism; schizophrenia; alcoholism; mood disorder ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; QUANTITATIVE TRAIT; MAJOR DEPRESSION; LINKAGE ANALYSIS; WORKING-MEMORY; RELATIVE RISK; SCHIZOPHRENIA; AUTISM; ENDOPHENOTYPES; HERITABILITY AB Despite its initial promise, there has been both progress and some set backs in genetic studies of the major psychiatric disorders of childhood and adulthood. Finding true susceptibility genes may be delayed because the most genetically informative phenotypes are not being used on a regular basis in linkage analysis and association studies. It is highly likely that using alternative phenotypes instead of DSM diagnostic categories will lead more rapid success in the search for these susceptibility genes. The objective of this paper is to describe the different types of informative phenotypes that can be employed in psychiatric genetic studies, to clarify their uses, to identify several methodologic issues the design and conduct of linkage and association studies that use alternative phenotypes and finally to suggest possible solutions to those difficulties. This is a conceptual review with a focus on methodological issues that may arise in psychiatric genetics and examples are taken from the literature on autism, schizophrenia, bipolar disorder, and alcoholism. (c) 2007 Wiley-Liss, Inc. C1 McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8N 3Z5, Canada. Univ Laval, Dept Psychiat, Quebec City, PQ, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. McGill Univ, Dept Psychiat, Montreal, PQ, Canada. RP Szatmari, P (reprint author), McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8N 3Z5, Canada. 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J. Med. Genet. B PD JUL 5 PY 2007 VL 144B IS 5 BP 581 EP 588 DI 10.1002/ajmg.b.30426 PG 8 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 187QU UT WOS:000247864000001 PM 17219386 ER PT J AU Adams, M Lucock, M Stuart, J Fardell, S Baker, K Ng, X AF Adams, Michelle Lucock, Mark Stuart, John Fardell, Sean Baker, Kerrie Ng, Xiaowei TI Preliminary evidence for involvement of the folate gene polymorphism 19 bp deletion-DHFR in occurrence of autism SO NEUROSCIENCE LETTERS LA English DT Article DE autism; folic acid; dihydrofolate reductase; glutamate ID NEURAL-TUBE DEFECTS; FOLIC-ACID; METHYLENETETRAHYDROFOLATE REDUCTASE; SPINA-BIFIDA; RISK-FACTOR; METHIONINE SYNTHASE; PIG-LIVER; INHIBITION; METABOLISM; HOMOCYSTEINE AB Folate has long been implicated in both the metabolism of neurotransmitter molecules, and as an agonist with a direct effect upon neuronal tissue. Folates mediate transfer of one-carbon units into major biosynthetic pathways. From a developmental perspective, the most important reactions 14 are de novo methionine and thymine synthesis, critical for DNA expression and elaboration, respectively. Dihydrofolate reductase (DHFR) is the sole enzyme responsible for maintaining the reduced state of the vitamin needed for these two pathways. Here, we report that the 19 bp-deletion polymorphism of DHFR acts independently (OR 2.69,95% CI; 1.00-7.28,p < 0.05) and in concert with related folate polymorphisms as a significant risk factor for autism. Possible consequences of this are discussed in the context of the interaction between folate and the glutamatergic nervous system, an area of promising candidate genes for contributing to autism. (c) 2007 Elsevier Ireland Ltd. All rights reserved. C1 Univ Newcastle, Sch Environm & Life Sci, Ourimbah, NSW 2258, Australia. John Hunter Childrens Hosp, Dept Paediat, Newcastle, NSW 2310, Australia. Kaleidoscope Child & Family Hlth Team, Wallsend, NSW 2287, Australia. RP Lucock, M (reprint author), Univ Newcastle, Sch Environm & Life Sci, POB 127,Brush Rd, Ourimbah, NSW 2258, Australia. 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Lett. PD JUL 5 PY 2007 VL 422 IS 1 BP 24 EP 29 DI 10.1016/j.neulet.2007.05.025 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 202BF UT WOS:000248875800005 PM 17597297 ER PT J AU Hayashi, ML Rao, BSS Seo, JS Choi, HS Dolan, BM Choi, SY Chattarji, S Tonegawa, S AF Hayashi, Mansuo L. Rao, B. S. Shankaranarayana Seo, Jin-Soo Choi, Han-Saem Dolan, Bridget M. Choi, Se-Young Chattarji, Sumantra Tonegawa, Susumu TI Inhibition of p21-activated kinase rescues symptoms of fragile X syndrome in mice SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE cortical long-term potentiation; spine morphology; trace fear conditioning; autism ID MENTAL-RETARDATION PROTEIN; SYNAPTIC PLASTICITY; MOUSE MODEL; DENDRITIC SPINES; MESSENGER-RNA; KNOCKOUT MICE; TRANSLATION; MUTATION; CORTEX; MEMORY AB Fragile X syndrome (FXS), the most commonly inherited form of mental retardation and autism, is caused by transcriptional silencing of the fragile X mental retardation 1 (FMR1) gene and consequent loss of the fragile X mental retardation protein. Despite growing evidence suggesting a role of specific receptors and biochemical pathways in FXS pathogenesis, an effective therapeutic method has not been developed. Here, we report that abnormalities in FMR1 knockout (KO) mice, an animal model of FXS, are ameliorated, at least partially, at both cellular and behavioral levels, by an inhibition of the catalytic activity of p21-activated kinase (PAK), a kinase known to play a critical role in actin polymerization and dendritic spine morphogenesis. Greater spine density and elongated spines in the cortex, morphological synaptic abnormalities commonly observed in FXS, are at least partially restored by postnatal expression of a dominant negative (dn) PAK transgene in the forebrain. Likewise, the deficit in cortical long-term potentiation observed in FMR1 KO mice is fully restored by the dnPA Ktransgene. Several behavioral abnormalities associated with FMR1 KO mice, including those in locomotor activity, stereotypy, anxiety, and trace fear conditioning are also ameliorated, partially or fully, by the dnPAK transgene. Finally, we demonstrate a direct interaction between PAK and fragile X mental retardation protein in vitro. Overall, our results demonstrate the genetic rescue of phenotypes in a FXS mouse model and suggest that the PAK signaling pathway, including the catalytic activity of PAK, is a novel intervention site for development of an FXS and autism therapy. C1 MIT, Picower Inst Learning & Memory, Howard Hughes Med Inst, RIKEN Massachusetts Inst Technol Neurosci Res Ctr, Cambridge, MA 02139 USA. MIT, Dept Biol, Cambridge, MA 02139 USA. MIT, Dept Brain & Cognit Sci, Cambridge, MA 02139 USA. Natl Inst Mental Hlth & Neurosci, Dept Neurophysiol, Bangalore 560029, Karnataka, India. Seoul Natl Univ, Coll Dent, Dept Physiol, Seoul 110749, South Korea. Tata Inst Fundamental Res, Natl Ctr Biol Sci, Bangalore 560065, Karnataka, India. RP Tonegawa, S (reprint author), MIT, Picower Inst Learning & Memory, Howard Hughes Med Inst, RIKEN Massachusetts Inst Technol Neurosci Res Ctr, 77 Massachusetts Ave, Cambridge, MA 02139 USA. 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Natl. Acad. Sci. U. S. A. PD JUL 3 PY 2007 VL 104 IS 27 BP 11489 EP 11494 DI 10.1073/pnas.0705003104 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 188DT UT WOS:000247900000065 PM 17592139 ER PT J AU Fernell, E Fagerberg, UL Hellstrom, PM AF Fernell, Elisabeth Fagerberg, Ulrika L. Hellstrom, Per M. TI No evidence for a clear link between active intestinal inflammation and autism based on analyses of faecal calprotectin and rectal nitric oxide SO ACTA PAEDIATRICA LA English DT Article DE autism; intestinal inflammation; nitric oxide; callprotectin ID LYMPHOCYTE CYTOKINE PROFILES; GASTROINTESTINAL SYMPTOMS; BOWEL-DISEASE; LANGUAGE REGRESSION; IMMUNE ACTIVATION; CHILDREN; DISORDERS; MEASLES; COMMON; MUMPS AB Aim: Due to parental concern regarding the child's bowel habits and the ongoing discussion whether there might be an association between autism and intestinal inflammation, two inflammatory markers were analysed in a group of children with autism. Methods: Twenty-four consecutive children with autism (3-13 years) of unknown aetiology were investigated with respect to faecal calprotectin and rectal nitric oxide (NO). Results: One child who previously had a severe Clostridium difficile infection displayed raised levels of both these inflammatory markers and one child with extreme constipation for whom only calprotectin was possible to measure had raised levels. The remaining children displayed results that did not indicate an active inflammatory status in the intestine when the two inflammatory markers were combined. Conclusion: By the use of two independent markers of inflammatory reactions in the gut, i.e. rectal NO and faecal calprotectin we were not able to disclose evidence of a link between the autistic disorder and active intestinal inflammation. C1 Karolinska Univ Hosp, Karolinska Inst, Astrid Lindgren Childrens Hosp, Dept Neuropaed, S-17175 Stockholm, Sweden. Karolinska Univ Hosp, Karolinska Inst, Astrid Lindgren Childrens Hosp, Dept Paediat Gastroenterol & Nutr, S-17176 Stockholm, Sweden. Karolinska Univ Hosp, Karolinska Inst, Dept Med, Unit Gastroenterol & Hepatol, S-17176 Stockholm, Sweden. RP Fernell, E (reprint author), Karolinska Univ Hosp, Karolinska Inst, Astrid Lindgren Childrens Hosp, Dept Neuropaed, S-17175 Stockholm, Sweden. 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PD JUL PY 2007 VL 96 IS 7 BP 1076 EP 1079 DI 10.1111/j.1651-2227.2007.00298.x PG 4 WC Pediatrics SC Pediatrics GA 184ZR UT WOS:000247681600030 PM 17465982 ER PT J AU Gonzalez, BP Menchaca, NF AF Gonzalez, B. Pay Menchaca, N. Fuentes TI Neurobiology of autism: neuropathology and neuroimaging studies SO ACTAS ESPANOLAS DE PSIQUIATRIA LA English DT Review DE autism; neuropathology; neuroimaging; neurobiology ID CEREBRAL-BLOOD-FLOW; CORPUS-CALLOSUM; INFANTILE-AUTISM; CHILDHOOD AUTISM; EMISSION-TOMOGRAPHY; POSTERIOR-FOSSA; BRAIN; CEREBELLUM; ADULTS; MRI AB Introduction. This study performs a review of the last studies in the field of neuropathology and neuroimaging of autism. Method. A search was done in Medline for articles on neuropathology and neuroimaging in autism and the most relevant articles of the last 10 years up to date were selected. Results. The existence of structural abnormalities in the brain of patients with autism, affecting different brain structures such as the cerebellum, limbic system, frontal and temporal cortexes, corpus callosum and basal ganglia seems to be demonstrated. Conclusion. The alterations found with the neuroimaging techniques are identified in the different brain structures. At present, there is almost generalized thinking that brain alterations in autism are not limited to a single brain area but involve different structures within a globally affected neuronal network. Future studies will allow us to increase knowledge on this disorder's pathophysiology. C1 CH Padre Manni, Programa Salud Mental Infanto Juvenil, Santander, Spain. RP Gonzalez, BP (reprint author), CSM Infanto Juvenil, Luis Vicente Velasco 1, Santander 39011, Spain. 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Psiquiatri. PD JUL-AUG PY 2007 VL 35 IS 4 BP 271 EP 276 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 195KR UT WOS:000248411600009 ER PT J AU Miles, JH Takahashi, TN AF Miles, Judith H. Takahashi, T. Nicole TI Lack of association between Rh status, Rh immune globulin in pregnancy and autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE autism; Rh; Rh immune globulin; thimerosal; RhoGam ID PERVASIVE DEVELOPMENTAL DISORDERS; FETAL GENOTYPE INCOMPATIBILITY; THIMEROSAL-CONTAINING VACCINES; SPECTRUM DISORDERS; PRESCHOOL-CHILDREN; RUBELLA VACCINE; MMR VACCINATION; HUMAN-DISEASE; SCHIZOPHRENIA; MERCURY AB Though causes of autism are considered largely genetic, considerable concern remains that exposure to Rh immune globulin (RhIg), which until 2001 in the United States contained the preservative thimerosal, can cause autism. To determine whether mothers of children with autism are more likely to be Rh negative (Rh-) or to have received RhIg preserved with thimerosal, which is 49.6% ethyl mercury, We surveyed families of children with an autism spectrum disorder (ASD) ascertained through a university-based autism clinic considered free of ascertainment biases related to type of autism or severity. Between 2004 and 2006, 305 mothers of 321 children with an ASD agreed to participate in a telephone interview. Analysis of complete records including the blood group status and RhIg exposure of 214 families showed that Rh- status is no higher in mothers of children with autism than in the general population, exposure to antepartum RhIg, preserved with thimerosal is no higher for children with autism and pregnancies are no more likely to be Rh incompatible. This was also true for autism subgroups defined by behavioral phenotype, gender, IQ, regressive onset, head circumference, dysmorphology, birth status, essential, or complex phenotype. These findings support the consensus that exposure to ethylmercury in thimerosal is not the cause of the increased prevalence of autism. These data are important not only for parents in this country but also for the international health community where thimerosal continues to be used to preserve multi-close vials which in turn makes vaccines affordable. (c) 2007 Wiley-Liss, Inc. C1 Univ Missouri Hosp & Clin, Dept Child Hlth, Thompson Ctr Autism & Neurodev Disorders, Columbia, MO 65212 USA. RP Miles, JH (reprint author), Univ Missouri Hosp & Clin, Dept Child Hlth, Thompson Ctr Autism & Neurodev Disorders, 1 Hosp Dr, Columbia, MO 65212 USA. 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A PD JUL 1 PY 2007 VL 143A IS 13 BP 1397 EP 1407 DI 10.1002/ajmg.a.31846 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 186DZ UT WOS:000247760600001 PM 17508426 ER PT J AU Baranek, GT Boyd, BA Poe, MD David, FJ Watson, LR AF Baranek, Grace T. Boyd, Brian A. Poe, Michele D. David, Fabian J. Watson, Linda R. TI Hyperresponsive sensory patterns in young children with autism, developmental delay, and typical development SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID WEAK CENTRAL COHERENCE; FRAGILE-X-SYNDROME; DISORDER; STIMULI; HYPERSENSITIVITY; DEFENSIVENESS; DISABILITIES; INDIVIDUALS; HABITUATION; PERFORMANCE AB The nature of hyperresponsiveness to sensory stimuli in children with autism, using a new observational measure, the SPA, was examined. Three groups of young participants were assessed (autism, developmental delay, typical). Across all groups, MA was a predictor of hyperresponsiveriess, such that aversion to multisensory toys decreased as MA increased. The two clinical groups displayed higher levels of sensory aversion than the typical group. The groups did not differ in the proportion of children habituating to an auditory stimulus; however, nonresponders were more prevalent in the autism group. These findings elucidate developmental influences on sensory features and the specificity of hyperresponsiveness to clinical groups. Implications for understanding pathogenesis, differentiating constructs of hypersensitivity, and planning treatment are discussed. C1 Univ N Carolina, Div Occupat Sci, Chapel Hill, NC 27599 USA. RP Baranek, GT (reprint author), Univ N Carolina, Div Occupat Sci, CB 7122,Bondurant Hall,Suite 2050, Chapel Hill, NC 27599 USA. EM gbaranek@med.unc.edu RI Poe, Michele/K-6615-2012; David, Fabian/K-6872-2013; David, Fabian/C-6028-2014 OI Poe, Michele/0000-0001-9693-3638; David, Fabian/0000-0002-3053-4295; David, Fabian/0000-0001-7780-788X CR Andres AM, 2004, BRIT J MATH STAT PSY, V57, P1, DOI 10.1348/000711004849268 Baranek G. 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J. Ment. Retard. PD JUL PY 2007 VL 112 IS 4 BP 233 EP 245 DI 10.1352/0895-8017(2007)112[233:HSPIYC]2.0.CO;2 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 184RM UT WOS:000247659500001 PM 17559291 ER PT J AU Keller-Bell, YD Abbeduto, LD AF Keller-Bell, Yolanda D. Abbeduto, Leonard D. TI Narrative development in adolescents and young adults with fragile X syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID SCHOOL-AGE-CHILDREN; DOWN-SYNDROME; LANGUAGE IMPAIRMENT; CONVERSATIONAL CHARACTERISTICS; WILLIAMS-SYNDROME; SKILLS; COMMUNICATION; INDIVIDUALS; AUTISM; STORY AB The narratives of 18 adolescents and young adults with fragile X syndrome were compared to those of 23 adolescents with Down syndrome and 21 typically developing children matched for nonverbal MA. Narratives were elicited using a wordless picture book and analyzed for use of narrative evaluation, linguistic productivity, and complexity. Results revealed that the individuals with fragile X syndrome produced significantly fewer different types of narrative evaluation, but more grammatically acceptable utterances than did the youth with Down syndrome. There was no significant difference between the participants with fragile X syndrome and their typically developing nonverbal-MA matches. Results suggest that a variety of language measures and contexts are needed to gain a full understanding of the language abilities of individuals with fragile X syndrome. C1 Univ Georgia, Dept Commun Sci & Special Educ, Athens, GA 30602 USA. Univ Wisconsin, Madison, WI USA. RP Keller-Bell, YD (reprint author), Univ Georgia, Dept Commun Sci & Special Educ, 565 Aderhold Hall, Athens, GA 30602 USA. 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Garrett-Mayer, Elizabeth TI Social and communication development in toddlers with early and later diagnosis of autism spectrum disorders SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID JOINT VISUAL-ATTENTION; YOUNG-CHILDREN; LANGUAGE-DEVELOPMENT; HOME MOVIES; REGRESSIVE AUTISM; EARLY RECOGNITION; 1ST YEAR; INFANTS; AGE; BRAIN AB Context: To our knowledge, no prospective studies of the developmental course of early and later diagnosis of autism spectrum disorders from 14 months of age exist. Objective: To examine patterns of development from 14 to 24 months in children with early and later diagnosis of autism spectrum disorders. Design: Prospective, longitudinal design in which 125 infants at high and low risk for autism were tested from age 14 to 36 months. Comprehensive standardized assessments included measures of social, communication, and play behavior. Setting: Testing occurred at a major medical and research institution as part of a large, ongoing longitudinal study. Participants: Low-risk controls (n=18) and siblings of children with autism, grouped on the basis of outcome diagnostic classification at 30 or 36 months: autism spectrum disorders (early diagnosis, n=16; later diagnosis, n=14), broader autism phenotype (n=19), and non broader autism phenotype (n=58). Main Outcome Measures: Social, communication, and symbolic abilities were assessed. Results: Social, communication, and play behavior in the early-diagnosis group differed from that in all other groups by 14 months of age. By 24 months, the later-diagnosis group differed from the non -autism spectrum disorder groups in social and communication behavior, but not from the early-diagnosis group. Examination of growth trajectories suggests that autism may involve developmental arrest, slowing, or even regression. Conclusion: This study provides insight into different patterns of development of children with early vs later diagnosis of autism spectrum disorders. 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TI The new neurobiology of autism - Cortex, connectivity, and neuronal organization SO ARCHIVES OF NEUROLOGY LA English DT Review ID HIGH-FUNCTIONING AUTISM; SENTENCE COMPREHENSION; HEAD CIRCUMFERENCE; CHILDREN; SPECTRUM; DISORDER; ABNORMALITIES; GRAY; MRI AB This review covers a fraction of the new research developments in autism but establishes the basic elements of the new neurobiologic understanding of autism. Autism is a polygenetic developmental neurobiologic disorder with multiorgan system involvement, though it predominantly involves central nervous system dysfunction. The evidence supports autism as a disorder of the association cortex, both its neurons and their projections. In particular, it is a disorder of connectivity, which appears, from current evidence, to primarily involve intrahemispheric connectivity. The focus of connectivity studies thus far has been on white matter, but alterations in functional magnetic resonance imaging activation suggest that intracortical connectivity is also likely to be disturbed. Furthermore, the disorder has a broad impact on cognitive and neurologic functioning. Deficits in high-functioning individuals occur in processing that places high demands on integration of information and coordination of multiple neural systems. Intact or enhanced abilities share a dependence on low information-processing demands and local neural connections. This multidomain model with shared characteristics predicts an underlying pathophysiologic mechanism that impacts the brain broadly, according to a common neurobiologic principle. The multiorgan system involvement and diversity of central nervous system findings suggest an epigenetic mechanism. C1 Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15260 USA. Duquesne Univ, Dept Speech Language Pathol, Pittsburgh, PA 15219 USA. RP Minshew, NJ (reprint author), Webster Hall,Suite 300,3811 OHara St, Pittsburgh, PA 15213 USA. 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Neurol. PD JUL PY 2007 VL 64 IS 7 BP 945 EP 950 DI 10.1001/archneur.64.7.945 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 188AZ UT WOS:000247892100004 PM 17620483 ER PT J AU Silverman Brosco AF Silverman Brosco TI Understanding autism: Parents and pediatricians in historical perspective (vol 161, pg 392, 2007) SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Correction CR SILVERMAN, 2007, ARCH PEDIAT ADOL MED, V161, P392 NR 1 TC 0 Z9 0 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD JUL PY 2007 VL 161 IS 7 BP 640 EP 640 PG 1 WC Pediatrics SC Pediatrics GA 185GI UT WOS:000247699000003 ER PT J AU Woo, EJ Ball, R Landa, R Zimmerman, AW Braun, MM AF Woo, Emily Jane Ball, Robert Landa, Rebecca Zimmerman, Andrew W. Braun, M. Miles CA VAERS Working Grp TI Developmental regression and autism reported to the vaccine adverse event reporting system SO AUTISM LA English DT Article DE adverse event; autism; regression; vaccine ID RUBELLA VACCINATION; CAUSAL ASSOCIATION; THIMEROSAL EXPOSURE; UNITED-KINGDOM; DISORDERS; POPULATION; MEASLES; MUMPS; CHILDREN; INFANTS AB We report demographic and clinical characteristics of children reported to the US Vaccine Adverse Event Reporting System (VAERS) as having autism or another developmental disorder after vaccination. We completed 124 interviews with parents and reviewed medical records for 31 children whose records contained sufficient information to evaluate the child's developmental history. Medical record review indicated that 2 7 of 3 1 (87%) children had autism/ASD and 19 (61.3%) had evidence of developmental regression (loss of social, language, or motor skills). The proportion of VAERS cases of autism with regression was greater than that reported in population based studies, based on the subset of VAERS cases with medical record confirmation. This difference may reflect preferential reporting to VAERS of autism with regression. In other respects, the children in this study appear to be similar to other children with autism. Further research might determine whether the pathogenesis of autism with developmental regression differs from that of autism without regression. C1 US FDA, Ctr Biol Evaluat & Res, Rockville, MD 20852 USA. Johns Hopkins Univ, Kennedy Krieger Inst, Baltimore, MD 21218 USA. RP Woo, EJ (reprint author), US FDA, Ctr Biol Evaluat & Res, HFM-222,1401 Rockville Pike, Rockville, MD 20852 USA. 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Mayes, Susan Dickerson Troxell, Lucinda B. Calhoun, Susan L. TI Assessing children with autism, mental retardation, and typical development using the Playground Observation Checklist SO AUTISM LA English DT Article DE autism; mental retardation; playground observations; typical children ID DSM; DELAY AB Elementary school children with normal intelligence and autism (n = 20), mental retardation and no autism (n = 24), and typical development (n = 37) were observed for 15 minutes during recess at school. Ten behaviors were scored as present or absent using the Playground Observation Checklist. Children with autism were distinguished from children with mental retardation and typical development by their social problems, whereas children with typical development and mental retardation did not differ significantly in social competency. The four social behaviors on the checklist correctly identified 94 percent of the children as having or not having autism. All of the children with autism and all of the typical children were correctly classified. Our pilot findings suggest that the Playground Observation Checklist has potential as a simple and clinically useful component of a comprehensive evaluation for possible autism. C1 Penn State Coll Med, Hershey, PA USA. Lincoln Intermediate Unit, New Oxford, PA USA. RP Mayes, SD (reprint author), Milton S Hershey Med Ctr, Dept Psychiat H073, POB 850, Hershey, PA 17033 USA. EM smayes@psu.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Farmer-Dougan V, 1999, ED PSYCHOL, V19, P429, DOI DOI 10.1080/0144341990190404 Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hobson RP, 1998, J AUTISM DEV DISORD, V28, P117, DOI 10.1023/A:1026088531558 LORD C, 1993, INF MENTAL HLTH J, V14, P234, DOI 10.1002/1097-0355(199323)14:3<234::AID-IMHJ2280140308>3.0.CO;2-F Mayes SD, 2001, AUTISM, V5, P81, DOI 10.1177/1362361301005001008 Mayes SD, 2001, J ABNORM CHILD PSYCH, V29, P263, DOI 10.1023/A:1010337916636 Mayes SD, 1999, INFANT YOUNG CHILD, V12, P90 MAYES SED, 2003, J DEV PHYS DISABIL, V16, P257 SIEGEL B, 1991, PLAY DIAGNOSIS ASSES, P331 SIGMAN MD, 1992, CHILD DEV, V63, P796, DOI 10.1111/j.1467-8624.1992.tb01662.x VanMeter L, 1997, J AUTISM DEV DISORD, V27, P557, DOI 10.1023/A:1025830110640 WING L, 1991, SOCIAL PSYCHIAT THEO, P113 NR 13 TC 10 Z9 10 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUL PY 2007 VL 11 IS 4 BP 311 EP 319 DI 10.1177/1362361307078129 PG 9 WC Psychology, Developmental SC Psychology GA 201RJ UT WOS:000248850000003 PM 17656396 ER PT J AU Reiter, S Vitani, T AF Reiter, Shunit Vitani, Taly TI Inclusion of pupils with autism - The effect of an intervention program on the regular pupils'burnout, attitudes and quality of mediation SO AUTISM LA English DT Article DE attitudes; autism; burnout; inclusion; quality of mediation ID CHILDRENS ATTITUDES; PEER; ACQUISITION AB An intervention program aimed at the improvement of the quality of inclusion of pupils with autism in a regular fourth grade classroom (average age of 9 years) was applied with 23 pupils. Two pupils with autism were included from first grade. The regular pupils displayed signs of burnout stemming from the inclusion. The aim of the study was to examine the effect of a specially designed intervention program on the regular pupils' level of burnout, attitude to the pupils with autism, and the quality of their mediation. Three questionnaires covering these variables were administered twice, at the beginning and at the end of the intervention program. The findings showed less burnout at the end of the program, significant improvement in the quality of mediation and more positive attitudes towards pupils with autism. Significant correlations were found between burnout, quality of tutoring and positive attitudes towards pupils with autism. C1 Univ Haifa, Fac Educ, IL-31905 Haifa, Israel. RimoN Sch, Kibbutz Mesilot, Israel. RP Reiter, S (reprint author), Univ Haifa, Fac Educ, IL-31905 Haifa, Israel. EM shunitr@construct.haifa.ac.il CR AINSCOW M, 4 ISEC C BIRM, P95 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BRAVERMAN M, 1989, J AUTISM DEV DISORD, V19, P301, DOI 10.1007/BF02211848 CARR EG, 1990, J AUTISM DEV DISORD, V20, P45, DOI 10.1007/BF02206856 CHARLOP MH, 1983, J ABNORM CHILD PSYCH, V11, P355, DOI 10.1007/BF00914244 Cherniss C., 1995, BURNOUT Culham A, 2003, J INTELLECT DEV DIS, V28, P65, DOI 10.1080/1366825031000086902 EGEL AL, 1988, BEHAV THERAPIST, V11, P7 Farber B. 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This systematic review considers the effectiveness of pharmacological treatment in managing autism spectrum disorder in adolescents and adults. Following a comprehensive search of literature published in English from 1980, methodological criteria were applied to identify studies designed to reliably assess treatment effectiveness. Only five double-blind, randomized controlled trials were eligible for appraisal. All had small sample sizes (mean = 3 0) and brief treatment duration of no more than 12 weeks. The paucity of trials and their methodological limitations means that there is only preliminary evidence about the short-term effectiveness of a few drug treatments for this age group. There was also a lack of reliable data reported on drug safety profiles. Methodological challenges and directions for future research are discussed. C1 Univ Otago, Christchurch Sch Med, Dept Publ Hlth & Gen Practice, NZHTA, Christchurch, New Zealand. RP Broadstock, M (reprint author), Univ Otago, Christchurch Sch Med, Dept Publ Hlth & Gen Practice, NZHTA, POB 4345, Christchurch, New Zealand. 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The children with autism were also subdivided into two groups according to intellectual functioning in order to analyze frequency and latency of social interaction in relation to degree of disability. The results showed a significant difference in frequency of social interaction between the typical children and those with autism. There was no difference between the groups on latency to initiate interaction. However, shorter latency was associated with higher frequency in the typical group but not in the group of children with autism. Significant differences in IQ and adaptive functioning were found between the children with autism who showed interaction and those who did not. The results for the typical children may be used as benchmark values for the assessment of treatment outcome for children with autism. RP Jahr, E (reprint author), Akershus Univ Sykehus, Seksjon Habilitering, POB 48, N-1474 Nordbyhagen, Norway. 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SO AUTISM LA English DT Article DE autism; behaviour modification; childhood play behaviour; childhood play development ID SYMBOLIC PLAY; GENERALIZED REDUCTION; SPECTRUM DISORDERS; APPROPRIATE PLAY; SELF-MANAGEMENT; SKILLS; SIBLINGS; DISABILITIES; STUDENTS AB Play is, by definition, internally motivated, flexible, spontaneous and voluntary. Yet some researchers claim to have taught children with autism to play using behavioural interventions that are heavily structured, repetitive and make use of external reinforcements. In the current systematic review, we examine the extent to which these claims are supported by the evidence presented by the researchers themselves. We conclude that the most effective behavioural intervent tions have been those which have built on children or have relied on the motivating nature of activities themselves rather than on external rewards. 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CR CHARMAN T, 2007, SOCIAL COMMUN DEV AU NR 1 TC 1 Z9 1 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD JUL PY 2007 VL 11 IS 4 BP 389 EP 390 DI 10.1177/1362361307082394 PG 2 WC Psychology, Developmental SC Psychology GA 201RJ UT WOS:000248850000008 ER PT J AU Johnson, CR Handen, BL Butter, E Wagner, A Mulick, J Sukhodolsky, DG Williams, S Swiezy, NA Arnold, LE Aman, MG Scahill, L Stigler, KA McDougle, CJ Vitiello, B Smith, T AF Johnson, Cynthia R. Handen, Benjamin L. Butter, Eric Wagner, Ann Mulick, James Sukhodolsky, Denis G. Williams, Susan Swiezy, Naomi A. Arnold, L. Eugene Aman, Michael G. Scahill, Lawrence Stigler, Kimberly A. McDougle, Christopher J. Vitiello, Benedetto Smith, Tristram TI Development of a parent training program for children with pervasive developmental disorders SO BEHAVIORAL INTERVENTIONS LA English DT Article ID INTENSIVE EARLY INTERVENTION; RANDOMIZED CONTROLLED-TRIAL; YOUNG-CHILDREN; BEHAVIORAL TREATMENT; PSYCHOSOCIAL INTERVENTIONS; PRESCHOOL-CHILDREN; AUTISM; RISPERIDONE; SYMPTOMS; PHARMACOTHERAPY AB Parent delivered interventions based on applied behavior analysis (ABA) for children with Pervasive Developmental Disorders (PDDs) have been evaluated using primarily single-subject design methodology or small case series. While the results of these evaluations are encouraging, an important next step is to standardize the interventions to allow for replication across sites, in studies with large samples and measures of long-term, clinically meaningful outcomes such as improvements in children's functioning and their relationships with parents. Accordingly, the Research Units on Pediatric Psychopharmacology and Psychosocial Interventions (RUPP Autism Network) assembled a detailed manual for a structured behavioral parent training (PT) program, developed treatment fidelity and training procedures, and conducted a pilot, feasibility study. The PT program is part of a large scale, multisite study intended to determine the efficacy of combined pharmacological treatment and behavioral intervention to improve behavior and adaptive ftincfioning in children with PDD. This paper discusses the rationale for this project. A companion paper provides the results of our feasibility study on the PT program. Copyright (c) 2007 John Wiley & Sons, Ltd. C1 Univ Pittsburgh, Childrens Hosp Pittsburgh, Sch Med, Autism Ctr, Pittsburgh, PA 15213 USA. Ohio State Univ, Columbus, OH 43210 USA. NIMH, Bethesda, MD 20892 USA. Yale Univ, New Haven, CT 06520 USA. Indiana Univ, Sch Med, Bloomington, IN 47405 USA. 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Intervent. PD JUL PY 2007 VL 22 IS 3 BP 201 EP 221 DI 10.1002/bin.237 PG 21 WC Psychology, Clinical SC Psychology GA 196WN UT WOS:000248513800002 ER PT J AU Kennedy, DP Semendeferi, K Courchesne, E AF Kennedy, Daniel P. Semendeferi, Katerina Courchesne, Eric TI No reduction of spindle neuron number in frontoinsular cortex in autism SO BRAIN AND COGNITION LA English DT Article DE Von Economo Neurons; postmortem; stereology; social cognition; emotion ID ANTERIOR CINGULATE CORTEX; BRAIN OVERGROWTH; CONNECTIVITY; DISORDER; TARGETS; HUMANS; UNIQUE; APES AB It has been suggested that spindle neurons, an evolutionarily unique type of neuron, might be involved in higher-order social, emotional, and cognitive functions. As such, it was hypothesized that these neurons may be particularly important to the pathophysiology of autism, a disease characterized in part by disruption of higher-order social and emotional processing. Therefore, we conducted the first stereological investigation of the number of spindle neurons in autism, using the optical fractionator technique. Our results did not provide evidence of a reduction in spindle neuron number in frontoinsular cortex in autism. However, this study provides the first quantitative stereological data on spindle neuron number in autism. Future postmortem studies with larger sample sizes will likely be critical in elucidating the spared and defective neural systems underlying the autistic phenotype. (c) 2007 Elsevier Inc. All rights reserved. C1 Univ Calif San Diego, Dept Anthropol, La Jolla, CA 92093 USA. Univ Calif San Diego, Grad Program Neurosci, La Jolla, CA 92093 USA. Childerns Hosp Res Ctr, Ctr Autism Res, La Jolla, CA 92037 USA. RP Semendeferi, K (reprint author), Univ Calif San Diego, Dept Anthropol, 9500 Gilman Dr, La Jolla, CA 92093 USA. 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PD JUL PY 2007 VL 64 IS 2 BP 124 EP 129 DI 10.1016/j.bandc.2007.01.007 PG 6 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 193DX UT WOS:000248255500002 PM 17353073 ER PT J AU Kayaalp, L Dervent, A Saltik, S Uluduz, D Kayaalp, IV Demirbilek, V Ghaziuddin, M AF Kayaalp, Levent Dervent, Aysin Saltik, Sema Uluduz, Derya Kayaalp, Inci Vural Demirbilek, Veysi Ghaziuddin, Mohammad TI EEG abnormalities in West syndrome: Correlation with the emergence of autistic features SO BRAIN & DEVELOPMENT LA English DT Article DE West syndrome; hypsarrhythmia; autism; frontal spike-wave ID PERVASIVE DEVELOPMENTAL DISORDERS; TUBEROUS SCLEROSIS COMPLEX; INFANTILE SPASMS; FOLLOW-UP; CHILDHOOD AUTISM; NORMAL-CHILDREN; EPILEPSY; SLEEP; PATTERNS; POPULATION AB Autism may develop in children with West syndrome. This study was conducted to determine if EEG abnormalities in patients with West syndrome predict the later onset of autism. Two groups of patients with West syndrome, older than 6 years of age, were studied. One group consisted of those with a past history of West syndrome plus autism (N = 14); the control group consisted of those with a past history of West syndrome but without autism (N = 14). Patients were followed at regular intervals and video-EEG recordings were done. A total of 108 (autistic group) and 123 (non-autistic group) video-EEGs were examined. The two groups were compared with respect to age, presence or absence of hypsarrhythmia, and characteristics and localization of the epileptogenic foci. chi(2) and Fisher's exact tests were used. The number of patients with at least one hypsarrhythmic EEG at the age of one year or later was significantly higher in autistic subjects (86%) than in non-autistic controls (29%). The incidence of EEGs with hypsarrhythmia was also higher in the autistic group, especially in older children (autistic, 49% versus non-autistic, 18% at age 3 years and later). Frontal predominance of the primary foci on EE-Gs with or without hypsarrhythmia was seen in 95.3% of the autistic group and 28.8% of the non-autistic group (p = 0.001). Frontal abnormalities on the EEGs, which were mainly bilateral, and the persistence of hypsarrhythmia were significantly related to the emergence of autistic behavior in patients with West syndrome. These findings suggest that paroxysmal discharges in the cortical areas undergoing rapid maturation may be involved in the development of autistic features. (C) 2006 Elsevier B.V. All rights reserved. C1 Istanbul Univ, Cerrahpasa Med Fac, Child Psychiat Dept, Istanbul, Turkey. Istanbul Univ, Cerrahpasa Med Fac, Dept Neurol, Istanbul, Turkey. Istanbul Goztepe Educ & Res Hosp, Dept Pediat, Istanbul, Turkey. Vali Konagi Cad Nisantasi Istandul 285, TR-34365 Istanbul, Turkey. Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA. 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In the case of Autism Spectrum Disorder (ASD), the determination of such a percentage remains a controversial matter; and when combined with educating these people, makes detection, identification and diagnosis of the disorder an important challenge. In this research a study of the prevalence of ASD is presented for the compulsory, school-age population of children in the city of Seville, Spain. The results were analysed as a function of age and gender of the subjects, the schooling type, and the different diagnostic categories that are considered within Autism Spectrum Disorder. These results demonstrate prevalence rates similar to those results recently obtained in other studies carried out both in and outside of Spain. C1 Univ Seville, Lecturer Res Grp Special Educat Needs & Cognit En, Dept Psicol evolut & Educ, Fac Psicol, Seville 41018, Spain. 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Using a research instrument devised by Mavropoulou and Padeliadu (2000), a study was carried out of all social workers working with disabled children in an English local authority. The results showed that though many workers had a good understanding of some aspects of the condition, there was also confusion about some key facts concerning ASD, the characteristics of ASD and scientific terminology, an inaccurate understanding of intervention approaches, and a more positive attitude towards the ability of generic services to meet need than was supported by the literature. Implications are discussed in terms of the provision of services to families of children with ASD in the UK, and the limitations of this study are recognized. C1 Univ Birmingham, Sch Educ, Birmingham B15 2TT, W Midlands, England. RP Jordan, R (reprint author), Univ Birmingham, Sch Educ, Birmingham B15 2TT, W Midlands, England. 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Psychiatr. N. Am. PD JUL PY 2007 VL 16 IS 3 BP 541 EP + DI 10.1016/j.chc.2007.03.003 PG 17 WC Psychiatry SC Psychiatry GA 188UI UT WOS:000247944400003 PM 17562578 ER PT J AU Feinstein, C Singh, S AF Feinstein, Carl Singh, Sonia TI Social phenotypes in neurogenetic syndromes SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Review ID FRAGILE-X-SYNDROME; PRADER-WILLI-SYNDROME; CARDIO-FACIAL SYNDROME; 22Q11 DELETION SYNDROME; AUTISM SPECTRUM DISORDERS; PREMATURE OVARIAN FAILURE; SMITH-MAGENIS-SYNDROME; DOWN-SYNDROME; TURNER-SYNDROME; BEHAVIORAL-PHENOTYPE AB Many of the known genetically based neurodevelopmental disorders are associated with a distinctive behavioral phenotype. As these behavioral phenotypes have been elucidated by clinical research, distinctive profiles of social traits have emerged as prominent syndromic features. This article reviews social phenotypic findings for fragile X syndrome, Down syndrome, Prader-Willi syndrome, Smith-Magenis syndrome, Turner syndrome, Williams syndrome, and velocardiofacial syndrome. An analysis of these social profiles raises several questions regarding the relationship between identified social impairments and autism and the relationship between social impairments in neurodevelopmental disorders and those found in normative child populations. The unique profile of certain of the known behavioral phenotypes also serves to distinguish several dimensions of sociability that are not readily observed in typical populations. C1 Lucile Packard Childrens Hosp, Dept Child & Adolescent Psychiat, Stanford, CA 94305 USA. RP Feinstein, C (reprint author), Lucile Packard Childrens Hosp, Dept Child & Adolescent Psychiat, 401 Quarry Rd,MC 5719, Stanford, CA 94305 USA. 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The study of individuals with FraX provides a unique window of understanding into important disorders such as autism, social phobia, cognitive disability, and depression. This review highlights the typical phenotypic features of individuals with FraX, discussing the apparent strengths and weaknesses in intellectual functioning, as evidenced from longitudinal follow-up studies. It also discusses recent neuroanatomic findings that may pave the way for more focused disease-specific pharmacologic and behavioral interventions. This article describes the results of an open-label trial of the antiglucocorticoid medication, mifepristone, that the authors have recently conducted in boys and men with FraX, as well as other medication trials designed to target symptoms associated with FraX It also describes some recent behavioral interventions that were conducted in the authors' laboratory. C1 Stanford Univ, Dept Psychiat & Behav Sci, Ctr Interdisciplinary Brain Sci Res, Stanford, CA 94305 USA. 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The behavioral phenotype of Prader-Willi syndrome affects four domains: food-seeking related behaviors; traits that indicate lack of flexibility; oppositional behaviors, and interpersonal problems. The management of the maladaptive behaviors is challenging and requires lifelong restrictive supervision (to prevent morbid obesity), addressing psychiatric comorbidity, psychopharmacologic management exacerbated by metabolic abnormalities, ongoing medical care, and, in many cases, institutional treatment. The multiple facets of the clinical problems demand a multidisciplinary approach with anticipatory medical and psychiatric care, oriented to enhancing the quality of life of individuals who have Prader-Willi syndrome. C1 Hadassah Univ Hosp, IL-91240 Jerusalem, Israel. Shaare Zedek Med Ctr, Neuropediat Unit, IL-91301 Jerusalem, Israel. RP Benarroch, F (reprint author), Hebrew Univ Jerusalem, Hadassah Med Ctr, Jerusalem, Israel. 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Psychiatr. N. Am. PD JUL PY 2007 VL 16 IS 3 BP 723 EP + DI 10.1016/j.chc.2007.03.004 PG 22 WC Psychiatry SC Psychiatry GA 188UI UT WOS:000247944400014 ER PT J AU Sharma, R Chandrakantha, EL Mold, B AF Sharma, R. Chandrakantha, E. L. Mold, B. TI National Autism Plan standards for assessment are achievable SO CHILD CARE HEALTH AND DEVELOPMENT LA English DT Letter C1 Northampton Gen Hosp, Northampton NN1 5BD, Northants, England. RP Sharma, R (reprint author), Northampton Gen Hosp, Northampton NN1 5BD, Northants, England. EM raman.sharma@ngh.nhs.uk CR *DEP HLTH, 2006, POP STAT CHILDR YOUN National Initiative for Autism: Screening and Assessment, 2003, NAT AUT PLAN CHILDR Preece PM, 2006, CHILD CARE HLTH DEV, V32, P559, DOI 10.1111/j.1365-2214.2006.00656.x 2006, SCH FAIL AUTISTIC CH NR 4 TC 2 Z9 2 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0305-1862 J9 CHILD CARE HLTH DEV JI Child Care Health Dev. PD JUL PY 2007 VL 33 IS 4 BP 500 EP 501 DI 10.1111/j.1365-2214.2007.00760.x PG 2 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 176VL UT WOS:000247112900020 PM 17584408 ER PT J AU Parish-Morris, J Hennon, EA Hirsh-Pasek, K Golinkoff, RM Tager-Flusberg, H AF Parish-Morris, Julia Hennon, Elizabeth A. Hirsh-Pasek, Kathy Golinkoff, Roberta Michnick Tager-Flusberg, Helen TI Children with autism illuminate the role of social intention in word learning SO CHILD DEVELOPMENT LA English DT Review ID HIGH-FUNCTIONING AUTISM; JOINT ATTENTION; SPECTRUM DISORDERS; BEHAVIORAL REENACTMENT; STIMULUS ENHANCEMENT; SOCIOECONOMIC-STATUS; ALTERNATIVE ACCOUNT; TYPICAL DEVELOPMENT; PRESCHOOL-CHILDREN; YOUNG-CHILDREN AB To what extent do children with autism (AD) versus typically developing children (TD) rely on attentional and intentional cues to learn words? Four experiments compared 17 AD children (M age = 5.08 years) with 17 language- and 17 mental-age-matched TD children (M ages = 2.57 and 3.12 years, respectively) on nonverbal enactment and word-learning tasks. Results revealed variability in all groups, but particularly within the AD group. Performance on intention tasks was the most powerful predictor of vocabulary in the AD group but not in the TD groups. These findings suggest that word learning cannot be explained exclusively by either attentional or intentional processes, and they provide evidence of a special role for intentional understanding in the vocabulary development of AD children. C1 Temple Univ, Philadelphia, PA 19122 USA. Univ Evansville, Evansville, IN USA. Univ Delaware, Newark, DE USA. Boston Univ, Sch Med, Boston, MA 02215 USA. RP Parish-Morris, J (reprint author), Dept Psychol, Weiss Hall,1701 N 13th St, Philadelphia, PA 19122 USA. 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In addition, they strongly regulate cortical development by modulating several cellular processes such as neuronal proliferation, migration, differentiation and connectivity. Not surprisingly, aberrant development of GABAergic circuits has been implicated in many neurodevelopmental disorders including schizophrenia, autism and Tourette's syndrome. Unfortunately, efforts directed towards the comprehension of the mechanisms regulating GABAergic circuits formation and function have been impaired by the strikingly heterogeneity, both at the morphological and functional level, of GABAergic interneurons. Recent technical advances, including the improvement of interneurons-specific labelling techniques, have started to reveal the basic principles underlying this process. This review summarizes recent findings on the mechanisms underlying the construction of GABAergic circuits in the cortex, with a particular focus on potential implications for brain diseases with neurodevelopmental origin. 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Genet. PD JUL PY 2007 VL 72 IS 1 BP 1 EP 8 DI 10.1111/j.1399-0004.2007.00822.x PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 183MB UT WOS:000247575800001 PM 17594392 ER PT J AU Kawakubo, Y Kasai, K Okazaki, S Hosokawa-Kakurai, M Watanabe, K Kuwabara, H Ishijima, M Yamasue, H Iwanami, A Kato, N Maekawa, H AF Kawakubo, Yuki Kasai, Kiyoto Okazaki, Shinji Hosokawa-Kakurai, Miyuki Watanabe, Kei-ichiro Kuwabara, Hitoshi Ishijima, Michiko Yamasue, Hidenori Iwanami, Akira Kato, Nobumasa Maekawa, Hisao TI Electrophysiological abnormalities of spatial attention in adults with autism during the gap overlap task SO CLINICAL NEUROPHYSIOLOGY LA English DT Article DE autism; spatial attention; event-related potentials; saccadic eye movement ID EVENT-RELATED POTENTIALS; PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-DENSITY ERP; VISUAL-ATTENTION; SELECTIVE ATTENTION; CHILDHOOD AUTISM; REACTION-TIME; RATING-SCALE; CHILDREN; SACCADES AB Objective: We evaluated event-related potentials (ERPs) elicited by attentional disengagement in individuals with autism. Methods: Sixteen adults with autism, 17 adults with mental retardation and 14 healthy adults participated in this study. We recorded the pre-saccade positive ERPs during the gap overlap task under which a peripheral stimulus was presented subsequent to a stimulus in the central visual field. Under the overlap condition, the central stimulus remained during the presentation of the peripheral stimulus and therefore participants need to disengage their attention intentionally in order to execute the saccade to the peripheral stimulus due to the preservation of the central stimulus. Results: The autism group elicited significantly higher pre-saccadic positivity during a period of 100-70 ms prior to the saccade onset than the other groups only underthe overlap condition. The higher amplitude of pre-saccadic positivity in the overlap condition was significantly correlated with more severe clinical symptoms within the autism group. Conclusions: These results demonstrate electrophysiological abnormalities of disengagement during visuospatial attention in adults with autism which cannot be attributed to their IQs. Significance: We suggest that adults with autism have deficits in attentional disengagement and the physiological substrates underlying deficits in autism and mental retardation are different. (c) 2007 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. C1 Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, Tokyo 1138655, Japan. Univ Tsukuba, Inst Disabil Sci, Tsukuba, Ibaraki 3058572, Japan. Fuji Tokoha Univ, Fac Educ & Care Early Childhood, Fuji, Shizuoka 4170801, Japan. Univ Tokyo, Sch Med, Dept Child Psychiat, Tokyo 1138655, Japan. Saitama Med Univ, Dept Neuropsychiat, Iruma 3500495, Japan. Showa Univ, Sch Med, Dept Psychiat, Tokyo 1428555, Japan. 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Neurophysiol. PD JUL PY 2007 VL 118 IS 7 BP 1464 EP 1471 DI 10.1016/j.clinph.2007.04.015 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 183PA UT WOS:000247583500005 PM 17532260 ER PT J AU Tervo, RC AF Tervo, Raymond C. TI Language proficiency, development, and behavioral difficulties in toddlers SO CLINICAL PEDIATRICS LA English DT Article DE parent report; language; development; behavioral; toddlers ID CHILD-DEVELOPMENT INVENTORY; PARENTS REPORTS; YOUNG-CHILDREN; DELAY; DISORDERS; COMMUNICATION; IMPAIRMENT; PREVALENCE; AUTISM AB The aim of this cross-sectional descriptive study was to explore the relation of language proficiency, behavioral difficulties, and development in infants and toddlers. Surveyed were 118 parents/caregivers of preschool children (76 boys, 42 girls). The children were a mean age of 27 months (range, 18-35 months), and 32 (27.1%) had no language delay, 8 (6.8%) had expressive delay, 14 (11.9%) had receptive delay, and 64 (54.2%) had mixed receptive-expressive delay. Children with expressive delay were more likely to have social-emotional problems. Those with receptive delay were more likely to have pervasive developmental problems. Children with receptive-expressive delay were more substantially delayed in all developmental domains; they were more withdrawn and more likely to have pervasive developmental problems. When parents of toddlers report problems, especially behavior problems, a search for delayed language is warranted as these children may be at risk for future social and emotional problems. C1 Gillette Childrens Specialty Healthcare, Pedait Sect, St Paul, MN 55101 USA. Univ Minnesota, Dept Pediat, Minneapolis, MN USA. 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Pediatr. PD JUL PY 2007 VL 46 IS 6 BP 530 EP 539 DI 10.1177/0009922806299154 PG 10 WC Pediatrics SC Pediatrics GA 180UC UT WOS:000247390600009 PM 17579106 ER PT J AU Aman, MG Vinks, AA Remmerie, B Mannaert, E Ramadan, Y Masty, J Lindsay, RL Malone, K AF Aman, Michael G. Vinks, Alexander A. Remmerie, Bart Mannaert, Erik Ramadan, Yaser Masty, Jessica Lindsay, Ronald L. Malone, Krista TI Plasma pharmacokinetic characteristics of risperidone and their relationship to saliva concentrations in children with psychiatric or neurodevelopmental disorders SO CLINICAL THERAPEUTICS LA English DT Article DE risperidone; children; pharmacokinetics; saliva; plasma; 9-hydroxyrisperidone enantiomers ID PSYCHOMOTOR PERFORMANCE; PSYCHOACTIVE MEDICINES; DRUG CONCENTRATION; AUTISM-SOCIETY; SEIZURE TYPE; CYP2D6 GENE; 9-HYDROXYRISPERIDONE; SCHIZOPHRENIA; PATTERNS; CARBAMAZEPINE AB Background: Risperidone is a second-generation antipsychotic agent widely used in the treatment of schizophrenia and other psychotic disorders in adults. Risperidone is probably the most frequently used atypical antipsychotic in the pediatric population. Objectives: The goals of this study were to estimate the pharmacokinetic parameters of risperidone and its enantiomers in a pediatric population and explore relationships between saliva and plasma concentrations. Methods: Eligible patients, between 4 and 15 years of age, included those taking a stable dose of oral risperidone ranging from 0.01 to 0.07 mg/kg BID for >= 4 weeks to treat psychiatric or neurodevelopmental conditions. A trough blood level and predose saliva sample were collected at study initiation; the regular risperidone dose was administered; and paired samples of blood and saliva were collected at 1, 2, 4, and 7 hours postdose. Plasma/saliva concentrations of risperidone and enantiomers of its principal active metabolite, 9-hydroxyrisperidone (9-OH-risperidone), were measured using a chiral liquid chromatography-tandem mass spectrometry assay. Standard pharmacokinetic parameters were calculated. Cytochrome P450 2D6 genotypes of *3,*4,*5 deletion and duplication were determined. Results: The study included 19 patients (age range, 4 years 2 months to 15 years 11 months). Mean (SD) values for C-max t(1/2), and AUC 0 to 12 hours for risperidone in plasma were 15.9 (22.2) ng/mL, 3.0 (2.3) h, and 92.1 (200.6) ng . h/mL, respectively. Corresponding values in saliva were 12.0 (21.0) ng/mL, 3.4 (3.2) h, and 27.8 (38.7) ng . h/mL, respectively. Mean (SD) plasma enantiomer values for C-max and AUC calculated up to the last observation were: (+)-9-OH-risperidone, 13.6 (10.0) ng/mL and 73.6 (52.3) ng . h/mL; (-)-9-OH-risperidone, 4.9 (3.1) ng/mL and 29.3 (19.1) ng . h/mL. Corresponding enantiomer values in saliva were: (+)-9-OH-risperidone, 5.2 (8.8) ng/mL and 15.6 (8.9) ng . h/mL; (-)-9-OH-risperidone, 5.0 (7.9) ng/mL and 15.6 (9.1) ng . h/mL, respectively. Large interindividual variability in risperidone and enantiomer concentrations was noted. A highly significant relationship between predose plasma and predose saliva risperidone concentrations was observed. The logarithmic regression model indicated that the log risperidone saliva concentration = -0.100 + 0.594 . log plasma concentration (R-2 = 0.93 [Spearman]). Conclusions: In this preliminary pharmacokinetic study of parameters for risperidone and the enantiomers of 9-OH-risperidone in a pediatric population, mean C-max, and t(1/2) of risperidone were generally similar to those previously described in adults. The highly significant relationship between predose plasma and predose saliva risperidone concentrations suggests that saliva measurements may be a viable alternative to plasma sampling in children. C1 Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. Cincinnati Childrens Hosp, Med Ctr, Pediat Pharmacol Res Unit, Cincinnati, OH USA. Univ Cincinnati, Dept Pediat, Cincinnati, OH 45221 USA. Johnson & Johnson Pharmaceut Res & Dev, Beerse, Belgium. Fordham Univ, Bronx, NY 10458 USA. St Josephs Hosp, Arizona Child Study Ctr, Phoenix, AZ 85013 USA. Hospice Cent Ohio, Newark, OH USA. 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TI Evidence of a divided-attention advantage in autism SO COGNITIVE NEUROPSYCHOLOGY LA English DT Article ID VISUAL-SEARCH; SHIFTING ATTENTION; OLDER ADULTS; USEFUL FIELD; PERCEPTION; COHERENCE; VIEW; LOCALIZATION; INFORMATION; SENSITIVITY AB People with autism spectrum disorders appear to have some specific advantages in visual processing, including an advantage in visual search tasks. However, executive function theory predicts deficits in tasks that require divided attention, and there is evidence that people with autism have difficulty broadening their attention (Mann & Walker, 2003). We wanted to know how robust the known attentional advantage is. Would people with autism have difficulty dividing attention between central and peripheral tasks, as is required in the Useful Field of View task, or would they show an advantage due to strengths in visual search? Observers identified central letters and localized peripheral targets under both focused- and divided-attention conditions. Participants were 20 adults with high-functioning autism and Asperger's syndrome and 20 adults matched to the experimental group on education, age, and IQ. Contrary to some predictions, individuals with autism tended to show relatively smaller divided-attention costs than did matched adults. These results stand in stark contrast to the predictions of some prevalent theories of visual and cognitive processing in autism. C1 McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON L8S 4K1, Canada. Univ Prince Edward Isl, Charlottetown, PE C1A 4P3, Canada. RP Rutherford, MD (reprint author), McMaster Univ, Dept Psychol Neurosci & Behav, 1280 Main St W, Hamilton, ON L8S 4K1, Canada. 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Neuropsychol. PD JUL PY 2007 VL 24 IS 5 BP 505 EP 515 DI 10.1080/02643290701508224 PG 11 WC Psychology; Psychology, Experimental SC Psychology GA 207JP UT WOS:000249247700003 PM 18416504 ER PT J AU Wang, LX Mottron, L Berthiaume, C Dawson, M AF Wang, Lixin Mottron, Laurent Berthiaume, Claude Dawson, Michelle TI Local bias and local-to-global interference without global deficit: A robust finding in autism under various conditions of attention, exposure time, and visual angle SO COGNITIVE NEUROPSYCHOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; PERCEPTUAL ORGANIZATION; ORIENTED PERCEPTION; SPECTRUM DISORDERS; COGNITIVE-STYLE; TASK; PERFORMANCE; CHILDREN; ABILITIES; STIMULI AB A wide variety of paradigms have shown that autistic individuals present with superior performance on visual tasks. Here, the impact of task constraints on visual hierarchical processing in autism was investigated. By employing free- and forced-choice procedures, global and local processing of Navon-type hierarchical numerals was examined in 15 autistic persons (13 males, 2 females) and a comparison group. In the free-choice condition, autistics chose global and local targets randomly, though they were faster responding to local than to global targets, regardless of visual angle and exposure duration. In contrast, the comparison group exhibited a global advantage in naming time, which was evident only for shorter exposures, as well as effects of visual angle. In the forced-choice condition, autistics presented with a more important local-to-global interference than global-to-local interference, whereas the comparison group exhibited global advantage and bidirectional interference. Overall, the autistic participants presented with atypical local-to-global interference and local advantage in incongruent conditions (where global and local targets differ), in naming time as well as accuracy. 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Neuropsychol. PD JUL PY 2007 VL 24 IS 5 BP 550 EP 574 DI 10.1080/13546800701417096 PG 25 WC Psychology; Psychology, Experimental SC Psychology GA 207JP UT WOS:000249247700006 PM 18416507 ER PT J AU Shalev, L AF Shalev, Lilach TI Do local bias and local-to-global interference reflect intact global processing in autism? SO COGNITIVE NEUROPSYCHOLOGY LA English DT Editorial Material C1 Hebrew Univ Jerusalem, Sch Educ, IL-91905 Jerusalem, Israel. RP Shalev, L (reprint author), Hebrew Univ Jerusalem, Sch Educ, IL-91905 Jerusalem, Israel. 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PD JUL PY 2007 VL 24 IS 5 BP 575 EP 577 DI 10.1080/02643290701541316 PG 3 WC Psychology; Psychology, Experimental SC Psychology GA 207JP UT WOS:000249247700007 PM 18416508 ER PT J AU Mottron, L Dawson, M Bertone, A Wang, LX AF Mottron, Laurent Dawson, Michelle Bertone, Armando Wang, Lixin TI Cognitive versatility in autism cannot be reduced to a deficit SO COGNITIVE NEUROPSYCHOLOGY LA English DT Editorial Material ID PERCEPTION; CHILDREN; MOTION; COMPLEXITY C1 Univ Montreal, Hop Rivieres Prairies, Montreal, PQ H1E 1A4, Canada. Univ Montreal, Visual Psychophys & Percept Lab, Montreal, PQ, Canada. Beijing Normal Univ, Sch Psychol, Beijing 100875, Peoples R China. RP Mottron, L (reprint author), Univ Montreal, Hop Rivieres Prairies, 7070 Bvd Perras, Montreal, PQ H1E 1A4, Canada. EM mottronl@istar.ca CR Bertone A, 2005, BRAIN, V128, P2430, DOI 10.1093/brain/awh561 Blake R, 2003, PSYCHOL SCI, V14, P151, DOI 10.1111/1467-9280.01434 Brosnan MJ, 2004, J CHILD PSYCHOL PSYC, V45, P459, DOI 10.1111/j.1469-7610.2004.00237.x Caron MJ, 2006, BRAIN, V129, P1789, DOI 10.1093/brain/awl072 Del Viva MM, 2006, VISION RES, V46, P1242, DOI 10.1016/j.visres.2005.10.018 Gernsbacher MA, 2006, BEHAV BRAIN SCI, V29, P413 GERNSBACHER MA, IN PRESS CHILD DEV P Happe F, 2006, J AUTISM DEV DISORD, V36, P5, DOI 10.1007/s10803-005-0039-0 Jemel B, 2006, J AUTISM DEV DISORD, V36, P91, DOI 10.1007/s10803-005-0050-5 Lahaie A, 2006, NEUROPSYCHOLOGY, V20, P30, DOI 10.1037/0894-4105.20.1.30 Mottron L, 2006, J AUTISM DEV DISORD, V36, P27, DOI 10.1007/s10803-005-0040-7 MOTTRON L, IN PRESS DIFFERENT M Rouse H, 2004, J CHILD PSYCHOL PSYC, V45, P1246, DOI 10.1111/j.1469-7610.2004.00317.x RUTHERFORD MD, 2007, COGNITIVE NEUROPSYCH Samson F, 2006, J AUTISM DEV DISORD, V36, P65, DOI 10.1007/s10803-005-0043-4 Shalev L, 2007, COGN NEUROPSYCHOL, V24, P575, DOI 10.1080/02643290701541316 SHEPPARD E, J AUTISM DEV DISORDE Soulieres I, 2007, J AUTISM DEV DISORD, V37, P481, DOI 10.1007/s10803-006-0172-4 Spencer J, 2000, NEUROREPORT, V11, P2765, DOI 10.1097/00001756-200008210-00031 Spencer JV, 2006, PERCEPTION, V35, P1047, DOI 10.1068/p5328 Wang LX, 2007, COGN NEUROPSYCHOL, V24, P550, DOI 10.1080/13546800701417096 NR 21 TC 3 Z9 3 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0264-3294 J9 COGN NEUROPSYCHOL JI Cogn. Neuropsychol. PD JUL PY 2007 VL 24 IS 5 BP 578 EP 580 DI 10.1080/02643290701541522 PG 3 WC Psychology; Psychology, Experimental SC Psychology GA 207JP UT WOS:000249247700008 ER PT J AU Mutter, J Naumann, J Guethlin, C AF Mutter, Joachim Naumann, Johannes Guethlin, Corina TI Comments on the article "The toxicology of mercury and its chemical compounds" by Clarkson and Magos (2006) SO CRITICAL REVIEWS IN TOXICOLOGY LA English DT Editorial Material DE amalgam; autism; ethylmercury; mercury; toxicity; thimerosal ID DENTAL AMALGAM FILLINGS; SILVER TOOTH FILLINGS; AMYOTROPHIC-LATERAL-SCLEROSIS; SHSY5Y NEUROBLASTOMA-CELLS; INDUCED OXIDATIVE STRESS; BETA-AMYLOID SECRETION; 1998 GERES-III; INORGANIC MERCURY; ALZHEIMERS-DISEASE; MULTIPLE-SCLEROSIS AB Clarkson and Magos (2006) provide their perspectives on the toxicology of mercury vapor and dental amalgam. As scientists who are involved in preparing a German federal guidline regarding dental amalgam, we welcome additional scientific data on this issue. However, Clarkson and Magos do not present all the relevant studies in their review. The additional data provided here show that: (a) Dental amalgam is the main source of human total mercury body burden, because individuals with amalgam have 2-12 times more mercury in their body tissues compared to individuals without amalgam; (b) there is not necessarily a correlation between mercury levels in blood, urine, or hair and in body tissues, and none of the parameters correlate with severity of symptoms; (c) the half-life of mercury deposits in brain and bone tissues could last from several years to decades, and thus mercury accumulates over time of exposure; (d) mercury, in particular mercury vapor, is known to be the most toxic nonradioactive element, and is toxic even in very low doses, and (e) some studies which conclude that amalgam fillings are safe for human beings have important methodogical flaws. Therefore, they have no value for assessing the safety of amalgam. C1 Univ Hosp Freiburg, Inst Environm Med & Hosp Epidemiol, D-79106 Freiburg, Germany. RP Mutter, J (reprint author), Univ Hosp Freiburg, Inst Environm Med & Hosp Epidemiol, Breisacherstr,115 B, D-79106 Freiburg, Germany. 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Rev. Toxicol. PD JUL PY 2007 VL 37 IS 6 BP 537 EP 549 DI 10.1080/10408440701385770 PG 13 WC Toxicology SC Toxicology GA 196TK UT WOS:000248504900004 PM 17661216 ER PT J AU Hazell, P AF Hazell, Philip TI Does the treatment of mental disorders in childhood lead to a healthier adulthood? SO CURRENT OPINION IN PSYCHIATRY LA English DT Editorial Material DE adolescent; child; mental disorders; treatment outcome ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; ANOREXIA-NERVOSA; FOLLOW-UP; STIMULANT TREATMENT; SUBSTANCE-ABUSE; CHILDREN; RISK; LIFE; PSYCHOPATHOLOGY; ADOLESCENTS AB Purpose of review To review mechanisms by which intervention for childhood mental disorders may exert an influence on mental health and wellbeing in adulthood, the challenges to demonstrating long-term benefit of harm from such intervention,existing evidence of long-term benefit, and strategies for improving the long-term benefit of treatment. Recent findings Intervention may improve long-term outcome through the promotion of protective interpersonal relationships, by enhancing scholastic and later occupational functioning, by arresting the progression of disorder, and by improving general health. Challenges to demonstrating benefits of harms in the long term include variability in the natural course of childhood mental disorders, heterotypic outcomes, and the influence of other variables over time on long-term functioning. Examples of demonstrated benefit include the lowering of risk for sub stance abuse seen with psychostimulant treatment for attention-devicit/hyperactivity disorder, improved outcomes for autism since the introduction of early interventions to address language impairment, and reduced mortality in anorexia nervosa. Summary There are feasible enduring benefits of treatment for childhood mental disorders. Treatment of complex problems may have a greater long-term impact than in conditions that follow a benign natural course. Success requires more assertive approaches to treatment than are traditionally employed by child and adolescent mental health services. C1 Univ Sydney, Sydney, NSW 2006, Australia. RP Hazell, P (reprint author), Thomas Walker Hosp Rivendell, Hosp Rd, Concord W, NSW 2138, Australia. 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PD JUL PY 2007 VL 20 IS 4 BP 315 EP 318 DI 10.1097/YCO.0b013e3281a7368d PG 4 WC Psychiatry SC Psychiatry GA 186IR UT WOS:000247772900001 PM 17551343 ER PT J AU Fazzi, E Rossi, M Signorini, S Rossi, G Bianchi, PE Lanzi, G AF Fazzi, E. Rossi, M. Signorini, S. Rossi, G. Bianchi, P. E. Lanzi, G. TI Leber's congenital amaurosis: is there an autistic component ? SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID BLIND-CHILDREN; DIAGNOSIS AB There is much evidence in the literature suggesting that children with congenital blindness can also present autistic like features. The aetiopathogenetic and clinical significance of this association is still unclear. Given the central role played by vision in development, we set out to establish the significance of autistic-like behaviours in children with early-onset severe visual impairment. Our sample comprised 24 children (13 males, 11 females; mean age 5y 2mo; range 2-11y) affected by Leber's congenital amaurosis (LCA). The results of our administration of a modified Childhood Austism Rating Scale - excluding item VII (Visual Responsiveness) - showed that only four of the children gave an overall score indicating the presence of autism (moreover, of mild/moderate degree). Hardly any of the children in our LCA sample presented major dysfunctions in their relationships with other people or in their social and emotional responsiveness, thus allowing us to exclude a genuine comorbidity with a picture of autism. Indeed, the risk facing the visually impaired child seems to concern their early interactive experiences, which may be affected by their inability to connect with others, and may be prevented through the development of specific strategies of intervention. C1 Univ Pavia, IRCCS, Neurol Inst C Mondino, Dept Child Neurol & Psychiat, I-27100 Pavia, Italy. IRCCS, Neurol Inst C Mondino, Dept Child Neurol & Psychiat, Pavia, Italy. St Matteo Hosp, IRCCS, Dept Ophthalmol, Pavia, Italy. RP Fazzi, E (reprint author), Univ Pavia, IRCCS, Neurol Inst C Mondino, Dept Child Neurol & Psychiat, Via Mondino 2, I-27100 Pavia, Italy. 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Med. Child Neurol. PD JUL PY 2007 VL 49 IS 7 BP 503 EP 507 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 181ZX UT WOS:000247476000008 PM 17593121 ER PT J AU Heilman, KJ Bal, E Bazhenova, OV Porges, SW AF Heilman, Keri J. Bal, Elgiz Bazhenova, Olga V. Porges, Stephen W. TI Respiratory sinus arrhythmia and tympanic membrane compliance predict spontaneous eye gaze behaviors in young children: A pilot study SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Article DE respiratory sinus arrhythmia; middle ear; tympanic membrane compliance; eye gaze; heart period; social behavior; children ID CARDIAC VAGAL TONE; SOCIAL-BEHAVIOR; OTITIS-MEDIA; POLYVAGAL THEORY; HEART-RATE; LANGUAGE IMPAIRMENT; SELECTIVE MUTISM; AUTISM; REACTIVITY; SKILLS AB The Polyvagal theory proposes the Social Engagement System as a theoretical model linking social behavior with the neural regulation of the heart (via the vagus) and the striated muscles of the face and head (via special visceral efferent pathways). The current pilot study tested the feasibility of this model with typically developing 3-5-year-old children by evaluating the relation between spontaneous social engagement behavior measured by eye gaze behaviors and the visceromotor (e.g., respiratory sinus arrhythmia) and somatomotor (e.g., right tympanic membrane compliance) components of the Social Engagement System. Regression analyses supported the hypothesis that the visceromotor and somatomotor components of the Social Engagement System significantly predict social behavior (indexed by spontaneous eye gazes). Future studies assessing indices of visceral regulation and middle ear muscle function may provide insights into neural mechanisms mediating features of developmental disorders, such as autism, that have deficits in spontaneous eye gaze, auditory processing, and social behavior (c) 2007 Wiley Periodicals, Inc. C1 Univ Illinois, Chicago, IL 60607 USA. RP Porges, SW (reprint author), Univ Illinois, Chicago, IL 60607 USA. 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PD JUL PY 2007 VL 49 IS 5 BP 531 EP 542 DI 10.1002/dev.20237 PG 12 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA 185MY UT WOS:000247716300009 PM 17577239 ER PT J AU Pellicano, E AF Pellicano, Elizabeth TI Links between theory of mind and executive function in young children with autism: Clues to developmental primacy SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article DE autism; theory of mind; executive function; cognitive development ID TO-MANAGE PRESCHOOLERS; FALSE BELIEF TASKS; WORKING-MEMORY; INHIBITORY CONTROL; INDIVIDUAL-DIFFERENCES; STRATEGIC DECEPTION; SPECTRUM DISORDERS; VERBAL-ABILITY; DYSFUNCTION; IMPAIRMENTS AB There has been much theoretical discussion of a functional link between theory of mind (ToM) and executive function (EF) in autism. This study sought to establish the relationship between ToM and EF in young children with autism (M = 5 years, 6 months) and to examine issues of developmental primacy. Thirty children with autism and 40 typically developing children, matched on age and ability, were assessed on a battery of tasks measuring ToM (1st- and 2nd-order false belief) and components of EF (planning, set shifting, inhibition). A significant correlation emerged between ToM and EF variables in the autism group, independent of age and ability, while ToM and higher order planning ability remained significantly related in the comparison group. Examination of the pattern of ToM-EF impairments in the autism group revealed dissociations in 1 direction only: impaired ToM with intact EF. These findings support the view that EF may be 1 important factor in the advancement of ToM understanding in autism. The theoretical implications of these findings are discussed. C1 Univ Oxford, Univ Coll, Oxford, England. Univ Western Australia, Sch Psychol, Crawley, WA, Australia. RP Pellicano, E (reprint author), Univ Bristol, Dept Expt Psychol, 12A Priory Rd, Bristol BS8 1TU, Avon, England. 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PD JUL 1 PY 2007 VL 41 IS 13 BP 4493 EP 4494 PG 2 WC Engineering, Environmental; Environmental Sciences SC Engineering; Environmental Sciences & Ecology GA 186MJ UT WOS:000247782500009 PM 17695885 ER PT J AU Kurian, JR Forbes-Lorman, RM Auger, AP AF Kurian, Joseph R. Forbes-Lorman, Robin M. Auger, Anthony P. TI Sex difference in Mecp2 expression during a critical period of rat brain development SO EPIGENETICS LA English DT Article DE Mecp2; development; sex-difference; epigenetics; autism; Rett syndrome ID AUTISM-SPECTRUM DISORDERS; CPG-BINDING-PROTEIN; RETT-SYNDROME; MOUSE MODEL; NERVOUS-SYSTEM; X-INACTIVATION; MESSENGER-RNA; NEONATAL-RAT; GENE; DIFFERENTIATION AB Pervasive developmental disorder is a classification covering five related conditions including the neurodevelopmental disorder Rett syndrome (RTT) and autism. Of these five conditions, only RTT has a known genetic cause with mutations in Methyl-CpG-binding protein 2 (MeCP2), a global repressor of gene expression, responsible for the majority of RTT cases. However, recent evidence indicates that reduced MeCP2 expression or activity is also found in autism and other disorders with overlapping phenotypes. Considering the sex difference in autism diagnosis, with males diagnosed four times more often than females, we questioned if a sex difference existed in the expression of MeCP2, in particular within the amygdala, a region that develops atypically in autism. We found that male rats express significantly less mecp2 mRNA and protein than females within the amygdala, as well as the ventromedial hypothalamus (VMH), but not within the preoptic area (POA) on post-natal day 1 (PN1). At PN10 these differences were gone; however, on this day males had more mecp2 mRNA than females within the POA. The transient sex difference of mecp2 expression during the steroid-sensitive period of brain development suggests that mecp2 may participate in normal sexual differentiation of the rat brain. Considering the strong link between MeCP2 and neurodevelopmental disorders, the lower levels of mecp2 expression in males may also underlie a biological risk for mecp2-related neural disorders. C1 [Kurian, Joseph R.; Forbes-Lorman, Robin M.; Auger, Anthony P.] Univ Wisconsin, Dept Psychol, Madison, WI 53706 USA. RP Auger, AP (reprint author), Univ Wisconsin, Dept Psychol, 1202 W Johnson St, Madison, WI 53706 USA. 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G. Ross, Louise TI Consequences of prenatal toxin exposure for mental health in children and adolescents SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Review DE prenatal; toxins; child; adolescent; neuro-development; mental health; ADHD; psychiatric disorder; risk factor; intra-uterine ID AUTISM SPECTRUM DISORDERS; MATERNAL SMOKING; BEHAVIORAL-PROBLEMS; COCAINE EXPOSURE; POLYCHLORINATED-BIPHENYLS; ACADEMIC-ACHIEVEMENT; ENVIRONMENTAL LEAD; PRESCHOOL-CHILDREN; ALCOHOL EXPOSURE; CONDUCT PROBLEMS AB Drug use during pregnancy is common and the developing foetus may be exposed to a range of environmental toxins that have long-term consequences for neurodevelopment. We conducted a systematic review of the literature to explore the results of longitudinal cohort studies that have examined this question. Out of 2,977 abstracts identified, 7 previous systematic reviews and 95 original articles met further selection criteria. These mostly addressed the neurodevelopmental effects of exposure to lead, polychlorinated biphenyls, mercury, cocaine, alcohol, marijuana, cigarettes and antidepressants. Radiation, opiates, steroids, amphetamines and caffeine have received much less attention. Findings are difficult to interpret because risk factors tend to cluster together and interact. However, some findings are consistent. Lead and PCB's have a general effect on brain development, whilst marijuana and alcohol appear to have long-term effects specifically on attentional skills. The effects of alcohol increase with maternal age and binge drinking is more important than average intake. The effects of cocaine diminish with age and are largely mediated through psychosocial factors, whilst the relation between smoking and later delinquency is largely mediated by genetically inherited factors. 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Child Adolesc. Psych. PD JUL PY 2007 VL 16 IS 4 BP 243 EP 253 DI 10.1007/s00787-006-0596-6 PG 11 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 178RT UT WOS:000247238500006 PM 17200791 ER PT J AU Lonardo, F Parenti, G Luquetti, DV Annunziata, I Della Monica, M Perone, L De Gregori, M Zuffardi, O Brunetti-Pierri, N Andria, G Scarano, G AF Lonardo, Fortunato Parenti, Giancarlo Luquetti, Daniela Varela Annunziata, Ida Della Monica, Matteo Perone, Lucia De Gregori, Manuela Zuffardi, Orsetta Brunetti-Pierri, Nicola Andria, Generoso Scarano, Gioacchino TI Contiguous gene syndrome due to an interstitial deletion in Xp22.3 in a boy with ichthyosis, chondrodysplasia punctata, mental retardation and ADHD SO EUROPEAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE ADHD; chondrodysplasia punctata; contiguous gene syndrome; ichthyosis; Xp22.3 microdeletion ID X-LINKED ICHTHYOSIS; VCX-A; FAMILY; MUTATIONS; DISORDER; AUTISM; MEMBER; NLGN4 AB Microdeletions of Xp22.3 can result in contiguous gene syndromes, showing the variable association of apparently unrelated clinical manifestations such as ichthyosis, chondrodysplasia punctata, hypogonadotropic hypogonadism, anosmia, ocular albinism, short stature and mental retardation. We report on a boy with ichthyosis, dysmorphic features and mental retardation with ADHD. The patient was born at term after a pregnancy complicated by threatened abortion; decreased fetal movements and low estriol serum levels were reported during the last trimester. The boy was referred to us at the age of 13 years. He presented with aggressive and hyperactive behavior. He had dry hair, a flat face, bilateral lens opacities, a small nose with hypoplastic tip, alae nasi and nares, a high-arched palate with a very small cleft, mixed dentition with 7 unerupted permanent teeth, left sensorineural and right mixed hearing loss with a calcified plaque of the tympanic membrane, marked shortness of terminal phalanges of hands and feet, ichthyosis of trunk and limbs. The genomic interval between AFM248th5 and KALI was investigated. PCR analysis showed a deletion in Xp22.3, with the distal breakpoint between the marker AFM248th5 and PABX and the proximal one between DXS278 and KALI. Array-CGH and FISH analysis confirmed the interstitial deletion (of about 5.5 Mb) and refined the breakpoints. We discuss the phenotype of our patient in relationship to the deleted segment and the possibility of mental retardation and ADHD genes in the region. (c) 2007 Elsevier Masson SAS. All rights reserved. C1 UOC Genet Med, AORN Gaetano Rummo, SS Citogenet Med & Genet Mol, I-82100 Benevento, Italy. Univ Naples Federico 2, Dipartimento Pediat, Naples, Italy. Telethon Inst Genet & Med, Naples, Italy. Univ Pavia, I-27100 Pavia, Italy. Policlin San Matteo, IRCCS, I-27100 Pavia, Italy. RP Lonardo, F (reprint author), UOC Genet Med, AORN Gaetano Rummo, SS Citogenet Med & Genet Mol, Via Angelo 1, I-82100 Benevento, Italy. 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J. Med. Genet. PD JUL-AUG PY 2007 VL 50 IS 4 BP 301 EP 308 DI 10.1016/j.ejmg.2007.04.005 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 202DM UT WOS:000248882200007 PM 17591464 ER PT J AU Gordon, N AF Gordon, Neil TI The cerebellum and cognition SO EUROPEAN JOURNAL OF PAEDIATRIC NEUROLOGY LA English DT Article DE cerebellum; ataxia; cognition; affect; causes ID POSTERIOR-FOSSA TUMORS; BRAIN ACTIVATION; MOTOR IMAGERY; DEFICITS; LESIONS; ATAXIA; DAMAGE; TASK AB The most important function of the cerebellum may be to coordinate motor function so that movements can be performed smoothly, but there are others. It has been shown that the cerebellum is involved in certain aspects of cognition and changes in affect. Also verbal deficits can be found after cerebellar lesions. The cerebellar cognitive affective syndrome is described, and the evidence for its existence discussed; in particular the use of neuroimaging studies. Different areas of the cerebellum have been identified as serving the various functions, and also their connections to the relevant parts of the cerebral cortex. Certain conditions merit special attention. The function of spatial navigation needs a major contribution from the cerebellum, and the problems of autism and impaired cognition are no doubt related to the enlarged cerebellum described in this disorder. The cognitive defects found in children with cerebellar ataxia supports its role in learning, and so does the study of music. (c) 2007 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved. RP Gordon, N (reprint author), Humtlywood,3 Styal Rd, Wilmslow SK9 4AE, Cheshire, England. 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J. Paediatr. Neurol. PD JUL PY 2007 VL 11 IS 4 BP 232 EP 234 DI 10.1016/j.ejpn.2007.02.003 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 181JK UT WOS:000247432800005 PM 17400009 ER PT J AU van Handel, M Swaab, H de Vries, LS Jongmans, MJ AF van Handel, Marielle Swaab, Hanna de Vries, Linda S. Jongmans, Marian J. TI Long-term cognitive and behavioral consequences of neonatal encephalopathy following perinatal asphyxia: a review SO EUROPEAN JOURNAL OF PEDIATRICS LA English DT Review DE asphyxia neonatorum; hypoxia; brain; hypoxia-ischemia; brain; neuropsychology; behavioral problems ID HYPOXIC-ISCHEMIC ENCEPHALOPATHY; DEFICIT-HYPERACTIVITY DISORDER; CEREBRAL-PALSY; NEWBORN ENCEPHALOPATHY; INTRAPARTUM ASPHYXIA; BIRTH ASPHYXIA; APGAR SCORES; BRAIN-INJURY; SCHOOL-AGE; INFANTS AB Neonatal encephalopathy (NE) following perinatal asphyxia (PA) is considered an important cause of later neurodevelopmental impairment in infants born at term. This review discusses long-term consequences for general cognitive functioning, educational achievement, neuropsychological functioning and behavior. In all areas reviewed, the outcome of children with mild NE is consistently positive and the outcome of children with severe NE consistently negative. However, children with moderate NE form a more heterogeneous group with respect to outcome. On average, intelligence scores are below those of children with mild NE and age-matched peers, but within the normal range. With respect to educational achievement, difficulties have been found in the domains reading, spelling and arithmetic/mathematics. So far, studies of neuropsychological functioning have yielded ambiguous results in children with moderate NE. A few studies suggest elevated rates of hyperactivity in children with moderate NE and autism in children with moderate and severe NE. Conclusion: Behavioral monitoring is required for all children with NE. In addition, systematic, detailed neuropsychological examination is needed especially for children with moderate NE. C1 Univ Utrecht, Med Ctr, Dept Neonatol, Wilhelmia Childrens Hosp, NL-3500 GA Utrecht, Netherlands. Leiden Univ, Dept Clin Child & Adolescent Studies, NL-2333 AK Leiden, Netherlands. Univ Utrecht, Med Ctr, Dept Neonatol, Wilhelmia Childrens Hosp, NL-3584 AE Utrecht, Netherlands. Univ Utrecht, Dept Gen & Special Educ, NL-3584 CS Utrecht, Netherlands. RP van Handel, M (reprint author), Univ Utrecht, Med Ctr, Dept Neonatol, Wilhelmia Childrens Hosp, Heidelberglaan 1,POB 85500, NL-3500 GA Utrecht, Netherlands. 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Psychiatr. PD JUL-SEP PY 2007 VL 72 IS 3 BP 421 EP 435 DI 10.1016/j.evopsy.2007.06.001 PG 15 WC Psychiatry SC Psychiatry GA 220PM UT WOS:000250168700003 ER PT J AU Hill, JM Cuasay, K Abebe, DT AF Hill, Joanna M. Cuasay, Katrina Abebe, Daniel T. TI Vasoactive intestinal peptide antagonist treatment during mouse embryogenesis impairs social behavior and cognitive function of adult male offspring SO EXPERIMENTAL NEUROLOGY LA English DT Review DE autism; neurodevelopmental disorder; sociability; social approach; cued and contextual fear conditioning; sex differences; neuropeptide ID DEPENDENT NEUROTROPHIC FACTOR; FETAL VALPROATE SYNDROME; EYE-MOVEMENT SLEEP; EMBRYONIC GROWTH; IGF-I; NEUROPROTECTIVE PEPTIDE; ENVELOPE PROTEIN; ALCOHOL SYNDROME; INBRED STRAINS; DEFICIENT MICE AB Vasoactive intestinal peptide (VIP) is a regulator of rodent ernbryogenesis during the period of neural tube closure. VIP enhanced growth in whole cultured mouse embryos; treatment with a VIP antagonist during embryogenesis inhibited growth and development. VIP antagonist treatment during embryogenesis also had permanent effects on adult brain chemistry and impaired social recognition behavior in adult male mice. The neurological deficits of autism appear to be initiated during neural tube closure and social behavior deficits are among the key characteristics of this disorder that is more common in males and is frequently accompanied by mental retardation. The current study examined the blockage of VIP during embryogenesis as a model for the behavioral deficits of autism. Treatment of pregnant mice with a VIP antagonist during embryonic days 8 through 10 had no apparent effect on the general health or sensory or motor capabilities of adult offspring. However, male offspring exhibited reduced sociability in the social approach task and deficits in cognitive function, as assessed through cued and contextual fear conditioning. Female offspring did not show these deficiencies. These results Suggest that this paradigm has usefulness as a mouse model for aspects of autism as it selectively impairs male offspring who exhibit the reduced social behavior and cognitive dysfunction seen in autism. Furthermore, the study indicates that the foundations of some aspects of social behavior are laid down early in mouse embryogenesis, are regulated in a sex specific manner and that interference with embryonic regulators such as VIP can have permanent effects on adult social behavior. Published by Elsevier Inc. C1 NIMH, Lab Behav Neurosci, NIH, Bethesda, MD 20892 USA. NICHD, Dev Neurobiol Lab, NIH, Bethesda, MD 21029 USA. RP Hill, JM (reprint author), NIMH, Lab Behav Neurosci, NIH, 35-1C903, Bethesda, MD 20892 USA. 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Neurol. PD JUL PY 2007 VL 206 IS 1 BP 101 EP 113 DI 10.1016/j.expneurol.2007.04.004 PG 13 WC Neurosciences SC Neurosciences & Neurology GA 187CN UT WOS:000247825000014 PM 17521630 ER PT J AU Grant, SFA Hakonarson, H AF Grant, Struan F. A. Hakonarson, Hakon TI Recent development in pharmacogenomics: from candidate genes to genome-wide association studies SO EXPERT REVIEW OF MOLECULAR DIAGNOSTICS LA English DT Review DE copy-number variation; genetics; genome-wide association; pharmacogenomics; single nucleotide polymorphism ID BONE-MINERAL DENSITY; SINGLE-NUCLEOTIDE POLYMORPHISMS; VITAMIN-D-RECEPTOR; HORMONE-REPLACEMENT THERAPY; TRANSCRIPTION-FACTOR-7-LIKE-2 TCF7L2 GENE; LEUKOTRIENE C-4 SYNTHASE; ADVERSE DRUG-REACTIONS; ACUTE LYMPHOBLASTIC-LEUKEMIA; ANTI HYPERTENSIVE TREATMENT; NEONATAL DIABETES-MELLITUS AB Genetic diversity, most notably through single nucleotide polymorphisms and copy-number variation, together with specific environmental exposures, contributes to both disease susceptibility and drug response variability. It has proved difficult to isolate disease genes that confer susceptibility to complex disorders, and as a consequence, even fewer genetic variants that influence clinical drug responsiveness have been uncovered. As such, the candidate gene approach has largely failed to deliver and, although the family-based linkage approach has certain theoretical advantages in dealing with common/complex disorders, progress has been slower than was hoped. More recently, genome-wide association studies have gained increasing popularity, as they enable scientists to robustly associate specific variants with the predisposition for complex disease, such as age-related macular degeneration, Type 2 diabetes, inflammatory bowel disease, obesity, autism and leukemia. This relatively new methodology has stirred new hope for the mapping of genes that regulate drug response related to these conditions, Collectively, these studies support the notion that modern high-throughput single nucleotide polymorphism genotyping technologies, when applied to large and comprehensively phenotyped patient cohorts, will readily reveal the most clinically relevant disease-modifying and drug response genes. This review addresses both recent advances in the genotyping field and highlights from genome-wide association studies, which have conclusively uncovered variants that underlie disease susceptibility and/or variability in drug response in common disorders. C1 Childrens Hosp Philadelphia, Ctr Appl Genom, Abramson Res Ctr 1216F, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Ctr Appl Genom, Abramson Res Ctr 1216E, Philadelphia, PA 19104 USA. RP Hakonarson, H (reprint author), Childrens Hosp Philadelphia, Ctr Appl Genom, Abramson Res Ctr 1216F, 3615 Civic Ctr Blvd, Philadelphia, PA 19104 USA. 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Cheung, Sau Wai TI Speech delay and autism spectrum behaviors are frequently associated with duplication of the 7q11.23 Williams-Beuren syndrome region SO GENETICS IN MEDICINE LA English DT Article DE 7q11.23; microduplication; language delay; autism spectrum disorder ID PSYCHIATRIC-DISORDERS; HUMAN GENOME; MENTAL-RETARDATION; MECHANISMS; DELETIONS; FEATURES; MICE; REARRANGEMENTS; MICRODELETION; ARCHITECTURE AB Purpose: Williams-Beuren syndrome is among the most well-characterized microdeletion syndromes, caused by recurrent de novo microdeletions at 7q11.23 mediated by nonallelic homologous recombination between low copy repeats flanking this critical region. However, the clinical phenotype associated with reciprocal microduplication of this genomic region is less well described. We investigated the molecular, clinical, neurodevelopmental, and behavioral features of seven patients with dup(7)(q11.23), including two children who inherited the microduplication from one of their parents, to more fully characterize this emerging microduplication syndrome. Methods: Patients were identified by array-based comparative genomic hybridization. Clinical examinations were performed on seven affected probands, and detailed cognitive and behavioral evaluations were carried out on four of the affected probands. Results: Our findings confirm initial reports of speech delay seen in patients with dup(7)(q11.23) and further delineate and expand the phenotypic spectrum of this condition to include communication, social interactions, and repetitive interests that are often observed in individuals diagnosed with autism spectrum disorders. Conclusions: Array-based comparative genomic hybridization is a powerful means of detecting genomic imbalances and identifying molecular etiologies in the clinic setting, including genomic disorders such as Williams-Beuren syndrome and dup(7)(q11.23). We propose that dup(7)(q11.23) syndrome may be as frequent as Williams-Beuren syndrome and a previously unrecognized cause of language delay and behavioral abnormalities. Indeed, these individuals may first be referred for evaluation of autism, even if they do not ultimately meet diagnostic criteria for an autism spectrum disorder. C1 Baylor Coll Med, Dept Mol & Human Genet, Kleberg Cytogenet Lab, Houston, TX 77030 USA. Texas Childrens Hosp, Houston, TX 77030 USA. Baylor Coll Med, Leopold Meyer Ctr Dev Pediat, Houston, TX 77030 USA. Baylor Coll Med, Med Genet Labs, Houston, TX 77030 USA. Univ Rochester, Med Ctr, Rochester, NY 14642 USA. Vanderbilt Univ, Med Ctr, Dept Pediat, Div Med Genet, Nashville, TN 37232 USA. Childrens Hosp Boston, Dev Med Ctr, Boston, MA USA. Childrens Hosp Boston, Dept Lab Med, Div Genet, Boston, MA USA. Childrens Hosp Boston, Dept Neurol, Boston, MA USA. Univ Arizona, Coll Med, Dept Pediat, Tucson, AZ USA. Texas Childrens Hosp, Baylor Coll Med, Dept Pediat, Sect Pediat Neurol & Dev Neurosci, Houston, TX 77030 USA. Illumina Inc, San Diego, CA USA. RP Cheung, SW (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Kleberg Cytogenet Lab, 1 Baylor Plaza,NAB 2015, Houston, TX 77030 USA. 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Hilger TI Array CGH identifies reciprocal 16p13.1 duplications and deletions that predispose to autism and/or mental retardation SO HUMAN MUTATION LA English DT Article DE autism; mental retardation; array CGH; copy number variant ID COMPARATIVE GENOMIC HYBRIDIZATION; END RULE PATHWAY; GENE-EXPRESSION OMNIBUS; COPY NUMBER VARIATION; SPECTRUM DISORDERS; DYSMORPHIC FEATURES; FISH ANALYSIS; MICE LACKING; REARRANGEMENTS; MICROARRAY AB Autism and mental retardation (MR) are often associated, suggesting that these conditions are etiologically related. Recently, array,based comparative genomic hybridization (array CGH) has identified submicroscopic deletions and duplications as a common cause of MR, prompting us to search for such genomic imbalances in autism. Here we describe a 1.5-Mb duplication on chromosome 16p13.1 that was found by high-resolution array CGH in four severe autistic male patients from three unrelated families. The same duplication was identified in several variably affected and unaffected relatives. A deletion of the same interval was detected in three unrelated patients with MR and other clinical abnormalities. In one patient we revealed a further rearrangement of the 16p13 imbalance that was not present in his unaffected mother. Duplications and deletions of this 1.5-Mb interval have not been described as copy number variants in the Database of Genomic Variants and have not been identified in > 600 individuals from other cohorts examined by high-resolution array CGH in our laboratory. Thus we conclude that these aberrations represent recurrent genomic imbalances which predispose to autism and/or MR. C1 Max Planck Inst Mol Genet, D-14195 Berlin, Germany. Univ Newcastle, GOLD Serv, Newcastle, NSW 2308, Australia. Rigshosp, Dept Clin Genet, DK-2100 Copenhagen, Denmark. Monash Univ, Dept Med Psychol, Melbourne, Vic 3004, Australia. 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Mutat. PD JUL PY 2007 VL 28 IS 7 BP 674 EP 682 DI 10.1002/humu.20546 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 184FT UT WOS:000247627200007 PM 17480035 ER PT J AU Maimburg, RD Vaeth, M AF Maimburg, Rikke Damkjaer Vaeth, Michael TI Do children born after assisted conception have less risk of developing infantile autism? SO HUMAN REPRODUCTION LA English DT Article DE autistic disorders; health behaviour; infertility treatment; pregnancy; assisted conception ID SPECTRUM DISORDERS; COHORT AB BACKGROUND: A Danish population based matched case-control study of perinatal risk factors in children with infantile autism has provided some interesting and surprising observations regarding infantile autism and children born after assisted conception. METHODS and RESULTS:: The cases (461) consisted of all children born between 1990 and 1999 and diagnosed with infantile autism in the Danish Psychiatric Central Register before February 2001. Matched controls were identified in the Danish Civil Registration System. The main exposure measures included obstetric risk factors for infantile autism. We found a 59% decreased risk for developing infantile autism among children conceived after assisted conception (odds ratio [OR] 0.41, 95% [0.19-0.89]) and a 63% decreased risk after adjusting for known risk factors for assisted conception and infantile autism (OR 0.37, 95% [0.14-0.98]). CONCLUSION: We found that children born after assisted conception had a lower risk of developing infantile autism then their matched controls. Our observations could possibly be explained by the mother's health status before and during early pregnancy. Our findings require further investigation in larger studies. C1 Univ Aarhus, Inst Publ Hlth, Dept Epidemiol, DK-8000 Aarhus C, Denmark. Univ Aarhus, Inst Publ Hlth, Dept Biostat, DK-8000 Aarhus, Denmark. 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PD JUL PY 2007 VL 22 IS 7 BP 1841 EP 1843 DI 10.1093/humrep/dem082 PG 3 WC Obstetrics & Gynecology; Reproductive Biology SC Obstetrics & Gynecology; Reproductive Biology GA 190IB UT WOS:000248051400007 PM 17456530 ER PT J AU Wahl, RUR AF Wahl, Roy U. Rojas TI G-protein coupled receptors & autism - Reflections on a double-edged sword at the example of the oxytocin receptor system SO INDIAN JOURNAL OF MEDICAL RESEARCH LA English DT Review DE ASD; autism; GPCR; oxytocin receptor ID SOCIAL-BEHAVIOR; VASOPRESSIN RECEPTOR; EARLY EXPERIENCE; AGONIST BINDING; MOLECULAR-BASIS; LIGAND-BINDING; DRUG DISCOVERY; DEFICIENT MICE; GENE OXTR; IN-VIVO AB G-protein coupled receptors (GPCR) tend to desensitize/internalize when exposed to excess agonist. Previously, we have supported the argument that in the case of the oxytocin receptor (OTR), excess agonist (oxytocin, OT) at birth could be implicated with behavioural disorders of the autistic spectrum. In this review, more recent evidence for this hypothesis is summarized, and it is juxtaposed against reports where exogenous OT was found beneficial in alleviating certain undesired behaviours. Facing this dichotomy, we suggest possible in silico drug discovery approaches to mitigate undesired side effect of OT administration/OTR desensitization, especially in the light of potentially emerging agonist therapies. For this, the most important structural features of OTR are reviewed, and we highlight here the need for higher level of theory studies at the easier approachable extracellular receptor side, where loop 3(e3) and the N-terminated strain of OTR appear to offer targets of particular interest for the development of an agent that conditions the action of excess OT. Another approach, based on the development of new agonists with an improved receptor activation to receptor phosphorylation ratio, is also discussed. Finally, the issue of OTR desensitization is put into the broader context of GPCR desensitization and possible implications for behavioural disorders, and the case is made for the usefulness of computational studies in this area. C1 Initiat Mol Studies Autism, Teaneck, NJ 07666 USA. RP Wahl, RUR (reprint author), Initiat Mol Studies Autism, Teaneck, NJ 07666 USA. 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We followed 102 families with children with disabilities for 15 years, listening to their descriptions of their daily lives. A major theme running through all the stories was accommodation-changes made or intentionally not made to the family's daily routine of activities due, at least in part, to their child with disabilities. Accommodations are usually adaptations to everyday routines, not responses to stress; are responsive to how children impact parents' daily routine, not to children's test scores; are related to parents' differing goals and values; do not fit a single script or model for what is good or bad parenting; and predict family sustainability of daily routines, rather than child outcomes. Accommodations can and do change-so interventions can indeed find their places. The practitioner participates in this "conversation" between the social structural constraints and opportunities of families and communities, the beliefs and values of parents, and the valuable contributions of the intervention. C1 Univ Calif Los Angeles, Ctr Culture & Hlth, Jane & Terry Semel Inst Neurosci & Human Behav, Dept Anthropol, Los Angeles, CA 90024 USA. RP Bernheimer, LP (reprint author), Univ Calif Los Angeles, Ctr Culture & Hlth, Jane & Terry Semel Inst Neurosci & Human Behav, Dept Anthropol, Box 62, Los Angeles, CA 90024 USA. 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Madera, Danielle TI A functional approach for ameliorating social skills deficits in young children with autism spectrum disorders SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autism; autism spectrum disorders; social skills; social skills assessment; social skills intervention ID PRESCHOOL-CHILDREN; PEER INTERACTIONS; INTERVENTIONS; INCLUSION; OUTCOMES; SCHOOL AB The number of children in school-based settings diagnosed with an autism spectrum disorder has been increasing, according to U.S. Department of Education (2002) statistics. Although many researchers have written extensively on the benefits of inclusion for children with autism spectrum disorder, social behavior idiosyncrasies exhibited by these children can limit its potential benefits. The purpose of this article is to describe a systematic, functional assessment approach for identifying environmental contextual factors related to the occurrence of peer-related social interactions and the outcomes (ie, functions) that maintain those behaviors. In particular, 2 descriptive assessment tools, the Social Skills Interview and the Snapshot Assessment Tool, both developed by the authors will be explained and illustrated. Both the tools were developed to be classroom-friendly instruments to assist with the objective description of environmental contextual factors that may influence the social behaviors of children with autism spectrum disorder. A case example is presented to demonstrate how the use of these 2 instruments led to the development of an assessment-based intervention to improve the social behaviors of a young child on the autism spectrum. C1 Virginia Commonwealth Univ, Dept Special Educ & Disabil Policy, Richmond, VA 23284 USA. 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PD JUL-SEP PY 2007 VL 20 IS 3 BP 242 EP 254 PG 13 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 183AQ UT WOS:000247545500006 ER PT J AU Stribling, P Rae, J Dickerson, P AF Stribling, Penny Rae, John Dickerson, Paul TI Two forms of spoken repetition in a girl with autism SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE autism; echolalia; palilalia; conversation analysis; social interaction ID IMMEDIATE ECHOLALIA; CHILDREN; LANGUAGE; SPEECH; CONVERSATIONS AB Background. The talk of persons with autistic spectrum disorders (ASD) often features distinctive forms of repetition (echophenomena). Although often characterized as meaningless or inappropriate, there is evidence that such practices can sometimes have communicative functions. Aims: To investigate the interactional organization of repetition practices found in the talk of an adolescent girl with an ASD. Methods & Procedures: As part of a project examining the interactional practices of children with ASD, we video-recorded 6 hours of activity in a school classroom for severe learning difficulty (SLD) children. This paper considers instances of repeated talk produced by a class pupil, 'Helen'. The analysis involved assembling a collection of examples of the repeated talk which were then transcribed in detail. Conversation Analysis was used to explore the sequential contexts in which they occur and precisely how they are produced. Outcomes & Results: Two forms of repetition occur very frequently in Helen's talk: first, repeats of turn-final lexical items from another speaker's immediately before talk (prior-turn repeats, a form of immediate echolalia), and second, repeats of the first item within a turn such that a turn is produced consisting entirely of repeated items (within-turn repeats). The latter appears to be a form of palilalia (repeats of one's on)own prior talk) that has not been widely reported in ASD. The prior turn repeats follow other speaker's initiating actions (e.g. questions) that are addressed specifically to Helen and make a response from her relevant. Helen apparently uses these to demonstrate that she has nevertheless heard, and is orienting to, that prior turn. Within-turn repeats are tied to and bounded by the accomplishment of non-vocal activities, e.g. handing an object to a co-participant, such that the repetitions cease when the object has reached its recipient. The two forms of repetition frequently co-occur to display on-going engagement with a recipient's prior turn. C1 Roehampton Univ, Whitelands Coll, Sch Human & Life Sci, Ctr Res Cogin Emot & Interact, London SW15 4JD, England. RP Stribling, P (reprint author), Roehampton Univ, Whitelands Coll, Sch Human & Life Sci, Ctr Res Cogin Emot & Interact, London SW15 4JD, England. EM P.Stribling@roehampton.ac.uk CR American Psychiatric Association, 1995, DIAGN STAT MAN MENT Baltaxe CA, 1977, J PEDIATR PSYCHOL, V2, P176, DOI DOI 10.1093/JPEPSY/2.4.176 Benke T, 2001, BRAIN LANG, V78, P62, DOI 10.1006/brln.2000.2445 CAMPBELL B, 1978, AM J MENT DEF, V82, P414 COGGINS TE, 1988, J AUTISM DEV DISORD, V18, P687, DOI 10.1007/BF02211886 Duchan J., 1983, SEMINARS SPEECH LANG, V4, P53 FAY WH, 1967, J SPEECH HEAR RES, V10, P305 FAY WH, 1968, J SPEECH HEAR RES, V11, P365 GOODWIN C, 1995, RES LANG SOC INTERAC, V28, P233, DOI 10.1207/s15327973rlsi2803_4 Heath Christian, 1986, BODY MOVEMENT SPEECH HOWLIN P, 1982, J CHILD PSYCHOL PSYC, V23, P281, DOI 10.1111/j.1469-7610.1982.tb00073.x Kanner L, 1943, NERV CHILD, V2, P217 KARMALI IAL, 2000, THESIS SCI ENG, V61, P3265 LOCAL J, 1995, CLIN LINGUIST PHONET, V9, P155, DOI 10.3109/02699209508985330 PRIZANT BM, 1981, J SPEECH HEAR DISORD, V46, P241 PRIZANT BM, 1984, J SPEECH HEAR RES, V27, P183 ROBERTS JMA, 1989, J AUTISM DEV DISORD, V19, P271, DOI 10.1007/BF02211846 RYDELL PJ, 1991, J AUTISM DEV DISORD, V21, P131, DOI 10.1007/BF02284756 SACKS H, 1974, LANGUAGE, V50, P696, DOI 10.2307/412243 SCHREIBMAN L, 1978, J APPL BEHAV ANAL, V11, P453, DOI 10.1901/jaba.1978.11-453 Tarplee C, 1999, CLIN LINGUIST PHONET, V13, P449 WOLFF S, 1965, J CHILD PSYCHOL PSYC, V6, P29, DOI 10.1111/j.1469-7610.1965.tb02152.x NR 22 TC 15 Z9 16 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. 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PD JUL-AUG PY 2007 VL 42 IS 4 BP 427 EP 444 DI 10.1080/13682820601183659 PG 18 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 199YF UT WOS:000248730400003 PM 17613098 ER PT J AU Spanoudis, G Natsopoulos, D Panayiotou, G AF Spanoudis, George Natsopoulos, Demetrios Panayiotou, Georgia TI Mental verbs and pragmatic language difficulties SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE pragmatics; mental verbs; Children's Communication Checklist; specific language impairment; pragmatic language difficulties ID CHILDRENS-COMMUNICATION-CHECKLIST; SOCIAL COGNITION; FALSE-BELIEF; IMPAIRMENT; AUTISM; DISORDERS; SLI; DIFFERENTIATE; COMPREHENSION; SUBGROUPS AB Background: Pragmatic language impairment has recently been the subject of a number of studies that attempted to illuminate classification and diagnostic issues, and identify the profile of children with pragmatic language difficulties. Although much progress has been made, the nature of pragmatic difficulties remains unclear. Aims: To contrast typically developing children with those with pragmatic difficulties and specific language impairment as well as their ability to produce and comprehend pragmatic inferences about given or presupposed knowledge in mental state verbs; and to explore the general hypothesis that children with pragmatic difficulties make some, but not all, of the pragmatic inferences necessary for successful communication. Methods & Procedures: Study groups consisted of 18 children with pragmatic language difficulties, 28 children with specific language impairment and 40 typically developing children. The groups were matched on non-verbal intelligence and age and differed in verbal intelligence, language achievement and pragmatic ability. Outcomes & Results: The language-impaired groups performed significantly more poorly than typically developing children on all mental verb measures. In addition, significant differences between specific language impairment and pragmatic difficulties groups were found in composite score performance, but not on individual test performance. Conclusions: Both inferential mental verb tasks (pragmatics) and non-inferential mental verb tasks (semantics) were more difficult for the children with language impairments compared with typically developing peers. Inferential and non-inferential abilities showed significant differences between the two language-impaired groups in favour of the children with specific language difficulties. Children's Communication Checklist scales in conjunction with mental verb measures were found to classify the three groups well. C1 Univ Cyprus, CY-1678 Nicosia, Cyprus. RP Spanoudis, G (reprint author), Univ Cyprus, POB 20537, CY-1678 Nicosia, Cyprus. EM spanoud@ucy.ac.cy CR Adams C, 2001, INT J LANG COMM DIS, V36, P289, DOI 10.1080/13682820119881 Astington J. 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R., 2000, PERCEPTION COGNITION, P245 NATSOPOULOS D, 1987, J PSYCHOLINGUIST RES, V16, P133, DOI 10.1007/BF01071999 Norbury CF, 2002, INT J LANG COMM DIS, V37, P227, DOI 10.1080/13682820210136269 Nunnaly J., 1978, PSYCHOMETRIC THEORY Petinou K., 2002, LANG ACQUIS, V10, P1, DOI 10.1207/S15327817LA1001_1 Rapin I, 1983, NEUROPSYCHOLOGY LANG, P155 Rapin I, 1996, J CHILD PSYCHOL PSYC, V37, P643, DOI 10.1111/j.1469-7610.1996.tb01456.x Redmond SM, 1998, J SPEECH LANG HEAR R, V41, P688 REEVES LM, 1998, PSYCHOLINGUISTICS, P157 Ruffman T., 2000, MINDS MAKING ESSAYS, P456 Schneider W., 2002, E PRIME USERS GUIDE Scholnick E. K., 1991, PERSPECTIVES LANGUAG, P397 Searle J., 1969, SPEECH ACTS ESSAY PH Shields J, 1996, DEV MED CHILD NEUROL, V38, P487 Stavrakaki S, 2001, BRAIN LANG, V77, P419, DOI 10.1006/brln.2000.2412 Tager-Flusberg H., 2000, UNDERSTANDING OTHER, P124 Tomblin JB, 2003, INT J LANG COMM DIS, V38, P235, DOI 10.1080/1368282031000086363 NR 49 TC 4 Z9 4 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1368-2822 EI 1460-6984 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD JUL-AUG PY 2007 VL 42 IS 4 BP 487 EP 504 DI 10.1080/13682820601010027 PG 18 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 199YF UT WOS:000248730400006 PM 17613101 ER PT J AU Trudgeon, C Carr, D AF Trudgeon, Clare Carr, Deborah TI The impacts of home-based early behavioural intervention programmes on families of children with autism SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE autism; children; early behavioural intervention; families ID PERVASIVE DEVELOPMENTAL DISORDER; INTENSIVE EARLY INTERVENTION; YOUNG-CHILDREN AB Background In the UK, Early Intensive Behavioural Intervention [EIBI] programmes typically are conducted within the homes of children with autism. Despite evidence for their effectiveness in producing appreciable developmental gains in children with autism, a concern expressed about EIBI programmes is that stressful effects from the high levels of demand they place on family resources could undermine their effectiveness [The Effectiveness of Early Interventions for Children with Autistic Spectrum Disorders (ASD). A report for the DfES South East Regional Special Educational Needs Partnership. SERSEN Website, 2004]. This study investigates the positive impacts and the stressors experienced by families running EIBI programmes. Method Sixteen parents from nine different families participated in semi-structured qualitative interviews on their experiences of running a home-based EIBI programme. Data were analysed using the Grounded Theory process. Results Positive and negative impacts of the programmes were reported. Analysis indicated that sources of support obtained through the programmes' benefits offset sources of stress through the programmes' demands. Conclusions The interaction between programme demands and benefits and the resources available to each family strongly influences the impact of running a home-based EIBI programme. C1 Univ Cardiff Wales, Welsh Ctr Learning Disabilities, Cardiff CF14 3BG, S Glam, Wales. Torfaen Community Healthcare Learning Disabil Tea, Cwmbran, Gwent, Wales. RP Carr, D (reprint author), Univ Cardiff Wales, Welsh Ctr Learning Disabilities, Meridian Court,N Rd, Cardiff CF14 3BG, S Glam, Wales. EM debcarr60@gmail.com RI turton, miranda/F-4682-2011 CR Abidin R, 1990, PARENTING STRESS IND Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 CHARLOP MH, 1985, J APPL BEHAV ANAL, V18, P155, DOI 10.1901/jaba.1985.18-155 Eikeseth S, 2002, BEHAV MODIF, V26, P49, DOI 10.1177/0145445502026001004 Hastings RP, 2001, J AUTISM DEV DISORD, V31, P327, DOI 10.1023/A:1010799320795 Howard JS, 2005, RES DEV DISABIL, V26, P359, DOI 10.1016/j.ridd.2004.09.005 Johnson E, 2002, CHILD CARE HLTH DEV, V28, P123 KOEGEL RL, 1988, J AUTISM DEV DISORD, V18, P525, DOI 10.1007/BF02211871 Koegel RL, 1998, J AUTISM DEV DISORD, V28, P241, DOI 10.1023/A:1026073522897 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MAURICE C, 1996, BEHAV INTERVENTION Y MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 MCGEE GG, 1985, J APPL BEHAV ANAL, V18, P17, DOI 10.1901/jaba.1985.18-17 MCGEE GG, 1992, J APPL BEHAV ANAL, V25, P117, DOI 10.1901/jaba.1992.25-117 Mudford OC, 2001, RES DEV DISABIL, V22, P173, DOI 10.1016/S0891-4222(01)00066-X National Initiative for Autism: Screening and Assessment (NIASA), 2003, NAT AUT PLAN CHILDR PIDGEON N, 1997, DOING QUALITATIVE AN, P243 Reed P., 2004, EFFECTIVENESS EARLY Sallows GO, 2005, AM J MENT RETARD, V110, P417, DOI 10.1352/0895-8017(2005)110[417:IBTFCW]2.0.CO;2 Shea V, 2004, AUTISM, V8, P349, DOI 10.1177/1362361304047223 Smith T, 2000, AM J MENT RETARD, V105, P269, DOI 10.1352/0895-8017(2000)105<0269:RTOIEI>2.0.CO;2 Smith T, 2000, RES DEV DISABIL, V21, P297, DOI 10.1016/S0891-4222(00)00043-3 Strauss A., 1990, BASICS QUALITATIVE R WOLF M, 1967, BEHAV RES THER, V5, P103, DOI 10.1016/0005-7967(67)90004-6 NR 24 TC 3 Z9 3 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PD JUL PY 2007 VL 20 IS 4 BP 285 EP 296 DI 10.1111/j.1468-3148.2006.00331.x PG 12 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 178NG UT WOS:000247226800001 ER PT J AU Pitetti, KH Rendoff, AD Grover, T Beets, MW AF Pitetti, Kenneth H. Rendoff, Andrew D. Grover, Travis Beets, Michael W. TI The efficacy of a 9-month treadmill walking program on the exercise capacity and weight reduction for adolescents with severe autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; adolescents; exercise capacity; body mass index ID MENTALLY-RETARDED ADULTS; CORONARY-HEART-DISEASE; PHYSICAL-FITNESS; CARDIOVASCULAR FITNESS; INAPPROPRIATE BEHAVIORS; VIGOROUS EXERCISE; RETARDATION; HEALTH; WOMEN; PREVENTION AB This study evaluated the efficacy of a 9-month treadmill walking (TW) program on exercise capacity and body mass index (BMI) for adolescents with severe autism. Ten youth residing in a residential/school treatment facility were assigned to either a supplemental treadmill walking (TW) or control group. Both groups continued to participate in their regular physical education curriculum. Monthly records were maintained for the following: (a) TW progression in frequency, duration, speed and elevation; (b) caloric expenditure; and (c) BMI. The TW program resulted in significant increases in mean monthly TW frequency, speed, elevation, and calories expended coupled with a reduction in BMI. C1 Wichita State Univ, Dept Phys Therapy, Coll Hlth Profess, Wichita, KS 67260 USA. Wichita State Univ, Dept Phys Assistant, Coll Hlth Profess, Wichita, KS 67260 USA. Oregon State Univ, Corvallis, OR 97331 USA. Heartspring, Wichita, KS USA. RP Pitetti, KH (reprint author), Wichita State Univ, Dept Phys Therapy, Coll Hlth Profess, Wichita, KS 67260 USA. 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Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 997 EP 1006 DI 10.1007/s10803-006-0238-3 PG 10 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300001 PM 17151799 ER PT J AU Eigsti, IM Bennetto, L Dadlani, MB AF Eigsti, Inge-Marie Bennetto, Loisa Dadlani, Mamta B. TI Beyond pragmatics: Morphosyntactic development in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; language acquisition; syntax; vocabulary; pragmatics ID HIGH-FUNCTIONING CHILDREN; BINET 4TH EDITION; LANGUAGE-ACQUISITION; SPECTRUM DISORDERS; ASPERGER-SYNDROME; GRAMMATICAL MORPHEMES; RETARDED-CHILDREN; INFANTILE-AUTISM; DISCOURSE; INDIVIDUALS AB Language acquisition research in autism has traditionally focused on high-level pragmatic deficits. Few studies have examined grammatical abilities in autism, with mixed findings. The present study addresses this gap in the literature by providing a detailed investigation of syntactic and higher-level discourse abilities in verbal children with autism, age 5 years. Findings indicate clear language difficulties that go beyond what would be expected based on developmental level; specifically, syntactic delays, impairments in discourse management and increased production of non-meaningful words (jargon). The present study indicates a highly specific pattern of language impairments, and importantly, syntactic delays, in a group of children with autism carefully matched on lexical level and non-verbal mental age with children with developmental delays and typical development. C1 Univ Connecticut, Dept Psychol, Unit 1020, Storrs, CT 06269 USA. Univ Massachusetts, Dept Psychol, Amherst, MA 01003 USA. Univ Rochester, Dept Clin & Social Sci Psychol, Rochester, NY USA. RP Eigsti, IM (reprint author), Univ Connecticut, Dept Psychol, Unit 1020, 406 Babbidge Rd, Storrs, CT 06269 USA. 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Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1007 EP 1023 DI 10.1007/s10803-006-0239-2 PG 17 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300002 PM 17089196 ER PT J AU Rutherford, MD Young, GS Hepburn, S Rogers, SJ AF Rutherford, M. D. Young, Gregory S. Hepburn, Susan Rogers, Sally J. TI A longitudinal study of pretend play in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pretend play; longitudinal study ID PERVASIVE DEVELOPMENTAL DISORDERS; EXECUTIVE FUNCTION DEFICITS; SYMBOLIC PLAY; FOLLOW-UP; INFANTILE-AUTISM; JOINT ATTENTION; COMMUNICATION DEFICITS; IMPAIRED CHILDREN; LANGUAGE; MIND AB This study describes a longitudinal design (following subjects described in Rutherford & Rogers [2003, Journal of Autism and Developmental Disorder, 33, 289-302]) to test for predictors of pretend play competence in a group of children with autism. We tested the hypothesis that developmental change in pretend play performance can be predicted by earlier measures of either executive function, intersubjectivity, imitation, or general development. Participants at the time of follow-up testing were 28 children with autistic disorder (mean chronological age (CA) 57.6 months), 18 children with other developmental disorders (mean CA 59.0 months), and 27 typically developing children (mean CA 30.1 months). Children with autism were profoundly delayed given both competence (prompted) measures as well as performance (spontaneous) measures. Joint attention at time 1 strongly and uniquely predicted pretend play development. C1 McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON L8S 4K1, Canada. Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. 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F., 2003, HDB PSYCHOL RES METH, V2, P115 Volkmar FR, 2004, J CHILD PSYCHOL PSYC, V45, P135, DOI 10.1046/j.0021-9630.2003.00317.x WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 WING L, 1977, J CHILD PSYCHOL PSYC, V18, P167, DOI 10.1111/j.1469-7610.1977.tb00426.x NR 69 TC 29 Z9 32 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1024 EP 1039 DI 10.1007/s10803-006-0240-9 PG 16 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300003 PM 17146707 ER PT J AU Beversdorf, DQ Narayanan, A Hillier, A Hughes, JD AF Beversdorf, David Q. Narayanan, Ananth Hillier, Ashleigh Hughes, John D. TI Network model of decreased context utilization in autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; neural network; false memory; semantic; memory; hippocampus ID CENTRAL COHERENCE; FALSE MEMORIES; CHILDREN; INDIVIDUALS; WORDS; MIND AB Individuals with autism spectrum disorders (ASD) demonstrate impaired utilization of context, which allows for superior performance on the "false memory" task. We report the application of a simplified parallel distributed processing model of context utilization to the false memory task. For individuals without ASD, experiments support a model wherein presentation of one word, e.g., "apple,'' strongly activates the neighboring nodes of closely related words such as "fruit,'' "tree,'' whereas in ASD these neighboring nodes are relatively less activated. We demonstrate this model to be consistent with the superior performance on recognition testing on the false memory test, but not on free recall. This may have an anatomic basis in diminished hippocampal neuronal arborization and the abnormal minicolumnar pathology in ASD. C1 Ohio State Univ, Dept Neurol, Med Ctr, Columbus, OH 43210 USA. Ohio State Univ, Integrated Biomed Sci Grad Program, Columbus, OH 43210 USA. Natl Naval Med Ctr, Bethesda, MD USA. RP Beversdorf, DQ (reprint author), Ohio State Univ, Dept Neurol, Med Ctr, Means Hall 469,1654 Upham Dr, Columbus, OH 43210 USA. EM david.beversdorf@osumc.edu CR Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 BAUMAN M, 1985, NEUROLOGY, V35, P866 Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 Beversdorf DQ, 2000, P NATL ACAD SCI USA, V97, P8734, DOI 10.1073/pnas.97.15.8734 Bowler DM, 2000, J ABNORM PSYCHOL, V109, P663, DOI 10.1037//0021-843X.109.4.663 Casanova MF, 2002, NEUROLOGY, V58, P428 COHEN IL, 1994, BIOL PSYCHIAT, V36, P5, DOI 10.1016/0006-3223(94)90057-4 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 GABRIELI JDE, 1988, BRAIN COGNITION, V7, P157, DOI 10.1016/0278-2626(88)90027-9 GOLDSTEIN G, 1994, J CLIN EXP NEUROPSYC, V16, P671, DOI 10.1080/01688639408402680 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x Happe FGE, 1997, BRIT J DEV PSYCHOL, V15, P1 HERMELIN B, 1967, BRIT J PSYCHOL, V58, P213 Just MA, 2004, BRAIN, V127, P1811, DOI 10.1093/brain/awh199 KEMPER TL, 1993, NEUROL CLIN, V11, P175 McClelland JL, 2000, J AUTISM DEV DISORD, V30, P497, DOI 10.1023/A:1005576229109 Mottron L, 2000, J CHILD PSYCHOL PSYC, V41, P1057, DOI 10.1017/S0021963099006253 OCONNOR N, 1967, J MENT DEFIC RES, V11, P126 ROEDIGER HL, 1995, J EXP PSYCHOL LEARN, V21, P803, DOI 10.1037/0278-7393.21.4.803 Rumelhart D. E., 1986, PARALLEL DISTRIBUTED, V1 Russell J N, 1997, Adv Data, P1 SHAH A, 1983, J CHILD PSYCHOL PSYC, V24, P613, DOI 10.1111/j.1469-7610.1983.tb00137.x SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x NR 23 TC 13 Z9 13 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1040 EP 1048 DI 10.1007/s10803-006-0242-7 PG 9 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300004 PM 17191098 ER PT J AU Loukusa, S Leinonen, E Kuusikko, S Jussila, K Mattila, ML Ryder, N Ebeling, H Moilanen, I AF Loukusa, Soile Leinonen, Eeva Kuusikko, Sanna Jussila, Katja Mattila, Marja-Leena Ryder, Nuala Ebeling, Hanna Moilanen, Irma TI Use of context in pragmatic language comprehension by children with Asperger syndrome or high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE pervasive developmental disorders; Asperger syndrome; high-functioning autism; pragmatic comprehension; context and language; relevance theory ID RELEVANCE THEORY; ADULTS; INDIVIDUALS; EXPLORATION; IMPAIRMENT; COMPETENCE; DISORDERS; SPECTRUM; MIND AB Utilizing relevance theory, this study investigated the ability of children with Asperger syndrome (AS) and high-functioning autism (HFA) to use context when answering questions and when giving explanations for their correct answers. Three groups participated in this study: younger AS/HFA group (age 7-9, n = 16), older AS/HFA group (age 10-12, n = 23) and a normally functioning control group (age 7-9, n = 23). The results indicated that the younger AS/HFA group did less well when answering contextually demanding questions compared to the control group, and the performance of the older AS/HFA group fell in between the younger AS/HFA group and the control group. Both AS/HFA groups had difficulties explaining their correct answers, suggesting that they are not always aware of how they have derived answers from the context. C1 Univ Oulu, Dept Finnish Informat Studies & Logoped, FIN-90014 Oulu, Finland. Univ Hertfordshire, Dept Psychol, Hatfield AL10 9AB, Herts, England. Univ Oulu, Clin Child Psychiat, FIN-90014 Oulu, Finland. Univ Hosp Oulu, Clin Child Psychiat, Oulu, Finland. RP Loukusa, S (reprint author), Univ Oulu, Dept Finnish Informat Studies & Logoped, POB 1000, FIN-90014 Oulu, Finland. 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Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1049 EP 1059 DI 10.1007/s10803-006-0247-2 PG 11 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300005 PM 17072751 ER PT J AU Macks, RJ Reeve, RE AF Macks, Ryan J. Reeve, Ronald E. TI The adjustment of non-disabled siblings of children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE families; children with autism; autistic children; psychosocial adjustment and development ID MENTAL HANDICAP; DOWN-SYNDROME; STRESS; FAMILY; BROTHERS; SISTERS; BOYS AB This study compared the psychosocial and emotional adjustment of siblings of children with autism and siblings of non-disabled children. In addition, differences between self and parent reports, as well as various demographic characteristics were examined. Fifty-one siblings of children with autism and 35 siblings of non-disabled children, between the ages of 7 and 17, along with one parent of each sibling, participated. Results indicated that the presence of a child with autism appears to enhance the psychosocial and emotional development of non-disabled siblings when demographic risk factors are limited. However, the presence of a child with autism appears to have an increasingly unfavorable impact on the non-disabled sibling as demographic risk factors increase. C1 Childrens Hosp, Med Ctr, Div Dev & Behav Pediat, Cincinnati, OH 45229 USA. Univ Virginia, Curry Programs Clin & Sch Psychol, Charlottesville, VA 22904 USA. RP Macks, RJ (reprint author), Childrens Hosp, Med Ctr, Div Dev & Behav Pediat, MLC 4002,3333 Burnet Ave, Cincinnati, OH 45229 USA. EM Ryan.Macks@cchmc.org CR BAGENHOLM A, 1991, J MENT DEFIC RES, V35, P291 BEBKO JM, 1987, J AUTISM DEV DISORD, V17, P565, DOI 10.1007/BF01486971 BERGER E, 1980, THESIS U CINCINNATI BIGBY C, 1997, J GERONTOLOGICAL SOC, V29, P2 Bristol M. 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V., 1984, PIERSHARRIS CHILDREN Randall P., 1999, SUPPORTING FAMILIES RODRIGUE JR, 1992, J AUTISM DEV DISORD, V22, P249, DOI 10.1007/BF01058154 RODRIGUE JR, 1993, J AUTISM DEV DISORD, V23, P665, DOI 10.1007/BF01046108 SCHWIRIAN PM, 1976, AM ANN DEAF, V121, P373 WOLF LC, 1989, J AUTISM DEV DISORD, V19, P157, DOI 10.1007/BF02212727 NR 29 TC 39 Z9 40 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1060 EP 1067 DI 10.1007/s10803-006-0249-0 PG 8 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300006 PM 17072750 ER PT J AU Yerys, BE Hepburn, SL Pennington, BF Rogers, SJ AF Yerys, Benjamin E. Hepburn, Susan L. Pennington, Bruce F. Rogers, Sally J. TI Executive function in preschoolers with autism: Evidence consistent with a secondary deficit SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE executive function; children; autism; cognitive flexibility ID DEVELOPMENTAL PSYCHOPATHOLOGY; IMPAIRED MEMORY; YOUNG-CHILDREN; DYSFUNCTION; MIND; INDIVIDUALS; ABILITY AB Recent research on executive function (EF) deficits in autism has led investigators to conclude that EF deficits are secondary to the disorder. The current study has two major goals: (1) Examine whether specific EF deficits are present in the youngest autism group to date (mean = 2.9 years), and (2) examine whether such deficits are secondary to autism, or act as an early non-specific cognitive risk factor for autism by comparing EF abilities of this autism group to a CA-matched typically developing group. Results from Experiment 1 suggest no specific EF deficits in autism relative to MA-matched controls, while results from Experiment 2 are consistent with the hypothesis that EF deficits may emerge as a secondary deficit in autism. Alternative hypotheses are also considered. C1 Univ Denver, Dept Psychol, Denver, CO 80208 USA. Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. RP Yerys, BE (reprint author), Univ Denver, Dept Psychol, 2155 S Race St, Denver, CO 80208 USA. EM byerys@nova.psy.du.edu CR Burack JA, 2002, DEV PSYCHOPATHOL, V14, P225 Carlson SM, 2004, J EXP CHILD PSYCHOL, V87, P299, DOI 10.1016/j.jecp.2004.01.002 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Dawson G, 1998, CHILD DEV, V69, P1276, DOI 10.2307/1132265 Dawson G, 2002, CHILD DEV, V73, P345, DOI 10.1111/1467-8624.00411 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Goldberg MC, 2005, J AUTISM DEV DISORD, V35, P279, DOI 10.1007/s10803-005-3291-4 Griffith EM, 1999, CHILD DEV, V70, P817, DOI 10.1111/1467-8624.00059 GRIFFITH EM, 2003, DISSERTATION ABSTR B, V63, P3473 Hill EL, 2004, DEV REV, V24, P189, DOI 10.1016/j.dr.2004.01.001 HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 HUGHES C, 2001, DEV AUTISM PERSPECTI HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 Joseph RM, 2004, DEV PSYCHOPATHOL, V16, P137, DOI 10.1017/S095457940404444X Kaufmann P, 1989, J CLIN EXPT NEUROPSY, V12, P69 Liss M, 2001, J CHILD PSYCHOL PSYC, V42, P261, DOI 10.1017/S0021963001006679 Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MCEVOY RE, 1993, J CHILD PSYCHOL PSYC, V34, P563, DOI 10.1111/j.1469-7610.1993.tb01036.x Minshew NJ, 2001, J CHILD PSYCHOL PSYC, V42, P1095, DOI 10.1111/1469-7610.00808 Mullen EM, 1992, MULLEN SCALES EARLY MULLEN EM, 1997, MANUAL MULLEN SCALES OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x OZONOFF S, 1995, NEUROPSYCHOLOGY, V9, P491, DOI 10.1037//0894-4105.9.4.491 Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x ROGERS SJ, 1997, UNPUB MODIFICATION W RUSSELL J, 1991, BRIT J DEV PSYCHOL, V9, P331 Rutherford MD, 2003, J AUTISM DEV DISORD, V33, P289, DOI 10.1023/A:1024406601334 Seltzer MM, 2004, J AUTISM DEV DISORD, V34, P41, DOI 10.1023/B:JADD.0000018073.92982.64 Swettenham J, 1998, J CHILD PSYCHOL PSYC, V39, P747, DOI 10.1017/S0021963098002595 WELSH MC, 1988, DEV NEUROPSYCHOL, V4, P199 WELSH MC, 1990, CHILD DEV, V61, P1697, DOI 10.1111/j.1467-8624.1990.tb03560.x Williams DL, 2005, ARCH CLIN NEUROPSYCH, V20, P1, DOI 10.1016/j.acn.2002.08.001 Williams DL, 2006, NEUROPSYCHOLOGY, V20, P21, DOI 10.1037/0894-4105.20.1.21 NR 34 TC 15 Z9 16 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1068 EP 1079 DI 10.1007/s10803-006-0250-7 PG 12 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300007 PM 17171455 ER PT J AU Tsakanikos, E Costello, H Holt, G Sturmey, P Bouras, N AF Tsakanikos, Elias Costello, Helen Holt, Geraldine Sturmey, Peter Bouras, Nick TI Behaviour management problems as predictors of psychotropic medication and use of psychiatric services in adults with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; behaviour management problems; challenging behaviour; intellectual disability/mental retardation; psychotropic medication; treatment interventions ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; INDIVIDUALS AB We examined behaviour management problems as predictors of psychotropic medication, use of psychiatric consultation and in-patient admission in a group of 66 adults with pervasive developmental disorder (PDD) and intellectual disability (ID) and 99 controls matched in age, gender and level of ID. Overall, people with PDD had higher rates of most DAS behaviour problems and more frequent use of anti-psychotics than matched controls. Logistic regression analyses showed that physical aggression and problems such as pestering staff independently predicted use of anti-psychotics. Physical aggression and overactivity predicted further involvement of psychiatric services. PDD diagnosis predicted admission to an in-patient unit. The results suggest that externalizing problem behaviours in adults with autism can predict type of treatment intervention. C1 Kings Coll London, Div Psychol Med, Inst Psychiat, Estia Ctr, London SE1 3SS, England. CUNY Queens Coll, Dept Psychol, New York, NY USA. RP Tsakanikos, E (reprint author), Kings Coll London, Div Psychol Med, Inst Psychiat, Estia Ctr, 66 Snowsfield, London SE1 3SS, England. EM e.tsakanikos@iop.kcl.ac.uk RI Tsakanikos, Elias/B-4881-2011 CR AMAN MG, 1995, AM J MENT RETARD, V99, P500 Billstedt E, 2005, J AUTISM DEV DISORD, V35, P351, DOI 10.1007/s10803-005-3302-5 Bouras N., 1999, PSYCHIAT BEHAV DISOR CARR EG, 1999, MONOGRAPH AM ASS MEN Didden R, 1997, AM J MENT RETARD, V101, P387 Dinca O, 2005, J PSYCHOPHARMACOL, V19, P521, DOI 10.1177/0269881105056541 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Grey IM, 2005, CURR OPIN PSYCHIATR, V18, P469, DOI 10.1097/01.yco.0000179482.54767.cf Hanson R. H., 2002, CRISIS PREVENTION RE Howlin P, 2003, J AUTISM DEV DISORD, V33, P3, DOI 10.1023/A:1022270118899 HOWLIN P, 1997, AUTISM PREPARATION A Kwok HWM, 2003, CURR OPIN PSYCHIATR, V16, P529, DOI 10.1097/01.yco.0000087259.35258.e9 McClintock K, 2003, J INTELL DISABIL RES, V47, P405, DOI 10.1046/j.1365-2788.2003.00517.x *NEW YORK DEP HLTH, 1999, PUB NEW YORK DEP HLT, V4217 Posey DJ, 2000, HARVARD REV PSYCHIAT, V8, P45, DOI 10.1093/hrp/8.2.45 SCOTTI JR, 1991, AM J MENT RETARD, V96, P233 Singh NN, 1997, J CHILD ADOL PSYCHOP, V7, P255, DOI 10.1089/cap.1997.7.255 Sturmey P, 1999, MENT RETARD, V37, P497, DOI 10.1352/0047-6765(1999)037<0497:LONABN>2.0.CO;2 NR 19 TC 25 Z9 25 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1080 EP 1085 DI 10.1007/s10803-006-0248-1 PG 6 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300008 PM 17053989 ER PT J AU Mazefsky, CA Oswald, DP AF Mazefsky, Carla A. Oswald, Donald P. TI Emotion perception in Asperger's syndrome and high-functioning autism: The importance of diagnostic criteria and cue intensity SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE emotion; nonverbal cues; Asperger's syndrome; high-functioning autism; diagnosis ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDS APPRAISAL; NORMAL ADULTS; EXPRESSIONS; ABILITIES; FACES; COMPREHENSION; LANGUAGE; DEFICITS; SKILLS AB This study compared emotion perception accuracy between children with Asperger's syndrome (AS) and high-functioning autism (HFA). Thirty children were diagnosed with AS or HFA based on empirically supported diagnostic criteria and administered an emotion perception test consisting of facial expressions and tone of voice cues that varied in intensity. Participants with AS and the typically developing standardization sample of the emotion perception instrument had the same mean emotion perception accuracy, whereas participants with HFA performed significantly worse. Results also provided preliminary evidence for a difference in accuracy perceiving low-intensity tone of voice cues between participants with HFA and AS. Future research to build on these initial findings should include attention to tone of voice, underlying processing, and cue intensity. C1 Childrens Hosp Pittsburgh, Child Dev Unit, Pittsburgh, PA 15213 USA. Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA 23298 USA. Virginia Commonwealth Univ, Dept Psychol, Richmond, VA 23284 USA. RP Mazefsky, CA (reprint author), Childrens Hosp Pittsburgh, Child Dev Unit, 3705 5th Ave, Pittsburgh, PA 15213 USA. EM Carla.Mazefsky@chp.edu CR Achenbach TM, 2001, MANUAL ASEBA SCH AGE Adolphs R, 2001, J COGNITIVE NEUROSCI, V13, P232, DOI 10.1162/089892901564289 American Psychiatric Association, 2000, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 BaronCohen S, 1997, VIS COGN, V4, P311, DOI 10.1080/713756761 Baum KM, 1998, J NONVERBAL BEHAV, V22, P89, DOI 10.1023/A:1022954014365 BRAVERMAN M, 1989, J AUTISM DEV DISORD, V19, P301, DOI 10.1007/BF02211848 Brown JR, 1996, CHILD DEV, V67, P789, DOI 10.1111/j.1467-8624.1996.tb01764.x Bruininks R., 1996, SCALES INDEPENDENT B Cohen J., 2003, APPL MULTIPLE REGR C Denham S. 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E., 1972, FACE EMOTION Klin A, 2005, J AUTISM DEV DISORD, V35, P221, DOI 10.1007/s10803-005-2001-6 Klin A, 2002, AM J PSYCHIAT, V159, P895, DOI 10.1176/appi.ajp.159.6.895 Koning C, 2001, AUTISM, V5, P23, DOI 10.1177/1362361301005001003 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 LORD C, 1993, INF MENTAL HLTH J, V14, P234, DOI 10.1002/1097-0355(199323)14:3<234::AID-IMHJ2280140308>3.0.CO;2-F MACDONALD H, 1989, J CHILD PSYCHOL PSYC, V30, P865, DOI 10.1111/j.1469-7610.1989.tb00288.x Macintosh KE, 2004, J CHILD PSYCHOL PSYC, V45, P421, DOI 10.1111/j.1469-7610.2004.00234.x MATTRON L, 2004, J AUTISM DEV DISORD, V34, P19 Miller GA, 2001, J ABNORM PSYCHOL, V110, P40, DOI 10.1037//0021-843X.110.1.40 Nijiokiktjien C., 2001, EUROPEAN CHILD ADOLE, V10, P79 NOWICKI S, 1993, J SOC PSYCHOL, V133, P749 NOWICKI S, 2003, UNPUB MANUAL RECEPTI, V2 NOWICKI S, 1992, J GENET PSYCHOL, V153, P385 ROSS DC, 1988, EDUC PSYCHOL MEAS, V48, P281, DOI 10.1177/0013164488482002 SCHOPLER E, 1998, CURRENT ISSUES AUTIS Serra M, 1999, EUR CHILD ADOLES PSY, V8, P301 SMITHMYLES B, 2002, FOCUS AUTISM OTHER D, V17, P132 TANTAM D, 1989, J CHILD PSYCHOL PSYC, V30, P623, DOI 10.1111/j.1469-7610.1989.tb00274.x Volkmar FR, 2000, AM J PSYCHIAT, V157, P262, DOI 10.1176/appi.ajp.157.2.262 VOLKMAR FR, 1996, UNPUB YALE SPECIAL I Wechsler D., 1991, MANUAL WECHSLER INTE WING L, 1981, PSYCHOL MED, V11, P115 NR 42 TC 35 Z9 36 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1086 EP 1095 DI 10.1007/s10803-006-0251-6 PG 10 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300009 PM 17180461 ER PT J AU Golan, O Baron-Cohen, S Hill, JJ Rutherford, MD AF Golan, Ofer Baron-Cohen, Simon Hill, Jacqueline J. Rutherford, M. D. TI The 'reading the mind in the voice' test-revised: A study of complex emotion recognition in adults with and without autism spectrum conditions SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE emotion recognition; complex emotions; voice perception; theory of mind; autism spectrum; adults ID HIGH-FUNCTIONING AUTISM; CEREBRAL-BLOOD-FLOW; ASPERGER-SYNDROME; SEX-DIFFERENCES; DEVELOPING-CHILDREN; FACIAL EXPRESSIONS; FACE; INFORMATION; PERCEPTION; DISORDERS AB This study reports a revised version of the 'Reading the Mind in the Voice' (RMV) task. The original task (Rutherford et al., (2002), Journal of Autism and Developmental Disorders, 32, 189-194) suffered from ceiling effects and limited sensitivity. To improve that, the task was shortened and two more foils were added to each of the remaining items. About 50 adults with Asperger Syndrome (AS) or High Functioning Autism (HFA) and 22 matched controls took the revised task. Results show the revised task has good reliability and validity, is harder, and more sensitive in distinguishing the AS/HFA group from controls. Verbal IQ was positively correlated with performance, and females performed worse than males in the AS/HFA group. Results are discussed with regard to multi modal empathizing deficits in autism spectrum conditions (ASC). C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON L8S 42K, Canada. RP Golan, O (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1096 EP 1106 DI 10.1007/s10803-006-0252-5 PG 11 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300010 PM 17072749 ER PT J AU Honey, E Leekam, S Turner, M McConachie, H AF Honey, Emma Leekam, Sue Turner, Michelle McConachie, Helen TI Repetitive behaviour and play in typically developing children and children with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; repetitive behaviours; play; parental report; questionnaire ID COMMUNICATION DISORDERS; DIAGNOSTIC INTERVIEW; PRETEND PLAY; RELIABILITY; LANGUAGE AB The view of a triad of impairments [(Wing and Gould (1979). Journal of Autism and Developmental Disorders, 9, 11-30] in which impaired imagination is linked with repetitive behaviour is widely accepted. However this categorisation differs from the international classification systems, which link imagination to communication impairments rather than to repetitive behaviours. To investigate this relationship, the Activities and Play Questionnaire-Revised was completed by 196 parents of 2-8-year-old children with autism spectrum disorders (ASD) and typical development. Results showed that repetitive behaviours were associated with play in ASD but not in typical development, supporting Wing and Gould's triad. However there was also an association between play, repetitive behaviour and language, confirming the international classification systems description of imagination as a component of language and communication difficulties. C1 Univ Durham, Dept Psychol, Durham DH1 3LE, England. Univ Newcastle Upon Tyne, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. RP Honey, E (reprint author), Univ Durham, Dept Psychol, Sci Site,S Rd, Durham DH1 3LE, England. EM e.j.honey@durham.ac.uk RI Leekam, Susan/A-1773-2010 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAILEY DB, 1993, DEV MED CHILD NEUROL, V35, P806 BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 BATES E, 1987, HDB INFANT DEV Bates E., 1979, EMERGENCE SYMBOLS CO Berkson G, 2000, J EARLY INTERVENTION, V23, P1, DOI 10.1177/10538151000230010401 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 CHARMAN T, 2000, INFANT DEV ESSENTIAL Evans DW, 1997, CHILD DEV, V68, P58, DOI 10.2307/1131925 Fenson L, 1993, MACARTHUR COMMUNICAT Frith U., 1989, AUTISM EXPLAINING EN HAPPE F, 1994, AUSTISM INTRO PSYCHO Hermelin B., 1963, BRIT J SOC CLIN PSYC, V2, P37, DOI 10.1111/j.2044-8260.1963.tb00373.x Jarrold C, 2003, AUTISM, V7, P379, DOI 10.1177/1362361303007004004 Jarrold C, 1996, BRIT J DEV PSYCHOL, V14, P275 Kanner L, 1943, NERV CHILD, V2, P217 Leekam SR, 2002, J CHILD PSYCHOL PSYC, V43, P327, DOI 10.1111/1469-7610.00024 LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 MCCUNE L, 1995, DEV PSYCHOL, V31, P198, DOI 10.1037//0012-1649.31.2.198 MCCUNENICOLICH L, 1981, CHILD DEV, V52, P785, DOI 10.2307/1129078 MORANS DW, 1997, HDB AUTISM PERVASIVE Piaget J, 1962, PLAY DREAMS IMITATIO PRIOR M, 1973, J AUTISM CHILD SCHIZ, V3, P154, DOI 10.1007/BF01537990 RUSSELL J, 1991, BRIT J DEV PSYCHOL, V9, P331 TURNER M, 1999, EXECUTIVE FUNCTION A, P57 *WHO, 1993, ICD10 CLASS MENT BEH, pP147 Williams RW, 2001, BEHAV GENET, V31, P61, DOI 10.1023/A:1010209925783 Wing L., 1996, AUTISTIC SPECTRUM Wing L, 2002, J CHILD PSYCHOL PSYC, V43, P307, DOI 10.1111/1469-7610.00023 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 34 TC 25 Z9 26 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1107 EP 1115 DI 10.1007/s10803-006-0253-4 PG 9 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300011 PM 17072748 ER PT J AU Kamio, Y Robins, D Kelley, E Swainson, B Fein, D AF Kamio, Yoko Robins, Diana Kelley, Elizabeth Swainson, Brook Fein, Deborah TI Atypical lexical/semantic processing in high-functioning autism spectrum disorders without early language delay SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger's disorder; high-functioning pervasive developmental disorder not otherwise specified; early language delay; semantic priming; phonological priming ID ASPERGER-SYNDROME; MEMORY; CHILDREN; ADULTS; INTELLIGENCE AB Although autism is associated with impaired language functions, the nature of semantic processing in high-functioning pervasive developmental disorders (HFPDD) without a history of early language delay has been debated. In this study, we aimed to examine whether the automatic lexical/semantic aspect of language is impaired or intact in these population. Eleven individuals with Asperger's Disorder (AS) or HFPDD-Not Otherwise Specified (NOS) and age-, IQ-, and gender-matched typically developing individuals performed a semantic decision task in four conditions using an indirect priming paradigm. Semantic priming effects were found for near-semantically related word pairs in the controls, whereas this was not the case in the AS or HFPDDNOS participants. This finding suggests similarities in the underlying semantic processing of language across PDD subtypes. C1 Natl Ctr Neurol & Psychiat, NIMH, Dept Child & Adolescent Mental Hlth, Kodaira, Tokyo 1878553, Japan. Georgia State Univ, Dept Psychol, Atlanta, GA 30303 USA. Univ Connecticut, Dept Psychol, Storrs, CT USA. RP Kamio, Y (reprint author), Natl Ctr Neurol & Psychiat, NIMH, Dept Child & Adolescent Mental Hlth, 4-1-1 Ogawahigashi, Kodaira, Tokyo 1878553, Japan. EM kamio@ncnp.go.np RI Robins, Diana/D-9959-2011 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x Beversdorf DQ, 2000, P NATL ACAD SCI USA, V97, P8734, DOI 10.1073/pnas.97.15.8734 Bishop D. V. M., 2000, ASPERGER SYNDROME, P254 Bowler DM, 1997, NEUROPSYCHOLOGIA, V35, P65, DOI 10.1016/S0028-3932(96)00054-1 Bryson S. 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Bakermans-Kranenburg, Marian J. van IJzendoorn, Marinus H. Dietz, Claudine van Daalen, Emma van Engeland, Herman TI Attachment in toddlers with autism and other developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; cortisol; physiology; strange situation procedure ID STRANGE SITUATION; YOUNG-CHILDREN; ADRENOCORTICAL RESPONSES; DISORGANIZED ATTACHMENT; MOTHER ATTACHMENT; SALIVARY CORTISOL; STRESS REACTIVITY; CARDIAC RESPONSES; HEART-RATE; BEHAVIOR AB Attachment was assessed in toddlers with Autistic Disorder (n = 20), Pervasive Developmental Disorder (n = 14), Mental Retardation (n = 12), Language Development Disorder (n = 16), and a non-clinical comparison group (n = 18), using the Strange Situation Procedure (SSP). Children in the clinical groups were more often disorganized and less often securely attached. Severity of autism was associated with more attachment insecurity, and lower developmental level increased the chance for disorganized attachment. Attachment disorganization was related to increased heart rate during the SSP. Controlling for basal cortisol and developmental level, more autistic symptoms predicted lower cortisol responses to the SSP. The findings support the importance of disorganized attachment for children with autism. C1 Leiden Univ, Dept Educ & Child Studies, Ctr Child & Family Studies, NL-2300 RB Leiden, Netherlands. Radboud Univ Nijmegen, Dept Psychiat, Nijmegen, Netherlands. Univ Utrecht, Rudolf Magnus Inst Neurosci, Dept Child & Adolescent Psychiat, Med Ctr, Utrecht, Netherlands. RP Naber, FBA (reprint author), Leiden Univ, Dept Educ & Child Studies, Ctr Child & Family Studies, POB 9555, NL-2300 RB Leiden, Netherlands. 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Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1123 EP 1138 DI 10.1007/s10803-006-0255-2 PG 16 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300013 PM 17160461 ER PT J AU Volden, J Magill-Evans, J Goulden, K Clarke, M AF Volden, Joanne Magill-Evans, Joyce Goulden, Keith Clarke, Margaret TI Varying language register according to listener needs in speakers with autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE pragmatics; language register; language style; communication ID IMPAIRED CHILDREN; MIND; COMMUNICATION; DEFICITS; CLARIFICATION; RESPONSES; REQUESTS; SCRIPTS AB The ability to adjust language register, or style, according to listener needs was assessed in 38 high-functioning children and adolescents with ASD. Participants were asked to explain the process of going to a restaurant to a series of listeners who varied in linguistic competence. Results showed that participants with ASD spontaneously simplified their language based on a listener's appearance and a brief introduction, but were not as adept at that adjustment as matched controls. Further stylistic adjustments were produced following increasingly specific prompts. C1 Univ Alberta, Edmonton, AB T6G 2G4, Canada. Univ Calgary, Calgary, AB, Canada. RP Volden, J (reprint author), Univ Alberta, Edmonton, AB T6G 2G4, Canada. EM joanne.volden@ualberta.ca CR Andersen E. 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Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1139 EP 1154 DI 10.1007/s10803-006-0256-1 PG 16 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300014 PM 17160460 ER PT J AU Christ, SE Holt, DD White, DA Green, L AF Christ, Shawn E. Holt, Daniel D. White, Desiree A. Green, Leonard TI Inhibitory control in children with autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE inhibitory control; autism; children; development; executive abilities ID DEFICIT HYPERACTIVITY DISORDER; OBSESSIVE-COMPULSIVE DISORDER; COLOR-WORD INTERFERENCE; EXECUTIVE FUNCTION; RESPONSE-INHIBITION; PREFRONTAL CORTEX; COGNITIVE CONTROL; CHILDHOOD AUTISM; WORKING-MEMORY; ATTENTION AB Impairments in executive abilities such as cognitive flexibility have been identified in individuals with autism spectrum disorder (ASD). It remains unclear, however, whether such individuals also experience impairments in another executive ability: inhibitory control. In the present study, we administered three inhibitory tasks to 18 children with ASD, 23 siblings of children with ASD, and 25 typically developing children. After controlling for individual differences in age, overall IQ, and processing speed, children with ASD demonstrated impaired performance on two of the three inhibitory tasks. Results suggest that children with ASD experience circumscribed deficits in some but not all aspects of inhibitory control. More generally, the findings underscore the importance of using multiple measures to assess a putative single cognitive ability. C1 Washington Univ, Dept Psychol, St Louis, MO 63130 USA. RP Christ, SE (reprint author), Univ Missouri, Dept Psychol Sci, 210 Mcalester Hall, Columbia, MO 65211 USA. 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Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1155 EP 1165 DI 10.1007/s10803-006-0259-y PG 11 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300015 PM 17066307 ER PT J AU Hume, K Odom, S AF Hume, Kara Odom, Sam TI Effects of an individual work system on the independent functioning of students with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE independence; on task behavior; teacher prompting; structured teaching ID PHOTOGRAPHIC ACTIVITY SCHEDULES; TEACHING-CHILDREN; SELF-MANAGEMENT; YOUNG-CHILDREN; PLAY; PROGRAM; BEHAVIOR; ENGAGEMENT; EDUCATION; SETTINGS AB This study examined the effects of a work system on the independent work and play skills of students with autism. Work systems, an element of structured teaching developed by Division TEACCH, are organized sets of visual information that inform a student about participation in work or play areas. A single subject withdrawal of treatment design, with replications across three participants, was used to assess the on-task behavior and work completion skills of the students in classroom and employment settings as a result of the intervention. Observational data indicated that all students showed increases in on-task behavior, increases in the number of tasks completed or play materials utilized, and reduction of teacher prompts. The results were maintained through the 1-month follow-up. C1 Indiana Univ, Sch Educ, Bloomington, IN 47405 USA. Univ N Carolina, Frank Porter Graham Child Dev Inst, Chapel Hill, NC USA. RP Hume, K (reprint author), Indiana Univ, Sch Educ, 201 N Rose Ave, Bloomington, IN 47405 USA. EM kahume@indiana.edu CR Alberto P. 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R., 1992, BEHAV ASSESSMENT SYS Roid G., 1997, LEITER INT PERFORMAN RUTTER M, 1973, J CHILD PSYCHOL PSYC, V14, P241 Schopler E., 1995, LEARNING COGNITION A, P243 SCHOPLER E, 1971, J AUTISM CHILD SCHIZ, V1, P87, DOI 10.1007/BF01537746 Schopler E., 1988, CHILDHOOD AUTISM RAT Schopler E, 1990, PSYCHOEDUCATIONAL PR Sparrow S, 1984, VINELAND ADAPTIVE BE STAHMER AC, 1992, J APPL BEHAV ANAL, V25, P447, DOI 10.1901/jaba.1992.25-447 STONE WL, 1990, PEDIATRICS, V86, P267 Tabor T., 1999, FOCUS AUTISM OTHER D, V14, P159 Terpstra J. E., 2002, FOCUS AUTISM OTHER D, V17, P119, DOI 10.1177/10883576020170020701 WEHMAN P, 1977, REHABIL LIT, V38, P98 Williams E, 2001, J AUTISM DEV DISORD, V31, P67, DOI 10.1023/A:1005665714197 NR 53 TC 27 Z9 27 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1166 EP 1180 DI 10.1007/s10803-006-0260-5 PG 15 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300016 PM 17072746 ER PT J AU de Bruin, EI de Nijs, PFA Verheij, F Hartman, CA Ferdinand, RF AF de Bruin, Esther I. de Nijs, Pieter F. A. Verheij, Fop Hartman, Catharina A. Ferdinand, Robert F. TI Multiple complex developmental disorder delineated from PDD-NOS SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE MCDD; pervasive developmental disorders; PDD-NOS; thought problems ID DIAGNOSTIC INTERVIEW SCHEDULE; OBSESSIVE-COMPULSIVE DISORDER; DSM-IV; INTERRATER RELIABILITY; BORDERLINE SYNDROME; AUTISTIC DISORDER; FIELD TRIAL; CHILDREN; CHILDHOOD; SCHIZOPHRENIA AB The objective of this study was to identify behavioral differences between children with multiple complex developmental disorder (MCDD) and those with pervasive developmental disorder-not otherwise specified (PDD-NOS). Twenty-five children (6-12 years) with MCDD and 86 children with PDD-NOS were compared with respect to psychiatric co-morbidity, psychotic thought problems and social contact problems using the child behavior checklist/4-18, the Dutch version of the diagnostic interview schedule for children-Version IV, the child and adolescent functional assessment scale, and the autism diagnostic observation schedule-generic. MCDD was associated with anxiety disorders, disruptive behavior, and psychotic thought problems. PDD-NOS was associated with deficits in social contact. MCDD differs from autistic disorder, and can also be delineated from PDD-NOS. C1 Rotterdam Sophia Childrens Hosp, Dept Child & Adolescent Psychiat, Erasmus Med Ctr, NL-3015 GD Rotterdam, Netherlands. Univ Groningen, Med Ctr, Dept Psychiat, Groningen, Netherlands. RP Ferdinand, RF (reprint author), Rotterdam Sophia Childrens Hosp, Dept Child & Adolescent Psychiat, Erasmus Med Ctr, Dr Molewaterpl 60, NL-3015 GD Rotterdam, Netherlands. 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Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1181 EP 1191 DI 10.1007/s10803-006-0261-4 PG 11 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300017 PM 17066306 ER PT J AU Yuill, N Strieth, S Roake, C Aspden, R Todd, B AF Yuill, Nicola Strieth, Sara Roake, Caroline Aspden, Ruth Todd, Brenda TI Brief report: Designing a playground for children with autistic spectrum disorders - Effects on playful peer interactions SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; play; peer-interaction; playground design ID INTERVENTIONS AB This study investigated possible changes in social play and initiations in eight boys (5 to 7-years-old) with autistic spectrum disorders (ASD) who were moving from an old to a new school playground that was designed specifically to enhance playful peer interaction. Each boy was observed for half an hour over three occasions in the old, then the new setting. The playgrounds differed in design, spatial density and identity of potential play partners. As hypothesised, frequency of group play and overall social initiations increased significantly in the new setting. We discuss how playgrounds with appropriate levels of physical challenge and support for both structured, imaginative play and solitary observation may support peer interactions in children with ASD. C1 Univ Sussex, Dept Psychol, Ctr Res Cognit Sci, Brighton BN1 9QH, E Sussex, England. St Anthonys Sch, Chichester, England. RP Yuill, N (reprint author), Univ Sussex, Dept Psychol, Ctr Res Cognit Sci, Brighton BN1 9QH, E Sussex, England. EM nicolay@sussex.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baker M. J., 2000, J POSIT BEHAV INTERV, V2, P66, DOI 10.1177/109830070000200201 Barbour AC, 1999, EARLY CHILD RES Q, V14, P75, DOI 10.1016/S0885-2006(99)80007-6 DOISE W, 1990, CHILDREN HELPING CHI Frost J. 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PD JUL PY 2007 VL 37 IS 6 BP 1192 EP 1196 DI 10.1007/s10803-006-0241-8 PG 5 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300018 PM 17063401 ER PT J AU Hilton, JC Seal, BC AF Hilton, Jane C. Seal, Brenda C. TI Brief report: Comparative ABA and DIR trials in twin brothers with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE ABA; DIR; evidence-based outcomes; CSBS; parent counseling; training programs ID CHILDREN AB Trial interventions in DIR and ABA with twin brothers with autism were offered to help the parents choose one of the programs for their sons. Pre- and post-test scores on the Communication and Symbolic Behavior Scales (CSBS) revealed a slight gain in the composite score of the ABA child and a slight loss in the score of the DIR child. Contrasted gains and losses occurred in six of the seven CSBS clusters. Results from this pilot research are discussed with additional communication and behavior data from the intervention period. Careful interpretation of CSBS outcomes in counseling parents and graduate students is strongly advised. Continued research in comparative outcomes for intervention programs is strongly encouraged. C1 James Madison Univ, Dept Commun Sci & Disorders, Harrisonburg, VA 22807 USA. RP Hilton, JC (reprint author), James Madison Univ, Dept Commun Sci & Disorders, MSC 4304, Harrisonburg, VA 22807 USA. EM hiltonjc@jmu.edu CR Greenspan S. I., 1998, CHILD SPECIAL NEEDS Greenspan SI, 1999, J ASSOC PERS SEVERE, V24, P147, DOI 10.2511/rpsd.24.3.147 Kasari C, 2002, J AUTISM DEV DISORD, V32, P447, DOI 10.1023/A:1020546006971 KOEGEL RL, 1979, J ABNORM PSYCHOL, V88, P418, DOI 10.1037/0021-843X.88.4.418 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Lovaas O. I., 1977, AUTISTIC CHILD LANGU Schreibman L, 2000, J AUTISM DEV DISORD, V30, P373, DOI 10.1023/A:1005535120023 Sherer MR, 2005, J CONSULT CLIN PSYCH, V73, P525, DOI 10.1037/0022-006X.73.3.525 WETHERBY AM, 1999, COMMUNICATION SYMBOL NR 9 TC 2 Z9 2 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD JUL PY 2007 VL 37 IS 6 BP 1197 EP 1201 DI 10.1007/s10803-006-0258-z PG 5 WC Psychology, Developmental SC Psychology GA 181VM UT WOS:000247464300019 PM 17072747 ER PT J AU Wishart, JG Cebula, KR Willis, DS Pitcairn, TK AF Wishart, J. G. Cebula, K. R. Willis, D. S. Pitcairn, T. K. TI Understanding of facial expressions of emotion by children with intellectual disabilities of differing aetiology SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE behavioural phenotypes; Down's syndrome; emotion recognition; fragile X syndrome; social cognition ID FRAGILE-X-SYNDROME; DOWN-SYNDROME; MENTAL-RETARDATION; BEHAVIORAL-PHENOTYPE; SOCIAL COGNITION; CONVERSATIONAL CHARACTERISTICS; WILLIAMS-SYNDROME; JOINT ATTENTION; RECOGNITION; AUTISM AB Background Interpreting emotional expressions is a socio-cognitive skill central to interpersonal interaction. Poor emotion recognition has been reported in autism but is less well understood in other kinds of intellectual disabilities (ID), with procedural differences making comparisons across studies and syndromes difficult. This study aimed to compare directly facial emotion recognition skills in children with fragile X syndrome (FXS), Down's syndrome (DS) and non-specific intellectual disability (NSID), contrasting ability and error profiles with those of typically developing (TD) children of equivalent cognitive and linguistic status. Methods Sixty children participated in the study: 15 FXS, 15 DS, 15 NSID and 15 TD children. Standardised measures of cognitive, language and socialisation skills were collected for all children, along with measures of performance on two photo-matching tasks: an 'identity-matching' task (to control for basic face-processing ability) and an 'emotion-matching' task (happiness, sadness, anger, surprise, fear or disgust). Results Identity-matching ability did not differ across the four child groups. Only the DS group performed significantly more poorly on the emotion-matching task and only in comparison to the TD group, with fear recognition an area of particular difficulty. Conclusion Findings support previous evidence of emotion recognition abilities commensurate with overall developmental level in children with FXS or NSID, but not DS. They also suggest, however, that syndrome-specific difficulties may be subtle and detectable, at least in smaller-scale studies, only in comparison with TD matches, and not always across syndromes. Implications for behavioural phenotype theory, educational interventions and future research are discussed. C1 Univ Edinburgh, Moray House Sch Educ, Edinburgh EH8 8AQ, Midlothian, Scotland. Napier Univ, Edinburgh EH14 1DJ, Midlothian, Scotland. RP Wishart, JG (reprint author), Univ Edinburgh, Moray House Sch Educ, Holyrood Rd, Edinburgh EH8 8AQ, Midlothian, Scotland. 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Intell. Disabil. Res. PD JUL PY 2007 VL 51 BP 551 EP 563 DI 10.1111/j.1365-2788.2006.00947.x PN 7 PG 13 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 172HJ UT WOS:000246794500008 PM 17537169 ER PT J AU Roy, M AF Roy, Meera TI Autism, brain and environment SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Book Review C1 S Birmingham Primary Care Trust, Birmingham, W Midlands, England. RP Roy, M (reprint author), S Birmingham Primary Care Trust, Birmingham, W Midlands, England. CR LATHE R, 2006, AUTISM BRAIN ENVIRON NR 1 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUL PY 2007 VL 51 BP 566 EP 567 DI 10.1111/j.1365-2788.2006.00914.x PN 7 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 172HJ UT WOS:000246794500010 ER PT J AU [Anonymous] AF [Anonymous] TI Yale child study center awarded NIH autism center of excellence status SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT News Item NR 0 TC 0 Z9 0 PU B C DECKER INC PI HAMILTON PA 50 KING STREET EAST, 2ND FLOOR, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JUL PY 2007 VL 55 IS 5 BP 215 EP 216 PG 2 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 214OK UT WOS:000249747800006 ER PT J AU Daneshi, A Hassanzadeh, S AF Daneshi, A. Hassanzadeh, S. TI Cochlear implantation in prelingually deaf persons with additional disability SO JOURNAL OF LARYNGOLOGY AND OTOLOGY LA English DT Article DE cochlear implants; outcome assessment; language development disorders; rehabilitation ID CHILDREN AB Objectives: We aimed to identify the frequency with which the following conditions were present as a second disability in cochlear-implanted, prelingually deaf persons: mild and moderate mental retardation; learning disability; attention deficit/hyperactivity disorder; cerebral palsy; congenital blindness; and autism. We also aimed to document the development of auditory perception in patients having one of these additional disabilities. Study design: A retrospective study was designed to pursue the above aims. Methods: We examined the records of 398 cochlear-implanted, prelingually deaf patients who had received a cochlear implant at least one year previously. Patients were selected who showed a delay in motor, cognitive or emotional development. The selected cases were referred for psychological evaluation in order to identify patients with additional disabilities. We then compared these patients' auditory perception prior to and one year following cochlear implantation. Results: A total of 60 (15 per cent) cochlear-implanted, prelingually deaf patients were diagnosed with additional disabilities. These were classified as: mild mental retardation in eight cases (13.33 per cent); moderate mental retardation in five (8.33 per cent); learning disability in 20 (33.33 per cent); attention deficit/hyperactivity disorder in 15 (25 per cent); cerebral palsy in five (8.33); congenital blindness in three (5 per cent); and autism in four (6.66 per cent). All patients showed significant development in speech perception, except for autistic and congenitally deaf-blind patients. Conclusion: Although cochlear implantation is not contraindicated in prelingually deaf persons with additional disabilities, congenitally deaf-blind and autistic patients showed limited development in auditory perception as a main outcome of cochlear implantation. These patients require unique rehabilitation in order to achieve more auditory development. C1 Iran Univ Med Sci, Dept Head & Neck Surg, Tehran, Iran. Res Inst Except Children, Dept Sensory Disabil, Tehran, Iran. RP Hassanzadeh, S (reprint author), Iran Cochlear Implant Ctr, 47 Eilvarshi Alley,Nejatollahi St,Enghelab Ave, Tehran, Iran. 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Betancur, C. Benyahia, B. Trouillard, O. Bouteiller, D. Verloes, A. LeGuern, E. Leboyer, M. Brice, A. TI Autism, language delay and mental retardation in a patient with 7q11 duplication SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID WILLIAMS-BEUREN-SYNDROME; DELETION; DISORDERS; PHENOTYPE; REGIONS; GENES; REARRANGEMENTS; ABNORMALITIES; MICRODELETION; PREVALENCE AB Background: Chromosomal rearrangements, arising from unequal recombination between repeated sequences, are found in a subset of patients with autism. Duplications involving loci associated with behavioural disturbances constitute an especially good candidate mechanism. The Williams-Beuren critical region (WBCR), located at 7q11.23, is commonly deleted in Williams-Beuren microdeletion syndrome (WBS). However, only four patients with a duplication of the WBCR have been reported to date: one with severe language delay and the three others with variable developmental, psychomotor and language delay. Objective and Methods: In this study, we screened 206 patients with autism spectrum disorders for the WBCR duplication by quantitative microsatellite analysis and multiple ligation-dependent probe amplification. Results: We identified one male patient with a de novo interstitial duplication of the entire WBCR of paternal origin. The patient had autistic disorder, severe language delay and mental retardation, with very mild dysmorphic features. Conclusion: We report the first patient with autistic disorder and a WBCR duplication. This observation indicates that the 7q11.23 duplication could be involved in complex clinical phenotypes, ranging from developmental or language delay to mental retardation and autism, and extends the phenotype initially reported. These findings also support the existence of one or several genes in 7q11.23 sensitive to gene dosage and involved in the development of language and social interaction. C1 Grp Hosp Pitie Salpetriere, INSERM U679, F-75013 Paris, France. Grp Hosp Pitie Salpetriere, APHP, Dept Genet Cytogenet & Embryol, F-75013 Paris, France. Univ Paris 06, Paris, France. Univ Paris 12, INSERM U513, Creteil, France. Hop Robert Debre, APHP, Dept Genet, F-75019 Paris, France. RP Brice, A (reprint author), Grp Hosp Pitie Salpetriere, INSERM U679, 47 Blvd Hop, F-75013 Paris, France. 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In addition to genetic influences, recent studies suggest that prenatal drug or chemical exposures are risk factors for autism. Terbutaline, a beta 2- adrenoceptor agonist used to arrest preterm labor, has been associated with increased concordance for autism in dizygotic twins. We studied the effects of terbutaline on microglial activation in different brain regions and behavioral outcomes in developing rats. Newborn rats were given terbutaline ( 10 mg/ kg) daily on postnatal days ( PN) 2 to 5 or PN 11 to 14 and examined 24 h after the last dose and at PN 30. Immunohistochemical studies showed that administration of terbutaline on PN 2 to 5 produced a robust increase in microglial activation on PN 30 in the cerebral cortex, as well as in cerebellar and cerebrocortical white matter. None of these effects occurred in animals given terbutaline on PN 11 to 14. In behavioral tests, animals treated with terbutaline on PN 2 to 5 showed consistent patterns of hyper-reactivity to novelty and aversive stimuli when assessed in a novel open field, as well as in the acoustic startle response test. Our findings indicate that beta 2-adrenoceptor overstimulation during an early critical period results in microglial activation associated with innate neuroinflammatory pathways and behavioral abnormalities, similar to those described in autism. This study provides a useful animal model for understanding the neuropathological processes underlying autism spectrum disorders. C1 Johns Hopkins Univ, Sch Med, Dept Neurol, Neuroimmunopathol Lab, Baltimore, MD 21287 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21287 USA. Kennedy Krieger Inst, Baltimore, MD USA. Duke Univ, Med Ctr, Dept Pharmacol & Canc Biol, Durham, NC USA. Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC USA. 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The study revealed that all of the clinicians surveyed (n = 16) were prescribing psychotropic medication; psychostimulants and major tranquillizers represented the most frequently prescribed classes and, respectively, methylphenidate, risperidone, melatonin, sodium valproate and carbamazepine were the most frequently employed specific agents. Most patients were receiving monotherapy. Many (14/16) clinicians reported difficulties in shared-care prescribing arrangements with General Practitioners. The study concludes that psychopharmacology is an established part of the psychiatric management of Learning disabled children but acknowledges the need for the elaboration of clinical governance standards to this area of practice. C1 Telford & Wrekin PCT, Shropshires Children & Young Peoples Serv, Serv Children & Young People, Shrewsbury SY1 3AS, Salop, England. 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Olovyannikova, Raissa Ya Hashii, Minako Yokoyama, Shigeru Koizumi, Keita Jin, Duo Liu, Hong-Xiang Lopatina, Olga Amina, Sarwat Islam, Mohammad Saharul Huang, Jian-Jun Noda, Mami TI Cyclic ADP-ribose as a universal calcium signal molecule in the nervous system SO NEUROCHEMISTRY INTERNATIONAL LA English DT Review DE beta-NAD(+); cADP-ribose; ADP-ribosyl cyclase; CD38; oxytocin; autism ID NICOTINAMIDE-ADENINE-DINUCLEOTIDE; METABOTROPIC GLUTAMATE RECEPTORS; INTRACELLULAR CA2+ MOBILIZATION; RAT CORTICAL ASTROCYTES; RYANODINE RECEPTOR; NG108-15 CELLS; CD38/ADP-RIBOSYL CYCLASE; INOSITOL TRISPHOSPHATE; NEUROBLASTOMA-CELLS; CARDIAC MYOCYTES AB beta-NAD(+) is as abundant as ATP in neuronal cells. beta-NAD(+) functions not only as a coenzyme but also as a substrate. beta-NAD(+)-utilizing enzymes are involved in signal transduction. We focus on ADP-ribosyl cyclase/CD38 which synthesizes cyclic ADP-ribose (cADPR), a universal Ca2+ mobilizer from intracellular stores, from beta-NAD(+). cADPR acts through activation/modulation of ryanodine receptor Ca2+ releasing Ca2+ channels. cADPR synthesis in neuronal cells is stimulated or modulated via different pathways and various factors. Subtype-specific coupling of various neurotransmitter receptors with ADP-ribosyl cyclase confirms the involvement of the enzyme in signal transduction in neurons and glial cells. Moreover, cADPR/CD38 is critical in oxytocin release from the hypothalamic cell dendrites and nerve terminals in the posterior pituitary. Therefore, it is possible that pharmacological manipulation of intracellular cADPR levels through ADP-ribosyl cyclase activity or synthetic cADPR analogues may provide new therapeutic opportunities for treatment of neurodevelopmental disorders. (c) 2007 Published by Elsevier Ltd. C1 Kanazawa Univ, Grad Sch Med, Dept Biophys Genet, Kanazawa, Ishikawa 9208640, Japan. Kanazawa Univ, 21st Century Ctr Excellence COE Program Innovat, Kanazawa, Ishikawa 920, Japan. Krasnoyarsk State Med Acad, Dept Biochem & Med Chem, Krasnoyarsk 660022, Russia. Kyushu Univ, Grad Sch Pharmaceut Sci, Dept Pathophysiol, Fukuoka 8128582, Japan. RP Higashida, H (reprint author), Kanazawa Univ, Grad Sch Med, Dept Biophys Genet, Kanazawa, Ishikawa 9208640, Japan. 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Int. PD JUL-SEP PY 2007 VL 51 IS 2-4 BP 192 EP 199 DI 10.1016/j.neuint.2007.06.023 PG 8 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 204WX UT WOS:000249075800014 PM 17664018 ER PT J AU Kim, SA Kim, JH Park, M Cho, IH Yoo, HJ AF Kim, Soon Ae Kim, Jin Hee Park, Mira Cho, In Hee Yoo, Hee Jeong TI Family-based association study between GRIK2 polymorphisms and autism spectrum disorders in the Korean trios SO NEUROSCIENCE RESEARCH LA English DT Article DE autism spectrum disorders (ASD); transmission disequilibrium test (TDT); glutamate receptor 6 (GRIK2); association ID GLUTAMATE-RECEPTOR-6 GENE; FOLLOW-UP; KAINATE; HIPPOCAMPUS; EPILEPSY; CHILDREN; LINKAGE; GLUR6; AGE AB Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder with strong genetic components. The present study comprises the detection of four single nucleotide polymorphisms (SNPs) in GRIK2 followed by a family-based association analysis of the SNPs in 126 Korean ASD trios by using the transmission disequilibrium test (TDT) and haplotype analysis. We found preferential transmission of the C allele at the rs3213607 (P < 0.001) of GRIK2 in ASD and haplotype analysis revealed that one haplotype demonstrated a significant association (P = 0.023). These results suggest a potential association between GRIK2 and ASD in the Korean population, (C) 2007 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved. C1 Seoul Natl Univ Bundang Hosp, Dept Psychiat, Songnam 463707, Kyunggi, South Korea. Eulji Univ, Sch Med, Dept Pharmacol, Taejon, South Korea. Eulji Univ, Sch Med, Div Biostat, Taejon, South Korea. Gachon Med Sch, Dept Neuropsychiat, Inchon, South Korea. RP Yoo, HJ (reprint author), Seoul Natl Univ Bundang Hosp, Dept Psychiat, 300 Gumi Dong, Songnam 463707, Kyunggi, South Korea. 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TI Pharmacotherapy of autism and related disorders SO PSYCHIATRIC ANNALS LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; RETROSPECTIVE ANALYSIS; BEHAVIORAL SYMPTOMS; SPECTRUM DISORDERS; INFANTILE-AUTISM; CROSSOVER TRIAL; CHILDREN; HALOPERIDOL C1 Indiana Univ, Sch Med, Riley Hosp Child & Adolescent Psychiat Clin, Dept Psychiat, Indianapolis, IN 46202 USA. James Whitcomb Riley Hosp Children, Christian Sarkine Autism Treatment Ctr, Indianapolis, IN USA. RP Posey, DJ (reprint author), Indiana Univ, Sch Med, Riley Hosp Child & Adolescent Psychiat Clin, Dept Psychiat, 702 Barnhill Dr,Room 4300, Indianapolis, IN 46202 USA. 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Ann. PD JUL PY 2007 VL 37 IS 7 BP 490 EP 500 PG 11 WC Psychiatry SC Psychiatry GA 193EU UT WOS:000248257900005 ER PT J AU Dvir, Y AF Dvir, Yael TI Unstrange minds: Remapping the world of autism SO PSYCHIATRIC SERVICES LA English DT Book Review C1 [Dvir, Yael] Univ Massachusetts, Sch Med, Dept Psychiat, Worcester, MA 01655 USA. RP Dvir, Y (reprint author), Univ Massachusetts, Sch Med, Dept Psychiat, Worcester, MA 01655 USA. CR Grinker R., 2006, UNSTRANGE MINDS REMA NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD JUL PY 2007 VL 58 IS 7 BP 1019 EP 1019 DI 10.1176/appi.ps.58.7.1019 PG 1 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 265LM UT WOS:000253360400031 ER PT J AU Frischen, A Bayliss, AP Tipper, SP AF Frischen, Alexandra Bayliss, Andrew P. Tipper, Steven P. TI Gaze cueing of attention: Visual attention, social cognition, and individual differences SO PSYCHOLOGICAL BULLETIN LA English DT Review DE attention; social cognition; gaze cueing; joint attention; face perception ID SUPERIOR TEMPORAL SULCUS; HIGH-FUNCTIONING AUTISM; MIRROR-NEURON SYSTEM; POSITRON-EMISSION-TOMOGRAPHY; UNINFORMATIVE SYMBOLIC CUES; MODULATES FACE RECOGNITION; SACCADE-RELATED ACTIVITY; WEAK CENTRAL COHERENCE; HUMAN FUSIFORM GYRUS; FRONTAL-LOBE DAMAGE AB During social interactions, people's eyes convey a wealth of information about their direction of attention and their emotional and mental states. This review aims to provide a comprehensive overview of past and current research into the perception of gaze behavior and its effect on the observer. This encompasses the perception of gaze direction and its influence on perception of the other person, as well as gaze-following behavior such as joint attention, in infant, adult, and clinical populations. Particular focus is given to the gaze-cueing paradigm that has been used to investigate the mechanisms of joint attention. The contribution of this paradigm has been significant and will likely continue to advance knowledge across diverse fields within psychology and neuroscience. C1 Macquarie Univ, Macquarie Ctr Cognit Sci, Sydney, NSW 2109, Australia. Univ Wales, Sch Psychol, Bangor, Gwynedd, Wales. RP Frischen, A (reprint author), Macquarie Univ, Macquarie Ctr Cognit Sci, Blsg C5A, Sydney, NSW 2109, Australia. 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National and sociopolitical contexts influence issue definition differently across nations. However, the degree to which nation-specific issue definition takes place has been insufficiently explored. In recent years, the growing incidence of autism has led to a quest for causal factors. One hypothesis posits that the use of mercury in vaccines may be a culprit. This paper examines the definition of the mercury and autism issue in Australia, Canada, the United Kingdom, and the United States. Insights into the comparative elements of issue definition are suggested by the case. These insights are of particular importance to administrators, as agencies are deeply involved as objects and actors in the process of issue definition and are often responsible for implementing new and redefined policies. C1 Wayne State Univ, Dept Polit Sci & Criminal Justice, Detroit, MI 48202 USA. Univ Missouri, Inst Publ Policy, Harry S Truman Sch Vet Affairs, Columbia, MO USA. 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PD JUL-AUG PY 2007 VL 67 IS 4 BP 757 EP 767 PG 11 WC Public Administration SC Public Administration GA 177SU UT WOS:000247173600014 ER PT J AU Goin-Kochel, RP Myers, BJ Mackintosh, VH AF Goin-Kochel, Robin P. Myers, Barbara J. Mackintosh, Virginia H. TI Parental reports on the use of treatments and therapies for children with autism spectrum disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Asperger's syndrome; PDD-NOS; Interventions; Drugs; Medications ID EARLY INTERVENTION; PATTERNS; COMPLEMENTARY; PREVALENCE AB Parents of children with autism spectrum disorders (ASD; N = 479) reported via web-based survey what pharmacological (drug), diet, and behavioral/educational/alternative therapies they had tried and were using now in the treatment of their children with ASD. Depending on type of ASD, children had tried, on average, between seven and nine therapies and were now using between four and six. 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PD JUL-SEP PY 2007 VL 1 IS 3 BP 195 EP 209 DI 10.1016/j.rasd.2006.08.006 PG 15 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89QU UT WOS:000206060000001 ER PT J AU Endicott, K Higbee, TS AF Endicott, Katie Higbee, Thomas S. TI Contriving motivating operations to evoke mands for information in preschoolers with autism SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Mands for information; Motivating operations; Autism AB Four preschoolers with autism participated in the study. Stimulus preference assessments were conducted to identify high and low preferred items, which were then hidden or given to an adult in order to contrive motivation for the information about the location of the items. The first experiment involved the manipulation of motivating operations to evoke the mand "Where is it?" Upon successful acquisition of this initial mand for information, students participated in a second experiment involving the manipulation of a motivating operation to evoke the mand "Who has it?" All participants successfully acquired the ability to mand for information. Published by Elsevier Ltd. C1 [Endicott, Katie; Higbee, Thomas S.] Utah State Univ, Dept Special Educ & Rehabil, Logan, UT 84322 USA. RP Higbee, TS (reprint author), Utah State Univ, Dept Special Educ & Rehabil, 2865 Old Main Hill, Logan, UT 84322 USA. EM tom.higbee@usu.edu RI Higbee, Thomas/F-5157-2010 CR Carr JE, 2000, J APPL BEHAV ANAL, V33, P353, DOI 10.1901/jaba.2000.33-353 Sundberg Mark L, 2002, Anal Verbal Behav, V18, P15 TAYLOR BA, 1995, J APPL BEHAV ANAL, V28, P3, DOI 10.1901/jaba.1995.28-3 TWARDOSZ S, 1973, J APPL BEHAV ANAL, V6, P655, DOI 10.1901/jaba.1973.6-655 Williams G, 2000, J APPL BEHAV ANAL, V33, P627, DOI 10.1901/jaba.2000.33-627 NR 5 TC 13 Z9 13 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1750-9467 J9 RES AUTISM SPECT DIS JI Res. Autism Spectr. Disord. PD JUL-SEP PY 2007 VL 1 IS 3 BP 210 EP 217 DI 10.1016/j.rasd.2006.10.003 PG 8 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89QU UT WOS:000206060000002 ER PT J AU La Malfa, G Lassi, S Salvini, R Giganti, C Bertelli, M Albertini, G AF La Malfa, Giampaolo Lassi, Stefano Salvini, Roberto Giganti, Chiara Bertelli, Marco Albertini, Giorgio TI The relationship between autism and psychiatric disorders in Intellectually Disabled Adults SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Intellectual Disability; Autism; Pervasive developmental disorders; Vulnerability; Psychiatric disorders AB Intellectual Disability (ID) shows a high comorbidity with psychiatric disorders with a great variability in the prevalence rates. An important subgroup is represented by subjects with ID and autism or other autistic spectrum disorders (PDD). The purpose of the present study was to assess PDD with specific screening tools in a population of people with ID and compare the groups with or without PDD through the administration of a psychopathological scale in order to verify the differences of psychiatric disorders' rates. The study was conducted on 90 subjects attending daily centres or residential centres in Florence, Italy. In order to assess the presence of PDD, the PDD-MRS was administrated, while for the assessment of the psychopathological aspects we have used the DASH-II. The presence of a psychiatric disorder has a significant effect on anxiety, depression and organic syndromes and statistically significant differences have been registered in many DASH-II subscales. The statistical comparison between the two groups shows that PDD was clearly correlated with an increased presence of psychiatric disorders. The variable PDD could be considered as a vulnerability factor for psychiatric disorders. However there was still the need to focus on categorical diagnoses, in order to increase our knowledge about the concept of vulnerability in people with ID. (C) 2006 Elsevier Ltd. All rights reserved. C1 [La Malfa, Giampaolo; Lassi, Stefano; Salvini, Roberto; Giganti, Chiara; Bertelli, Marco] Univ Florence, Careggi Hosp, Psychiat Unit, Dept Neurol & Psychiat Sci, Florence, Italy. [Albertini, Giorgio] IRCCS San Raffaele Pisana, Rome, Italy. RP La Malfa, G (reprint author), SIRM, I-5850127 Florence, Italy. EM gplamalfa@videosoft.it CR American Association on Mental Retardation, 2002, MENT RET DEF CLASS S American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bamburg JW, 2001, J DEV PHYS DISABIL, V13, P319, DOI 10.1023/A:1012218611103 BORTHWICKDUFFY SA, 1994, J CONSULT CLIN PSYCH, V62, P17, DOI 10.1037//0022-006X.62.1.17 Bradley EA, 2004, J AUTISM DEV DISORD, V34, P151, DOI 10.1023/B:JADD.0000022606.97580.19 Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 de Bildt A, 2004, J AUTISM DEV DISORD, V34, P129 de Bildt A, 2003, J AUTISM DEV DISORD, V33, P595, DOI 10.1023/B:JADD.0000005997.92287.a3 DILAVORE RC, 1995, J AUTISM DEV DISORD, V25, P355 DOSEN A, J INTELLECT IN PRESS Dosen A, 2001, TREATING MENTAL ILLNESS AND BEHAVIOR DISORDERS IN CHILDREN AND ADULTS WITH MENTAL RETARDATION, P3 Gadow KD, 2004, J AUTISM DEV DISORD, V34, P379, DOI 10.1023/B:JADD.0000037415.21458.93 Glahn DC, 2004, BIPOLAR DISORD, V6, P171, DOI 10.1111/j.1399-5618.2004.00113.x Glenn E, 2003, J AUTISM DEV DISORD, V33, P69, DOI 10.1023/A:1022282521625 Gottesman II, 2003, AM J PSYCHIAT, V160, P636, DOI 10.1176/appi.ajp.160.4.636 Guaraldi Gian Paolo, 2002, Quaderni Italiani di Psichiatria, V21, P39 Hemmings CP, 2006, J INTELL DISABIL RES, V50, P269, DOI 10.1111/j.1365-2788.2006.00827.x Hessl D, 2002, PSYCHONEUROENDOCRINO, V27, P855, DOI 10.1016/S0306-4530(01)00087-7 HILL J, RES DEV DIS IN PRESS KONSTANTAREOS MM, 2001, J AUTISM DEV DISORD, V34, P19 KRAIJER D, 2006, STAD DI SCALA VALUTA Kraijer D. W., 1997, AUTISM AUTISTIC LIKE Krug D. A., 1980, AUTISM SCREENING INS Kurita H, 2004, J DEV PHYS DISABIL, V16, P377, DOI 10.1007/s10882-004-0693-8 La Malfa G, 2004, J INTELL DISABIL RES, V48, P262, DOI 10.1111/j.1365-2788.2003.00567.x Landis J. R., 1977, BIOMETRICS, V33, P174 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Matson J. L., 1995, DIAGNOSTIC ASSESSMEN MATSON JL, 1991, J NERV MENT DIS, V179, P553, DOI 10.1097/00005053-199109000-00006 Matson JL, 1997, RES DEV DISABIL, V18, P39, DOI 10.1016/S0891-4222(96)00036-4 Matson JL, 1997, RES DEV DISABIL, V18, P457, DOI 10.1016/S0891-4222(97)00022-X Matson JL, 1998, J AUTISM DEV DISORD, V28, P77, DOI 10.1023/A:1026019221036 Matson JL, 1997, RES DEV DISABIL, V18, P221, DOI 10.1016/S0891-4222(97)00005-X Morgan C. N., 2002, PSYCHIAT B, V26, P127, DOI 10.1192/pb.26.4.127 Morgan C. 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R., 1995, BIOMETRY PRINCIPLES, V3rd SPARROW SS, 2003, VINELAND ADAPTATIVE Stahlberg O, 2004, J NEURAL TRANSM, V111, P891, DOI 10.1007/s00702-004-0115-1 Towbin KE, 2005, J CHILD ADOL PSYCHOP, V15, P452, DOI 10.1089/cap.2005.15.452 Tsai LY, 1996, J AUTISM DEV DISORD, V26, P159, DOI 10.1007/BF02172004 TSAKANIKOS E, J AUTISM DE IN PRESS Wechsler D, 1981, WECHSLER ADULT INTEL WING K, 1989, HOSP CLOSURE EFFECTS WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Yirmiya N, 2005, J CHILD PSYCHOL PSYC, V46, P69, DOI 10.1111/j.1469-7610.2004.00334.x NR 50 TC 21 Z9 21 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1750-9467 J9 RES AUTISM SPECT DIS JI Res. Autism Spectr. Disord. PD JUL-SEP PY 2007 VL 1 IS 3 BP 218 EP 228 DI 10.1016/j.rasd.2006.10.004 PG 11 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89QU UT WOS:000206060000003 ER PT J AU Machalicek, W O'Reilly, MF Beretvas, N Sigafoos, J Lancioni, GE AF Machalicek, Wendy O'Reilly, Mark F. Beretvas, Natasha Sigafoos, Jeff Lancioni, Guilio E. TI A review of interventions to reduce challenging behavior in school settings for students with autism spectrum disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Review DE Challenging behavior; Autism spectrum disorders; Schools AB This review evaluates research oil the treatment of challenging behavior in school settings for Students with autism spectrum disorders (ASD). Electronic database searches were carried out to identify Studies published between 1995 and 2005. Twenty-Six Studies were identified. A variety of procedures were implemented in these studies to decrease challenging behavior in classrooms. These procedures were classified into four groups: (a) antecedent manipulations, (b) change in instructional context, (c) differential reinforcement, and (d) self-management techniques. The results of these Studies indicated that till four classes of procedures were generally effective in reducing challenging behavior. These results are discussed ill relation to four issues: (a) the characteristics of the participants, (b) assessment procedures carried out prior to intervention, (c) the feasibility of classroom treatment, and (d) the social validity of intervention procedures. Surprisingly, the effectiveness of a procedure did not seem to be related to completion of a prior functional behavior assessment (FBA). Also, the reported measures of social validity ill the studies reviewed here have elicited positive reports froth stakeholders, but the utility of these measures, as they have been conceptualized, is questioned. The findings of this review suggest future research directions that are also examined. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Machalicek, Wendy; O'Reilly, Mark F.; Beretvas, Natasha] Univ Texas Austin, Dept Special Educ, Austin, TX 78712 USA. [Sigafoos, Jeff] Univ Tasmania, Hobart, Tas 7001, Australia. [Lancioni, Guilio E.] Univ Bari, I-70121 Bari, Italy. RP O'Reilly, MF (reprint author), Univ Texas Austin, Dept Special Educ, 1 Univ Stn,D5300, Austin, TX 78712 USA. EM markoreilly@mail.utexas.edu CR Agosta E, 2004, INTERV SCH CLIN, V39, P276, DOI 10.1177/10534512040390050401 Baghdadli A, 2003, J INTELL DISABIL RES, V47, P622, DOI 10.1046/j.1365-2788.2003.00507.x Braithwaite KL, 2000, BEHAV INTERVENT, V15, P21, DOI 10.1002/(SICI)1099-078X(200001/03)15:1<21::AID-BIN45>3.3.CO;2-R Brownell MD, 2002, J MUSIC THER, V39, P117 Buggey T., 2005, FOCUS AUTISM OTHER D, V20, P52, DOI DOI 10.1177/10883576050200010501 CARR EG, 1991, J APPL BEHAV ANAL, V24, P523, DOI 10.1901/jaba.1991.24-523 Conroy M. A., 2005, FOCUS AUTISM OTHER D, V20, P223, DOI DOI 10.1177/10883576050200040401 Conroy MA, 2005, TOP EARLY CHILD SPEC, V25, P157, DOI 10.1177/02711214050250030301 DERBY KM, 1992, J APPL BEHAV ANAL, V25, P713, DOI 10.1901/jaba.1992.25-713 Dooley P., 2001, J POSIT BEHAV INTERV, V3, P57, DOI 10.1177/109830070100300108 DURAND M, 1999, J APPL BEHAV ANAL, V3, P247 Durand M, 1992, MOTIVATION ASSESSMEN DURAND VM, 1988, J AUTISM DEV DISORD, V18, P99 FAWCETT SB, 1991, J APPL BEHAV ANAL, V24, P235, DOI 10.1901/jaba.1991.24-235 FINNEY JW, 1991, J APPL BEHAV ANAL, V24, P245, DOI 10.1901/jaba.1991.24-245 Gray C. A., 1993, FOCUS AUTISTIC BEHAV, V8, P1, DOI DOI 10.1177/108835769300800101 Hastings RP, 2004, RES DEV DISABIL, V25, P139, DOI 10.1016/j.ridd.2004.01.002 Hastings RP, 2002, MENT RETARD, V40, P148, DOI 10.1352/0047-6765(2002)040<0148:CSATIO>2.0.CO;2 HAWKINS RP, 1991, J APPL BEHAV ANAL, V24, P205, DOI 10.1901/jaba.1991.24-205 Heckaman K. A., 1998, J BEHAV ED, V8, P171, DOI 10.1023/A:1022883523915 Hirsch N., 1996, FOCUS AUTISM OTHER D, V11, P222 Horner RH, 2002, J AUTISM DEV DISORD, V32, P423, DOI 10.1023/A:1020593922901 Jones KM, 2000, J EDUC PSYCHOL CONS, V11, P323, DOI 10.1207/S1532768XJEPC113&4_03 KEELING K, 2003, FOCUS AUTISM OTHER D, V18, P103 Kennedy CH, 2000, J APPL BEHAV ANAL, V33, P559, DOI 10.1901/jaba.2000.33-559 KIERNAN C, 1994, MENT HANDICAP RES, V7, P177, DOI DOI 10.1111/J.1468-3148.1994.TB00126.X KUOCH H, 2003, FOCUS AUTISM OTHER D, V18, P1088 Kuttler S., 1998, FOCUS AUTISM OTHER D, V13, P176, DOI DOI 10.1177/108835769801300306 Lancioni GE, 2002, RES DEV DISABIL, V23, P309, DOI 10.1016/S0891-4222(02)00138-5 Mancina C, 2000, J AUTISM DEV DISORD, V30, P599, DOI 10.1023/A:1005695512163 Massey NG, 2000, EDUC TRAIN MENT RET, V35, P326 MATSON J, 1994, AUTISM CHILDREN ADUL, P244 McClintock K, 2003, J INTELL DISABIL RES, V47, P405, DOI 10.1046/j.1365-2788.2003.00517.x Miltenberger R. G., 1997, BEHAV INTERVENT, V12, P105, DOI 10.1002/(SICI)1099-078X(199707)12:3<105::AID-BRT172>3.0.CO;2-4 Murphy G, 1999, J INTELL DISABIL RES, V43, P149, DOI 10.1046/j.1365-2788.1999.00183.x Murphy GH, 2005, J AUTISM DEV DISORD, V35, P405, DOI 10.1007/s10803-005-5030-2 Murray JB, 1996, J PSYCHOL, V130, P145 NORTHUP J, 1994, J APPL BEHAV ANAL, V27, P33, DOI 10.1901/jaba.1994.27-33 Nuzzolo-Gomez R, 2002, J POSIT BEHAV INTERV, V4, P80, DOI 10.1177/109830070200400203 ODOM S, 2003, FOCUS AUTISM OTHER D, V10, P166 OLIVER C, 1987, J MENT DEFIC RES, V31, P147 O'Reilly M, 2005, J AUTISM DEV DISORD, V35, P305, DOI 10.1007/s10803-005-3294-1 Orr T., 1998, FOCUS AUTISM OTHER D, V13, P163 Peterson S. M., 2001, FOCUS AUTISM OTHER D, V16, P240 PRUPAS A, 2001, ED TRAINING MENTAL R Reichle J., 1990, NAT WORK C POS APPR Reynhout G, 2006, J AUTISM DEV DISORD, V36, P445, DOI 10.1007/s10803-006-0086-1 Scattone D, 2002, J AUTISM DEV DISORD, V32, P535, DOI 10.1023/A:1021250813367 Schilling DL, 2004, J AUTISM DEV DISORD, V34, P423, DOI 10.1023/B:JADD.0000037418.48587.f4 Schindler HR, 2005, AM J MENT RETARD, V110, P36, DOI 10.1352/0895-8017(2005)110<36:GROPBO>2.0.CO;2 Schmit J, 2000, MENT RETARD, V38, P131, DOI 10.1352/0047-6765(2000)038<0131:EOUAPC>2.0.CO;2 SCHWARTZ IS, 1991, J APPL BEHAV ANAL, V24, P189, DOI 10.1901/jaba.1991.24-189 Taylor BA, 2005, BEHAV INTERVENT, V20, P239, DOI 10.1002/bin.200 Vittimberga G. L, 2001, J POSIT BEHAV INTERV, V3, P194, DOI 10.1177/109830070100300401 WOLF MM, 1978, J APPL BEHAV ANAL, V11, P203, DOI 10.1901/jaba.1978.11-203 NR 55 TC 47 Z9 47 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1750-9467 J9 RES AUTISM SPECT DIS JI Res. Autism Spectr. Disord. PD JUL-SEP PY 2007 VL 1 IS 3 BP 229 EP 246 DI 10.1016/j.rasd.2006.10.005 PG 18 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89QU UT WOS:000206060000004 ER PT J AU Gillett, JN LeBlanc, LA AF Gillett, Jill N. LeBlanc, Linda A. TI Parent-implemented natural language paradigm to increase language and play in children with autism SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Parent training; Language; Play; Spontaneous; Natural language paradigm AB Three parents of children with autism were taught to implement the Natural Language Paradigm (NLP). Data were collected on parent implementation, multiple measures of child language, and play. The parents were able to learn to implement the NLP procedures quickly and accurately with beneficial results for their children. Increases in the overall rate of vocalizations were observed for all three children with a shift from imitative language at the beginning of intervention to spontaneous language at the end of intervention. Clear improvements in play were observed for two of three children while ceiling effects were observed for a third child who already played effectively. In response to a social validity questionnaire, parents indicated that they found the study useful and the NLP procedures simple to implement and that that they would continue to use NLP at home following the conclusion of the study. (C) 2006 Elsevier Ltd. All rights reserved. C1 [LeBlanc, Linda A.] Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. RP LeBlanc, LA (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. EM linda.leblanc@wmich.edu CR CELIBERTI DA, 1993, BEHAV THER, V24, P573, DOI 10.1016/S0005-7894(05)80319-3 CHARLOPCHRISTY MH, 1999, AUTISM BEHAV ANAL PE Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd Gilliam J. E., 1995, GILLIAM AUTISM RATIN Kamps D, 2002, EXCEPT CHILDREN, V68, P173 Koegel LK, 1999, J ASSOC PERS SEVERE, V24, P174, DOI 10.2511/rpsd.24.3.174 KOEGEL RL, 1987, J AUTISM DEV DISORD, V17, P187, DOI 10.1007/BF01495055 Koegel RL, 2001, J CLIN CHILD PSYCHOL, V30, P19, DOI 10.1207/S15374424JCCP3001_4 Koegel RL, 2003, EVIDENCE-BASED PSYCHOTHERAPIES FOR CHILDREN AND ADOLESCENTS, P341 LASKI KE, 1988, J APPL BEHAV ANAL, V21, P391, DOI 10.1901/jaba.1988.21-391 Leblanc Linda A, 2006, Anal Verbal Behav, V22, P49 LEONARD LB, 1984, J SPEECH HEAR DISORD, V45, P336 SCHWARTZ IS, 1989, J ASSOC PERS SEVERE, V14, P48 Skinner B. F., 1957, VERBAL BEHAV STOKES TF, 1977, J APPL BEHAV ANAL, V10, P349, DOI 10.1901/jaba.1977.10-349 STOKES TF, 1989, BEHAV THER, V20, P337, DOI 10.1016/S0005-7894(89)80054-1 NR 16 TC 24 Z9 24 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1750-9467 J9 RES AUTISM SPECT DIS JI Res. Autism Spectr. Disord. PD JUL-SEP PY 2007 VL 1 IS 3 BP 247 EP 255 DI 10.1016/j.rasd.2006.09.003 PG 9 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89QU UT WOS:000206060000005 ER PT J AU Carminati, GG Gerber, F Baud, MA Baud, O AF Carminati, Giuliana Galli Gerber, Fabienne Baud, Marc Andre Baud, Olivier TI Evaluating the effects of a structured program for adults with autism spectrum disorders and intellectual disabilities SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Adults; Autism Spectrum Disorders (ASD); Intellectual disability; Residential setting; Aberrant Behaviour Checklist (ABC); Behavioural disorders AB This study observes the evolution of persons with pervasive developmental disorders (PDD) and profound intellectual disabilities living in residences with a Program for Residents with Autism Spectrum Disorders (ASD) characterised by a different educator's presence ratio and different logistic accommodations. This population is characterised by the need to live in a very structured and predictable environment and greatly benefits froth specific programs in residential settings. We evaluated the evolution during 2.5 years of 2 groups of 10 residents using the Aberrant Behaviour Checklist (ABC) and the Children Autism Rating Scale (CARS). Evolution appears to be slow and irregular but we observed significant changes in social withdrawal along the study for one group. Possible implications of this study are discussed. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Carminati, Giuliana Galli; Gerber, Fabienne] UPDM, HUG, Div Adult Psychiat, Unit Mental Dev Psychiat, CH-1225 Chene Bourg, Switzerland. [Baud, Marc Andre; Baud, Olivier] Publ Socioeduc Inst EPSE, Geneva, Switzerland. RP Gerber, F (reprint author), UPDM, HUG, Div Adult Psychiat, Unit Mental Dev Psychiat, Ch Petit Bel Air 2, CH-1225 Chene Bourg, Switzerland. EM fabienne.gerber@hcuge.ch CR AMAN MG, 1995, AM J MENT RETARD, V100, P283 AMAN MG, 1985, AM J MENT DEF, V89, P485 AMAN MG, 1987, AM J MENT RETARD, V92, P237 AMAN MG, 1985, AM J MENT DEF, V89, P492 *ASS INT AUT EUR, 2000, DESCR AUT CARMINATI GG, LONGITUDINAL S UNPUB Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 HOLT G, 2002, AUTISM RELATED DISOR MARSHBURN EC, 1992, J AUTISM DEV DISORD, V22, P357, DOI 10.1007/BF01048240 Mesibov G, 1997, PROFIL PSYCHOEDUCATI MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 ROGE B, 2003, AUTISME COMPRENDRE A ROJAHN J, 1991, J AUTISM DEV DISORD, V21, P17, DOI 10.1007/BF02206994 Rojahn J, 2003, RES DEV DISABIL, V24, P391, DOI 10.1016/S0891-4222(03)00055-6 Schopler E., 1988, CHILDHOOD AUTISM RAT Schopler E., 2001, RES BASIS AUTISM INT SCHOPLER E, 1985, AUTISM ADOLESCENTS A Schopler E, 1994, PROFIL PSYCHOEDUCATI Van Bourgondien ME, 2003, J AUTISM DEV DISORD, V33, P131, DOI 10.1023/A:1022931224934 Van Bourgondien ME, 2001, RESEARCH BASIS FOR AUTISM INTERVENTION, P187 VANBOURGONDIEN ME, 1990, J AUTISM DEV DISORD, V20, P299 World Health Organisation, 1994, ICD 10 CLASS MENT BE NR 22 TC 9 Z9 9 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1750-9467 J9 RES AUTISM SPECT DIS JI Res. Autism Spectr. Disord. PD JUL-SEP PY 2007 VL 1 IS 3 BP 256 EP 265 DI 10.1016/j.rasd.2006.11.001 PG 10 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89QU UT WOS:000206060000006 ER PT J AU Ray, E Schlottmann, A AF Ray, Elizabeth Schlottmann, Anne TI The perception of social and mechanical causality in young children with ASD SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Perceptual causality; ASD ID AUTISTIC-CHILDREN; ASPERGER-SYNDROME; CENTRAL COHERENCE; MIND; INFANTS; ABILITY; ATTENTION; TASK; RECOGNITION; PERFORMANCE AB This study investigated perceptual causality in launch and reaction events in children with ASD (CA = 8.4, VMA = 5.1) and mental age matched controls with typical development and learning difficulties. This is of interest because difficulties with global processing in autism suggest that individuals with ASD may not 'see' causal Gestalts in general, and specific difficulties with reaction perception could be related to difficulties with TOM. Participants matched pictures depicting mechanical and psychological cause and non-causality to computer animated launch and reaction events and delayed control events. Children with ASD showed the typical response to reaction events, matching them with the picture for psychological cause, but they were impaired in launch perception compared to control participants. We discuss the possibility that event duration may be the critical difference between the causal events. The information allowing identification of a reaction is conveyed over a longer time frame (600 m here) than in launching (21 ms here). This may allow for the deployment of global processes and/or attentional shifts in reaction, but not launch perception. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Ray, Elizabeth; Schlottmann, Anne] UCL, Dept Psychol, London WC1E 6BT, England. RP Ray, E (reprint author), UCL, Dept Psychol, Gower St, London WC1E 6BT, England. 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Autism Spectr. Disord. PD JUL-SEP PY 2007 VL 1 IS 3 BP 266 EP 280 DI 10.1016/j.rasd.2006.11.002 PG 15 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89QU UT WOS:000206060000007 ER PT J AU Matson, JL Nebel-Schwalm, MS AF Matson, Johnny L. Nebel-Schwalm, Marie S. TI Comorbid psychopathology with autism spectrum disorder in children: An overview SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE comorbidity; autism spectrum disorder; psychopathology ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTALLY-RETARDED CHILDREN; SCHOOL-AGE-CHILDREN; ASPERGER-SYNDROME; BEHAVIORAL TREATMENT; GENERAL-POPULATION; EATING-DISORDERS; DOWN-SYNDROME; ADI-R; DEPRESSION AB Comorbidity, the co-occurrence of two or more disorders in the same person, has been a topic receiving considerable attention in the child psychopathology literature overall. Despite many publications in the ADHD, depression and other child literatures, autism spectrum disorder has not received such scrutiny. The purpose of this review will be to discuss the available evidence. We address specific variables in diagnosis and classification of comorbid symptoms, and propose potential avenues for research and practice with respect to differential diagnosis. A brief discussion of the implications for treatment is also provided. (c) 2006 Elsevier Ltd. All rights reserved. C1 Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA. RP Matson, JL (reprint author), Louisiana State Univ, Dept Psychol, Baton Rouge, LA 70803 USA. 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Dev. Disabil. PD JUL-SEP PY 2007 VL 28 IS 4 BP 341 EP 352 DI 10.1016/j.ridd.2005.12.004 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 184PY UT WOS:000247655400002 PM 16765022 ER PT J AU Zimbelman, M Paschal, A Hawley, SR Molgaard, CA StRomain, T AF Zimbelman, Merilee Paschal, Angelia Hawley, Suzanne R. Molgaard, Craig A. StRomain, Theresa TI Addressing physical inactivity among developmentally disabled students through visual schedules and social stories SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE developmental disabilities; visual schedules; social stories; physical education ID EXCHANGE COMMUNICATION-SYSTEM; AUTISM; CHILDREN; BEHAVIORS; DISABILITIES; SKILLS AB Introduction: This project tested visual schedules and social stories in a physical education setting in order to increase the physical activity of developmentally disabled students. Method: This cohort study design involved 17 physical education teachers in a training course with an initial survey and 7-month post-survey. The initial survey assessed participant experience with developmentally disabled students, visual schedules and social stories. The post-survey assessed usage of, effectiveness of, and satisfaction with visual schedules and social stories in a physical education setting. Results: On the initial survey, 100% of the participants reported that they work with developmentally disabled students and 24% reported little to no training in working with this population. On the post-survey, 75% of the participants reported using visual schedules in their teaching and 64% found them to be "effective" or "very effective". Six percent used social stories in their teaching, reporting them as 100%, "very effective". Conclusion: There is an indication that visual schedules and social stories are effective learning tools in the physical education setting, increasing opportunities for developmentally disabled students to be physically active. However, additional resources and training are needed in order for physical education teachers to implement these tools widely in their classes. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ Kansas, Sch Med, Dept Prevent Med & Publ Hlth, Wichita, KS 67214 USA. RP Hawley, SR (reprint author), Univ Kansas, Sch Med, Dept Prevent Med & Publ Hlth, 1010 N Kansas, Wichita, KS 67214 USA. EM shawley@kumc.edu CR Agosta E, 2004, INTERV SCH CLIN, V39, P276, DOI 10.1177/10534512040390050401 Barry L. 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Dev. Disabil. PD JUL-SEP PY 2007 VL 28 IS 4 BP 386 EP 396 DI 10.1016/j.ridd.2006.03.004 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 184PY UT WOS:000247655400005 PM 16765023 ER PT J AU Balconi, M Carrera, A AF Balconi, Michela Carrera, Alba TI Emotional representation in facial expression and script - A comparison between normal and autistic children SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE facial expressions; autism; emotion; script ID KNOWLEDGE AB The paper explored conceptual and lexical skills with regard to emotional correlates of facial stimuli and scripts. In two different experimental phases normal and autistic children observed six facial expressions of emotions (happiness, anger, fear, sadness, surprise, and disgust) and six emotional scripts (contextualized facial expressions). In the second place, the effect of emotional domain (different emotions) in decoding was explored. A semantic grid was applied to conversational line, including two levels of data: the lexical adequacy index (correct decoding of emotion) and the emotional vocabulary (such as the causal representation and the hedonic valence of the stimulus). Log-linear analysis showed different representations across the subjects, as a function of emotion, task and pathology. Specifically, childrens' lexical competence was well developed for some emotions (such as happiness, anger, and fear), and as a function of type of task, that is script was better represented than face. Between the main linguistic indexes, causal relation was a prototypical index for emotional conceptualization. Finally, pathology affected children's performance, with an increased "facilitation effect" for autistic children in the script condition. (c) 2006 Elsevier Ltd. All rights reserved. C1 Catholic Univ Milan, Dept Psychol, Lab Cognit Psychol, I-20123 Milan, Italy. RP Balconi, M (reprint author), Catholic Univ Milan, Dept Psychol, Lab Cognit Psychol, Largo Gemelli 1, I-20123 Milan, Italy. 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H., 1994, NATURE EMOTION FUNDA, P59 Gepner B, 1996, CHILD NEUROPSYCHOL, V2, P123, DOI 10.1080/09297049608401357 Hillier A, 2002, AUTISM, V6, P299, DOI 10.1177/1362361302006003007 Kanner L, 1943, NERV CHILD, V2, P217 Lazarus R. S., 1999, HDB COGNITION EMOTIO, P3 ROJAHN J, 1995, RES DEV DISABIL, V16, P393, DOI 10.1016/0891-4222(95)00019-J Russel J. A., 1986, MEASURING EMOTIONS I, V2, P203 Russell JA, 2002, INT J BEHAV DEV, V26, P97, DOI 10.1080/01650250042000582 Want SC, 2001, CHILD DEV, V72, P431, DOI 10.1111/1467-8624.00288 Widen SC, 2004, COGNITIVE DEV, V19, P111, DOI 10.1016/j.cogdev.2003.11.004 Widen SC, 2003, DEV PSYCHOL, V39, P114, DOI 10.1037//0012-1649.39.1.114 NR 27 TC 26 Z9 26 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD JUL-SEP PY 2007 VL 28 IS 4 BP 409 EP 422 DI 10.1016/j.ridd.2006.05.001 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 184PY UT WOS:000247655400007 PM 16828256 ER PT J AU Chung, KM Reavis, S Mosconi, M Drewry, J Matthews, T Tasse, MJ AF Chung, Kyong-Mee Reavis, Shaye Mosconi, Matt Drewry, Josiah Matthews, Todd Tasse, Marc J. TI Peer-mediated social skills training program for young children with high-functioning autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE social skills training; high-functioning autism; video feedback; peer-mediated; social communication ID INTERVENTIONS; INITIATIONS AB One of the most prevailing characteristics of children with autism is their deficit in social communication skills. The purpose of this study was to evaluate the effectiveness of a peer-mediated social skills training (SST) program combined with video feedback, positive reinforcement and token system in increasing social communication skills in young children with high-functioning autism. Four boys with high-functioning autism, ages 6-7 years, participated in the study. The social skills training, lasting 12 weeks, targeted six communication skills, selected after parent interviews and behavioral observation during a pre-training assessment period. One SST session was conducted each week, each session lasted 90 min and had six structured activities. The training effectiveness was evaluated through direct observation of a structured interaction period, using an observational coding system. Improvement was observed in three out of four children, although individual differences among children were seen for changes in two global scales as well as subscales. These results suggest that the social skills training was effective in improving social communication skills for some children with high-functioning autism. Clinical and research implications and future directions for social skills training as well as this study's limitations are discussed. (c) 2006 Elsevier Ltd. All rights reserved. C1 Yonsei Univ, Coll Arts & Sci, Dept Psychol, Seoul 120749, South Korea. Univ N Carolina, Dept Psychol, Chapel Hill, NC USA. Univ N Carolina, Ctr Dev & Learning, Chapel Hill, NC USA. RP Chung, KM (reprint author), Yonsei Univ, Coll Arts & Sci, Dept Psychol, 134 Shinchon Dong, Seoul 120749, South Korea. 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TI Using the Natural Language Paradigm (NLP) to increase vocalizations of older adults with cognitive impairments SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE Natural Language Paradigm; cognitive impairment; language; older adults ID CHILDREN; INTERVENTION; DEMENTIA; AUTISM; SPEECH AB The Natural Language Paradigm (NLP) has proven effective in increasing spontaneous verbalizations for children with autism. This study investigated the use of NLP with older adults with cognitive impairments served at a leisure-based adult day program for seniors. Three individuals with limited spontaneous use of functional language participated in a multiple baseline design across participants. Data were collected on appropriate and inappropriate vocalizations with appropriate vocalizations coded as prompted or unprompted during baseline and treatment sessions. All participants experienced increases in appropriate speech during NLP with variable response patterns. Additionally, the two participants with substantial inappropriate vocalizations showed decreases in inappropriate speech. Implications for intervention in day programs are discussed. (c) 2006 Elsevier Ltd. All rights reserved. C1 Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. RP LeBlanc, LA (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. 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Osborne, Susan TI An evolution of virtual reality training designs for children with autism and fetal alcohol spectrum disorders SO TOPICS IN LANGUAGE DISORDERS LA English DT Article ID PREVENTION; INJURIES; EXPOSURE; SAFETY; CARE; VR AB This article describes an evolution of training programs to use first-person interaction in virtual reality (VR) situations to teach safety skills to children with autism spectrum disorder (ASD) and fetal alcohol spectrum disorder (FASD). Multiple VR programs for children aged 2 to 9 were built and tested between 1992 and 2007. Based on these results, a learning design evolved that uses practice in virtual space with guidance and correction by an animated character, strategic limitations on allowed actions to force correct patterning, and customization of worlds and responses to simplify user controls. This article describes program evolution by comparing design details and results as variations in behavioral responses between disorders, differences in skill set complexity between different safety skills being taught, and improved technology required changes in the virtual training methodology. A series of research projects are summarized in which the VR programs proved effective for teaching children with ASD and FASD new skills in the virtual space and, where measured, most children generalized the actions to the real world. C1 Do2Learn, Raleigh, NC 27607 USA. N Carolina State Univ, Dept Comp Sci, Raleigh, NC USA. N Carolina State Univ, Dept Educ, Raleigh, NC USA. Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA USA. RP Strickland, DC (reprint author), Do2Learn, 3204 Churchill Rd, Raleigh, NC 27607 USA. 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Lang. Disord. PD JUL-SEP PY 2007 VL 27 IS 3 BP 226 EP 241 PG 16 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 204LE UT WOS:000249044500004 ER PT J AU Self, T Scudder, RR Weheba, G Crumrine, D AF Self, Trisha Scudder, Rosalind R. Weheba, Gamal Crumrine, Daiquirie TI A virtual approach to teaching safety skills to children with autism spectrum disorder SO TOPICS IN LANGUAGE DISORDERS LA English DT Article AB Recent advancements in the development of hardware/software configurations for delivering virtual reality (VR) environments to individuals with disabilities have included approaches for children with autism spectrum disorder (ASD). This article describes a study comparing benefits of using VR to benefits of an integrated/visual treatment model when teaching safety skills to children with ASD in a public school setting. Participants were 8 children diagnosed with ASD who were randomly assigned to receive either VR or an integrated/visual treatment model to learn fire and tornado safety skills. Both groups improved in their learning and transfer of safety skills. The VR group, however, learned these skills in considerably less time. Implications and suggestions for the use of VR in educational settings are presented. C1 Wichita State Univ, Dept Commun Sci & Disorders, Wichita, KS 67260 USA. Wichita State Univ, Dept Ind & Mfg Engn, Wichita, KS 67260 USA. Wichita State Univ, Wichita Publ Sch, Wichita, KS 67260 USA. RP Self, T (reprint author), Wichita State Univ, Dept Commun Sci & Disorders, 1845 Fairmount, Wichita, KS 67260 USA. 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A., 2006, AUTISM SPECTRUM DISO SELF T, 2003, AM SPEECH LANG HEAR SELF T, 2005, AM SPEECH LANG HEAR Strickland D, 1996, J AUTISM DEV DISORD, V26, P651, DOI 10.1007/BF02172354 STRICKLAND DC, 2007, TOP LANG DISORD, V27, P222 WATSON L. R., 1989, TEACHING SPONTANEOUS NR 24 TC 16 Z9 16 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0271-8294 J9 TOP LANG DISORD JI Top. Lang. Disord. PD JUL-SEP PY 2007 VL 27 IS 3 BP 242 EP 253 PG 12 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 204LE UT WOS:000249044500005 ER PT J AU Rutherford, MD Clements, KA Sekuler, AB AF Rutherford, M. D. Clements, Kathleen A. Sekuler, Allison B. TI Differences in discrimination of eye and mouth displacement in autism spectrum disorders SO VISION RESEARCH LA English DT Article DE face perception; autism; feature displacement ID PERVASIVE DEVELOPMENTAL DISORDERS; UPSIDE-DOWN FACES; FACIAL EXPRESSIONS; CHILDREN; RECOGNITION; INDIVIDUALS; INVERSION; PERCEPTION; FIXATION; DEFICITS AB Individuals with Autism Spectrum Disorders (ASD) have been found to have impairments in some face recognition tasks [e.g., Boucher, J., & Lewis, V. (1992). Unfamiliar face recognition in relatively able autistic children. Journal of Child Psychology and Psychiatry, 33, 843-859.], and it has been suggested that this impairment occurs because these individuals do not spontaneously attend to the eyes [e.g., Pelphrey, K. A., Sasson, N. J., Reznick, J. S., Paul, G., Goldman, B. D., & Piven, J. (2002). Visual scanning of faces in autism. Journal of Autism and Developmental Disorders, 32, 249-261.], or attend selectively to the mouth [e.g., Langdell, T. (1978). Recognition of faces-approach to study of autism. Journal of Child Psychology and Psychiatry and Allied Disciplines, 19, 255-268; Joseph, R. M., & Tanaka J. (2003). Holistic and part-based face recognition in children with autism. Journal of Child Psychology and Psychiatry, 44, 529542.]. Here, we test whether the eyes or the mouth are attended to preferentially by 16 males with ASD and 19 matched controls. Participants discriminated small spatial displacements of the eyes and the mouth. If the mouth region were attended to preferentially by individuals with ASD, we would expect ASD observers to be better at detecting subtle changes in mouth than eye displacements, relative to controls. Further, following Barton Barton, J. J. S., Keenan, J. P., & Bass, T. (2001). Discrimination of spatial relations and features in faces: Effects of inversion and viewing duration. British Journal of Psychology, 92, 527-549.], we would expect to see differences in inversion effects as a function of feature manipulation between ASD and control groups. We found that individuals with ASD performed significantly differently than controls for the eye, but not the mouth, trials. However, we found no difference in inversion effects between the two groups of observers. Furthermore, we found evidence of distinct subclasses of individuals with ASD: those who performed normally, and those who were impaired. These results suggests that typical individuals are better able to make use of information in the eyes than some individuals with ASD, but that there is no clear autism "advantage" in the use of information in the mouth region. (C) 2007 Elsevier Ltd. All rights reserved. C1 McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON L8S 4K1, Canada. RP Rutherford, MD (reprint author), McMaster Univ, Dept Psychol Neurosci & Behav, 1280 Main St W, Hamilton, ON L8S 4K1, Canada. 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PD JUL PY 2007 VL 47 IS 15 BP 2099 EP 2110 DI 10.1016/j.visres.2007.01.029 PG 12 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA 190RW UT WOS:000248077700012 PM 17559905 ER PT J AU Im, SH Park, ES Kim, DY Song, DH Lee, JD AF Im, Sang-Hee Park, Eun Sook Kim, Deog Young Song, Dong Ho Lee, Jong Doo TI The neuroradiological findings of children with developmental language disorder SO YONSEI MEDICAL JOURNAL LA English DT Article DE developmental language disorder; attention-deficit hyperactivity disorder; positron emission tomography; statistical parametric mapping ID CEREBRAL PERFUSION ABNORMALITIES; POSITRON EMISSION TOMOGRAPHY; BRAIN MATURATION; LEFT-HEMISPHERE; IMPAIRMENT; SPECT; PREVALENCE; DYSLEXIA; AUTISM; DELAY AB Purpose: To investigate the general characteristics of glucose metabolism distribution and the functional deficit in the brain of children with developmental language delay (DLD), we compared functional neuroradiological studies such as positron emission tomography (PET) of a patient group of DLD children and a control group of attention-deficit hyperactivity disorder (ADHD) children. Patients and Methods: Seventeen DLD children and 10 ADHD children under 10 years of age were recruited and divided into separate groups consisting of children less than 5 years of age or between 5 and 10 years of age. The PET findings of 4 DLD children and 6 control children whose ages ranged from 5 to 10 years were compared by Statistical Parametric Mapping (SPM) analysis. Results: All of the DLD children revealed grossly normal findings in brain MRIs, however, 87.5% of them showed grossly abnormal findings in their PET studies. Abnormal findings were most frequent in the thalamus. The patient group showed significantly decreased glucose metabolism in both frontal, temporal and right parietal areas (p < 0.005) and significantly increased metabolism in both occipital areas (p < 0.05) as compared to the control group. Conclusion: This study reveals that DLD children may show abnormal findings on functional neuroradiological studies, even though structural neuroradiological studies such as a brain MRI do not show any abnormal findings. Frequent abnormal findings on functional neuroradiological studies of DLD children, especially in the subcortical area, suggests that further research with quantitative assessments of functional neuroradiological studies recruiting more DLD children and age-matched normal controls could be helpful for understanding the pathophysiology of DLD and other disorders confined to the developmental disorder spectrum. C1 Yonsei Univ, Coll Med, Res Inst Rehabil Med, Dept Rehabil Med, Seoul, South Korea. Yonsei Univ, Coll Med, Dept Psychiat, Seoul, South Korea. Yonsei Univ, Coll Med, Dept Diagnost Radiol, Div Nucl Med, Seoul, South Korea. RP Park, ES (reprint author), Yonsei Univ, Coll Med, Dept Phys Med, 250 Seongsanno, Seoul 120752, South Korea. 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PD JUN 23 PY 2007 VL 194 IS 2609 BP 6 EP 7 DI 10.1016/S0262-4079(07)61544-9 PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 182YB UT WOS:000247538800002 ER PT J AU Chubykin, AA Atasoy, D Etherton, MR Brose, N Kavalali, ET Gibson, JR Sudhof, TC AF Chubykin, Alexander A. Atasoy, Deniz Etherton, Mark R. Brose, Nils Kavalali, Ege T. Gibson, Jay R. Suedhof, Thomas C. TI Activity-dependent validation of excitatory versus inhibitory synapses by neuroligin-1 versus neuroligin-2 SO NEURON LA English DT Article ID NMDA RECEPTOR SUBUNITS; CELL-ADHESION MOLECULE; ALPHA-NEUREXINS; SILENT SYNAPSES; BETA-NEUREXINS; PSD-95; AUTISM; TRANSMISSION; MUTATION; BINDING AB Neuroligins enhance synapse formation in vitro, but surprisingly are not required for the generation of synapses in vivo. We now show that in cultured neurons, neuroligin-1 overexpression increases excitatory, but not inhibitory, synaptic responses, and potentiates synaptic NMDAR/AMPAR ratios. In contrast, neuroligin-2 overexpression increases inhibitory, but not excitatory, synaptic responses. Accordingly, deletion of neuroligin-1 in knockout mice selectively decreases the NMDAR/AMPAR ratio, whereas deletion of neuroligin-2 selectively decreases inhibitory synaptic responses. Strikingly, chronic inhibition of NMDARs or CaM-Kinase 11, which signals downstream of NMDARs, suppresses the synapse-boosting activity of neuroligin-1, whereas chronic inhibition of general synaptic activity suppresses the synapse-boosting activity of neuroligin-2. Taken together, these data indicate that neuroligins do not establish, but specify and validate, synapses via an activity-dependent mechanism, with different neuroligins acting on distinct types of synapses. This hypothesis reconciles the overexpression and knockout phenotypes and suggests that neuroligins contribute to the use-dependent formation of neural circuits. C1 Univ Texas, SW Med Ctr, Dept Neurosci, Dallas, TX 75390 USA. 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Tannan, V. Cascio, C. J. Baranek, G. T. Whitsel, B. L. TI Vibrotactile adaptation fails to enhance spatial localization in adults with autism SO BRAIN RESEARCH LA English DT Article DE somatosensory; autism; spatial localization; vibrotactile; adaptation; tactile ID HUMAN HAIRY SKIN; SOMATOSENSORY CORTEX; DISCRIMINATION; STIMULATION; SENSITIVITY; PERCEPTION; FREQUENCY; AMPLITUDE; PARIETAL; CHILDREN AB A recent study [Tannan, V., Tommerdahl, M., Whitsel, B.L., 2006. Vibrotactile adaptation enhances spatial localization. Brain Res. 1102(1), 109-116 (Aug 2)] showed that pre-exposure of a skin region to a 5 s 25 Hz flutter stimulus ("adaptation") results in an approximately 2-fold improvement in the ability of neurologically healthy human adults to localize mechanical stimulation delivered to the same skin region that received the adapting stimulation. Tannan et al. [Tannan, V., Tommerdahl, M., Whitsel, B.L., 2006. Vibrotactile adaptation enhances spatial localization. Brain Res. 1102(1), 109-116 (Aug 2)] proposed that tactile spatial discriminative performance is improved following adaptation because adaptation is accompanied by an increase in the spatial contrast in the response of contralateral primary somatosensory cortex (SI) to mechanical skin stimulation-an effect identified in previous imaging studies of Sl cortex in anesthetized non-human primates [e.g., Simons, S.B., Tannan, V., Chiu, J., Favorov, O.V., Whitsel, B.L., Tommerdahl, M, 2005. Amplitude -dependency of response of Sl cortex to flutter stimulation. BMC Neurosci. 6(1), 43 Gun 21); Tommerdahl, M., Favorov, O.V., Whitsel, B.L., 2002. optical imaging of intrinsic signals in somatosensory cortex. Behav. Brain Res. 135, 83-91; Whitsel, B.L., Favorov, O.V., Tommerdahl, M., Diamond, M., Juliano, S., Kelly, D., 1989. Dynamic processes govern the somatosensory cortical response to natural stimulation. In: Lund, J.S., (Ed.), Sensory Processing in the Mammalian Brain. Oxford Univ. Press, New York, 79-107]. In the experiments described in this report, a paradigm identical to that employed previously by Tarman et al. [Tannan, V., Tommerdahl, M., Whitsel, B.L., 2006. Vibrotactile adaptation enhances spatial localization. Brain Res. 1102(1), 109-116 (Aug 2)] was used to study adults with autism. The results demonstrate that although cutaneous localization performance of adults with autism is significantly better than the performance of control subjects when the period of adapting stimulation is short (i.e., 0.5 s), tactile spatial discriminative capacity remained unaltered in the same subjects when the duration of adapting stimulation was increased (to 5 s). Both the failure of prior history of tactile stimulation to alter tactile spatial localization in adults with autism, and the better- than-normal tactile localization performance of adults with autism when the period of adaptation is short are concluded to be attributable to the deficient cerebral cortical GABAergic inhibitory neurotransmission characteristic of this disorder. (C) 2007 Elsevier B.V. All rights reserved. C1 Univ N Carolina, Dept Biomed Engn, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Allied Hlth Sci, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Cellular & Mol Physiol, Chapel Hill, NC 27599 USA. Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. RP Tommerdahl, M (reprint author), Univ N Carolina, Dept Biomed Engn, Chapel Hill, NC 27599 USA. 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The condition that defines BIC is the detection of an intelligence quotient between 71 and 84. Unlike MR, patients with BIC have received little attention in medical journals and hence the cognitive characteristics of this group are still poorly defined. Aims. The purpose of this study was to assess the different neurodevelopmental disorders associated with BIC. Patients and methods. A group of 87 patients who had been diagnosed with BIC were selected, together with a control group. The clinical diagnoses were analysed and the results of the CBCL/6-18 survey from the two groups were compared. Results. The group of patients was found to have a high prevalence of neurocognitive disorders, such as attention deficit hyperactivity disorder (ADHD), learning difficulties and pervasive developmental disorders. The most frequent medical diagnosis was the effects of alcohol on the foetus. 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The aims of the Study were to descride their systemic and functional defects, especially autism spectrum disorders, and to search for possible etiologic risk factors, Available medical records were studied and the mothers answered a questionnaire on history of prenatal events. A clinical examination evaluating systemic findings, vision, hearing, speech, oral and swallowing function, and neuropsychiatric function, especially autism, was made. Eighteen patients, (11 males, 7 females) aged 8 months to 17 years with OAV were studied. Most frequent systemic malformations included, ear ahnormalities (100%), ocular malformations (72%), vertebral deformities (67%), cerebral anomalies (50%), and congenital heart defects (33%). Functional defects consisted of hearing impairment (83%), visual impairment (28%), both visual and hearing impairment (28%), difficulties in feeding/eating (50%), speech (53%), mental retardation (39%), and severe autistic symptoms (11%). Three children were born following assisted fertilization (two intracytoplasmatic sperm injection, one in vitro fertilization), two mothers reported early bleedings, and six (33%) mothers had smoked during pregnancy. (c) 2007 Wiley-Liss, Inc. C1 Univ Gothenburg, Dept Ophthalmol, Sahlgrenska Acad, Gothenburg, Sweden. Univ Illinois, Eye & Ear Infirm, Dept Ophthalmol & Visual Sci, Chicago, IL 60612 USA. Univ Gothenburg, Dept Odontol, Mun H Ctr, Sahlgrenska Acad, Gothenburg, Sweden. Skaraborg Hosp, Dept Pediat, Skovde, Sweden. Univ Gothenburg, Dept Pediat, Sahlgrenska Acad, Gothenburg, Sweden. Univ Gothenburg, Dept Pediat, Sahlgrenska Acad, Gothenburg, Sweden. Univ Gothenburg, Sahlgrenska Acad, Dept Otorhinolaryngol Head & Neck Surg, Gothenburg, Sweden. RP Stromland, K (reprint author), Univ Gothenburg, Dept Ophthalmol, Dept Pediat Ophthalmol, Queen Silvia Childrens Hosp,Sahlgrenska Acad, S-41685 Gothenburg, Sweden. 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We investigated event-related potentials response to visual elements that either formed perceptually coherent illusory contour or were arranged in a noncoherent way. The results showed that in healthy boys the illusory contour as compared with control stimulus elicited enhanced negativity of NI peak (C effect), which has been previously found in adults. Autistic boys demonstrated the reliable inverted illusory contour effect, that is, more positive NI amplitude to illusory contour. We hypothesized that boys with autism were sensitive to difference between illusory contour and control figures basing on collinearity processing mechanisms implemented in neural circuitry of primary visual cortex. C1 [Stroganova, Tatiana A.; Prokofyev, Andrey O.] Moscow Univ Psychol & Educ, Fac Clin & Abnormal Psychol, Moscow 103051, Russia. [Stroganova, Tatiana A.; Posikera, Irina N.] Russian Acad Educ, Inst Psychol, Moscow, Russia. 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In this study, the MECP2 gene was scanned in a Portuguese autistic population, hypothesizing that the phenotypic spectrum of mutations extends beyond the traditional diagnosis of RTT and X-linked mental retardation, leading to a nonlethal phenotype in male autistic patients. The coding region, exon-intron boundaries, and the whole 3'UTR were scanned in 172 patients and 143 controls, by Detection of Virtually All Mutations-SSCP (DOVAM-S). Exon 1 was sequenced in 103 patients. We report 15 novel variants, not found in controls: one missense, two intronic, and 12 in the 3'UTR (seven in conserved nucleotides). The novel missense change, c.617G > C (p.G206A), was present in one autistic male with severe mental retardation and absence of language, and segregates in his maternal family. This change is located in a highly conserved residue within a region involved in an alternative transcriptional repression pathway, and likely alters the secondary structure of the MeCP2 protein. It is therefore plausible that it leads to a functional modification of MeCP2. MECP2 mRNA levels measured in four patients with 3'UTR conserved changes were below the control range, suggesting an alteration in the stability of the transcripts. Our results suggest that MECP2 can play a role in autism etiology, although very rarely, supporting the notion that MECP2 mutations underlie several neurodevelopmental disorders. (c) 2007 Wiley-Liss, Inc. C1 Inst Nacl Saude Dr Ricardo Jorge, P-1649016 Lisbon, Portugal. Inst Gulbenkian Ciencias, Oeiras, Portugal. Hosp Pediat Coimbra, Coimbra, Portugal. City Hope Natl Med Ctr, Dept Mol Genet, Duarte, CA 91010 USA. Beckman Res Inst, Duarte, CA USA. Direccao Reg Educ Regiao Ctr, Coimbra, Portugal. Hosp Divino Espirito Santo, Unidade Genet & Patol Mol, Azores, Portugal. Hosp Sto Antonio, Oporto, Portugal. Univ Minho, ICVS, Escola Ciencias Saude, Braga, Portugal. Univ Porto, ICBAS, P-4100 Oporto, Portugal. RP Vicente, AM (reprint author), Inst Nacl Saude Dr Ricardo Jorge, Av Padre Cruz, P-1649016 Lisbon, Portugal. 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Hollander, Eric Leboyer, Marion Gillberg, Christopher Verloes, Alain Betancur, Catalina TI Mutation screening of the PTEN gene in patients with autism spectrum disorders and macrocephaly SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE Cowden syndrome; Bannayan-Riley-Ruvalcaba syndrome; polydactyly; sequence analysis; multiplex ligation-dependent probe; amplification ID RILEY-RUVALCABA-SYNDROME; TUMOR-SUPPRESSOR PTEN; COWDEN-SYNDROME; DIAGNOSTIC INTERVIEW; HEAD CIRCUMFERENCE; MENTAL-RETARDATION; CELL-MIGRATION; C2 DOMAIN; KINASE; FEATURES AB Mutations in the PTEN gene are associated with a broad spectrum of disorders, including Cowden syndrome (CS), Bannayan-Riley-Ruvaleaba syndrome, Proteus syndrome, and Lhermitte-Duclos disease. In addition, PTEN mutations have been described in a few patients with autism spectrum disorders (ASDs) and macrocephaly. In this study, we screened the PTEN gene for mutations and deletions in 88 patients with ASDs and macrocephaly (defined as >= 2 SD above the mean). Mutation analysis was performed by direct sequencing of all exons and flanking regions, as well as the promoter region. Dosage analysis of PTEN was carried out using multiplex ligation-dependent probe amplification (MLPA). No partial or whole gene deletions were observed. We identified a de novo missense mutation (D326N) in a highly conserved amino acid in a 5-year-old boy with autism, mental retardation, language delay, extreme macrocephaly (+ 9.6 SD) and polydactyly of both feet. Polydactyly has previously been described in two patients with Lhermitte-Duclos disease and CS and is thus likely to be a rare sign of PTEN mutations. Our findings suggest that PTEN mutations are a relatively infrequent cause of ASDs with macrocephaly. Screening of PTEN mutations is warranted in patients with autism and pronounced macrocephaly, even in the absence of other features of PTEN-related tumor syndromes. (c) 2007 Wiley-Liss, Inc. C1 Fac Med, INSERM U513, F-94010 Creteil, France. Mt Sinai Sch Med, Lab Mol Neuropsychiat, New York, NY USA. Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY USA. Hop Robert Debre, APHP, Serv Psychopathol Enfant & Adolescent, F-75019 Paris, France. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Hop Henri Mondor, Dept Psychiat, APHP, F-94010 Creteil, France. Hop Albert Chenevier, Creteil, France. St George Hosp, Sch Med, Dept Psychiat, London, England. Hop Robert Debre, APHP, Dept Genet, F-75019 Paris, France. RP Betancur, C (reprint author), Fac Med, INSERM U513, 8 Rue Gen Sarrail, F-94010 Creteil, France. 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NRP2 has been demonstrated to both guide axons and to control neuronal migration in the central nervous system. It has been reported that NRP2 may be required in vivo for sorting migrating cortical and striatal interneurons to their correct destination. We examine the association between the NRP2 gene and autism using a cohort of 169 Chinese Han family trios. Four single nucleotide polymorphisms (SNPs) were genotyped by the polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) analyses. The transmission disequilibrium. tests (TDT) of SNPs and haplotype association were carried out using the TDTPHASE program. We found significant genetic association between autism and two of the SNPs of the NRP2 gene (rs849578: P = 0.017, rs849563: P = 0.027), as well as specific haplotypes, especially those formed by rs849563. Furthermore, haplotypes constructed with all markers showed significant excess transmission in both global and individual haplotype analyses (P=0.004 and 0.017, respectively). The polymorphisms in the NR.P2 gene are associated with autism, implying that the NRP2 gene may render individuals to be predisposed to autism. (c) 2007 Wiley-Liss, Inc. C1 Peking Univ, Inst Mental Hlth, Beijing 100083, Peoples R China. RP Yang, XL (reprint author), Peking Univ, Inst Mental Hlth, 51,Hua Yuan Bei Rd, Beijing 100083, Peoples R China. 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TI A quantitative trait locus analysis of social responsiveness in multiplex autism families (vol 164, pg 656, 2007) SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Correction EM Dhg@ucla.edu CR Duvall JA, 2007, AM J PSYCHIAT, V164, P656, DOI 10.1176/appi.ajp.164.4.656 NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD JUN PY 2007 VL 164 IS 6 BP 980 EP 980 PG 1 WC Psychiatry SC Psychiatry GA 176ZE UT WOS:000247122600037 ER PT J AU Dover, CJ Le Couteur, A AF Dover, Clare J. Le Couteur, Ann TI How to diagnose autism SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; OBSERVATION SCHEDULE; MENTAL-RETARDATION; MEDICAL DISORDERS; CHILDREN; INTERVIEW; PREVALENCE; REGRESSION; MEASLES AB Over the past two decades, there has been an explosion of interest in autism and autism spectrum disorders. Knowledge and awareness of the condition has grown exponentially at all levels among the general public, parents, health professionals, the research community and, more recently, at parliamentary level. Alongside the increased understanding of these complex and disabling conditions is the acknowledgment of a broadening of the diagnostic criteria away from a narrow definition of autism to the autism spectrum with less clear diagnostic boundaries. Growing evidence of the importance of early diagnosis and intervention demands knowledge and skills from all professionals working with young children and in particular those involved in recognising early concerns about a child's development. This article outlines current clinical and research findings in relation to early diagnosis and considers the role of the paediatrician in this process. Reference is also made to the National Autism Plan for Children. C1 Northumberland Tyne & Wear NHS Trust, Fleming Nuffield Unit, Newcastle Upon Tyne NE2 3AE, Tyne & Wear, England. Univ Newcastle Upon Tyne, Sch Clin Med Sci Child & Adolescent Psychiat, Sir James Spence Inst, Royal Victoria Infirm, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. RP Le Couteur, A (reprint author), Northumberland Tyne & Wear NHS Trust, Fleming Nuffield Unit, Burdon Terrace, Newcastle Upon Tyne NE2 3AE, Tyne & Wear, England. 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Dis. Child. PD JUN PY 2007 VL 92 IS 6 BP 540 EP 545 DI 10.1136/adc.2005.086280 PG 6 WC Pediatrics SC Pediatrics GA 170JI UT WOS:000246659100024 PM 17515625 ER PT J AU Wang, AT Lee, SS Sigman, M Dapretto, M AF Wang, A. Ting Lee, Susan S. Sigman, Marian Dapretto, Mirella TI Reading affect in the face and voice - Neural correlates of interpreting communicative intent in children and adolescents with autism spectrum disorders SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article; Proceedings Paper CT 4th International Meeting for Autism Research CY MAY 06-07, 2005 CL Boston, MA ID HIGH-FUNCTIONING AUTISM; CEREBRAL-BLOOD-FLOW; ASPERGER-SYNDROME; INTERMODAL PERCEPTION; DIAGNOSTIC INTERVIEW; CROSSMODAL BINDING; NORMAL ADULTS; MIND; INDIVIDUALS; RECOGNITION AB Context: Understanding a speaker's communicative intent in everyday interactions is likely to draw on cues such as facial expression and tone of voice. Prior research has shown that individuals with autism spectrum disorders (ASD) show reduced activity in brain regions that respond selectively to the face and voice. However, there is also evidence that activity in key regions can be increased if task demands allow for explicit processing of emotion. Objectives: To examine the neural circuitry underlying impairments in interpreting communicative intentions in ASD using irony comprehension as a test case, and to determine whether explicit instructions to attend to facial expression and tone of voice will elicit more normative patterns of brain activity. Design, Setting, and Participants: Eighteen boys with ASD (aged 7-17 years, full-scale IQ > 70) and 18 typically developing (TD) boys underwent functional magnetic resonance imaging at the Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles. Main Outcome Measures: Blood oxygenation level-dependent brain activity during the presentation of short scenarios involving irony. Behavioral performance (accuracy and response time) was also recorded. Results: Reduced activity in the medial prefrontal cortex and right superior temporal gyrus was observed in children with ASD relative to TD children during the perception of potentially ironic vs control scenarios. Importantly, a significant group X condition interaction in the medial prefrontal cortex showed that activity was modulated by explicit instructions to attend to facial expression and tone of voice only in the ASD group. Finally, medial prefrontal cortex activity was inversely related to symptom severity in children with ASD such that children with greater social impairment showed less activity in this region. Conclusions: Explicit instructions to attend to facial expression and tone of voice can elicit increased activity in the medial prefrontal cortex, part of a network important for understanding the intentions of others, in children with ASD. These findings suggest a strategy for future intervention research. C1 Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Ahmanson Lovelace Brain Mapping Ctr, Los Angeles, CA 90024 USA. RP Wang, AT (reprint author), Mt Sinai Sch Med, Seaver & New York Autism Ctr Excellence, Dept Psychiat, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA. 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Gen. Psychiatry PD JUN PY 2007 VL 64 IS 6 BP 698 EP 708 DI 10.1001/archpsyc.64.6.698 PG 11 WC Psychiatry SC Psychiatry GA 175HQ UT WOS:000247005100008 PM 17548751 ER PT J AU Wassink, TH Hazlett, HC Epping, EA Arndt, S Dager, SR Schellenberg, GD Dawson, G Piven, J AF Wassink, Thomas H. Hazlett, Heather C. Epping, Eric A. Arndt, Stephan Dager, Stephen R. Schellenberg, Gerard D. Dawson, Geraldine Piven, Joseph TI Cerebral cortical gray matter overgrowth and functional variation of the serotonin transporter gene in autism SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID RIGID-COMPULSIVE BEHAVIORS; BRAIN-DEVELOPMENT; MESSENGER-RNA; HIPPOCAMPAL VOLUMES; HUMAN AMYGDALA; MR-IMAGES; POLYMORPHISM; DISORDER; PROMOTER; SLC6A4 AB Context: Autism is a heritable neurodevelopmental disorder characterized biologically by enlargement of the head and brain and abnormalities of serotonin neurotransmission. Objective: To evaluate whether 5-HTTLPR, a functional promoter polymorphism of the serotonin transporter gene SLC6A4, influences cerebral cortical structure volumes in young male children with autism. Design: Association study of a genetic variant with quan titative traits. Setting: Autism research centers at the University of North Carolina (UNC), Chapel Hill, and the University of Washington (UW), Seattle. Participants: Forty-four male children, 2 to 4 years old, with autism participating in longitudinal brain magnetic resonance imaging studies. Main Outcome Measures: Cerebral cortical and cerebellar gray and white matter volumes. Results: We found that 5-HTTLPR genotype influenced gray matter volumes of the cerebral cortex (F-2,F-23=7.29, P=.004) and of 3 lobe-based subregions in the UNC sample of 29 children (frontal lobe gray matter: F-2,(23)=6.36, P=.01). The 5-HTTLPR short allele appeared to be additively associated with increasing gray matter volumes, an observation affirmed by tests of linear genotype effects (cortical gray matter: F-1,(24)= 14. 11, P=.001; frontal lobe gray matter: F-1,F-24= 13.20, P=.001). Genotype did not influence cerebellar volumes. Confirmation was pursued by means of the UW sample of 15 children. While effects were not significant in the UW sample alone, the patterns of adjusted means resembled those found in the UNC sample. Positive Cochran-Mantel-Haenszel test results supported the concordance of relationships across the 2 sites, and analyses of covariance of the combined sample that included a site covariate showed significant linear genotype effects on structure volumes (cortical gray matter: F-1,(38)=5.73, P=.02; frontal lobe gray matter: F1,(38)= 11.73, P=.002). Effect sizes of 5-HTTLPR genotype on total cortical and frontal lobe gray matter volumes were 10% and 16%, respectively. Conclusion: The SLC6A4 promoter polyinorphism 5-HTTLPR influences cerebral cortical gray, matter volumes in young male children with autism. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Dept Psychiat, Chapel Hill, NC 27599 USA. Univ Iowa, Coll Publ Hlth, Dept Biostat, Iowa City, IA USA. Univ Iowa, Dept Psychiat, Roy J & Lucille A Carver Coll Med, Iowa City, IA USA. Univ Washington, Autism Ctr, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. Univ Washington, Dept Radiol, Seattle, WA 98195 USA. Univ Washington, Dept Bioengn, Seattle, WA 98195 USA. Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. Univ Washington, Dept Gerontol & Geriatr Med, Seattle, WA 98195 USA. Univ Washington, Dept Neurol, Seattle, WA 98195 USA. Univ Washington, Dept Pharmacol, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Puget Sound Vet Affairs Med Ctr, Geriatr Res Educ & Clin Ctr, Seattle, WA USA. RP Piven, J (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, Neurosci Hosp 7011, Campus Box 3366, Chapel Hill, NC 27599 USA. 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Psychiatry PD JUN PY 2007 VL 64 IS 6 BP 709 EP 717 DI 10.1001/archpsyc.64.6.709 PG 9 WC Psychiatry SC Psychiatry GA 175HQ UT WOS:000247005100009 PM 17548752 ER PT J AU Steiner, CE Acosta, AX Guerreiro, MM Marques-De-Faria, AP AF Steiner, Carlos Eduardo Acosta, Angelina Xavier Guerreiro, Marilisa Mantovani Marques-de-Faria, Antonia Paula TI Genotype and natural history in unrelated individuals with phenylketonuria and autistic behavior SO ARQUIVOS DE NEURO-PSIQUIATRIA LA English DT Article DE autism; natural history; pervasive developmental disorders; phenylalanine hydroxilase; phenylketonuria ID PHENYLALANINE-HYDROXYLASE DEFICIENCY; INFANTILE-AUTISM; DISORDERS; MUTATIONS; SPECTRUM; PAH AB We describe three unrelated individuals, two males (ages 35 and 9) and a female (age 8) presenting with late diagnosed phenylketonuria (PKU) and autistic behavior, all showing poor adhesion to the dietary treatment resulting in high plasmatic phenylalanine levels, particularly in the oldest subject. Clinical findings included hair hypopigmentation, microcephaly, severe mental retardation with absent development of verbal language and autistic symptoms in all three patients, whereas variable neurological signs such as seizures, spasticity, ataxia, aggressivity, and hyperactivity were individually found. Homozygosity for the IVS10nt11g/a (IVS10nt546) was found in all. This is the first report of molecular findings in subjects with PKU also presenting with autistic features. The authors discuss if this mutation is particularly involved in the association of autistic symptoms in untreated PKU individuals. C1 Univ Estadual Campinas, Fac Ciencias Med, Dept Med Genet, BR-13081970 Campinas, SP, Brazil. Univ Fed Bahia, Fac Med Bahia, Dept Pediat, Salvador, BA, Brazil. Univ Estadual Campinas, Fac Ciencias Med, Dept Neurol, Campinas, SP, Brazil. RP Steiner, CE (reprint author), Univ Estadual Campinas, Fac Ciencias Med, Dept Med Genet, Rua Tessalia Vieira de Camargo 126, BR-13081970 Campinas, SP, Brazil. 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Neuro-Psiquiatr. PD JUN PY 2007 VL 65 IS 2A BP 202 EP 205 DI 10.1590/S0004-282X2007000200003 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 177FA UT WOS:000247137800003 PM 17607414 ER PT J AU Abel, CG Stein, G Galarregui, M Garretto, N Mangone, C Genovese, O Allegri, RF Sica, REP AF Abel, Carlos G. Stein, Gustavo Galarregui, Marina Garretto, Nelida Mangone, Carlos Genovese, Osvaldo Allegri, Ricardo F. Sica, Roberto E. P. TI Social cognition and theory of mind assessment in non-demented patients with isolated cerebellar degeneration SO ARQUIVOS DE NEURO-PSIQUIATRIA LA English DT Article DE cerebellum; degenerative cerebellar disease; executive cognition; cognition; social cognition; theory of mind ID ASPERGER-SYNDROME; SCHIZOPHRENIA; INDIVIDUALS; INVOLVEMENT; ACTIVATION; INVENTORY; AUTISM AB Aim: To investigate whether the cerebellum could participate in social cognition (SC). Method: General neuropsychological tests, executive tests (EF), social cognition tests, which assess the ability to infer other peoples' mental states, and the Beck Depression Inventory were given to 10 non-demented patients with isolated cerebellar degenerative disease, and to 10 healthy controls matched for sex, age, and years of education. ANOVA and correlation coefficients were employed for the statistical analysis. Results: Patients within the cerebellar group were significantly impaired (p <= 0.05) in EF test [Wisconsin Card Sorting Test (WSCT)] and belief questions (BQ) from Theory of Mind (ToM) tests. Performance in control questions (CQ) from ToM tests was similar for both groups. Lower scores in BQ correlated with a lower conceptual ability, the severity of apathy (NPI) and static ataxia. CQ correlated with measures of attention and free recall. 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The present article explores the notion that the understanding of social competitive emotions is particularly impaired in patients with ventromedial (VM) prefrontal lesions. By manipulating a simple Theory of Mind (ToM) task, we tested the ability of patients with localized lesions to understand 'fortune of others' emotions: envy and gloating (schadenfreude). Patients were also assessed for their ability to recognize control physical and identification conditions. While envy is an example of a negative experience in the face of another's fortunes, gloat is thought to be a positive experience in the face of another's misfortune. Whereas in schadenfreude and envy the emotion of the self and the protagonist may be opposite, identification involves matching between the protagonist's and the observer's emotions. Patients with VM (N = 10) lesions (particularly in the right hemisphere), although showing intact performance on a basic first order ToM condition, and relatively preserved understanding of identification, did not recognize envy (F[6,76] = 3.491, P = 0.004) and gloating (F[6,76] = 3.738, P = 0.003). Impaired recognition of gloating involved additionally lesions in the inferior parietal lobule (P = 0.001). Furthermore, while patients with lesions in the left hemisphere were more impaired in recognizing gloating (a positive emotion), right hemisphere patients were more impaired in recognizing envy (a negative emotion), suggesting that the valence of these emotions may also be affected by the asymmetry of the lesion (F[6,68] = 2.002, P = 0.011). In addition, the ability to identify these emotions was related to perspective-taking abilities and ToM. 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PD JUN PY 2007 VL 29 IS 5 BP 257 EP 272 DI 10.1016/j.braindev.2006.09.003 PG 16 WC Clinical Neurology SC Neurosciences & Neurology GA 164TL UT WOS:000246257200001 PM 17084999 ER PT J AU van Vliet, J Oates, NA Whitelaw, E AF van Vliet, J. Oates, N. A. Whitelaw, E. TI Epigenetic mechanisms in the context of complex diseases SO CELLULAR AND MOLECULAR LIFE SCIENCES LA English DT Review DE epigenetics; DNA methylation; histone modifications; complex diseases; cancer; schizophrenia; autism; systemic lupus erythematosus ID ASSISTED REPRODUCTIVE TECHNOLOGIES; BECKWITH-WIEDEMANN-SYNDROME; GENOMIC DNA METHYLATION; CPG-ISLAND METHYLATION; IN-VITRO FERTILIZATION; BIPOLAR DISORDER; HUMAN CANCER; PROMOTER HYPERMETHYLATION; GERMLINE EPIMUTATION; SPECTRUM DISORDERS AB Complex diseases arise from a combination of heritable and environmental factors. The contribution made by environmental factors may be mediated through epigenetics. Epigenetics is the study of changes in gene expression that occur without a change in DNA sequence and are meiotically or mitotically heritable. Such changes in gene expression are achieved through the methylation of DNA, the post-translational modifications of histone proteins, and RNA-based silencing. Epigenetics has been implicated in complex diseases such as cancer, schizophrenia, bipolar disorder, autism and systemic lupus erythematosus. The prevalence and severity of these diseases may be influenced by factors that affect the epigenotype, such as ageing, folate status, in vitro fertilization and our ancestors' lifestyles. Although our understanding of the role played by epigenetics in complex diseases remains in its infancy, it has already led to the development of novel diagnostic methods and treatments, which augurs well for its future health benefits. C1 Queensland Inst Med Res, Div Populat Studies & Human Genet, Herston, Qld 4006, Australia. RP Whitelaw, E (reprint author), Queensland Inst Med Res, Div Populat Studies & Human Genet, 300 Herston Rd, Herston, Qld 4006, Australia. 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TI Altered neocortical cell density and layer thickness in serotonin transporter knockout mice: A quantitation study SO CEREBRAL CORTEX LA English DT Article DE apoptosis; cerebral cortex; optical fractionator proliferation; stereology ID PERVASIVE DEVELOPMENTAL DISORDERS; NEURONS IN-VITRO; THALAMIC NEURONS; PLATELET SEROTONIN; MONOAMINE-OXIDASE; BRAIN-SEROTONIN; CORTICAL DEVELOPMENT; HEAD CIRCUMFERENCE; NEURITE OUTGROWTH; INFANTILE-AUTISM AB The neurotransmitter serotonin (5-HT) plays morphogenetic roles during development, and their alteration could contribute to autism pathogenesis in humans. To further characterize 5-HT's contributions to neocortical development, we assessed the thickness and neuronal cell density of various cerebral cortical areas in serotonin transporter (5-HTT) knockout (ko) mice, characterized by elevated extracellular 5-HT levels. The thickness of layer IV is decreased in 5-HTT ko mice compared with wild-type (wt) mice. The overall effect on cortical thickness, however, depends on the genetic background of the mice. Overall cortical thickness is decreased in many cortical areas of 5-HTT ko mice with a mixed c129-CD1-C57BL/6J background. Instead, 5-HTT ka mice backcrossed into the C57BL/6J background display increases in supragranular and infragranular layers, which compensate entirely for decreased layer IV thickness, resulting in unchanged or even enhanced cortical thickness. Moreover, significant increases in neuronal cell density are found in 5-HTT ko mice with a C57BL/6J background (wt:hz:ko ratio = 1.00:1.04:1.17) but not in the mixed c129-CD1-C57BL/6J 5-HTT ko animals. These results provide evidence of 5-HTT gene effects on neocortical morphology in epistatic interaction with genetic variants at other loci and may model the effect of functional 5-HTT gene variants on neocortical development in autism. C1 Univ Rome, Lab Mol Psychiat & Neurogenet, I-00155 Rome, Italy. 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Cortex PD JUN PY 2007 VL 17 IS 6 BP 1394 EP 1401 DI 10.1093/cercor/bhl051 PG 8 WC Neurosciences SC Neurosciences & Neurology GA 169VO UT WOS:000246620400015 PM 16905592 ER PT J AU Nopoulos, P Richman, L Andreasen, NC Murray, JC Schutte, B AF Nopoulos, P. Richman, L. Andreasen, N. C. Murray, J. C. Schutte, B. TI Abnormal brain structure in adults with Van der Woude syndrome SO CLINICAL GENETICS LA English DT Article DE brain; cleft lip/palate; magnetic resonance imaging; Van der Woude syndrome ID PRENATAL CRANIOFACIAL DEVELOPMENT; ISOLATED CLEFT-LIP; AND/OR PALATE; CHILDREN; MORPHOLOGY; MALES; DYSFUNCTION; AUTISM; VOLUME; MRI AB Van der Woude syndrome (VWS) is an autosomal dominant disorder manifested in cleft lip and/or palate and lip pits. Isolated clefts of the lip and/or palate (ICLP) have both genotype and phenotype overlap with VWS. Subjects with ICLP have abnormalities in brain structure and function. Given the similarities between VWS and ICLP, the current study was designed to evaluate the pattern of brain structure of adults with VWS. Fourteen adults with VWS were compared to age- and gender-matched healthy controls. Brain structure was evaluated using magnetic resonance imaging. All subjects with VWS had enlarged volumes of the anterior regions of the cerebrum. Men with VWS had reduced volumes of the posterior cerebrum. Anterior cerebrum volume was negatively correlated with intelligent quotient in the subjects with VWS indicating that the enlargement of this brain region was 'pathologic.' The pattern of brain structure in VWS is nearly identical to those seen in ICLP. In addition, men are affected more severely. Pathologic enlargement of the tissue and a gender effect with men affected more severely are common features of neurodevelopmental disorders supporting the notion that the brain structure of VWS and ICLP may be because of abnormal brain development. C1 Univ Iowa, Coll Med, Iowa Neuroimaging Ctr, Dept Psychiat, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Iowa Neuroimaging Ctr, Dept Pediat, Iowa City, IA 52242 USA. RP Nopoulos, P (reprint author), Univ Iowa, Coll Med, Iowa Neuroimaging Ctr, Dept Psychiat, 200 Hawkins Dr,W278 GH, Iowa City, IA 52242 USA. 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Genet. PD JUN PY 2007 VL 71 IS 6 BP 511 EP 517 DI 10.1111/j.1399-0004.2007.00799 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 174CE UT WOS:000246918000004 PM 17539900 ER PT J AU Soden, SE Lowry, JA Garrison, CB Wasserman, GS AF Soden, Sarah E. Lowry, Jennifer A. Garrison, Carol B. Wasserman, Gary S. TI 24-Hour provoked urine excretion test for heavy metals in children with autism and typically developing controls, a pilot study SO CLINICAL TOXICOLOGY LA English DT Article DE autism; chelation; heavy metal; mercury; provoked excretion ID MESO-2,3-DIMERCAPTOSUCCINIC ACID; MERCURY EXPOSURE; DMSA; CHELATION AB Introduction. The complementary and alternative medicine practice of prescribing chelators to children with autism is based on the premise that the chronic symptoms of autism can be ameliorated by reducing heavy metal body burden. However, there has not been definitive evidence, published to date, to support the assertion that children with autism are at increased risk of an excess chelatable body burden of heavy metals. The oral chelator meso-2,3-dimercaptosuccinic acid (DMSA) can be used diagnostically to mobilize heavy metals from extravascular pools, enhancing the identification of individuals who have a chelatable body burden. Methods. Seventeen children with autism and five typically developing children were enrolled in a pilot study to test for chelatable body burden of Arsenic (As), Cadmium (Cd), Lead (Pb), and Mercury (Hg). Evaluation included a questionnaire regarding potential exposure to heavy metals, diet restrictions, a baseline 24-hour urine collection, and a DMSA-provoked urine collection. Urine collections were sent for As, Cd, Ph, and Hg quantification by Inductively Coupled Plasma-Mass Spectrometry. Unprovoked reference ranges were used in the interpretation of all collections. Results. Fifteen autistic children and four typically developing children completed the study. Three autistic subjects excreted one metal in greater quantity during the provoked excretion than baseline. Two of these were very close to the limit of detection. In the third case, the provoked excretion of mercury was between the upper limit of normal and lower limit of the potentially toxic reference range. Fish was removed from this child's diet for greater than one month, and the provoked excretion test repeated. The repeat excretion of mercury was within the normal range. Conclusion. In the absence a proven novel mode of heavy metal toxicity, the proportion of autistic participants in this study whose DMSA provoked excretion results demonstrate an excess chelatable body burden of As, Cd, Pb, or Hg is zero. The confidence interval for this proportion is 0-22%. C1 Childrens Mercy Hosp, Sect Behav & Dev Sci, Kansas City, MO 64106 USA. Univ Missouri, Kansas City Sch Med, Kansas City, MO USA. Univ Kansas, Ctr Med, Dept Pediat, Kansas City, KS USA. Childrens Mercy Hosp, Div Clin Pharmacol & Med Toxicol, Kansas City, MO 64106 USA. RP Soden, SE (reprint author), Childrens Mercy Hosp, Sect Behav & Dev Sci, 2401 Gilham Rd, Kansas City, MO 64106 USA. 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Toxicol. PD JUN-AUG PY 2007 VL 45 IS 5 BP 476 EP 481 DI 10.1080/15563650701338195 PG 6 WC Toxicology SC Toxicology GA 185SV UT WOS:000247731600011 PM 17503250 ER PT J AU Mouridsen, SE Rich, B Isager, T Nedergaard, NJ AF Mouridsen, Svend Erik Rich, Bente Isager, Torben Nedergaard, Niels Jorgen TI Autoimmune diseases in parents of children with infantile autism: a case-control study SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID SPECTRUM DISORDERS; REGISTER; AGE AB This register study compared the rates and types of autoimmune disease in the parents of 111 patients (82 males, 29 females; mean age at diagnosis 5y 5mo [SD 2y 6mo]) with infantile autism (IA) with a matched control group of parents of 330 children from the general population. All parents were screened through the nationwide Danish National Hospital Register. We inquired about 35 autoimnune diseases during an observation period of 27 years. At follow-up the case and control mothers were identical in age (65Y 7mo [SDs 9Y 7mo and 9y respectively]). For case and control fathers the figures were 70 years 2 months (SD 10y 2mo) and 69 years 1 month (SD 10Y 1mo) respectively. A similar proportion of case and control mothers had a diagnosis of any autoimmune disease: 10.8% versus 9.1%. For case fathers the proportion was 8.6% versus 4.6%. Two autoimmune conditions were associated with IA: ulcerative colitis in mothers (p=0.05) and type 1 diabetes in fathers (p=0.02). Additional studies are required to determine whether there is a true association between a parental history of autoimmune disease and pervasive developmental disorder in their offspring. C1 Bispebjerg Hosp, Dept Child & Adolescent Psychiat, Copenhagen, Denmark. Glostrup Univ Hosp, Ctr Child & Adolescent Psychiat, Glostrup, Denmark. Aarhus Univ Hosp, Psychiat Hosp Children & Adolescents, DK-8000 Aarhus, Denmark. 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Med. Child Neurol. PD JUN PY 2007 VL 49 IS 6 BP 429 EP 432 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 180EY UT WOS:000247346300009 PM 17518928 ER PT J AU Rajendran, G Mitchell, P AF Rajendran, Gnanathusharan Mitchell, Peter TI Cognitive theories of autism SO DEVELOPMENTAL REVIEW LA English DT Review DE autism; Asperger syndrome; autistic spectrum disorders; cognitive theories ID HIGH-FUNCTIONING AUTISM; WEAK CENTRAL COHERENCE; FRONTAL-LOBE DAMAGE; THEORY-OF-MIND; ASPERGER-SYNDROME; EXECUTIVE FUNCTION; SPECTRUM DISORDER; DEVELOPMENTAL PSYCHOPATHOLOGY; CHILDS THEORY; NEUROPSYCHOLOGICAL EVIDENCE AB This article considers three theories of autism: The Theory of Mind Deficit, Executive Dysfunction and the Weak Central Coherence accounts. It outlines each along with studies relevant to their emergence, their expansion, their limitations and their possible integration. 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While there has been some attention given to the issue of identity and disability, there has been little attention paid to the process of identity construction for individuals with autism, in large part because of the assumption that social worlds hold little importance. This ethnographic study, which focuses on the process of identity construction for one young man with autism, was conducted over nine months using participant observation and interviews to construct an in-depth narrative. Using the works of anthropologists and the literary scholar Bahktin as an interpretive framework, this article illustrates that constructing identities requires creativity and ingenuity. It is hard work, in many ways a struggle to orchestrate conflicting discourses in an attempt to author oneself and construct multiple identities. C1 Univ So Calif, Dept Occupat Sci & Therapy, Los Angeles, CA 90089 USA. 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PD JUN PY 2007 VL 22 IS 4 BP 413 EP 426 DI 10.1080/09687590701337967 PG 14 WC Rehabilitation; Social Sciences, Interdisciplinary SC Rehabilitation; Social Sciences - Other Topics GA 185RL UT WOS:000247728000006 ER PT J AU Nelson, C McDonnell, AP Johnston, SS Crompton, A Nelson, AR AF Nelson, Catherine McDonnell, Andrea P. Johnston, Susan S. Crompton, Angie Nelson, Andrew R. TI Keys to play: a strategy to increase the social interactions of young children with autism and their typically developing peers SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID EARLY INTERVENTION; INITIATIONS; PRESCHOOLERS; DISABILITIES; INSTRUCTION; SETTINGS; BEHAVIOR AB Crucial to the successful inclusion of young children with disabilities is the premise that benefit occurs when children socialize with peers and are actively involved in preschool activities including play. Playgroups are often primary to learning in typical preschool classrooms since it is within playgroups that preschool-age children learn both preacademic and social skills. However, this critical avenue of learning is often closed to young children with autism who may have difficulty initiating play interactions with other children. This study examined the effects of a visual intervention strategy on the play initiations of four young children with autism in inclusive preschool classes. The strategy was successful in increasing the play initiations of the participating young children with autism. At the same time, the children's engagement time within playgroups concomitantly increased, as did the sophistication level of their play. C1 Univ Utah, Dept Special Educ, Salt Lake City, UT 84112 USA. Westminster Coll, Fulton, MO USA. RP Nelson, C (reprint author), Univ Utah, Dept Special Educ, 1705 E Campus Ctr Dr,Rm 221, Salt Lake City, UT 84112 USA. EM Cathy.Nelson@ed.utah.edu CR Achenbach T., 1991, CHILD BEHAV CHECKLIS American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bondy A. S., 1994, FOCUS AUTISTIC BEHAV, V9, P1, DOI DOI 10.1177/108835769400900301 Bricker D., 1998, ACTIVITY BASED APPRO Bruner J, 1986, ACTUAL MINDS POSSIBL Carpenter M., 2000, AUTISM SPECTRUM DISO, P31 COSARO WA, 1979, LANG SOC, V8, P315 COSARO WA, 1995, DEV CHILDRENS FRIEND, P207 CRAIG HK, 1993, J SPEECH HEAR RES, V36, P322 Daugherty S, 2001, TOP EARLY CHILD SPEC, V21, P213, DOI 10.1177/027112140102100402 DODGE KA, 1983, MERRILL PALMER QUART, V29, P309 Gilliam J. E., 1995, GILLIAM AUTISM RATIN GOLDSTEIN H, 1992, J APPL BEHAV ANAL, V25, P289, DOI 10.1901/jaba.1992.25-289 Harris S. L., 1997, HDB AUTISM PERVASIVE, P665 Hemmeter ML, 2000, TOP EARLY CHILD SPEC, V20, P56, DOI 10.1177/027112140002000110 HODGDON LA, 2000, VISUAL STRATEGIES IM Horn E, 2000, TOP EARLY CHILD SPEC, V20, P208, DOI 10.1177/027112140002000402 Johnston S., 2003, AUGMENTATIVE ALTERNA, V19, P86, DOI 10.1080/0743461031000112016 JOLLY AC, 1993, J ASSOC PERS SEVERE, V18, P46 Kazdin A. E., 1982, SINGLE CASE RES DESI KELLEGREW DH, 1995, TEACHING CHILDREN AU, P127 Koegel LK, 1999, J ASSOC PERS SEVERE, V24, P174, DOI 10.2511/rpsd.24.3.174 Kohler F. W., 1997, FOCUS AUTISM OTHER D, V12, P196 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 LAYTON T., 1995, TEACHING CHILDREN AU, P73 Lord C., 2000, AUTISM DIAGNOSTIC OB MACE F, 1993, COMMUNICATIVE APPROA MCGEE GG, 2001, PRESCHOOL ED PROGRAM, V2, P157 McGee GG, 1999, J ASSOC PERS SEVERE, V24, P133, DOI 10.2511/rpsd.24.3.133 MCWILLIAM RA, 1985, ANAL INTERVENTION DE, V5, P33 MIRENDA P, 2000, AUTISM SPECTRUM DISO, P333 Mullen E, 1995, MULLEN SCALES EARLY ODOM SL, 1984, AM J ORTHOPSYCHIAT, V54, P544 Parten MB, 1932, J ABNORM SOC PSYCH, V27, P243, DOI 10.1037/h0074524 PRIOR MR, 1976, J AUTISM CHILD SCHIZ, V6, P121, DOI 10.1007/BF01538055 Prizant B., 2000, AUTISM SPECTRUM DISO, P193 QUILL K, 1995, TEACHING CHILDREN AU, P163 Quill Kathleen A., 1998, Seminars in Speech and Language, V19, P407, DOI 10.1055/s-2008-1064057 Quill K. A., 2000, DO WATCH LISTEN SAY Quill K. A., 1995, FOCUS AUTISTIC BEHAV, V10, P10, DOI DOI 10.1177/108835769501000302 Quill KA, 1997, J AUTISM DEV DISORD, V27, P697, DOI 10.1023/A:1025806900162 ROGERS SJ, 2001, PRESCHOOL ED PROGRAM, P95 Sandall S. R., 2002, BUILDING BLOCKS TEAC Sandall S. R., 2000, DEC RECOMMENDED PRAC Schopler E., 1988, CHILDHOOD AUTISM RAT SCHULER A, 1995, TEACHING CHILDREN AU SCHULER AL, 2000, AUTISM SPECTRUM DISO, P251 Schwartz IS, 1998, TOP EARLY CHILD SPEC, V18, P144 Shabani DB, 2002, J APPL BEHAV ANAL, V35, P79, DOI 10.1901/jaba.2002.35-79 SIGMAN M, 1997, HDB AUTISM PERVASIVE, P248 Simpson RL, 1999, J ASSOC PERS SEVERE, V24, P218, DOI 10.2511/rpsd.24.3.218 STRAIN PS, 1983, ANAL INTERVEN DEVEL, V3, P23, DOI 10.1016/0270-4684(83)90024-1 Tawney J. W., 1984, SINGLE SUBJECT RES S Wetherby Amy M., 2000, AUTISM SPECTRUM DISO, P109 WOLFBERG PJ, 1995, TEACHING CHILDREN AU, P193 WOLFBERG PJ, 1993, J AUTISM DEV DISORD, V23, P467, DOI 10.1007/BF01046051 Zanolli K, 1996, J AUTISM DEV DISORD, V26, P407, DOI 10.1007/BF02172826 ZIMMERMAN I, 1991, PRESCHOOL LANGUAGE S, V3 NR 58 TC 11 Z9 12 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 1547-0350 J9 EDUC TRAIN DEV DISAB JI Educ. Train. Dev. Disabil. PD JUN PY 2007 VL 42 IS 2 BP 165 EP 181 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 171EH UT WOS:000246717200005 ER PT J AU Spriggs, AD Gast, DL Ayres, KM AF Spriggs, Amy D. Gast, David L. Ayres, Kevin M. TI Using picture activity schedule books to increase on-schedule and on-task behaviors SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID PHOTOGRAPHIC ACTIVITY SCHEDULES; INTELLECTUAL DISABILITIES; AUTISM; CHILDREN; ACQUISITION; ENGAGEMENT; STUDENTS AB The purpose of this study was to evaluate the effectiveness of using picture activity schedule books to increase on-schedule and on-task behaviors of children with moderate intellectual disabilities. Four students enrolled in a self-contained classroom participated in the study. Graduated guidance, system of least prompts, and verbal prompting were used to teach students how to use the picture schedules. Percentage of on-schedule steps completed and Percentage of intervals on-task were evaluated within the context of an A-BC-B-A-B withdrawal design. Stimulus generalization was assessed with novel activities in a different location and at different times during the academic day. Results showed increases in on-schedule and on-task behavior only when using the picture activity schedules. Students' on-schedule and on-task behavior generalized to novel activities, settings, and times when using the picture activity schedule books. C1 Univ Georgia, Dept Commun Sci & Special Educ, Chicago, IL 60602 USA. RP Spriggs, AD (reprint author), Univ Georgia, Dept Commun Sci & Special Educ, 537 Aderhold Hall, Chicago, IL 60602 USA. CR Bevill AR, 2001, J EARLY INTERVENTION, V24, P129 BILLINGSLEY F, 1980, BEHAV ASSESS, V2, P229 Bryan LC, 2000, J AUTISM DEV DISORD, V30, P553, DOI 10.1023/A:1005687310346 Copeland SR, 2000, EDUC TRAIN MENT RET, V35, P294 HALL LJ, 1995, EDUC TRAIN MENT RET, V30, P208 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P137, DOI 10.1901/jaba.1993.26-137 Lancioni GE, 2000, BEHAV MODIF, V24, P700, DOI 10.1177/0145445500245005 MACDUFF GS, 1993, J APPL BEHAV ANAL, V26, P89, DOI 10.1901/jaba.1993.26-89 Massey NG, 2000, EDUC TRAIN MENT RET, V35, P326 Mechling LC, 1997, EDUC TRAIN MENT RET, V32, P138 Morse TW, 2000, EXCEPT CHILDREN, V66, P273 Rivera MA, 2000, INT J HYDROGEN ENERG, V25, P197, DOI 10.1016/S0360-3199(99)00045-2 Spohn J. R., 1999, EDUC TREAT CHILD, V22, P1 Tawney J. W., 1984, SINGLE SUBJECT RES S Wolery M., 1992, TEACHING STUDENTS MO NR 15 TC 12 Z9 12 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 1547-0350 J9 EDUC TRAIN DEV DISAB JI Educ. Train. Dev. Disabil. PD JUN PY 2007 VL 42 IS 2 BP 209 EP 223 PG 15 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 171EH UT WOS:000246717200008 ER PT J AU Osaka, H Ogiwara, I Mazaki, E Okamura, N Yamashita, S Iia, M Yamada, M Kurosawa, K Iwamoto, H Yasui-Furukori, N Kaneko, S Fujiwara, T Inoue, Y Yamakawa, K AF Osaka, Hitoshi Ogiwara, Ikuo Mazaki, Emi Okamura, Nami Yamashita, Sumimasa Iia, Mizue Yamada, Michiko Kurosawa, Kenji Iwamoto, Hiroko Yasui-Furukori, Norio Kaneko, Sunao Fujiwara, Tateki Inoue, Yushi Yamakawa, Kazuhiro TI Patients with a sodium channel alpha 1 gene mutation show wide phenotypic variation SO EPILEPSY RESEARCH LA English DT Article DE SCN1A; epilepsy; sodium channel ID FEBRILE SEIZURES PLUS; SEVERE MYOCLONIC EPILEPSY; GENERALIZED EPILEPSY; SCN1A MUTATION; MISSENSE MUTATIONS; AUTISM; DISORDERS; FAMILIES; GEFS(+); INFANCY AB We investigated the roles of mutations in voltage-gated sodium channel alpha 1 subunit gene (SCN1A) in epilepsies and psychiatric disorders. The SCN1A gene was screened for mutations in three unrelated Japanese families with generalized epilepsy with febrile seizure plus (GEFS+), febrile seizure with myoclonic seizures, or intractable childhood epilepsy with generalized tonic-clonic seizures (ICEGTC). In the family with GEFS+, one individual was affected with panic disorder and seizures, and another individual was diagnosed with Asperger syndrome and seizures. The novel mutation V13661 was found in all probands and patients with psychiatric disorders of the three families. These results suggest that SCN1A mutations may confer susceptibility to psychiatric disorders in addition to variable epileptic seizures. Unidentified modifiers may play critical roles in determining the ultimate phenotype of patients with sodium channel mutations. (c) 2007 Elsevier B.V. All rights reserved. C1 Kanagawa Childrens Med Ctr, Div Neurol, Yokohama, Kanagawa 2328555, Japan. Kanagawa Canc Ctr, Res Inst, Mol Pathol & Genet Div, Yokohama, Kanagawa 2410815, Japan. RIKEN, Brain Sci Inst, Neurogenet Lab, Wako, Saitama 3510198, Japan. Kanagawa Childrens Med Ctr, Div Genet, Yokohama, Kanagawa 2328555, Japan. Yokohama Ryoiku Iryou Ctr, Div Pediat Neurol, Yokohama, Kanagawa 2410014, Japan. Hirosaki Univ, Sch Med, Dept Neuropsychiat, Hirosaki, Aomori 0368562, Japan. Shizuoka Inst Epilepsy & Neurol Disorders, Natl Epilepsy Ctr, Shizuoka 4208688, Japan. RP Osaka, H (reprint author), Kanagawa Childrens Med Ctr, Div Neurol, Yokohama, Kanagawa 2328555, Japan. EM kcmc_ho@cameo.plala.or.jp; yamakawa@brain.riken.jp CR Abou-Khalil B, 2001, NEUROLOGY, V57, P2265 Annesi G, 2003, EPILEPSIA, V44, P1257, DOI 10.1046/j.1528-1157.2003.22503.x Bonanni P, 2004, EPILEPSIA, V45, P149, DOI 10.1111/j.0013-9580.2004.04303.x Ceulemans BPGM, 2004, PEDIATR NEUROL, V30, P236, DOI 10.1016/j.pediatrneurol.2003.10.012 Commission on Classification and Terminology of the International League Against Epilepsy, 1989, EPILEPSIA, V30, P389 Escayg A, 2001, AM J HUM GENET, V68, P866, DOI 10.1086/319524 Fujiwara T, 2003, BRAIN, V126, P531, DOI 10.1093/brain/awg053 Gerard F, 2002, EPILEPSIA, V43, P581, DOI 10.1046/j.1528-1157.2002.43001.x Goldin AL, 2001, ANNU REV PHYSIOL, V63, P871, DOI 10.1146/annurev.physiol.63.1.871 Ito M, 2002, EPILEPSY RES, V48, P15, DOI 10.1016/S0920-1211(01)00313-8 Kolevzon A, 2006, J CLIN PSYCHIAT, V67, P407 Lerche H, 2001, NEUROLOGY, V57, P1191 Meisler MH, 2005, J CLIN INVEST, V115, P2010, DOI 10.1172/JCI25466 Meisler MH, 2002, NOVART FDN SYMP, V241, P72 Morimoto M, 2006, EPILEPSIA, V47, P1732, DOI 10.1111/j.1528-1167.2006.00645.x Piven J, 1999, AM J PSYCHIAT, V156, P557 Scheffer IE, 1997, BRAIN, V120, P479, DOI 10.1093/brain/120.3.479 Singh R, 1999, ANN NEUROL, V45, P75, DOI 10.1002/1531-8249(199901)45:1<75::AID-ART13>3.0.CO;2-W Spampanato J, 2003, NEUROSCIENCE, V116, P37, DOI 10.1016/S0306-4522(02)00698-X Sugawara T, 2001, NEUROLOGY, V57, P703 Wallace RH, 2001, AM J HUM GENET, V68, P859, DOI 10.1086/319516 Wallace RH, 2002, NEUROLOGY, V58, P1426 Weiss LA, 2003, MOL PSYCHIATR, V8, P186, DOI 10.1038/sj.mp.4001241 Yamakawa K, 2005, NEUROREPORT, V16, P1, DOI 10.1097/00001756-200501190-00001 NR 24 TC 21 Z9 23 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-1211 J9 EPILEPSY RES JI Epilepsy Res. PD JUN PY 2007 VL 75 IS 1 BP 46 EP 51 DI 10.1016/j.eplepsyres.2007.03.018 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 186CP UT WOS:000247757000006 PM 17507202 ER PT J AU Reed, P Osborne, LA Corness, M AF Reed, Phil Osborne, Lisa A. Corness, Mark TI The real-world effectiveness of early teaching interventions for children with autism spectrum disorder SO EXCEPTIONAL CHILDREN LA English DT Article; Proceedings Paper CT Conference of the Behavioural-Association-of-Ireland CY 2004 CL Galway, IRELAND SP Behav Assoc Ireland ID PERVASIVE DEVELOPMENTAL DISORDER; INTENSIVE BEHAVIORAL TREATMENT; YOUNG-CHILDREN; PRESCHOOL-CHILDREN; SCHOOL; PROGRAMS; PROGRESS AB The effectiveness of 3 early teaching interventions (applied behavior analysis [ABA], special nursery placement, and portage) for children with autism spectrum disorder was studied in a community-based sample over 10 months. Measures of autism severity as well as intellectual, educational and adaptive behavioral function were administered. In contrast to reports in some previous research (Lovaqs, 1987), there was no evidence of recovery from autism. Children in the ABA condition made greater intellectual and educational gains than children in the portage program. They also made greater educational gains than students in the nursery program. Furthermore, the nursery program produced larger gains than the portage program in adaptive functioning. C1 Univ Swansea, Dept Psychol, Swansea SA2 8PP, W Glam, Wales. Children Young People & Families Directorate, Oxford, England. RP Reed, P (reprint author), Univ Swansea, Dept Psychol, Singleton Pk, Swansea SA2 8PP, W Glam, Wales. EM p.reed@swansea.ac.uk CR Cameron RJ, 1997, CHILD CARE HLTH DEV, V23, P11, DOI 10.1046/j.1365-2214.1997.838838.x Charman T, 2004, AUTISM, V8, P89, DOI 10.1177/1362361304040641 Conners C. 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Child. PD SUM PY 2007 VL 73 IS 4 BP 417 EP 433 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 180CS UT WOS:000247338200004 ER PT J AU Bonnet-Brilhault, F Lemonnier, E Roux, S Barthelemy, C AF Bonnet-Brilhault, F. Lemonnier, E. Roux, S. Barthelemy, C. TI Barin growth in autism: first study of evidence of prenatal overgrowth SO FUNDAMENTAL & CLINICAL PHARMACOLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0767-3981 J9 FUND CLIN PHARMACOL JI Fundam. Clin. Pharmacol. PD JUN PY 2007 VL 21 SU 1 MA 460 BP 93 EP 93 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 150QT UT WOS:000245232000455 ER PT J AU Kalueff, AV Fox, MA Gallagher, PS Murphy, DL AF Kalueff, A. V. Fox, M. A. Gallagher, P. S. Murphy, D. L. TI Hypolocomotion, anxiety and serotonin syndrome-like behavior contribute to the complex phenotype of serotonin transporter knockout mice SO GENES BRAIN AND BEHAVIOR LA English DT Article DE activity; anxiety; behavioral phenotype; knockout mice; serotonin syndrome-like behavior; serotonin transporter ID AUTISM SPECTRUM DISORDERS; 5-HT TRANSPORTER; DEFICIENT MICE; MUTANT MICE; OUT MICE; REUPTAKE TRANSPORTER; SOCIAL-INTERACTION; MONOAMINE-OXIDASE; TEST BATTERIES; ANIMAL-MODEL AB Although mice with a targeted disruption of the serotonin transporter (SERT) have been studied extensively using various tests, their complex behavioral phenotype is not yet fully understood. Here we assess in detail the behavior of adult female SERT wild type (+/+), heterozygous (+/-) and knockout (-/-) mice on an isogenic C57BL/6J background subjected to a battery of behavioral paradigms. Overall, there were no differences in the ability to find food or a novel object, nest-building, self-grooming and its sequencing, and horizontal rod balancing, indicating unimpaired sensory functions, motor co-ordination and behavioral sequencing. In contrast, there were striking reductions in exploration and activity in novelty-based tests (novel object, sticky label and open field tests), accompanied by pronounced thigmotaxis, suggesting that combined hypolocomotion and anxiety (rather than purely anxiety) influence the SERT -/- behavioral phenotype. Social interaction behaviors were also markedly reduced. In addition, SERT -/- mice tended to move close to the ground, frequently displayed spontaneous Straub tail, tics, tremor and backward gait - a phenotype generally consistent with 'serotonin syndrome'-like behavior. In line with replicated evidence of much enhanced serotonin availability in SERT -/- mice, this serotonin syndrome-like state may represent a third factor contributing to their behavioral profile. An understanding of the emerging complexity of SERT -/- mouse behavior is crucial for a detailed dissection of their phenotype and for developing further neurobehavioral models using these mice. C1 NIMH, Clin Sci Lab, Intramural Res Program, Bethesda, MD 20892 USA. RP Kalueff, AV (reprint author), NIMH, Clin Sci Lab, Intramural Res Program, Bldg 10,Room 3D41,10 Ctr Dr MSC 1264, Bethesda, MD 20892 USA. 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Neuroimaging endophenotypes are quantitative indicators of brain structure or function that index genetic liability for an illness. These indices will significantly improve gene discovery and help us to understand the functional consequences of specific genes at the level of systems neuroscience. Here, we review the feasibility of using neuroanatomic and neuropsychological measures as endophenotypes for brain-related disorders. Specifically, we examine specific indices of brain structure or function that are genetically influenced and associated with neurological and psychiatric illness. In addition, we review genetic approaches that capitalize on the use of quantitative traits, including those derived from brain images. C1 Univ Texas, Hlth Sci Ctr, Dept Psychiat, San Antonio, TX 78229 USA. Univ Texas, Hlth Sci Ctr, Res Imaging Ctr, San Antonio, TX 78229 USA. Univ Calif Los Angeles, Dept Neurol, Lab Neuro Imaging, Los Angeles, CA 90024 USA. 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Brain Mapp. PD JUN PY 2007 VL 28 IS 6 BP 488 EP 501 DI 10.1002/hbm.20401 PG 14 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 169YV UT WOS:000246628900005 PM 17440953 ER PT J AU Noriega, G AF Noriega, Gerardo TI Self-organizing maps as a model of brain mechanisms potentially linked to autism SO IEEE TRANSACTIONS ON NEURAL SYSTEMS AND REHABILITATION ENGINEERING LA English DT Article DE autism; self-organizing maps; sensory abnormalities AB The application of artificial neural networks in the study of psychopathological syndromes has great potential. Several computational models of acquired and developmental disorders, including autism, have been proposed recently. In this paper, we use the framework of self-organizing maps to study several aspects of autism, by modeling abnormalities in the learning process in biologically plausible manners. We then interpret the resulting feature maps with reference to autistic characteristics. The effects of manipulating the physical structure and size of self-organizing maps were measured and compared with the general characteristics of neural growth abnormalities in autistic children. We find no effect on stimuli coverage, but a negative impact on map unfolding, dependant on the intensity of the abnormality, but not the time of onset. We analyze sensory issues by introducing the concept of attention functions, used to model hypersensitivities and hyposensitivities. The issue of focus on details rather than the whole is analyzed through a model in which distant neighbors are explicitly rejected; we show the model may lead to improved coverage of finely-shaped areas or isolated stimuli, but poorer map unfolding. Finally, we consider effects of noisy communication channels on the development of maps, and show a strong sensitivity of both coverage and unfolding of maps. C1 RMS Instruments Ltd, Mississauga, ON L4V IL9, Canada. RP Noriega, G (reprint author), RMS Instruments Ltd, Mississauga, ON L4V IL9, Canada. EM g.noriega@ieee.org CR [Anonymous], 2001, ED CHILDREN AUTISM Aylward EH, 2002, NEUROLOGY, V59, P175 BALKENIUS C, 2004, P 4 INT WORKSH EP RO, P27 Bauman M.L., 1996, J NEUROPATHOL EXP NE, V55, P613, DOI 10.1097/00005072-199605000-00048 Bauman ML, 2005, INT J DEV NEUROSCI, V23, P183, DOI 10.1016/j.ijdevneu.2004.09.006 Bogdashina O, 2003, SENSORY PERCEPTUAL I Cohen I., 1998, NEURAL NETWORKS PSYC, P274, DOI DOI 10.1017/CBO9780511547195.012 COHEN IL, 1994, BIOL PSYCHIAT, V36, P5, DOI 10.1016/0006-3223(94)90057-4 Courchesne E, 2001, NEUROLOGY, V57, P245 Courchesne E, 1999, NEUROLOGY, V52, P1057 Dakin S, 2005, NEURON, V48, P497, DOI 10.1016/j.neuron.2005.10.018 de Carvalho L. A. V., 1999, P 4 BRAZ C NEUR NETW, P344 Frith U., 2003, AUTISM EXPLAINING EN Gustafsson L, 1997, BIOL PSYCHIAT, V42, P1138, DOI 10.1016/S0006-3223(97)00141-8 Gustafsson L, 2004, J AUTISM DEV DISORD, V34, P189, DOI 10.1023/B:JADD.0000022609.31371.4d Gustafsson L., 2002, P INT C NEUR INF PRO, P1815 Haykin S., 1999, NEURAL NETWORKS COMP, V2nd Kandel E. R., 2000, PRINCIPLES NEURAL SC Kohonen T, 1997, SELF ORG MAPS McClelland JL, 2000, J AUTISM DEV DISORD, V30, P497, DOI 10.1023/A:1005576229109 Oliver A, 2000, DEVELOPMENTAL SCI, V3, P1, DOI 10.1111/1467-7687.00094 O'Loughlin C, 2000, MIND LANG, V15, P375 PAPLINSKI AP, 2004, P IEEE INT JOINT C N, P34 Reggia J. A., 1996, NEURAL MODELING BRAI Ritter H, 1992, NEURAL COMPUTATION S Sirosh J., 1993, P IEEE INT C NEUR NE, P1360 SPITZER M, 1995, COMPR PSYCHIAT, V36, P83, DOI 10.1016/S0010-440X(95)90103-5 Volkmar F. R., 2005, HDB AUTISM PERVASIVE NR 28 TC 7 Z9 8 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855 USA SN 1534-4320 J9 IEEE T NEUR SYS REH JI IEEE Trans. Neural Syst. Rehabil. Eng. PD JUN PY 2007 VL 15 IS 2 BP 217 EP 226 DI 10.1109/TNSRE.2007.897031 PG 10 WC Engineering, Biomedical; Rehabilitation SC Engineering; Rehabilitation GA 179YW UT WOS:000247327700009 PM 17601191 ER PT J AU Fahmi, R Elbaz, A Hassan, H Farag, AA Casanova, MF AF Fahmi, Rachid Elbaz, Ayman Hassan, Hossam Farag, Aly A. Casanova, Manuel F. TI Structural MRI-based discrimination between autistic and typically developing brain SO INTERNATIONAL JOURNAL OF COMPUTER ASSISTED RADIOLOGY AND SURGERY LA English DT Article DE Autism; Magnetic resonance imaging (MRI); Distance map; Image registration AB Autism is a neurodevelopmental disorder characterized by marked deficits in communication, social interaction, and interests. Various studies of autism have suggested abnormalities in several brain regions, with an increasing agreement on the abnormal anatomy of the white matter (WM) and on deficits in the size of the corpus callosum (CC) and its sub-regions in autism. In this paper, we aim at using these abnormalities in order to devise robust classification methods of autistic vs. typically developing brains by analyzing their respective MRIs. Our analysis is based on shape descriptions and geometric models. We compute the 3D distance map to describe the shape of the WM, and use it as a statistical feature to discriminate between the two groups. We also use our recently proposed non-rigid registration technique to devise another classification approach by statistically analyzing and comparing the deformation fields generated from registering segmented CC's onto each others. The proposed techniques are tested on postmortem and on in-vivo brain MR data. At the 85% confidence level the WM-based classification algorithm correctly classified 14/14 postmortem-autistics and 12/12 in-vivo autistics, a 100% accuracy rate, and 13/15 postmortem controls (86% accuracy rate) and 30/30 in-vivo controls (100% accuracy rate). The technique based on the analysis of the CC was applied only on the in vivo data. At the 85% confidence rate, this technique correctly classified 10/15 autistics, a 0.66 accuracy rate, and 29/30 controls, a 0.96 accuracy rate. These results are very promising and show that, contrary to traditional methods, the proposed techniques are less sensitive to age and volume effects. C1 [Fahmi, Rachid; Hassan, Hossam; Farag, Aly A.] Univ Louisville, CVIP Lab, Louisville, KY 40292 USA. [Elbaz, Ayman] Univ Louisville, Dept Bioengn, Louisville, KY 40292 USA. [Casanova, Manuel F.] Univ Louisville, Dept Psychiat & Behav Sci, Louisville, KY 40292 USA. RP Fahmi, R (reprint author), Univ Louisville, CVIP Lab, Louisville, KY 40292 USA. CR Casanova MF, 2006, ACTA NEUROP IN PRESS Courchesne E, 2001, NEUROLOGY, V57, P245 Courchesne R, 2003, JAMA-J AM MED ASSOC, V290, P337 Fahmi R, 2006, IEEE EMBS 06 NEW YOR, P3041 Farag A, 2004, LECT NOTES COMPUT SC, V3216, P143 Herbert MR, 2004, ANN NEUROL, V55, P530, DOI 10.1002/ana.20032 Mountcastle VB, 2003, CEREB CORTEX, V13, P2, DOI 10.1093/cercor/13.1.2 Schumann CM, 2001, J AUTISM DEV DISORD, V31, P561, DOI 10.1023/A:1013294927413 Vidal CN, 2006, BIOL PSYCHIAT, V60, P218, DOI 10.1016/j.biopsych.2005.11.011 NR 9 TC 0 Z9 0 PU SPRINGER HEIDELBERG PI HEIDELBERG PA TIERGARTENSTRASSE 17, D-69121 HEIDELBERG, GERMANY SN 1861-6410 EI 1861-6429 J9 INT J COMPUT ASS RAD JI Int. J. Comput. Assist. Radiol. Surg. PD JUN PY 2007 VL 2 SU 1 BP S24 EP S26 PG 3 WC Engineering, Biomedical; Radiology, Nuclear Medicine & Medical Imaging; Surgery SC Engineering; Radiology, Nuclear Medicine & Medical Imaging; Surgery GA V32ZD UT WOS:000208988200014 ER PT J AU Dane, S Balci, N AF Dane, Senol Balci, Nese TI Handedness, eyedness and nasal cycle in children with autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE autism; handedness; eyedness; nasal cycle ID INTRAOCULAR-PRESSURE; HAND PREFERENCE; INFANTILE-AUTISM; HEMISPHERE ADVANTAGE; PLANUM TEMPORALE; HEALTHY-SUBJECTS; AIR-FLOW; BRAIN; SCHIZOPHRENIA; PERFORMANCE AB Objective: Autism is referred to as cerebral lateralization abnormality. In this study, the possible relationships among handedness, eyedness and nasal cycle in autism have been investigated. Materials and methods: Thirty-seven children with autism and 20 controls were included in the study. The patient group included 27 boys and 10 girls who ranged in age from 5 to 20 years. For hand preference, hand used to write and throw a ball was accepted as dominant hand. For eye preference or dominance, eye used to look through keyhole of a door was accepted as dominant eye. Nasal dominance was assessed by a method of measuring the nasal airflow. Results: The rates of left-handedness and left-eyedness were higher in children with autism compared to normal populations. A majority of children with autism had left nasal dominance. Conclusion: Autism and early language impairment may be associated with left handedness, eyedness and nasal dominance.(c) 2007 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Ataturk Univ, Fac Med, Dept Physiol, TR-25240 Erzurum, Turkey. Psycho Acad, Psikolojik Danismanlik Refleksoloji Merkezi, Izmir, Turkey. RP Dane, S (reprint author), Ataturk Univ, Fac Med, Dept Physiol, TR-25240 Erzurum, Turkey. 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PD JUN PY 2007 VL 25 IS 4 BP 223 EP 226 DI 10.1016/j.ijdevneu.2007.03.005 PG 4 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 183BY UT WOS:000247548900004 PM 17462849 ER PT J AU Ahearn, WH Clark, KM MacDonald, RPF Chung, BI AF Ahearn, William H. Clark, Kathy M. MacDonald, Rebecca P. F. Chung, Bo In TI Assessing and treating vocal stereotypy in children with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article; Proceedings Paper CT 28th Annual Meeting of the Association-for-Behavior-Analysis CY MAY, 2002 CL TORONTO, CANADA SP Assoc Behav Anal DE vocal stereotypy; automatic reinforcement; response interruption; autism ID SELF-STIMULATORY BEHAVIORS; AUTOMATIC REINFORCEMENT; RESPONSE BLOCKING; DEVELOPMENTAL-DISABILITIES; REPETITIVE BEHAVIOR; FUNCTIONAL-ANALYSIS; SENSORY EXTINCTION; INJURIOUS-BEHAVIOR; DISORDERS AB Previous research implies that stereotypic behavior tends to be maintained by the sensory consequences produced by engaging in the response. Few investigations, however, have focused on vocal stereotypy. The current study examined the noncommunicative vocalizations of 4 children with an autism spectrum disorder. First, functional analyses were conducted in an attempt to identify the function of each child's behavior. For each of the participants, it was found that vocal stereotypy was likely not maintained by the social consequences. Following assessment, response interruption and redirection (RIRD) was implemented in an ABAB design to determine whether vocal stereotypy could be successfully redirected. RIRD involved a teacher issuing a series of vocal demands the child readily complied with during regular academic programming. Vocal demands were presented contingent on the occurrence of vocal stereotypy and were continuously presented until the child complied with three consecutively issued demands without emitting vocal stereotypy. For each child, RIRD produced levels of vocal stereotypy substantially lower than those observed in baseline. For 3 of the children, an increase in appropriate communication was also observed. The children's teachers were trained to implement RIRD. Brief follow-up probes and anecdotal information implied that the treatment had a positive impact in the natural environment. C1 New England Ctr Children, Southborough, MA 01772 USA. Northeastern Univ, Boston, MA 02115 USA. Yonsei Univ, Seoul 120749, South Korea. RP Ahearn, WH (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. EM Bahearn@necc.org CR Ahearn WH, 2005, J APPL BEHAV ANAL, V38, P247, DOI 10.1901/jaba.2005.36-04 Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 DORSEY MF, 1982, J APPL BEHAV ANAL, V15, P217, DOI 10.1901/jaba.1982.15-217 DUNLAP G, 1983, AM J MENT DEF, V88, P194 Falcomata TS, 2004, J APPL BEHAV ANAL, V37, P83, DOI 10.1901/jaba.2004.37-83 FAVELL JE, 1982, ANAL INTERVEN DEVEL, V2, P83, DOI 10.1016/0270-4684(82)90007-6 Fay W. 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Appl. Behav. Anal. PD SUM PY 2007 VL 40 IS 2 BP 263 EP 275 DI 10.1901/jaba.2007.30-06 PG 13 WC Psychology, Clinical SC Psychology GA 176TS UT WOS:000247108400005 PM 17624067 ER PT J AU Dib, N Sturmey, P AF Dib, Nancy Sturmey, Peter TI Reducing student stereotypy by improving teachers' implementation of discrete-trial teaching SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; children; discrete-trial teaching; staff training; teacher training; stereotypy AB Discrete-trial teaching is an instructional method commonly used to teach social and academic skills to children with an autism spectrum disorder. The purpose of the current study was to evaluate the indirect effects of discrete-trial teaching on 3 students' stereotypy. Instructions, feedback, modeling, and rehearsal were used to improve 3 teaching aides' implementation of discrete-trial teaching in a private school for children with autism. Improvements in accurate teaching were accompanied by systematic decreases in students' levels of stereotypy. C1 CUNY, Grad Ctr, New York, NY USA. CUNY Queens Coll, New York, NY USA. RP Dib, N (reprint author), 15 S Hamilton St,Apt 2D, Poughkeepsie, NY 12601 USA. EM DibNancy@aol.com CR KOEGEL RL, 1977, J APPL BEHAV ANAL, V10, P197, DOI 10.1901/jaba.1977.10-197 Sarokoff RA, 2004, J APPL BEHAV ANAL, V37, P535, DOI 10.1901/jaba.2004.37-535 NR 2 TC 30 Z9 30 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2007 VL 40 IS 2 BP 339 EP 343 DI 10.1901/jaba.2007.52-06 PG 5 WC Psychology, Clinical SC Psychology GA 176TS UT WOS:000247108400013 PM 17624075 ER PT J AU Delano, ME AF Delano, Monica E. TI Improving written language performance of adolescents with Asperger syndrome SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE adolescents; autism; academic behavior; video modeling; writing ID SELF; STUDENTS; VIDEO; INSTRUCTION; BEHAVIOR; CHILDREN; AUTISM; DIFFICULTIES; SKILLS AB The effects of a multicomponent intervention involving self-regulated strategy development delivered via video self-modeling on the written language performance of 3 students with Asperger syndrome were examined. During intervention sessions, each student watched a video of himself performing strategies for increasing the number of words written and the number of functional essay elements. He then wrote a persuasive essay. The number of words written and number of functional essay elements included in each essay were measured. Each student demonstrated gains in the number of words written and number of functional essay elements. Maintenance of treatment effects at follow-up varied across targets and participants. Implications for future research are suggested. C1 Florida State Univ, Tallahassee, FL 32306 USA. RP Delano, ME (reprint author), Florida State Univ, 205 Stone Bldg, Tallahassee, FL 32306 USA. 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H., 2005, WRITING BETTER EFFEC Hitchcock CH, 2004, LEARN DISABILITY Q, V27, P89, DOI 10.2307/1593644 Klin A., 2005, HDB AUTISM PERVASIVE, V1, P88 MYLES BS, 2001, ASPERGER SYNDROME DI Myles BS, 2003, EDUC TRAIN MENT RET, V38, P362 SCHUNK DH, 1989, J EDUC PSYCHOL, V81, P155, DOI 10.1037//0022-0663.81.2.155 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 Troia G., 1999, EXCEPT CHILDREN, V65, P235 NR 21 TC 34 Z9 34 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2007 VL 40 IS 2 BP 345 EP 351 DI 10.1901/jaba.2007.50-06 PG 7 WC Psychology, Clinical SC Psychology GA 176TS UT WOS:000247108400014 PM 17624076 ER PT J AU Petursdottir, AL McComas, J McMaster, K Horner, K AF Petursdottir, Anna-Lind McComas, Jennifer McMaster, Kristen Horner, Kathy TI The effects of scripted peer tutoring and programming common stimuli on social interactions of a student with autism spectrum disorder SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; generalization; peer tutoring; programming common stimuli; social interaction ID INTERACTION SKILLS; TEACHING-CHILDREN; FADING PROCEDURE AB This study examined the effects of scripted peer-tutoring reading activities, with and without programmed common play-related stimuli, on social interactions between a kindergartner with autism spectrum disorder and his typically developing peer-tutoring partners during free play. A withdrawal design with multiple baselines across peers showed no effects of peer tutoring on social interactions. A withdrawal design with I peer and continuing baselines across the other 2 peers showed that adding play-related common stimuli to the peer-tutoring activity increased social interactions during free play. C1 Univ Minnesota, Minneapolis, MN 55455 USA. Minneapolis Publ Sch, Minneapolis, MN USA. RP Petursdottir, AL (reprint author), Reykjavik City Dept Educ, Frikirkjuvegi 1, IS-101 Reykjavik, Iceland. EM annalind.petursdottir@reykjavik.is CR Esbenshade P. H., 2001, J POSIT BEHAV INTERV, V3, P199, DOI 10.1177/109830070100300402 Fuchs D., 2001, PEER ASSISTED LEARNI Fuchs D, 2001, J EDUC PSYCHOL, V93, P251, DOI 10.1037//0022-0663.93.2.251 KAMPS DM, 1994, J APPL BEHAV ANAL, V27, P49, DOI 10.1901/jaba.1994.27-49 Krantz PJ, 1998, J APPL BEHAV ANAL, V31, P191, DOI 10.1901/jaba.1998.31-191 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 MCGEE GG, 1992, J APPL BEHAV ANAL, V25, P117, DOI 10.1901/jaba.1992.25-117 Pollard NL, 1998, CHILD FAM BEHAV THER, V20, P1 Sarokoff RA, 2001, J APPL BEHAV ANAL, V34, P81, DOI 10.1901/jaba.2001.34-81 STOKES TF, 1977, J APPL BEHAV ANAL, V10, P349, DOI 10.1901/jaba.1977.10-349 NR 10 TC 12 Z9 12 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD SUM PY 2007 VL 40 IS 2 BP 353 EP 357 DI 10.1901/jaba.2007.160-05 PG 5 WC Psychology, Clinical SC Psychology GA 176TS UT WOS:000247108400015 PM 17624077 ER PT J AU Oswald, DP Sonenklar, NA AF Oswald, Donald P. Sonenklar, Neil A. TI Medication use among children with autism-spectrum disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PSYCHOACTIVE MEDICINES; PATTERNS; PREVALENCE; INDIVIDUALS; SOCIETY AB The study characterizes the use of psychoactive medications among children and youth with autism-spectrum disorders over the course of a calendar year. Eighty-three percent of the sample had at least one drug claim during the year. Prescribed drugs came from 125 different therapeutic classes. The seven most frequently prescribed classes of psychoactive drugs were antidepressants, stimulants, tranquilizers/antipsychotics, anticonvulsants, hypotensive agents, anxiolytic/sedative/hypnotics, and benzodiazepines. The data on other relevant diagnoses indicate that children and youth are frequently treated with medication under an autism-spectrum diagnosis, even though the target symptoms may be commonly associated with other mental disorders. Age data indicate that about 70% of children with autism-spectrum disorders age 8 yr and up receive some form of psychoactive medication in a given year. C1 Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA 23298 USA. RP Oswald, DP (reprint author), Virginia Commonwealth Univ, Dept Psychiat, Box 980489, Richmond, VA 23298 USA. EM doswald@vcw.edu CR Aman MG, 2005, J CHILD ADOL PSYCHOP, V15, P116, DOI 10.1089/cap.2005.15.116 Aman MG, 2003, J AUTISM DEV DISORD, V33, P527, DOI 10.1023/A:1025883612879 AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 American Psychiatric Association, 2000, DIAGN STAT MAN MENT Filipek Pauline A, 2006, NeuroRx, V3, P207, DOI 10.1007/BF03207050 Langworthy-Lam KS, 2002, J CHILD ADOL PSYCHOP, V12, P311, DOI 10.1089/104454602762599853 Martin A, 1999, J AM ACAD CHILD PSY, V38, P923, DOI 10.1097/00004583-199907000-00024 *MULT INF SERV INC, 2003, WEB LEX DAT DRUG PRO NR 8 TC 59 Z9 59 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD JUN PY 2007 VL 17 IS 3 BP 348 EP 355 DI 10.1089/cap.2006.17303 PG 8 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 190CE UT WOS:000248034700012 PM 17630868 ER PT J AU Mraz, KD Green, J Dumont-Mathieu, T Makin, S Fein, D AF Mraz, Krista D. Green, James Dumont-Mathieu, Thyde Makin, Sarah Fein, Deborah TI Correlates of head circumference growth in infants later diagnosed with autism spectrum disorders SO JOURNAL OF CHILD NEUROLOGY LA English DT Article DE autism; head circumference ID PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIORAL TREATMENT; HORMONE RESPONSE; BRAIN OVERGROWTH; CEREBRAL-CORTEX; 1ST YEAR; CHILDREN; LIFE; AGE; ABNORMALITIES AB Previous research has demonstrated that children diagnosed with autism spectrum disorder show an abnormal acceleration of head growth during the first year of life. This study attempts to replicate these findings and to determine whether over-growth is associated with clinical outcome. Measurements of head circumference, body length, and body weight taken during the first 2 years of life were obtained from a sample of 35 children diagnosed with autism spectrum disorder and compared to both national normative data (Centers for Disease Control and Prevention) and a control group of 37 healthy infants. Results demonstrated that compared to national averages, infants who were later diagnosed with autism spectrum disorder had a significantly smaller head circumference at birth to 2 weeks and a significantly larger head circumference by 10 to 14 months. Children with autism spectrum disorder were also significantly longer and heavier beginning at 1 to 2 months. However, when overall length and weight were controlled, head circumference was not bigger in the autistic spectrum disorder group compared to local controls. Correlations between head circumference and clinical outcome were significant for 5 of the 30 clinical variables that were run, suggesting that there appears to be no simple or straightforward relationship between head circumference and clinical outcome. Smaller head circumference at birth to 2 weeks was associated with a greater number of symptoms related to social impairment and a greater total number of autism spectrum disorder symptoms based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria. Larger head circumference at 15 to 25 months was also associated with a greater number of symptoms of social impairment. In addition, greater head circumference change during the first 2 years was associated with poorer performance on the visual reception subtest of the Mullen Scales of Early Learning and a smaller number of stereotyped and repetitive behaviors and interests based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition criteria. These findings support previous findings of accelerated brain growth during the first year of life in autism spectrum disorder and question whether growth factors might contribute to both accelerated brain growth and overall body growth. C1 Univ Connecticut, Dept Psychol, Unit 1020, Storrs, CT 06269 USA. RP Mraz, KD (reprint author), Univ Connecticut, Dept Psychol, Unit 1020, 406 Babbidge Rd, Storrs, CT 06269 USA. 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Child Neurol. PD JUN PY 2007 VL 22 IS 6 BP 700 EP 713 DI 10.1177/0883073807304005 PG 14 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 188BH UT WOS:000247892900004 PM 17641255 ER PT J AU Fanciulli, G Azara, E Wood, TD Delitala, G Marchetti, M AF Fanciulli, Giuseppe Azara, Emanuela Wood, Troy D. Delitala, Giuseppe Marchetti, Mauro TI Liquid chromatography-mass spectrometry assay for quantification of Gluten Exorphin B5 in cerebrospinal fluid SO JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES LA English DT Article DE cerebrospinal fluid; Gluten Exorphin B5; liquid chromatography-mass spectrometry ID OPIOID-PEPTIDES; ENKEPHALIN; PROLACTIN; AUTISM; RATS AB A sensitive, precise and accurate method for the quantification of the alimentary opioid peptide Gluten Exorphin 135 (GE-B5, Tyr-Gly-Gly-TrpLeu) in cerebrospinal fluid (CSF) was developed using liquid chromatography-mass spectrometry (LC-MS). Aliquots (10 mu L) of sheep CSF were injected into a LC-MS instrument equipped with a reversed-phase C12 column at a flow rate of 250 mu L/min. The mobile phase consisted of Eluent A water with 0.01% acetic acid as an ion-pairing reagent, and Eluent B acetonitrile. The LC-MS system was programmed to divert column flow to waste for 3.5 min after injection, after which time flow was directed into the mass spectrometer that operated in positive ion mode. DADLE (Tyr-D-Ala-Gly-Phe-D-Leu) was used as Internal Standard. No significant interfering peaks were detected at the retention times of GE-B5 in CSF blanks. The calibration curves were linear in the range of 0.39-78.00 ng/mL. The lower limit of detection and the lower limit of quantitation values for GE-B5 in CSF were established at 0.30 and 0.78 ng/mL, respectively. The intra-day and inter-day precision values were < 12% relative standard deviation. The intra-day and inter-day accuracy were 99.46-100.86% and 98.95-100.02%, respectively. Recovery of GE-135 in CSF samples was greater than 80%. Stability studies indicate that GE-B5 in CSF undergoes significant degradation (> 55% after 600 min), which is reduced by the addition of protease inhibitors. This is the first reported method for the quantification of GE-135 in CSF. (c) 2007 Elsevier B.V. All rights reserved. C1 Univ Sassari, Dipartimento Strutt Clin Med Patol Speciale Med, I-07100 Sassari, Italy. CNR, Ist Chim Biomol, Sezione Sassari, I-07100 Sassari, Italy. SUNY Buffalo, Dept Chem, Buffalo, NY 14260 USA. RP Fanciulli, G (reprint author), Univ Sassari, Dipartimento Strutt Clin Med Patol Speciale Med, Viale San Pietro 8, I-07100 Sassari, Italy. EM gfanciu@uniss.it CR BLOOM FE, 1983, PSYCHIAT CLIN N AM, V6, P365 Fanciulli G, 2003, PHARMACOL RES, V47, P53, DOI 10.1016/S1043-6618(02)00267-0 FANCIULLI G, 2006, J CHROMATOGR B, V883, P204 Fanciulli G, 2002, LIFE SCI, V71, P2383, DOI 10.1016/S0024-3205(02)02036-2 FROETSCHEL A, 1997, ANN REPORT UGA ANIMA, P130 Fukudome S, 1997, FEBS LETT, V412, P475, DOI 10.1016/S0014-5793(97)00829-6 FUKUDOME S, 1992, FEBS LETT, V296, P107, DOI 10.1016/0014-5793(92)80414-C Hunter LC, 2003, DEV MED CHILD NEUROL, V45, P121, DOI 10.1017/S0012162203000227 IZQUIERDO I, 1980, BEHAV BRAIN RES, V1, P451 MUCK WM, 1989, J CHROMATOGR-BIOMED, V495, P41, DOI 10.1016/S0378-4347(00)82608-0 Reichelt KL, 2003, NUTR NEUROSCI, V6, P19, DOI 10.1080/1028415021000042839 Rossi S, 2002, J CHROMATOGR B, V772, P73, DOI 10.1016/S1570-0232(02)00058-2 Shattock Paul, 2002, Expert Opin Ther Targets, V6, P175 Takahashi M, 2000, JPN J PHARMACOL, V84, P259, DOI 10.1254/jjp.84.259 WOOD TD, 2006, 34 NE REG M AM CHEM, P14 Yang JZ, 2002, J PHARMACOL EXP THER, V303, P840, DOI 10.1124/jpet.102.037135 NR 16 TC 9 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1570-0232 J9 J CHROMATOGR B JI J. Chromatogr. B PD JUN 1 PY 2007 VL 852 IS 1-2 BP 485 EP 490 DI 10.1016/j.jchromb.2007.02.012 PG 6 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 179JV UT WOS:000247286700067 PM 17336169 ER PT J AU Cabovska, B Cox, SL Vinks, AA AF Cabovska, B. Cox, S. L. Vinks, A. A. TI Determination of risperidone and enantiomers of 9-hydroxyrisperidone in plasma by LC-MS/MS SO JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES LA English DT Article DE risperidone; 9-hydroxyrisperidone enantiomers; LC-MS/MS method; matrix effects ID ACTIVE METABOLITE 9-HYDROXYRISPERIDONE; TANDEM MASS-SPECTROMETRY; LIQUID-CHROMATOGRAPHY; SCHIZOPHRENIC-PATIENTS; PHARMACOKINETICS; AUTISM; CYP2D6 AB A robust and validated liquid-liquid extraction LC-MS/MS method was developed for population pharmacokinetic analysis and therapeutic drug monitoring of risperidone and the enantiomers of its major active metabolite (+)-and (-)9-hydroxyrisperidone in pediatric patients. The method was rapid, sensitive and used a low sample amount (200 mu L), which is very desirable for the pediatric population. The assay was validated from 0.2 to 50 ng/mL in plasma for all analytes. LLOQ for all analytes was 0.2 ng/mL. The extracts were analyzed by normal phase LC-MS/MS. The sample run time was 8 min. Intra- and interday precision for all analytes was <= 6%; method accuracy was between 89 and 99%. Additional experiments were performed to analyze matrix effects and identify a proper internal standard for each analyte. The validated method was used to study risperidone and its enantiomer metabolites in plasma as part of a population pharmacokinetic study in pediatric patients with pervasive developmental disorder (PDD). (c) 2007 Elsevier B.V. All rights reserved. C1 Childrens Hosp, Med Ctr, PPRU, Lab Appl Pharmacokinet & Therapeut Drug Managemen, Cincinnati, OH 45229 USA. RP Cabovska, B (reprint author), Childrens Hosp, Med Ctr, PPRU, Lab Appl Pharmacokinet & Therapeut Drug Managemen, 3333 Burnet Ave,MLC 6018, Cincinnati, OH 45229 USA. EM Baiba.Cabovska@cchmc.org CR [Anonymous], 2001, GUID IND BIOAN METH Aravagiri M, 2003, THER DRUG MONIT, V25, P657, DOI 10.1097/00007691-200312000-00003 Aravagiri M, 1998, PHARMACOPSYCHIATRY, V31, P102, DOI 10.1055/s-2007-979308 Aravagiri M, 2000, J MASS SPECTROM, V35, P718, DOI 10.1002/1096-9888(200006)35:6<718::AID-JMS999>3.0.CO;2-O Avenoso A, 2000, J CHROMATOGR B, V746, P173, DOI 10.1016/S0378-4347(00)00323-6 Balant-Gorgia AE, 1999, THER DRUG MONIT, V21, P105, DOI 10.1097/00007691-199902000-00017 Bhatt J, 2006, RAPID COMMUN MASS SP, V20, P2109, DOI 10.1002/rcm.2537 HE H, 1995, INT CLIN PSYCHOPHARM, V10, P19, DOI 10.1097/00004850-199503000-00003 HEYKANTS J, 1994, J CLIN PSYCHIAT, V55, P13 HUANG ML, 1993, CLIN PHARMACOL THER, V54, P257 Jessome LL, 2006, LC GC N AM, V24, P498 Keegan D, 1994, CAN J PSYCHIAT, V39, P46 Matuszewski BK, 2006, J CHROMATOGR B, V830, P293, DOI 10.1016/j.jchromb.2005.11.009 McDougle CJ, 2005, AM J PSYCHIAT, V162, P1142, DOI 10.1176/appi.ajp.162.6.1142 Moody DE, 2004, J ANAL TOXICOL, V28, P494 Remmerie BMM, 2003, J CHROMATOGR B, V783, P461, DOI 10.1016/S1570-0232(02)00715-8 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Yasui-Furukori N, 2003, J CLIN PHARMACOL, V43, P122, DOI 10.1177/0091270002239819 Yasui-Furukori N, 2001, DRUG METAB DISPOS, V29, P1263 Zhang L, 2005, CHROMATOGRAPHIA, V61, P245, DOI 10.1365/s10337-005-0506-y Zuddas A, 2000, J CHILD ADOL PSYCHOP, V10, P79, DOI 10.1089/cap.2000.10.79 NR 21 TC 24 Z9 25 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 1570-0232 J9 J CHROMATOGR B JI J. Chromatogr. B PD JUN 1 PY 2007 VL 852 IS 1-2 BP 497 EP 504 DI 10.1016/j.jchromb.2007.02.007 PG 8 WC Biochemical Research Methods; Chemistry, Analytical SC Biochemistry & Molecular Biology; Chemistry GA 179JV UT WOS:000247286700069 PM 17344104 ER PT J AU Niederhofer, H AF Niederhofer, Helmut TI Glutamate antagonists seem to be slightly effective in psychopharmacologic treatment of autism SO JOURNAL OF CLINICAL PSYCHOPHARMACOLOGY LA English DT Letter C1 Gen Hosp Bolzano, Dept Pediat, Bolzano, Italy. RP Niederhofer, H (reprint author), Gen Hosp Bolzano, Dept Pediat, Bolzano, Italy. EM helmutniederhofer@yahoo.de CR AMMAN MG, 1985, AM J MENT DEFIC, V99, P492 Chez MG, 2004, J CHILD NEUROL, V19, P165 Hertzman M, 2003, INT J PSYCHIAT MED, V33, P395, DOI 10.2190/JE5Q-1NFT-FL40-7PMW NR 3 TC 27 Z9 27 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0271-0749 J9 J CLIN PSYCHOPHARM JI J. Clin. Psychopharmacol. PD JUN PY 2007 VL 27 IS 3 BP 317 EP 318 DI 10.1097/01.jcp.0000270082.30500.69 PG 2 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 171BX UT WOS:000246711000024 PM 17502791 ER PT J AU Vig, S AF Vig, Susan TI Young children's object play: A window on development SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE object play; early childhood development; young children; developmental disabilities ID SYMBOLIC PLAY; MENTAL-RETARDATION; REPRESENTATIONAL PLAY; COMMUNICATION-SKILLS; LANGUAGE IMPAIRMENT; VISUAL IMPAIRMENTS; MASTERY MOTIVATION; DOWN-SYNDROME; AUTISM; PRESCHOOLERS AB Adults can learn a great deal about young children's development by watching them play with toys or other objects. Insights derived from theoretical and empirical explorations of object play are particularly useful for early childhood professionals who assess the development of preschool children with disabilities. The following discussion reviews theoretical and empirical literature relevant to young children's object play and suggests implications of research findings for practitioners. The review emphasizes the cognitive prerequisites for object play, the sequential development of object play, the relationship between play and language, and the characteristics of object play in young children with developmental disabilities. C1 Yeshiva Univ Albert Einstein Coll Med, Childrens Evaluat & Rehabil Ctr, Rose F Kennedy Ctr, Dept Pediat, Bronx, NY 10461 USA. RP Vig, S (reprint author), Yeshiva Univ Albert Einstein Coll Med, Childrens Evaluat & Rehabil Ctr, Rose F Kennedy Ctr, Dept Pediat, 1410 Pelham Pkwy S, Bronx, NY 10461 USA. 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PD JUN PY 2007 VL 19 IS 3 BP 201 EP 215 DI 10.1007/s10882-007-9048-6 PG 15 WC Rehabilitation SC Rehabilitation GA 178GF UT WOS:000247208500004 ER PT J AU Dyck, MJ Piek, JP Hay, DA Hallmayer, JF AF Dyck, Murray J. Piek, Jan P. Hay, David A. Hallmayer, Joachim F. TI The relationship between symptoms and abilities in autism SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; intelligence; empathy; motor coordination; language ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME; SELECTIVE ATTENTION; REVISED VERSION; CHILDREN; MIND; ADULTS; COMMUNICATION; COHERENCE AB We assessed if autism symptoms relate to ability deficits and achievement discrepancies in 29 children aged 4-13 years with a diagnosis of Autistic Disorder. Symptoms, intelligence, language, motor coordination and social cognition were assessed. Children with autism underachieve on all ability measures. There were significant achievement discrepancies between Performance IQ and theory of mind, fine and gross motor coordination. The most common discrepancy was between Performance IQ scores and motor coordination scores, which was observed in 86% of children. Early developmental abnormalities related to most abilities, social interaction symptoms related to motor coordination and receptive language, and symptoms related to discrepancies between PIQ and social cognitive abilities. C1 Griffith Univ, Sch Psychol, Gold Coast, Qld 9726, Australia. Curtin Univ Technol, Sch Psychol, Bentley, WA, Australia. Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. RP Dyck, MJ (reprint author), Griffith Univ, Sch Psychol, PMB50, Gold Coast, Qld 9726, Australia. 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Dev. Phys. Disabil. PD JUN PY 2007 VL 19 IS 3 BP 251 EP 261 DI 10.1007/s10882-007-9055-7 PG 11 WC Rehabilitation SC Rehabilitation GA 178GF UT WOS:000247208500008 ER PT J AU Danforth, S Naraian, S AF Danforth, Scot Naraian, Srikala TI Use of the machine metaphor within autism research SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE student-machine; autism; machine metaphor ID YOUNG-CHILDREN; SPECTRUM AB Traditionally, metaphor has been viewed a literary trope standing in opposition to literal forms of writing in the natural and social sciences. In recent decades, however, a multi-disciplinary field of cognitive linguistic research has developed. This research finds metaphor at the heart of both everyday and scientific thinking. Metaphor is understood to be vital to the development of useful theories within the sciences. 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Dev. Phys. Disabil. PD JUN PY 2007 VL 19 IS 3 BP 273 EP 290 DI 10.1007/s10882-007-9061-9 PG 18 WC Rehabilitation SC Rehabilitation GA 178GF UT WOS:000247208500010 ER PT J AU de Fockert, J Davidoff, J Fagot, J Parron, C Goldstein, J AF de Fockert, Jan Davidoff, Jules Fagot, Joel Parron, Carole Goldstein, Julie TI More accurate size contrast judgments in the Ebbinghaus illusion by a remote culture SO JOURNAL OF EXPERIMENTAL PSYCHOLOGY-HUMAN PERCEPTION AND PERFORMANCE LA English DT Article DE Ebbinghaus illusion; local precedence; size contrast judgments; cross-cultural ID WEAK CENTRAL COHERENCE; VISUAL-PERCEPTION; AUTISM; SIMILARITY; CHILDREN; CATEGORIES AB The Ebbinghaus (Titchener) illusion was examined in a remote culture (Himba) with no words for geometric shapes. The illusion was experienced less strongly by Himba compared with English participants, leading to more accurate size contrast judgments in the Himba. The study included two conditions of inducing stimuli. The illusion was weaker when the inducing stimuli were dissimilar (diamonds) to the target (circle) compared with when they were similar (circles). However, the illusion was weakened to the same extent in both cultures. It is argued that the more accurate size judgments of the Himba derive from their tendency to prioritize the analysis of local details in visual processing of multiple objects, and not from their impoverished naming. C1 Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. Univ Aix Marseille 2, CNRS, Inst Neurosci Cognit Mediterranee, Marseille, France. RP de Fockert, J (reprint author), Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. 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Exp. Psychol.-Hum. Percept. Perform. PD JUN PY 2007 VL 33 IS 3 BP 738 EP 742 DI 10.1037/0096-1523.33.3.738 PG 5 WC Psychology; Psychology, Experimental SC Psychology GA 172DU UT WOS:000246785100017 PM 17563234 ER PT J AU Allen, DG Lowe, K Moore, K Brophy, S AF Allen, D. G. Lowe, K. Moore, K. Brophy, S. TI Predictors, costs and characteristics of out of area placement for people with intellectual disability and challenging behaviour SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE challenging behaviour; out of area placement ID SUPPORT AB Background Out of area placements for people with challenging behaviour represent an expensive and often ineffective strategy for meeting the needs of this service user group. Methods More than 800 agencies and service settings in a large area of South Wales were screened to identify children and adults with challenging behaviour against a number of defined operational criteria. Detailed data on identified individuals and the services they received were collected by interviewing key informants. Univariate and multivariate statistics were employed to identify predictors of out of area placement. Results In total, 1458 people were identified. Full data were available for 901 participants, 97 of whom were placed out of area. Predictors of out of area placement included behaviours resulting in physical injury and exclusion from service settings, a history of formal detention under the mental health act, the presence of mental health problems, a diagnosis of autism and higher total score on the Adaptive Behaviour Scale. Out of area placements were typically of high cost, and associated with only limited evidence of improved service quality. Conclusions Identifying predictors for out of area placement can be used to highlight deficiencies in local services and individuals at increased risk of exclusion from local services. C1 Bro Morgannwg NHS Trust, Special Projects Team, Cardiff, Wales. Univ Glamorgan, Pontypridd CF37 1DL, M Glam, Wales. RP Allen, DG (reprint author), 58-62 Cowbridge Rd W, Cardiff CF5 5BS, Wales. EM david.allen@bromor-tr-wales.nhs.uk CR Alborz A., 1994, CHALLENGING BEHAV SU Allen D, 1998, J APPL RES INTELLECT, V11, P156 ALLEN D, 2004, ALLENING DISABILITY, V7, P16 Allen D., 1989, MENT HANDICAP RES, V2, P18 Allen D, 1991, M CHALLENGE SOME UK ALLEN D, 2000, LEARNING DISABILITY, V117, P5 ALLEN D, 1995, J INTELL DISABIL RES, V39, P67 BLUNDEN R, 1987, 74 KING EDW HOSP FUN Chan J. 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PD JUN PY 2007 VL 51 BP 409 EP 416 DI 10.1111/j.1365-2788.2006.00877.x PN 6 PG 8 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 164OL UT WOS:000246243300001 PM 17493024 ER PT J AU Zarcone, J Napolitano, D Peterson, C Breidbord, J Ferraioli, S Caruso-Anderson, M Holsen, L Butler, MG Thompson, T AF Zarcone, J. Napolitano, D. Peterson, C. Breidbord, J. Ferraioli, S. Caruso-Anderson, M. Holsen, L. Butler, M. G. Thompson, T. TI The relationship between compulsive behaviour and academic achievement across the three genetic subtypes of Prader-Willi syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE academic achievement; compulsion; obsessive-compulsive disorder; Prader-Willi syndrome ID MATERNAL UNIPARENTAL DISOMY; SYMPTOM DIMENSIONS; COMORBIDITY; DISORDERS; AUTISM; PEOPLE; SCALE; PHENOMENOLOGY; RELIABILITY; PREVALENCE AB Background Prader - Willi syndrome (PWS) is a genetic syndrome associated with several physical, cognitive and behavioural characteristics. For many individuals with this syndrome, compulsive behaviour is often noted in both food and non-food situations. The focus of this paper is on the non-food-related compulsions in individuals with PWS and comparing differences across the three genetic subtypes of the syndrome. Methods Compulsive behaviours in.. people with PWS were assessed using the Yale-Brown Obsessive Compulsive Scale and the Compulsive Behavior Checklist. Compulsive behaviour and its relation to IQ and academic achievement also were evaluated. Phenotypic differences were characterized for the three most common genetic subtypes of the disorder: 16 individuals with the long Type I ( TI) 15q deletion, 26 individuals with the short Type II (TII) 15q deletion and 31 individuals with maternal disomy 15. Results There appeared to be important differences between the two deletion subtypes. Specifically, individuals with the TI deletion had more compulsions regarding personal cleanliness (i.e. excessive bathing/ grooming), and their compulsions were more difficult to interrupt and interfered with social activities more than the other subtypes. Individuals with the TII deletion were more likely to have compulsions related to specific academic areas (i.e. rereading, erasing answers and counting objects or numbers). Conclusions These findings may help clinicians and researchers identify possible intervention strategies and supports based on the behavioural phenotype associated with genetic subtype in individuals with PWS. C1 Univ Rochester, Med Ctr, Strong Ctr Dev Disabil, Rochester, NY 14642 USA. Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Baltimore, MD USA. Univ Wisconsin, Waisman Ctr Mental Retardat & Human Dev, Madison, WI 53706 USA. Univ Missouri, Childrens Mercy Hosp & Clin, Kansas City, MO 64108 USA. Univ Minnesota, Minneapolis, MN USA. RP Zarcone, J (reprint author), Univ Rochester, Med Ctr, Strong Ctr Dev Disabil, 601 Elmwood Ave,Box 671, Rochester, NY 14642 USA. EM Jennifer_Zarcone@URMC.Rochester.edu CR Bittel D. 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Intell. Disabil. Res. PD JUN PY 2007 VL 51 BP 478 EP 487 DI 10.1111/j.1365-2788.2006.00916.x PN 6 PG 10 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 164OL UT WOS:000246243300007 PM 17493030 ER PT J AU Lucyshyn, JM Albin, RW Horner, RH Mann, JC Mann, JA Wadsworth, G AF Lucyshyn, Joseph M. Albin, Richard W. Horner, Robert H. Mann, Jane C. Mann, James A. Wadsworth, Gina TI Family implementation of positive behavior support for a child with autism: Longitudinal, single-case, experimental, and descriptive replication and extension SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID ACTIVITY SETTINGS; INTERVENTION; PERSPECTIVES; DISABILITIES; AGGRESSION; ECOLOGY; CONTEXT; INJURY AB This study examined the efficacy, social validity, and durability of a positive behavior support (PBS) approach with the family of a girl with autism and severe problem behavior. The study was conducted across a 10-year period beginning when the child was 5 years old. A multiple baseline across family routines design evaluated the functional relationship between parent implementation of a PBS plan and longitudinal improvements in child behavior and successful participation in routines. Daily indicator behavior data allowed us to assess generalized improvements in child behavior. An inventory of monthly community activities allowed us to assess changes in child quality of life. In addition, social validity and contextual fit were assessed. Results document that the intervention was associated with a 75% reduction in problem behavior, and that the effects were maintained across a 6-month to 7-year follow-up period. Associated outcomes included generalized improvements in child behavior and enhanced community activity patterns. Parents also rated the social validity and contextual fit of the approach highly. Results verify the efficacy and social validity of the approach and offer preliminary descriptive evidence of its durability. Contributions to the literature, implications, and future directions are discussed. C1 Univ British Columbia, Fac Educ, Dept Educ & Counseling Psychol & Special Educ, Vancouver, BC V6Z 1Z4, Canada. Univ Oregon, Coll Educ, Eugene, OR 97403 USA. 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P., 2006, FAMILIES PROFESSIONA Turnbull AP, 1997, EXCEPT CHILDREN, V63, P211 Turnbull AP, 1996, MENT RETARD, V34, P280 Turnbull AP, 1998, J ASSOC PERS SEVERE, V23, P178, DOI 10.2511/rpsd.23.3.178 Vaughn BJ, 1997, J APPL BEHAV ANAL, V30, P713, DOI 10.1901/jaba.1997.30-713 Vaughn BJ, 2002, J POSIT BEHAV INTERV, V4, P38, DOI 10.1177/109830070200400107 Vaughn BJ, 1997, J ASSOC PERS SEVERE, V22, P186 Wechsler D., 1989, WPPSI R MANUAL Whyte W. F., 1991, PARTICIPATORY ACTION NR 50 TC 20 Z9 20 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD SUM PY 2007 VL 9 IS 3 BP 131 EP 150 DI 10.1177/10983007070090030201 PG 20 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 180TH UT WOS:000247388400002 ER PT J AU Hundert, JP AF Hundert, Joel P. TI Training classroom and resource preschool teachers to develop inclusive class interventions for children with disabilities: Generalization to new intervention targets SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID SOCIAL-SKILLS; INTEGRATED PRESCHOOLS; ACTIVITY SCHEDULES; PEER INTERACTION; AUTISM; EDUCATION; BEHAVIORS; IMPLEMENTATION; CONSULTATION; INSTRUCTION AB Four preschool supervisors were individually trained in a collaborative team approach in which classroom and resource teachers together developed a plan to increase the peer interactions of the entire class, including children with disabilities. The purpose of the research was to assess the generalization of effects to a new program target (children's on-task behavior during circle time) and over time (3 months). The experimental phases of baseline, supervisor training, and follow-up were introduced in a multiple-baseline design across four preschool classes, each containing 2 children with disabilities. Behaviors of teachers, 8 children with disabilities, and 8 comparison children were measured during daily 20-min training sessions (indoor play periods) and generalization sessions (circle time). Results indicated that following supervisor training, teachers increased their focus on groups of children that included children with disabilities in both training and generalization sessions. After supervisor training, children with disabilities and comparison children increased their peer interactions during training sessions and their on-task behavior during circle time. Changes in teachers' and children's behaviors in both settings were maintained at the 3-month follow-up observation. Implications for teacher training and consultation are discussed. C1 McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8S 4L8, Canada. RP Hundert, JP (reprint author), Behav Inst, 57 Young St, Hamilton, ON L8N 1V1, Canada. EM hundert@mcmaster.ca CR Bryan LC, 2000, J AUTISM DEV DISORD, V30, P553, DOI 10.1023/A:1005687310346 BURGIO LD, 1983, J APPL BEHAV ANAL, V16, P37, DOI 10.1901/jaba.1983.16-37 Carr EG, 2002, J POSIT BEHAV INTERV, V4, P4, DOI 10.1177/109830070200400102 CARTA JJ, 1986, UNPUB MANUAL CHANDLER LK, 1992, J APPL BEHAV ANAL, V25, P249, DOI 10.1901/jaba.1992.25-249 CHANDLER LK, 1992, J APPL BEHAV ANAL, V25, P415, DOI 10.1901/jaba.1992.25-415 Chiara L, 1995, J EARLY INTERVENTION, V19, P203 FOX JJ, 1993, BEHAV MODIF, V17, P339, DOI 10.1177/01454455930173006 Gadow KD, 2005, AUTISM, V9, P392, DOI 10.1177/1362361305056079 GRADEN JL, 1985, EXCEPT CHILDREN, V51, P487 Greenwood C. 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PD SUM PY 2007 VL 9 IS 3 BP 159 EP 173 DI 10.1177/10983007070090030401 PG 15 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 180TH UT WOS:000247388400004 ER PT J AU McGuinness, TM AF McGuinness, Teena M. TI How young is too young for psychotropic medication? SO JOURNAL OF PSYCHOSOCIAL NURSING AND MENTAL HEALTH SERVICES LA English DT Article ID UNITED-STATES; CHILDREN; PRESCHOOLERS; CLONIDINE; SECRETIN; DISORDER; AUTISM; TRENDS; ADHD AB Approximately 1.5% of pre-school-age children receive prescribed psychiatric medications, and most of these prescirptions are written for off-label indications. These circumstances create numerous ethical issues. Few studies support the use of psychotropic medications in children younger than age 6. In addition, the effects of these medications are not fully understood in young children with rapidly maturing brains and bodies. Suggestions for nurses are offered. C1 Univ Alabama, Sch Nursing, Birmingham, AL 35294 USA. RP McGuinness, TM (reprint author), Univ Alabama, Sch Nursing, Birmingham, AL 35294 USA. 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Psychosoc. Nurs. Ment. Health Serv. PD JUN PY 2007 VL 45 IS 6 BP 20 EP 23 PG 4 WC Nursing SC Nursing GA 356MF UT WOS:000259781600011 PM 17601156 ER PT J AU Luyster, R Qiu, SP Lopez, K Lord, C AF Luyster, Rhiannon Qiu, Shanping Lopez, Kristina Lord, Catherine TI Predicting outcomes of children referred for autism using the MacArthur-Bates communicative development inventory SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE autism spectrum disorders; communication; language; outcome ID DIAGNOSTIC OBSERVATION SCHEDULE; RECEPTIVE LANGUAGE DISORDER; DOWN-SYNDROME; SPECTRUM DISORDERS; PRESCHOOL-CHILDREN; JOINT ATTENTION; YOUNG-CHILDREN; 2ND YEAR; VOCABULARY; TODDLERS AB Purpose: Autism spectrum disorders (ASD) are characterized by early impairments in language and related social communication skills. This investigation explored whether scores on the MacArthur-Bates Communicative Development Inventory (CDI) at ages 2 and 3 years predict outcome at age 9 years in children with ASD and developmental delay (DD). Method: Sixty-two children referred for possible autism at age 2 years, and 19 children with DD, were followed to age 9 years. Vocabulary, prespeech, and gestures scores on CDIs administered at ages 2 and 3 years were used to predict follow-up IQ, language adaptive skills and scores on diagnostic measures. Results: CDI scores at ages 2 and 3 did not predict outcome for the DD group. For the ASD sample, CDI receptive and expressive language and late gestures at ages 2 and 3 years predicted a number of follow-up variables, although scores at age 3 years were generally more predictive than scores at age 2 years. 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H., 1992, CLIN EVALUATION LANG Woods JJ, 2003, LANG SPEECH HEAR SER, V34, P180, DOI 10.1044/0161-1461(2003/015) Zwaigenbaum L, 2005, INT J DEV NEUROSCI, V23, P143, DOI 10.1016/j.ijdevneu.2004.05.001 NR 64 TC 30 Z9 31 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 1092-4388 J9 J SPEECH LANG HEAR R JI J. Speech Lang. Hear. Res. PD JUN PY 2007 VL 50 IS 3 BP 667 EP 681 DI 10.1044/1092-4388(2007/047) PG 15 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 177NM UT WOS:000247159800010 PM 17538108 ER PT J AU Brinton, B Spackman, MP Fujiki, M Ricks, J AF Brinton, Bonnie Spackman, Matthew P. Fujiki, Martin Ricks, Jenny TI What should Chris say? The ability of children with specific language impairment to recognize the need to dissemble emotions in social situations SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE specific language impairment; social competence; dissemblance; emotion understanding; emotional intelligence ID DISPLAY RULES; PEER ACCEPTANCE; BEHAVIOR; COMPETENCE; KNOWLEDGE; ACCESS; RESPONSIVENESS; PRESCHOOLERS; EXPRESSION; AUTISM AB Purpose: In this study, the authors examined the ability of children with specific language impairment (SLI) and ee s to when an experienced their typical judge emotion should be dissembled (hidden) in accord with social display rules. Method: Participants included 19 children with SLI and 19 children with typical language skills, both groups ranging in age from 7;9 (years;months) to 10;10, with a mean age of 9;1. Children were presented with 10 hypothetical social situations in which a character, Chris, experienced an emotion that should be dissembled for social purposes. The participants' responses were categorized as to whether or not they dissembled or displayed the emotion. Results: Although the task was difficult for many participants, children with SLl indicated that the experienced emotion should be dissembled significantly less often than did their typical peers. Children in the 2 groups did not significantly differ in their judgments of the social display rules governing these situations. Conclusion: These results suggested that the children with SLI did not understand the impact of displaying emotion on relationships in the same way as did their typical peers. In this respect, they seemed to lag behind the typical children in their developing emotion knowledge. C1 Brigham Young Univ, Provo, UT 84602 USA. RP Brinton, B (reprint author), Brigham Young Univ, B-380 ASB, Provo, UT 84602 USA. EM bonnie_brinton@byu.edu CR Banerjee M, 1997, SOC COGNITION, V15, P107 Boucher J, 2000, J CHILD PSYCHOL PSYC, V41, P847, DOI 10.1017/S0021963099006149 BRACKEN BA, 2003, UNIVERSAL NONVERBAL Brinton B, 1998, J SPEECH LANG HEAR R, V41, P927 Brinton B, 1997, J SPEECH LANG HEAR R, V40, P1011 Brinton B, 2005, TOP LANG DISORD, V25, P338 BRINTON B, 1986, J SPEECH HEAR DISORD, V51, P370 Carrow-Woolfolk E, 1999, COMPREHENSIVE ASSESS COLE PM, 1986, CHILD DEV, V57, P1309, DOI 10.1111/j.1467-8624.1986.tb00459.x Conti-Ramsden G, 2004, J SPEECH LANG HEAR R, V47, P145, DOI 10.1044/1092-4388(2004/013) CRAIG HK, 1993, J SPEECH HEAR RES, V36, P322 Denham S. A., 1998, EMOTIONAL DEV YOUNG Denham S. 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PD JUN PY 2007 VL 50 IS 3 BP 798 EP 811 DI 10.1044/1092-4388(2007/055) PG 14 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 177NM UT WOS:000247159800018 PM 17538116 ER PT J AU Getchell, N Lynch, A AF Getchell, Nancy Lynch, Amy TI Motor Competencies in children with Autism spectrum disorders SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Delaware, Newark, DE 19716 USA. NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2007 VL 29 SU S BP S6 EP S7 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 180EQ UT WOS:000247345500014 ER PT J AU Glazebrook, CM Gonzalez, D Elliott, D AF Glazebrook, Cheryl M. Gonzalez, David Elliott, Digby TI The role of vision for online control of aiming movements in persons with autism SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract C1 McMaster Univ, Hamilton, ON L8S 4L8, Canada. NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2007 VL 29 SU S BP S75 EP S76 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 180EQ UT WOS:000247345500127 ER PT J AU Jensen, JL AF Jensen, Jody L. TI The empirical evidence for the efficacy of neurosensory approaches to the treatment of autism spectrum disorders SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Texas, Austin, TX 78712 USA. NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2007 VL 29 SU S BP S7 EP S7 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 180EQ UT WOS:000247345500015 ER PT J AU Pope, M Lantero, D AF Pope, Michelle Lantero, Dawn TI Autism: Issues in measurement and research design SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2007 VL 29 SU S BP S6 EP S6 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 180EQ UT WOS:000247345500013 ER PT J AU Ray, MC Welsh, T Weeks, D Dewey, D Elliott, D AF Ray, Matthew C. Welsh, Tim Weeks, Daniel Dewey, Deborah Elliott, Digby TI Between- and within-person inhibition of return effects in the movements of people with autism SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Calgary, Calgary, AB T2N 1N4, Canada. Simon Fraser Univ, Burnaby, BC V5A 1S6, Canada. McMaster Univ, Hamilton, ON L8S 4L8, Canada. NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2007 VL 29 SU S BP S119 EP S120 PG 2 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 180EQ UT WOS:000247345500201 ER PT J AU [Anonymous] AF [Anonymous] TI Motor development symposia - Autism spectrum disorders and motor development: It is not just about language and social interaction SO JOURNAL OF SPORT & EXERCISE PSYCHOLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU HUMAN KINETICS PUBL INC PI CHAMPAIGN PA 1607 N MARKET ST, PO BOX 5076, CHAMPAIGN, IL 61820-2200 USA SN 0895-2779 J9 J SPORT EXERCISE PSY JI J. Sport Exerc. Psychol. PD JUN PY 2007 VL 29 SU S BP S6 EP S6 PG 1 WC Hospitality, Leisure, Sport & Tourism; Psychology, Applied; Psychology; Sport Sciences SC Social Sciences - Other Topics; Psychology; Sport Sciences GA 180EQ UT WOS:000247345500012 ER PT J AU Wazana, A Bresnahan, M Kline, J AF Wazana, Ashley Bresnahan, Michaeline Kline, Jennie TI The autism epidemic: Fact or artifact? SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; pervasive developmental disorders; epidemiology; time trends; prediction model ID PERVASIVE DEVELOPMENTAL DISORDERS; DSM-III-R; SPECTRUM DISORDERS; DIAGNOSTIC SUBSTITUTION; CHANGING PREVALENCE; PRESCHOOL-CHILDREN; CHILDHOOD AUTISM; RUBELLA VACCINE; DOWN-SYNDROME; FIELD TRIAL AB Objective: We provide an illustration of how changes in methodological factors may produce variations in the frequency of autistic disorder (AD) over time and project how much of the observed increase in the frequency of AD may be explained by methodological factors. Method: Using a prediction analysis, we calculate how broadening diagnostic criteria, younger age at diagnosis, and improved efficiency of case ascertainment could produce temporal trends in the incidence and prevalence of AD, measured by calendar year and by year of birth, in a hypothetical population of children 0 to 18 across the years 1950 to 2020. Results: Time trend studies report an increase as large as 11.0-fold over a 13-year period for AD. Conservative changes in the three methodological factors produced increases in the frequency of AD ranging from 2.1-to 28.8-fold. Measures of frequency by year of birth show the largest magnitude of increase; predicted prevalence by calendar year and to age 4 by year of birth are influenced by changes in the distribution of age at diagnosis, but 1-year incidence and prevalence to age 12 are not. Discussion: Methodological factors may explain the observed increases in AD over time. To increase confidence in reports of time trends, we recommend particular frequency measures and study circumstances. C1 Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3Z 1P2, Canada. New York State Psychiat Inst & Hosp, Epidemiol Dev Brain Disorders Dept, New York, NY 10032 USA. Columbia Univ, Mailman Sch Publ Hlth, Dept Epidemiol, New York, NY USA. RP Wazana, A (reprint author), Montreal Childrens Hosp, Dept Psychiat, 4018 Rue St Catherine Ouest, Montreal, PQ H3Z 1P2, Canada. 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Am. Acad. Child Adolesc. Psychiatr. PD JUN PY 2007 VL 46 IS 6 BP 721 EP 730 DI 10.1097/chi.0b013e31804a7f3b PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 171KD UT WOS:000246733900006 PM 17513984 ER PT J AU Eapen, V Mabrouk, AA Zoubeidi, T Yunis, F AF Eapen, Valsamma Mabrouk, Abdul Azim Zoubeidi, Taoufik Yunis, Feisal TI Prevalence of pervasive developmental disorders in preschool children in the UAE SO JOURNAL OF TROPICAL PEDIATRICS LA English DT Article ID AUTISM; POPULATION; EPIDEMIOLOGY AB Available evidence from the literature suggests that the prevalence of autistic disorder may be on the rise world wide, but no prevalence studies have been carried out till date in the Arabian Gulf region. A representative random sample of 694 three-year-old United Arab Emirates national children was evaluated in a two-stage study in the community. In the first stage, using Autism Screening Questionnaire, 58 per 10000 children were noted to have autistic features. In the second stage using clinical interview, the weighted prevalence was estimated to be 29 per 10 000 for a DSM-IV diagnosis of pervasive developmental disorder (PDD). However, none of these children had been diagnosed prior to the study. Presence of autistic features was associated with male gender, presence of bebavioural problems and a family history of developmental delay. The rate of PDD observed in the UAE is comparable with that reported from western countries. However, the lack of recognition of these disorders suggests the need for a comprehensive screening program, as early diagnosis can open the door for early intervention which in turn may improve the prognosis. C1 UAE Univ, Fac Med, Al Ain, U Arab Emirates. Sch Hlth Serv, Dept Pediat, Al Ain, U Arab Emirates. UAE Univ, Dept Stat, Al Ain, U Arab Emirates. Cairo Univ, Dept Psychol, Cairo, Egypt. RP Eapen, V (reprint author), UAE Univ, Fac Med & Hlth Sci, POB 17666, Al Ain, U Arab Emirates. 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We screened eleven clock/clock-related genes in a predominantly high-functioning Autism Genetic Resource Exchange sample of strictly diagnosed autistic disorder progeny and their parents (110 trios) for association of clock gene variants with autistic disorder. We found significant association (P<0.05) for two single-nucleotide polymorphisms in per1 and two in npas2. Analysis of all possible combinations of two-marker haplotypes for each gene showed that in npas2 40 out of the 136 possible two-marker combinations were significant at the P<0.05 level, with the best result between markers rs1811399 and rs2117714, P=0.001. Haplotype analysis within per1 gave a single significant result: a global P=0.027 for the markers rs2253820-rs885747. No two-marker haplotype was significant in any of the other genes, despite the large number of tests performed. Our findings support the hypothesis that these epistatic clock genes may be involved in the etiology of autistic disorder. 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The present experiments employed a new social approach task for mice which is designed to detect low levels of sociability, representing the first diagnostic criterion for autism. Two lines of oxytocin knockout mice were tested, the National Institute of Mental Health line in Bethesda, and the Baylor/Emory line at the University of North Carolina in Chapel Hill. Similar methods were used for each line to evaluate tendencies to spend time with a stranger mouse versus with an inanimate novel object with no social valence. Adult C57BL/6J males were tested identically, as controls to confirm the robustness of the methods used in the social task. Comprehensive phenotyping of general health, neurological reflexes, olfactory and other sensory abilities, and motor functions was employed to assess both lines. No genotype differences were detected in any of the control measures for either line. Normal sociability, measured as time spent with a novel stranger mouse as compared to time spent with a novel object, was seen in both the NIMH and the Baylor/Emory lines of oxytocin null mutants, heterozygotes.. and wild-type littermate controls. Normal preference for social novelty, measured as time spent with a second novel stranger as compared to time spent with a more familiar mouse, was seen in both the NIMH and the Baylor/Emory lines of oxytocin null mutants, heterozygotes, and wild-type littermate controls, with minor exceptions. Similar behavioral results from two independent targeted gene mutations. generated with different targeting vectors, bred on different genetic backgrounds, and tested in different laboratory environments, corroborates the negative findings on sociability in oxytocin mutant mice. Intact tendencies to spend time with another mouse versus with a novel object, in both lines of oxytocin knockouts, supports an interpretation that oxytocin plays a highly specific role in social memory, but is not essential for general spontaneous social approach in mice. (C) 2007 Elsevier Ltd. All rights reserved. C1 NIMH, Intramural Res Program, Lab Behav Neurosci, Bethesda, MD 20892 USA. Univ N Carolina, Sch Med, Mouse Behav Phenotyping Lab, Neurodev Disorders Res Ctr, Chapel Hill, NC USA. Univ N Carolina, Sch Med, Autism Res Ctr, Chapel Hill, NC USA. Univ N Carolina, Sch Med, Dept Genet, Chapel Hill, NC USA. Emory Univ, Sch Med, Yerkes Natl Primate Ctr, Ctr Behav Neurosci, Atlanta, GA 30322 USA. Emory Univ, Sch Med, Yerkes Natl Primate Ctr, Dept Psychiat, Atlanta, GA 30322 USA. NIMH, Intramural Res Program, Sect Neural Gene Express, Bethesda, MD 20892 USA. RP Crawley, JN (reprint author), NIMH, Intramural Res Program, Lab Behav Neurosci, Bethesda, MD 20892 USA. 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Liu, Y. Sadamatsu, M. Tsutsumi, S. Akaike, M. Ushijima, H. Kato, N. TI Perinatal bisphenol A affects the behavior and SRC-1 expression of male pups but does not influence on the thyroid hormone receptors and its responsive gene SO NEUROSCIENCE RESEARCH LA English DT Article DE hyperactivity; impaired special memory; hippocampus; RC3/neurogranin; ADHD; autism; thyroid hormone receptor alpha ID DEVELOPING RAT-BRAIN; SEXUAL-DIFFERENTIATION; NEONATAL-HYPOTHYROIDISM; ENDEMIC CRETINISM; NERVOUS-SYSTEM; EXPOSURE; FETAL; THYROXINE; HYPERACTIVITY; COACTIVATOR AB Bisphenol A (BPA) has been shown to interfere with thyroid hormone receptors (THRs) and to influence the expression of THR-responsive elements in vivo and in vitro, while some studies reported hyperactivity induced by BPA treatment. In the present study, our purpose was to investigate the effect of BPA exposure on behavioral alteration and its mechanism of action, especially focusing on the thyroid hormone pathway. Significant sexual difference on behaviors was observed in perinatal BPA exposure, as manifested by hyperactivity and impaired spatial learning/ memory in male pups after matured. Dams treated with 0.1 mg/l BPA showed transient hypothyroidism, while male pups were found to exhibit a transient hyperthyroidism followed by hypothyroidism. Furthermore, significant up-regulated expression levels of mRNA and protein of SRC-1 in the hippocampus were observed in male pups by 0.1 mg/l BPA treatment. However the expression of THR alpha/beta and RC3/neurogranin were not affected by BPA treatment. These results indicate that perinatal BPA exposure at a very low level may influence thyroid function and then consequently affects brain development, but at the same time, suggest that thyroid hormone receptor may not be a direct target of BPA action, but instead, another factor may be involved in this action. (c) 2007 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved. C1 Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, Tokyo 1130033, Japan. Univ Tokyo, Grad Sch Med, Inst Int Hlth, Dept Dev Med Sci, Tokyo 1130033, Japan. Shiga Univ Med Sci, Dept Psychiat, Shiga 5202192, Japan. GlaxoSmithKline Pharmaceut Co Ltd, Safety Assessment Dept, Tokyo 1518566, Japan. RP Kato, N (reprint author), Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. 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Res. PD JUN PY 2007 VL 58 IS 2 BP 149 EP 155 DI 10.1016/j.neures.2007.02.011 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 185BG UT WOS:000247685700009 PM 17412439 ER PT J AU Meyer, U Yee, BK Feldon, J AF Meyer, Urs Yee, Benjamin K. Feldon, Joram TI The neurodevelopmental impact of prenatal infections at different times of pregnancy: The earlier the worse? SO NEUROSCIENTIST LA English DT Review DE autism; cytokines; infection; neurodevelopment; pregnancy; schizophrenia ID AUTISM SPECTRUM DISORDERS; MIDBRAIN DOPAMINERGIC-NEURONS; DISRUPTED LATENT INHIBITION; MATERNAL IMMUNE ACTIVATION; ANIMAL-MODEL; VIRAL-INFECTION; IN-UTERO; BRAIN-DEVELOPMENT; NEONATAL MICE; PHARMACOLOGICAL CHANGES AB Environmental insults taking place in early brain development may have long-lasting consequences for adult brain functioning. There is a large body of epidemiological data linking maternal infections during pregnancy to a higher incidence of psychiatric disorders with a presumed neurodevelopmental origin in the offspring, including schizophrenia and autism. Although specific gestational windows may be associated with a differing vulnerability to infection-mediated disturbances in normal brain development, it still remains debatable whether and/or why certain gestation periods may confer maximal risk for neurodevelopmental disturbances following the prenatal exposure to infectious events. In this review, the authors integrate both epidemiological and experimental findings supporting the hypothesis that infection-associated immunological events in early fetal life may have a stronger neurodevelopmental impact compared to late pregnancy infections. This is because infections in early gestation may not only interfere with fundamental neurodevelopmental events such as cell proliferation and differentiation, but it may also predispose the developing nervous system to additional failures in subsequent cell migration, target selection, and synapse maturation, eventually leading to multiple brain and behavioral abnormalities in the adult offspring. The temporal dependency of the epidemiological link between maternal infections during pregnancy and a higher risk for brain disorders in the offspring may thus be explained by specific spatiotemporal events in the course of fetal brain development. C1 ETH, Lab Behav Neurobiol, CH-8603 Schwerzenbach, Switzerland. RP Yee, BK (reprint author), ETH, Lab Behav Neurobiol, Schorenstr 16, CH-8603 Schwerzenbach, Switzerland. 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115 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 1073-8584 J9 NEUROSCIENTIST JI Neuroscientist PD JUN PY 2007 VL 13 IS 3 BP 241 EP 256 DI 10.1177/1073858406296401 PG 16 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 169VM UT WOS:000246620200014 PM 17519367 ER PT J AU Schum, RL AF Schum, Robert L. TI Language screening in the pediatric office setting SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID PRESCHOOL-CHILDREN; SPEECH; IMPAIRMENT; DISORDERS; DELAY; COMMUNICATION; TRANSIENT; DIAGNOSIS; AUTISM AB This article discusses screening of language development in a pediatric office setting. It describes the relationship between language delay and various developmental disorders. It provides recent recommendations regarding the efficacy of formal language screening instruments, and suggests developmental guidelines for clinical observations. Referrals for specialty evaluations and services for evaluation and treatment are presented. The article offers suggestions for counseling parents when a language disorder is suspected. C1 Childrens Hosp Wisconsin, Child Dev Ctr, Milwaukee, WI 53201 USA. Med Coll Wisconsin, Dept Pediat, Sect Child Dev, Milwaukee, WI 53226 USA. RP Schum, RL (reprint author), Childrens Hosp Wisconsin, Child Dev Ctr, PO Box 1997 MS 744, Milwaukee, WI 53201 USA. 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Clin. N. Am. PD JUN PY 2007 VL 54 IS 3 BP 425 EP + DI 10.1016/j.pcl.2007.02.010 PG 13 WC Pediatrics SC Pediatrics GA 187JD UT WOS:000247842800003 PM 17543903 ER PT J AU Tager-Flusberg, H Caronna, E AF Tager-Flusberg, Helen Caronna, Elizabeth TI Language disorders: Autism and other pervasive developmental disorders SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; MENTAL-RETARDATION; ASPERGER-SYNDROME; JOINT ATTENTION; CHILDREN; INFANTS; DIAGNOSIS; ADULTS; COMMUNICATION AB This article summarizes current knowledge about language and communication impairments in children who have autism spectrum disorders. 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Clin. N. Am. PD JUN PY 2007 VL 54 IS 3 BP 469 EP + DI 10.1016/j.pcl.2007.02.011 PG 14 WC Pediatrics SC Pediatrics GA 187JD UT WOS:000247842800005 PM 17543905 ER PT J AU Russell, RL AF Russell, Robert L. TI Social communication impairments: Pragmatics SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID CONVERSATIONAL CHARACTERISTICS; LANGUAGE DISORDER; TEACHER REPORT; CHILDREN; CHECKLIST; AUTISM; FMRI; SPEECH; PARENT; DAMAGE AB Social communication or pragmatic impairments are characterized and illustrated as involving inappropriate or ineffective use of language and gesture in social contexts. Three clinical vignettes illustrate different pragmatic impairments and the wealth of diagnostic information that can be garnered from observation of a child's social communicationbehavior. Definitions of, and developmental milestones in, domains of pragmatic competence are provided. Several screening instruments are suggested for use in assessing pragmatic competence within the time-frame of a pediatric examination. Frequent comorbid psychiatric conditions are described and a sample of current neurobiologic research is briefly summarized. C1 Med Coll Wisconsin, Milwaukee, WI 53226 USA. Childrens Hosp Wisconsin, Child Dev Ctr, MEB, Milwaukee, WI 53226 USA. RP Russell, RL (reprint author), Med Coll Wisconsin, 8701 Watertown Plank Rd, PO Box 26509, Milwaukee, WI 53226 USA. 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H., 1988, TEST LANGUAGE COMPET WIIG EH, 1990, CRITERION REFERENCED NR 58 TC 4 Z9 4 PU W B SAUNDERS CO-ELSEVIER INC PI PHILADELPHIA PA 1600 JOHN F KENNEDY BOULEVARD, STE 1800, PHILADELPHIA, PA 19103-2899 USA SN 0031-3955 J9 PEDIATR CLIN N AM JI Pediatr. Clin. N. Am. PD JUN PY 2007 VL 54 IS 3 BP 483 EP + DI 10.1016/j.pcl.2007.02.016 PG 25 WC Pediatrics SC Pediatrics GA 187JD UT WOS:000247842800006 PM 17543906 ER PT J AU Herbert, MR Kenet, T AF Herbert, Martha R. Kenet, Tal TI Brain abnormalities in language disorders and in autism SO PEDIATRIC CLINICS OF NORTH AMERICA LA English DT Review ID CORPUS-CALLOSUM SIZE; EVENT-RELATED POTENTIALS; CEREBRAL WHITE-MATTER; NON-SPEECH SOUNDS; DEVELOPMENTAL DYSLEXIA; HEAD CIRCUMFERENCE; SPECTRUM DISORDERS; ASSOCIATION CORTEX; MOTION PERCEPTION; EVOKED POTENTIALS AB It has been speculated that autism and specific language impairment share common underlying neural substrates because of the overlap in language impairment issues and evidence suggesting parallels in other domains and implying a possible shared genetic risk. Anatomically the two sets of disorders have generally been studied using different methodologies, but when identical methodologies have been used substantial similarities have been noted. Functionally there is a growing body of literature suggesting sensory perception abnormalities that have parallels in both conditions and that may be upstream of language abnormalities. Finding upstream mechanisms that impact language and non-language abnormalities in autism and specific language impairment would impact the orientation taken by translational attempts to use science to design treatments. C1 Massachusetts Gen Hosp, Dept Neurol, Charlestown, MA 02129 USA. Harvard Univ, Sch Med, Ctr Child & Adolescent Dev, TRANSCEND Res Program, Medford, MA 02155 USA. RP Herbert, MR (reprint author), Massachusetts Gen Hosp, Dept Neurol, 149 13th St, Charlestown, MA 02129 USA. 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Clin. N. Am. PD JUN PY 2007 VL 54 IS 3 BP 563 EP + DI 10.1016/j.pcl.2007.02.007 PG 22 WC Pediatrics SC Pediatrics GA 187JD UT WOS:000247842800010 PM 17543910 ER PT J AU Chez, MG Dowling, T Patel, PB Khanna, P Kominsky, M AF Chez, Michael G. Dowling, Tim Patel, Pikul B. Khanna, Pavan Kominsky, Matt TI Elevation of tumor necrosis factor-alpha in cerebrospinal fluid of autistic children SO PEDIATRIC NEUROLOGY LA English DT Article ID TNF-ALPHA; BRAIN; AUTOANTIBODIES; ANTIBODIES; DISORDERS; CYTOKINES AB Recent reports implicating elevated cytokines in the central nervous system in a small number of patients studied with autism have reported clinical regression. These studies have not focused on tumor necrosis factor-alpha as a possible marker for inflammatory damage. A series of 10 children with autism had clinical evaluation of their serum and spinal fluid for inflammatory changes and possible metabolic disease as part of their neurological evaluation. Elevation of cerebrospinal fluid levels of tumor necrosis factor-alpha was significantly higher (mean 1.04.10 pg/mL) than concurrent serum levels (mean 2.78 pg/mL) in all of the patients studied. The ratio of the cerebrospinal fluid levels to serum levels averaged 53.7:1. This ratio is significantly higher than the elevations reported for other pathological states for which cerebrospinal fluid and serum tumor necrosis factor-alpha levels have been simultaneously measured. This observation may offer a unique insight into central nervous system inflammatory mechanisms that may contribute to the onset of autism and may serve as a potential clinical marker. More controlled study of this potentially important observation may prove valuable. (c) 2007 by Elsevier Inc. All rights reserved. C1 Rosalind Franklin Univ, Dept Neurol, Chicago Med Sch, N Chicago, IL USA. Sutter Hosp, Sutter Neurosci Inst, Sacramento, CA USA. Illinois State Univ, Dept Educ Psychol, Normal, IL 61761 USA. 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Neurol. PD JUN PY 2007 VL 36 IS 6 BP 361 EP 365 DI 10.1016/j.pediatrneurol.2007.01.012 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 183AE UT WOS:000247544300002 PM 17560496 ER PT J AU Parikh, NA Lasky, RE Kennedy, KA Tyson, JE AF Parikh, Nehal A. Lasky, Robert E. Kennedy, Kathleen A. Tyson, Jon E. TI Early autism identification - In reply SO PEDIATRICS LA English DT Letter ID MEDICAL HOME C1 New York Med Coll, Dept Pediat, New York, NY 10029 USA. Kennedy Krieger Inst, Div Neurol & Dev Med, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21287 USA. RP Parikh, NA (reprint author), New York Med Coll, Dept Pediat, New York, NY 10029 USA. CR *AM AC PED, 2005, AAP NEWS, V26, P34 Sia CJ, 2002, PEDIATRICS, V110, P184 Sandler AD, 2001, PEDIATRICS, V107, P1155 Duby JC, 2006, PEDIATRICS, V118, P405, DOI 10.1542/peds.2006-1231 Jacobson J, 1998, BEHAV INTERVENT, V13, P201, DOI DOI 10.1002/(SICI)1099-078X National Research Council, 2001, ED CHILDR AUT OLLEY JG, 2005, HDB AUTISM PERVASIVE, P863 NR 7 TC 0 Z9 0 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUN PY 2007 VL 119 IS 6 BP 1253 EP 1254 DI 10.1542/peds.2007-0725 PG 8 WC Pediatrics SC Pediatrics GA 174NL UT WOS:000246948900040 ER PT J AU Pivalizza, PJ AF Pivalizza, Penelope J. TI Early autism identification SO PEDIATRICS LA English DT Letter ID CHILDREN C1 Baylor Coll Med, Houston, TX 77030 USA. Texas Childrens Hosp, Houston, TX 77030 USA. RP Pivalizza, PJ (reprint author), Baylor Coll Med, Houston, TX 77030 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Duby JC, 2006, PEDIATRICS, V118, P405, DOI 10.1542/peds.2006-1231 Gupta VB, 2007, PEDIATRICS, V119, P152, DOI 10.1542/peds.2006-2026 NR 3 TC 1 Z9 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD JUN PY 2007 VL 119 IS 6 BP 1253 EP 1253 DI 10.1542/peds.2007-0509 PG 1 WC Pediatrics SC Pediatrics GA 174NL UT WOS:000246948900039 PM 17545403 ER PT J AU Jobe, LE White, SW AF Jobe, Lisa E. White, Susan Williams TI Loneliness, social relationships, and a broader autism phenotype in college students SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE autism; Asperger's syndrome; friendships; dating; personality; autism phenotype; Autism Spectrum Quotient ID SPECTRUM QUOTIENT AQ; ADOLESCENCE; CHILDREN; SCALE AB Impaired social functioning is a hallmark of autism spectrum conditions. The purpose of this study was to investigate possible relationship between social functioning and a broader autism phenotype. With a sample of non-clinical undergraduate students from a large, urban university (N = 97; mean age = 19.4 +/- 2 years), characteristics associated with autism were measured as well as self-reported dating and friendship history, feelings of loneliness, and social motivation. Results indicate that those individuals with a stronger autism phenotype (e.g., rigidity, preference for sameness, high attention to detail) report significantly more loneliness (r =.52, p < 0.01) and fewer and shorter duration friendships. Also, for participants in romantic relationships, a stronger phenotype was moderately and positively correlated with length of relationship (r = .34, p < 0.05). Findings support the view that individuals with characteristics of autism and related conditions do not necessarily prefer aloneness, as once assumed, but rather experience increased levels of loneliness related to lack of social skill and understanding. Significance and limitations of these findings are discussed and future directions for research and possibilities for social skills training in this population are explored. (c) 2006 Elsevier Ltd. All rights reserved. C1 Virginia Commonwealth Univ, Sch Med, Richmond, VA 23284 USA. RP Jobe, LE (reprint author), Virginia Commonwealth Univ, Sch Med, Richmond, VA 23284 USA. 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Individ. Differ. PD JUN PY 2007 VL 42 IS 8 BP 1479 EP 1489 DI 10.1016/j.paid.2006.10.021 PG 11 WC Psychology, Social SC Psychology GA 174GH UT WOS:000246929700004 ER PT J AU Carr, JE LeBlanc, LA AF Carr, James E. LeBlanc, Linda A. TI Autism spectrum disorders in early childhood: An overview for practicing physicians SO PRIMARY CARE LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; INTENSIVE BEHAVIORAL TREATMENT; HYPERBARIC-OXYGEN THERAPY; FOLLOW-UP; SLEEP PROBLEMS; GASTROINTESTINAL SYMPTOMS; RUBELLA VACCINATION; MENTAL-RETARDATION; MODIFIED CHECKLIST; MMR VACCINATION AB Autism spectrum disorders (ASDs) affect approximately 1 in 166 children in the United States, making it likely for the average physician to encounter patients with ASDs in his or her practice. In particular, pediatricians and developmental neurologists play a critical role in early identification, resource referrals, and management of a variety of comorbid physical and medical concerns. This article reviews the current literature on ASDs and provides recommendations for practice in areas critical to the provision of medical services. C1 Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. RP Carr, JE (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. 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The IIH suggests that individuals with efficient inhibition skills perform better on working memory tasks because they are able to keep out irrelevant information from working memory. Children with SLI show processing capacity limitations. This study examined whether the working memory limitations are impacted by inhibition problems in this population. Working memory capacity was measured with a listening span task and children's inhibition errors were categorized. These errors reflected either immediate or delayed inhibition problems and they indicated either contextual distractions or perseverations. Children with SLI produced more inhibition errors than their peers in most categories. The results show an association between inhibition control and working memory capacity, but the direction of causality is not clear. C1 CUNY Brooklyn Coll, Brooklyn, NY 11210 USA. CUNY, New York, NY 10021 USA. Eotvos Lorand Univ, H-1364 Budapest, Hungary. 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Queens Coll, London, England. RP Koegel, LK (reprint author), Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. CR Asperger H., 1944, AUTISM ASPERGER SYND WING L, 1981, PSYCHOL MED, V11, P115 NR 2 TC 0 Z9 0 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SUM PY 2007 VL 32 IS 2 BP 87 EP 88 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 211QG UT WOS:000249537800001 ER PT J AU Klin, A Danovitch, JH Merz, AB Volkmar, FR AF Klin, Ami Danovitch, Judith H. Merz, Amanda B. Volkmar, Fred R. TI Circumscribed interests in higher functioning individuals with autism spectrum disorders: An exploratory study SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE Asperger syndrome; autism; restricted; interests; circumscribed interests ID ASPERGER-SYNDROME; CHILDREN; OBSESSIONS; BEHAVIORS; COGNITION; DOMAINS; TASK AB Circumscribed interests are a fascinating and an understudied phenomenon in some individuals with autism spectrum disorders (ASD). Research in this area is likely to contribute to our understanding of ASDs and to advancing developmental knowledge on learning processes used to adapt to the demands of everyday social life. This study reports on a survey of special interests in 96 children and adolescents with higher functioning ASD. The survey included listing of up to three special interests for each child, and the rating of level of interference of a given interest upon children's activities when by themselves and when in contact with family members, peers, and other adults. This information was collected for both preschool and elementary school years. Special interests were classified into eight categories in terms of their nature (rather than topic), which included the ways through which the interest was manifest and pursued. Results indicated that circumscribed interests (a) are the norm rather than the exception in this population (75 % and 88 % of the sample for the younger and the older age periods, respectively), (b) most frequently involve verbal learning and memorization of facts (65 % and 81 % for the younger and the older age periods, respectively), (c) often involve an element of interest in letters and numbers in the preschool years (35% of the sample), (d) greatly interfere with activities pursued by oneself or with others, and (e) level of interference is predictive of lower social and communicative adaptive behavior later in life. Given the ubiquity of circumscribed interests in this population, their verbal nature, and the passion that children with ASD invest in these pursuits, we suggest the need for studies that will trace the longitudinal course of learning profiles from early childhood and possible interventions that may address these areas. 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Kasari, Connie Freeman, Stephanny Paparella, Tanya TI The acquisition and generalization of joint attention and symbolic play skills in young children with autism SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE joint attention; symbolic play; naturalistic teaching methods; autism ID PRESCHOOL-CHILDREN; BEHAVIOR; DEFICITS AB For children with autism, acquiring and generalizing new skills can be particularly difficult and may be affected by child characteristics. Forty-one preschool children with autism were recruited from an existing early intervention program and then randomized to one of two treatments, a targeted intervention for symbolic play skills or one for joint attention skills. Interventions involved Applied Behavior Analysis (ABA) approaches, in two teaching contexts that included similar prompt hierarchies, natural rewards (access to item), expansion, and corrective feedback. However, in the first ABA context, Naturalistic 1, the children sat at the table. Components, such as scaffolding in play, greater pause times, and imitation of the child were included in the second ABA context, Naturalistic H. Mastery of children's first treatment goal was analyzed, and results indicate that children with autism generally acquired and mastered their first joint attention or symbolic play skill with the Naturalistic I approach before generalizing the skill to novel objects and activities to the Naturalistic II context. However, these findings are qualified by teaching domain and child characteristics. Overall, children had an easier time learning play skills than joint attention skills, but the mastery using the Naturalistic I methods was greater for play skills than for joint attention skills. Finally, children with higher mental and language ages reached performance mastery criteria faster than children with lower scores. 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Pract. Pers. Sev. Disabil. PD SUM PY 2007 VL 32 IS 2 BP 101 EP 109 PG 9 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 211QG UT WOS:000249537800003 ER PT J AU Carr, EG AF Carr, Edward G. TI Social skills that are not always social and problems that are not always problems SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Editorial Material DE autism; social skills; problem behavior; social motivation; idiosyncratic interests ID BEHAVIOR C1 SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA. RP Carr, EG (reprint author), SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA. EM Edward.Carr@sunysb.edu CR Carr EG, 2007, J POSIT BEHAV INTERV, V9, P3, DOI 10.1177/10983007070090010201 Jones E.A., 2004, FOCUS AUTISM OTHER D, V19, P13, DOI 10.1177/10883576040190010301 JONES EA, 2007, BEHAV MODIF, V30, P782 Klin A, 2007, RES PRACT PERS SEV D, V32, P89 Koegel R. L., 2006, PIVOTAL RESPONSE TRE McLaughlin DM, 2005, J POSIT BEHAV INTERV, V7, P68 Rogers SJ, 2000, J AUTISM DEV DISORD, V30, P399, DOI 10.1023/A:1005543321840 Wong CS, 2007, RES PRACT PERS SEV D, V32, P101 NR 8 TC 1 Z9 1 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SUM PY 2007 VL 32 IS 2 BP 110 EP 111 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 211QG UT WOS:000249537800004 ER PT J AU Mcgee, GG Daly, T AF McGee, Gail G. Daly, Teresa TI Incidental teaching of age-appropriate social phrases to children with autism SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE autism; social communication; language instruction ID ACQUISITION; AFFECTION AB Successful inclusion is facilitated when children with autism fit in and interact in meaningful ways with their typical peers. However, deficits in conversational language likely limit the social attractiveness of children with autism to their classmates. This study evaluated an incidental teaching approach to promoting use of age-appropriate social phrases by three preschool-aged boys with autism. A multiple baseline design demonstrated that introduction of incidental teaching yielded immediate use of the targeted social phrases ("All right" and "You know what?") during instructional sessions, and children transferred use of the new social phrases to unprompted conditions. Initial instruction required somewhat artificial stimulus-response relationships to compensate for the lack of responsiveness to social consequences that characterizes autism. However, as in other studies in which conversational language was successfully taught to children with autism, systematic fading procedures facilitated transfer of stimulus control from the contrived cues needed to teach a child with autism to say age-appropriate social phrases to conditions that call for comments and queries in everyday situations. C1 Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Emory Autism Ctr, Atlanta, GA 30322 USA. RP Mcgee, GG (reprint author), Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Emory Autism Ctr, 1551 Shoup Court, Atlanta, GA 30322 USA. 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TI The modifier model of autism and social development in higher functioning children SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Review DE phenotypic variability; comorbity; self-monitoring; motivation and attributional processes; autism ID ERROR-RELATED NEGATIVITY; MEDIAL-FRONTAL-CORTEX; ASPERGER-SYNDROME; SEROTONIN TRANSPORTER; SPECTRUM DISORDERS; CHILDHOOD AUTISM; BEHAVIORAL-INHIBITION; ANTERIOR CINGULATE; PSYCHIATRIC-DISORDERS; BRAIN ACTIVATION AB The study of phenotypic variability in social impairments and comorbid emotional disorders in autism is important because it provides information on phenotypic differences that currently complicate diagnosis, research, and treatment of this disorder Currently, though, relatively little is known about the processes that contribute to individual differences in social impairments and comorbidity in autism. In this paper, we present a model that suggests modifier processes (MPs), which are not necessarily specific to the syndrome, refract or alter the expression of autism and contribute to fundamental behavioral and psychological differences in children diagnosed with this disorder One MPs involves the somewhat surprising tendency of some children with higher functioning autism (HFA) to make attributions about other peoples thoughts, although they have social cognitive deficits. Just as in other children, the attributions of children with HFA are linked to some of their behavioral problems. Another MP involves the influence of differences in motivation associated with the behavioral activation and inhibition systems that can be assessed with measures of anterior EEG asymmetry. This dimension of motivation may be linked to how active but inappropriate and withdrawn children with HFA may appear. Third, differences in the self-monitoring of errors among children with HEA appear to be related to individual differences in IQ and social symptom severity in these children. The possible role of these MPs in diagnostic subgroups and differences in treatment responses among children with HFA are discussed. In addition, the role of MPs in understanding the effects associated with specific genetic functions in autism, such as those associated with the serotonin transporter gene (5-HTTLPR), is discussed. A conclusion of this paper is that the varied expression of autism may require that we understand how autism interacts with other non-syndrome-specific processes that are related to individual differences in all people. C1 Univ Miami, Dept Psychol, Marino Autism Res Inst, Coral Gables, FL 33124 USA. RP Mundy, PC (reprint author), Univ Miami, Dept Psychol, Marino Autism Res Inst, POB 248185 0751, Coral Gables, FL 33124 USA. 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TI Social development in individuals with high functioning autism and Asperger disorder SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Editorial Material DE autism; social behavior; neuroscience; physiological; intervention C1 Univ Calif Santa Barbara, Koegel Autism Ctr, Santa Barbara, CA 93106 USA. RP Koegel, RL (reprint author), Univ Calif Santa Barbara, Koegel Autism Ctr, Santa Barbara, CA 93106 USA. EM koegel@education.ucsb.edu CR Kanner L, 1943, NERV CHILD, V2, P217 Koegel R. L., 2006, PIVOTAL RESPONSE TRE Mcgee GG, 2007, RES PRACT PERS SEV D, V32, P112 Mundy PC, 2007, RES PRACT PERS SEV D, V32, P124 NR 4 TC 3 Z9 3 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SUM PY 2007 VL 32 IS 2 BP 140 EP 141 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 211QG UT WOS:000249537800007 ER PT J AU Bryson, SE Koegel, LK Koegel, RL Openden, D Smith, IM Nefdt, N AF Bryson, Susan E. Koegel, Lynn K. Koegel, Robert L. Openden, Daniel Smith, Isabel M. Nefdt, Nicolette TI Large scale dissemination and community implementation of pivotal response treatment: Program description and preliminary data SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE pivotal response treatment; autism; parent education; trainer-of-trainer; translational research; early intervention; systems change ID NONVERBAL AUTISTIC-CHILDREN; PRESCHOOL-CHILDREN; YOUNG-CHILDREN; BEHAVIORAL TREATMENT; PARENT EDUCATION; EARLY INTERVENTION; PARTNERSHIPS; DISORDERS; SUPPORT; AGE AB This paper describes a collaborative effort aimed at province-wide dissemination and implementation of pivotal response treatment (PRT) for young children with autism spectrum disorder (ASD) in Nova Scotia, Canada. Three critical components of the associated training model are described (1) direct training of treatment teams (parents, one-to-one interventionists, and clinical supervisors/ leaders); (2) training of trainers, and (3) follow-up and monitoring of treatment fidelity and child progress. A major goal of the Dalhousie University/IWK Health Centre-University of California at Santa Barbara partnership was to optimize effectiveness when translating PRT from the "lab" for dissemination in large geographical areas with community service providers. Finally, we provide data on stakeholder satisfaction with the training workshops and end by identifying features that may have contributed to our success thus far. C1 IWK Hlth Ctr, Halifax, NS B3K 6R8, Canada. Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. RP Bryson, SE (reprint author), IWK Hlth Ctr, 5850 Univ Ave, Halifax, NS B3K 6R8, Canada. 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PD SUM PY 2007 VL 32 IS 2 BP 142 EP 153 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 211QG UT WOS:000249537800008 ER PT J AU McMahon, CR Malesa, EE Yoder, PJ Stone, WL AF McMahon, Caitlin R. Malesa, Elizabeth E. Yoder, Paul J. Stone, Wendy L. TI Parents of children with autism spectrum disorders have merited concerns about their later-born infants SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Article DE parent concerns; autism; siblings; infant development; cognitive development ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNGER SIBLINGS; BEHAVIOR; IDENTIFICATION; COMMUNICATION; MANAGEMENT; INTERVIEW; LANGUAGE; VALIDITY; VERSION AB Infant siblings of children with autism spectrum disorders (ASD) are at elevated risk for social, cognitive, and language delays which may cause parents to become hypervigilant (i.e., excessively worried) about their infant's development. The extent to which parental concern is related to actual cognitive or language impairment in these infants is currently unknown. This study compared the developmental concerns of two groups of parents: those whose infants have an older sibling with ASD (Sibs-ASD) and those whose infants have an older sibling with typical development (Sibs-TD). The association between parental concerns and infant's actual cognitive and language levels was also examined within and across groups. Forty-nine Sibs-ASD and 27 Sibs-TD, ages 12-24 months, participated in this study. Results revealed that parents of Sibs-ASD had higher levels of concern about their infant's development than did parents of Sibs-TD. 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Pract. Pers. Sev. Disabil. PD SUM PY 2007 VL 32 IS 2 BP 154 EP 160 PG 7 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 211QG UT WOS:000249537800009 ER PT J AU Dunlap, G AF Dunlap, Glen TI Some thoughts on the evolving arena of autism services SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Editorial Material DE autism; families; systems change ID YOUNG-CHILDREN; BEHAVIOR C1 Univ S Florida, Dept Child & Family Studies, Div Appl Res & Educ Support, Reno, NV 89509 USA. RP Dunlap, G (reprint author), Univ S Florida, Dept Child & Family Studies, Div Appl Res & Educ Support, 2778 Mayberry Dr, Reno, NV 89509 USA. 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P., 2001, FAMILIES PROFESSIONA WOLF MM, 1965, BEHAV RES THER, V3, P113 NR 18 TC 1 Z9 1 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD SUM PY 2007 VL 32 IS 2 BP 161 EP 163 PG 3 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 211QG UT WOS:000249537800010 ER PT J AU Guevara-Campos, J Guevara, LG AF Guevara-Campos, J. Gonzalez-de Guevara, L. TI Landau-Kleffner syndrome: An analysis of 10 cases in Venezuela SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE ACTH; aphasia; autism; epilepsy; epileptic status; Landau-Kleffner syndrome ID ELECTRICAL STATUS EPILEPTICUS; SLOW-WAVE SLEEP; ACQUIRED APHASIA; CONVULSIVE DISORDER; CONTINUOUS SPIKE; EEG; EPILEPSY; CHILDREN; ENCEPHALOPATHY; REGRESSION AB Introduction. Landau-Kleffner syndrome is characterised by acquired aphasia and encephalographic alterations that may or may not be accompanied by epileptic seizures. Aim. To analyse the clinical and encephalographic features and response to treatment of 10 patients with Landau-Kleffner syndrome. Patients and methods. We reviewed the patient records, encephalograms and treatment administered to patients catalogued as having Landau-Meffner syndrome. Results. The mean age of the patients was 44 months. Of these cases, 60% presented epilepsy when the diagnosis was established and 70% were found to have epileptic status during slow-wave sleep in the encephalographic study. Results showed that 40% corresponded to variants of Landau-Kleffner syndrome. No cause of the disease could be established in any of the patients. In the neuroimaging study, only one patient displayed abnormalities in the magnetic resonance imaging of the brain. All the patients received adrenocorticotropic hormone (ACTH)-based treatment, at a dose of 1 IU/kg/day for one month, administered together with antiepileptic drugs,such as valproic acid and clobazam. Convulsive seizures and epileptic status during slow-wave sleep disappeared in all the patients. In the patients without epileptic status, epileptic activity became lessfrequent, although it did not completely disappear Aphasia improved considerably, which meant that all the patients were able to enrol in normal schools. Conclusions. We believe that early diagnosis, together with suitable and timely management of aphasic patients with encephalographic alterations that allow ACTH to be used at low doses, make it possible to offer an early education so as to provide maximum recovery from the disease. C1 Ctr Clin Cientif Esperanza Paraco, Unidad Epilepsia & Encefalografia, El Tigre Anzoategui, Venezuela. 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Neurologia PD JUN 1 PY 2007 VL 44 IS 11 BP 652 EP 656 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 181AP UT WOS:000247409400004 PM 17557221 ER PT J AU Muraru, O Honjo, S Murase, S Kaneko, H Nomura, K Ishii, T Koishi, S Ishikawa, N Ozaki, N AF Muraru, Oana Honjo, Shuji Murase, Satomi Kaneko, Hitoshi Nomura, Kenji Ishii, Takashi Koishi, Seiji Ishikawa, Naoko Ozaki, Norio TI The aggressive behavior of autistic patients. Some general considerations SO ROMANIAN JOURNAL OF LEGAL MEDICINE LA Rumanian DT Article DE autism; aggressive behavior ID ANTISOCIAL-BEHAVIOR; FRONTAL-CORTEX; AMYGDALA; SEROTONIN; INJURY; SYSTEM AB The present paper addresses the particularities of aggressive behavior, characteristic to autistic patients. The neuroanatomical and physiological mechanisms that regulate aggressiveness in normal population are briefly presented. Then we describe the particular disturbances of these mechanisms induced by autistic pathology and their behavioral consequences. We also briefly review the main theories that explain human aggressive behavior, particularizing the discussion for autistic aggressive behavior. Our intention is to identify the factors that are responsible for the development of autistic aggressive behavior. This might be useful in order to correctly interpret the autistic aggressiveness and to prevent it from becoming a chronic manifestation. C1 [Muraru, Oana; Nomura, Kenji; Ishii, Takashi; Koishi, Seiji; Ishikawa, Naoko; Ozaki, Norio] Nagoya Univ, Grad Sch Med, Dept Psychiat Parents & Children, Showa Ku, Nagoya, Aichi 4668555, Japan. [Honjo, Shuji; Murase, Satomi; Kaneko, Hitoshi] Nagoya Univ, Ctr Dev Clin Psychol & Psychiat, Nagoya, Aichi 4668555, Japan. RP Muraru, O (reprint author), Nagoya Univ, Grad Sch Med, Dept Psychiat Parents & Children, Showa Ku, 65 Tsurumai Cho, Nagoya, Aichi 4668555, Japan. 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J. Leg. Med. PD JUN PY 2007 VL 15 IS 2 BP 127 EP 134 PG 8 WC Medicine, Legal SC Legal Medicine GA 311GW UT WOS:000256589700009 ER PT J AU Pelphrey, KA Morris, JP McCarthy, G Labar, KS AF Pelphrey, Kevin A. Morris, James P. McCarthy, Gregory Labar, Kevin S. TI Perception of dynamic changes in facial affect and identity in autism SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE LA English DT Article DE autism; amygdala; emotion; face processing; fMRI ID FUSIFORM FACE AREA; SPECTRUM DISORDER; ASPERGER-SYNDROME; SOCIAL-PERCEPTION; CHILDS APPRAISAL; FUNCTIONAL MRI; EMOTION; EXPRESSIONS; RECOGNITION; BRAIN AB Despite elegant behavioral descriptions of abnormalities for processing emotional facial expressions and biological motion in autism, identification of the neural mechanisms underlying these abnormalities remains a critical and largely unmet challenge. We compared brain activity with dynamic and static facial expressions in participants with and without high-functioning autism using event-related functional magnetic resonance imaging (fMRI) and three classes of face stimuli-emotion morphs (fearful and angry), identity morphs and static images (fearful, angry and neutral). We observed reduced activity in the amygdala (AMY) and fusiform gyrus (FFG) to dynamic emotional expressions in people with autism. There was also a lack of modulation by dynamic compared with static emotional expressions of social brain regions including the AMY, posterior superior temporal sulcus (STS) region and FFG. We observed equivalent emotion and identity morph-evoked activity in participants with and without autism in a region corresponding to the expected location of the more generally motion-sensitive area MT or V5. 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TI Measuring expressive language growth in young children with autism spectrum disorders SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID CURRICULUM-BASED MEASUREMENT; CHILDHOOD SPECIAL-EDUCATION; GENERAL OUTCOME MEASURE; INTERVENTION PROGRAMS; PRESCHOOL-CHILDREN; VARIABLES; TODDLERS; INFANTS AB This study explored the use of the Picture Naming Individual Growth and Development Indicator (Picture Naming IGDI; Early Childhood Research Institute on Measuring Growth and Development [ECRI-MGD], 1998) with 11 preschoolers who have autism spectrum disorders (ASD). Children completed the Picture Naming IGDI on 7 occasions in 12 weeks. Results indicated Picture Naming was both a valid and reliable measure of language skills for young children with ASD. Hierarchical linear modeling revealed Picture Naming was sensitive to growth for children with ASD between 39 and 69 months old. 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PD SUM PY 2007 VL 27 IS 2 BP 110 EP 118 DI 10.1177/02711214070270020101 PG 9 WC Education, Special SC Education & Educational Research GA 225XE UT WOS:000250550700004 ER PT J AU Zeng, XK Sun, MK Liu, L Chen, F Wei, LC Xie, W AF Zeng, Xiankun Sun, Mingkuan Liu, Li Chen, Fading Wei, Liuchan Xie, Wei TI Neurexin-1 is required for synapse formation and larvae associative learning in Drosophila SO FEBS LETTERS LA English DT Article ID ALPHA-NEUREXINS; NERVOUS-SYSTEM; AUTISM; GENES; NEUROLIGINS; BINDING; PROTEIN; NLGN4 AB Neurexins are highly polymorphic cell-surface adhesive molecules in neurons. In cultured mammalian cell system, they were found to be involved in synaptogenesis. Here, we report for the first time that Drosophila neurexin is required for synapse formation and associative learning in larvae. Drosophila genome encodes a single functional neurexin (CG7050; Neurexin-1 or Nrx-1), which is a homolog of vertebrate a-neurexin. Neurexin-1 is expressed in central nervous system and highly enriched in synaptic regions of the ventral ganglion and brain. Neurexin-1 null mutants are viable and fertile, but have shortened lifespan. The synapse number is decreased in central nervous system in Neurexin-1 null mutants. In addition, Neurexin-1 null mutants exhibit associative learning defect in larvae. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. C1 SE Univ, Sch Med, Dept Genet & Dev Biol,Minist Educ, Genet Res Ctr,Key Lab Dev Genes & Human Dis, Nanjing 210009, Jiangsu Prov, Peoples R China. RP Xie, W (reprint author), SE Univ, Sch Med, Dept Genet & Dev Biol,Minist Educ, Genet Res Ctr,Key Lab Dev Genes & Human Dis, 87 Dingjiaqiao Rd, Nanjing 210009, Jiangsu Prov, Peoples R China. 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PD MAY 29 PY 2007 VL 581 IS 13 BP 2509 EP 2516 DI 10.1016/j.febslet.2007.04.068 PG 8 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 176LW UT WOS:000247087600021 PM 17498701 ER PT J AU McInnes, LA Ouchanov, L Nakamine, A Jimenez, P Esquivel, M Fallas, M Monge, S Bondy, P Manghi, ER AF McInnes, Lynne A. Ouchanov, Leonid Nakamine, Alisa Jimenez, Patricia Esquivel, Marcela Fallas, Marietha Monge, Silvia Bondy, Pamela Manghi, Elina R. TI The NRGI exon II missense variant is not associated with autism in the Central Valley of Costa Rica SO BMC PSYCHIATRY LA English DT Article ID 22Q11.2 DELETION SYNDROME; SCHIZOPHRENIA; NEUREGULIN-1; SYMPTOMS; CHILDREN AB Background: We are conducting a genetic study of autism in the isolated population of the Central Valley of Costa Rica (CVCR). A novel Neuregulin 1 (NRG1) missense variant ( exon 11 G > T) was recently associated with psychosis and schizophrenia (SCZ) in the same population isolate. Methods: We genotyped the NRG1 exon 11 missense variant in 146 cases with autism, or autism spectrum disorder, with CVCR ancestry, and both parents when available (N = 267 parents) from 143 independent families. Additional microsatellites were genotyped to examine haplotypes bearing the exon 11 variant. Results: The NRG1 exon 11 G> T variant was found in 4/146 cases including one de novo occurrence. The frequency of the variant in case chromosomes was 0.014 and 0.045 in the parental non-transmitted chromosomes. At least 6 haplotypes extending 0.229 Mb were associated with the T allele. Three independent individuals, with no personal or family history of psychiatric disorder, shared at least a 1 megabase haplotype 5' to the T allele. Conclusion: The NRG1 exon 11 missense variant is not associated with autism in the CVCR. 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Y. Davies, William TI The 39,XO mouse as a model for the neurobiology of Turner syndrome and sex-biased neuropsychiatric disorders SO BEHAVIOURAL BRAIN RESEARCH LA English DT Review DE ADHD; amygdala; autism; brain; genomic imprinting; haploinsufficiency; X-inactivation; X chromosome ID DEFICIT HYPERACTIVITY DISORDER; PREMATURE OVARIAN FAILURE; MUS-MUSCULUS L; PAR X-GENE; COGNITIVE FUNCTION; IMPRINTED GENES; WORKING-MEMORY; FRAGILE-X; NEURODEVELOPMENTAL CHANGES; FUNCTIONAL NEUROANATOMY AB Turner syndrome (TS) is a developmental disorder most frequently arising from the loss of a complete X chromosome (karyotype 45,XO). The disorder is characterised by physiological abnormalities (notably short stature and ovarian dysfunction), emotional anomalies (including heightened anxiety) and by a neuropsychological profile encompassing deficits in visuospatial skills, memory, attention, social cognition and emotion recognition. Moreover, TS subjects are at significantly increased risk of developing attention deficit hyperactivity disorder (ADHD) and autism. At the neuroanatomical level, TS subjects display abnormalities across a number of brain structures, including the amygdala, hippocampus and orbitofrontal cortex. The TS phenotype arises due to reduced dosage of X-linked genes, and may also be modulated by parental origin of the single X chromosome. In this review, we discuss the utility of a mouse model of TS, the 39,XO mouse, in which the parental origin of the single X chromosome can be varied. This model provides the opportunity to investigate the effects of X-linked gene dosage/parent-of-origin effects on neurobiology in the absence of gross physiological abnormalities. Initial findings indicate that several features of the TS behavioural phenotype may be accurately recapitulated in the mouse. 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To determine the gestational time window when stress exposure produces the greatest impact on cognition, dams were exposed to chronic variable stress (CVS) early, mid-, or late in gestation and offspring learning performance and navigation strategies assessed. These studies utilized a modified version of the Barnes maze to allow investigation of coping responses to stress stimuli. In our study, males exposed to early gestational stress showed significantly impaired learning performance, requiring twice as long to locate the target following training. In stark contrast, early prenatal stress enhanced female performance, where these females located the target in a quarter of the time required by controls. Differences in search strategies whether cued, random, or serial accounted for divergent performances between sex and CVS groups. While control males' behavior expectedly evolved to a cued strategy, the early stressed offspring continued to rely on serial and random searching. 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Behav. PD MAY 16 PY 2007 VL 91 IS 1 BP 55 EP 65 DI 10.1016/j.physbeh.2007.01.017 PG 11 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA 171NT UT WOS:000246743400008 PM 17367828 ER PT J AU Smith, A Yarwood, J Salisbury, DM AF Smith, Alan Yarwood, Joanne Salisbury, David M. TI Tracking mothers' attitudes to MMR immunisation 1996-2006 SO VACCINE LA English DT Article DE immunisation; MMR; attitudes; media ID RUBELLA VACCINE; MEASLES-VIRUS; MUMPS; CHILDREN; PARENTS; SCHEDULE; DISORDER; COVERAGE; BLOOD; UK AB This paper presents the findings of surveys that have tracked mothers' attitudes towards MMR over the period 1996-2006. The main aim was to demonstrate how attitudes in relation to MMR have evolved over the last 10 years incorporating the periods of time before, during and after the height of the MMR controversy within the UK. MMR vaccine remains the number one 'top of mind' vaccination issue for parents. The proportion of parents believing MMR to be a greater risk than the diseases it protects against has fallen from 24% in 2002 to 14% in 2006. The proportion of 'hard-core rejectors' of MMR vaccine remains stable at 6%. There has been a gradual and sustained increase in the proportion of parents across all social groups saying MMR was completely safe/slight risk rising from 60% in 2002 to a current level of 74%. There now appears to be a sustained move away from fears over MMR safety and belief in the unfounded link to autism towards a more positive perception of the vaccine. (C) 2007 Elsevier Ltd. All rights reserved. C1 Dept Hlth, Immunisat Policy Monitoring & Surveillance, London SE1 8UG, England. RP Salisbury, DM (reprint author), Dept Hlth, Immunisat Policy Monitoring & Surveillance, Wellington House,133-155 Waterloo Rd, London SE1 8UG, England. 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Eng. News PD MAY 14 PY 2007 VL 85 IS 20 BP 32 EP 35 DI 10.1021/cen-v085n020.p032 PG 4 WC Chemistry, Multidisciplinary; Engineering, Chemical SC Chemistry; Engineering GA 168UD UT WOS:000246548600039 ER PT J AU Fernell, E Karagiannakis, A Edman, G Bjerkenstedt, L Wiesel, FA Venizelos, N AF Fernell, Elisabeth Karagiannakis, Aristea Edman, Gunnar Bjerkenstedt, Lars Wiesel, Frits-Axel Venizelos, Nikolaos TI Aberrant amino acid transport in fibroblasts from children with autism SO NEUROSCIENCE LETTERS LA English DT Article DE autism; amino acid transport; fibroblasts; tyrosine; alanine ID PERVASIVE DEVELOPMENTAL DISORDERS; TISSUE EXPRESSION PATTERN; TYROSINE TRANSPORT; FUNCTIONAL-CHARACTERISTICS; SYSTEM; SCHIZOPHRENIA; BRAIN; CHILDHOOD; PHENYLKETONURIA; ATTENTION AB Autism is a developmental, cognitive disorder clinically characterized by impaired social interaction, communication and restricted behaviours. The present study was designed to explore whether an abnormality in transport of tyrosine and/or alanine is present in children with autism. Skin biopsies were obtained from 11 children with autism (9 boys and 2 girls) fulfilling the DSM-IV diagnostic criteria for autistic disorder and 11 healthy male control children. Transport of amino acids tyrosine and alanine across the cell membrane of cultured fibroblasts was studied by the cluster tray method. The maximal transport capacity, V-max and the affinity constant of the amino acid binding sites, K-m, were determined. ;Significantly increased V-max, for alanine (p = 0.014) and increased K-m for tyrosine (p = 0.007) were found in children with autism. The increased transport capacity of alanine across the cell membrane and decreased affinity for transport sites of tyrosine indicates the involvement of two major amino acid transport systems (L- and A-system) in children with autism. This may influence the transport of several other amino acids across the blood-brain-barrier. The significance of the findings has to be further explored. (c) 2007 Elsevier Ireland Ltd. All rights reserved. C1 Univ Orebro, Dept Clin Med, SE-70182 Orebro, Sweden. Karolinska Univ Hosp, Dept Neuropaediat, Astrid Lindgren Childrens Hosp, SE-17176 Stockholm, Sweden. Danderyd Hosp, Dept Psychiat, R&D Sect, SE-18287 Danderyd, Sweden. Karolinska Univ Hosp, Dept Clin Neurosci, SE-17176 Stockholm, Sweden. Univ Uppsala Hosp, Dept Neurosci, SE-75017 Uppsala, Sweden. RP Venizelos, N (reprint author), Univ Orebro, Dept Clin Med, SE-70182 Orebro, Sweden. 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PD MAY 10 PY 2007 VL 502 IS 2 BP 309 EP 324 DI 10.1002/cne.21304 PG 16 WC Neurosciences; Zoology SC Neurosciences & Neurology; Zoology GA 156ZO UT WOS:000245688600010 PM 17348015 ER PT J AU Marui, T Koishi, S Funatogawa, I Yamamoto, K Matsumoto, H Hashimoto, O Ishijima, M Nanba, E Nishida, H Sugiyama, T Kasai, K Watanabe, K Kano, Y Kato, N Sasaki, T AF Marui, Tetsuya Koishi, Shinko Funatogawa, Ikuko Yamamoto, Kenji Matsumoto, Hideo Hashimoto, Ohiko Ishijima, Michiko Nanba, Eiji Nishida, Hisami Sugiyama, Toshiro Kasai, Kiyoto Watanabe, Keiichiro Kano, Yukiko Kato, Nobumasa Sasaki, Tsukasa TI No association between the Neuronal Pentraxin II gene polymorphism and autism SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE association study; autistic disorder; chromosome 7q; haplotype block; NPTX2 gene; SNPs ID BINDING PROTEIN 49; TWIN; RECEPTORS; TAIPOXIN; ETIOLOGY; DISORDER; FAMILY; NARP AB Autism (MIM 209850) is a neurodevelopmental disorder characterized by difficulties with verbal and non-verbal communication, impairments in reciprocal social interactions, and displays of stereotypic behaviors, interests and activities. Twin and family studies have indicated a robust role of genetic factors in the development of autism. Neuronal Pentraxin II (NPTX2) is located in chromosome 7q21.3-q22.1, where it is a candidate region for autism. NPTX2 promotes neuritic outgrowth and is suggested to mediate uptake of degraded synaptic material during synapse formation and remodeling. NPTX2 is also associated with the clustering of synaptic AMPA receptors. It was reported that glutamate systems including AMPA receptor was associated to the pathophysiology of autism. Thus, the NPTX2 gene is involved in neuritic outgrowth, synapse remodeling and the aggregation of neurotransmitter receptors at synapses. These functions play an important role in the mechanisms of learning and brain development. In the present study, we tested for the presence of the association of four single nucleotide polymorphisms (SNPs) of NPTX2 and haplotypes consisting of the SNPs with autism, between autistic patients (n = 170) and normal controls (n = 214) in a Japanese population. No significant difference was observed in the allele, genotype or haplotype frequencies between the patients and controls. Thus, the NPTX2 locus is not likely to play a major role in the development of autism. However, further studies with larger sample size and sequencing of NPTX2 gene are needed to exclude a role of NPTX2 gene in autism. (c) 2007 Elsevier Inc. All rights reserved. C1 Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, Tokyo 113, Japan. Aichi Childrens Hlth & Med Ctr, Obu, Japan. Teikyo Univ, Sch Med, Dept Hyg & Publ Hlth, Tokyo 173, Japan. Kitasato Univ, Sch Med, Dept Psychiat, Sagamihara, Kanagawa 228, Japan. Tokai Univ, Sch Med, Dept Psychiat, Isehara, Kanagawa 25911, Japan. Aino Univ, Fac Nursing & Rehabil, Dept Occupat Therapy, Ibaraki, Japan. Tottori Univ, Gene Res Ctr, Yonago, Tottori 683, Japan. Asumaro Hosp Child & Adolescent Psychiat, Tsu, Mie, Japan. Univ Tokyo, Hlth Serv Ctr, Dept Psychiat, Tokyo 106, Japan. RP Marui, T (reprint author), Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, 7-3-1 Hongo, Tokyo 113, Japan. 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Neuro-Psychopharmacol. Biol. Psychiatry PD MAY 9 PY 2007 VL 31 IS 4 BP 940 EP 943 DI 10.1016/j.pnpbp.2007.02.016 PG 4 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 174GW UT WOS:000246931200021 PM 17408830 ER PT J AU Murphy, M AF Murphy, Marina TI PCB link to autism? SO CHEMISTRY & INDUSTRY LA English DT News Item NR 0 TC 0 Z9 0 PU SOC CHEMICAL INDUSTRY PI LONDON PA 14 BELGRAVE SQUARE, LONDON SW1X 8PS, ENGLAND SN 0009-3068 J9 CHEM IND-LONDON JI Chem. Ind. PD MAY 7 PY 2007 IS 9 BP 6 EP 6 PG 1 WC Chemistry, Applied SC Chemistry GA 174IX UT WOS:000246936700005 ER PT J AU Yip, J Soghomonian, JJ Blatt, GJ AF Yip, Jane Soghomonian, Jean-Jacques Blatt, Gene J. TI Decreased GAD67 mRNA levels in cerebellar purkinje cells in autism: pathophysiological implications SO ACTA NEUROPATHOLOGICA LA English DT Article DE glutamic acid decarboxylase (GAD) 67 mRNA; autism; purkinje cells; GABA; pathophysiology ID GLUTAMIC-ACID DECARBOXYLASE; GAMMA-AMINOBUTYRIC-ACID; RECEPTOR SUBUNIT GENES; INSITU HYBRIDIZATION; BIPOLAR DISORDER; MULTIPLE INNERVATION; INFANTILE-AUTISM; CLIMBING FIBERS; HUMAN-BRAIN; 2 FORMS AB The recent identification of decreased protein levels of glutamate decarboxylase (GAD) 65 and 67 isoforms in the autistic cerebellar tissue raises the possibility that abnormal regulation of GABA production in individual neurons may contribute to the clinical features of autism. Reductions in Purkinje cell number have been widely reported in autism. It is not known whether the GAD changes also occur in Purkinje cells at the level of transcription. 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Prospective follow-up of 219 children from preschool age to mid-childhood SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE pervasive developmental disorder; autism; follow-up; prognosis; preschool children; outcome ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING CHILDREN; ADAPTIVE-BEHAVIOR SCALE; AUTISTIC-CHILDREN; INFANTILE PSYCHOSIS; YOUNG-CHILDREN; PREDICTORS; DISABILITIES; CONTINUITY; STABILITY AB Objective: To describe the psychological development of children with pervasive developmental disorders over a period of 3 years and to identify the factors linked to their developmental paths. Method: The study was a collaborative and prospective follow-up study of 219 preschoolers. Retrospective data and enrollment data were collected at the beginning of the study and 3 years later. Results: We observed high variability in the short-term outcomes of preschoolers. 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PD MAY PY 2007 VL 115 IS 5 BP 403 EP 412 DI 10.1111/j.1600-0447.2006.00898.x PG 10 WC Psychiatry SC Psychiatry GA 152VM UT WOS:000245390100010 PM 17430419 ER PT J AU Flanders, SC Engelhart, L Pandina, GJ McCracken, JT AF Flanders, Scott C. Engelhart, Luella Pandina, Gahan J. McCracken, James T. TI Direct health care costs for children with Pervasive Developmental Disorders: 1996-2002 SO ADMINISTRATION AND POLICY IN MENTAL HEALTH AND MENTAL HEALTH SERVICES RESEARCH LA English DT Article DE autism; cost; health care; cost of illness ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; SPECTRUM DISORDER; ECONOMIC BURDEN; AUTISM; PREVALENCE; EXPENDITURES; DISABILITIES; ADOLESCENTS; POPULATION; SERVICES AB We compared direct costs of treatment of Pervasive Developmental Disorder (PDD), asthma, and diabetes in children aged 3-17 years. A retrospective, claims-based study was conducted using the California Medicaid (Medi-Cal) database (1996-2002). Seven hundred and thirty-one children with PDD were identified and matched for sex with an equal number of randomly selected children with asthma and diabetes. Mean total health care costs for PDD were two- to threefold higher than for asthma and diabetes post-diagnosis ($4,815 vs. $1,469 vs. $2,404, respectively, P < 0.0001). Children with PDD incur significantly greater health care costs when compared with children with other chronic pediatric diseases. C1 Ortho McNeil Janssen Sci Affairs LLC, Reg Outcomes Res, Grayslake, IL 60030 USA. Cordis Corp, Hlth Econ & Reimbursement, Warren, NJ 07059 USA. Janssen Pharmaceut Prod LP, Med Affairs Div, CNS Clin Dev, Titusville, NJ 08560 USA. Univ Calif Los Angeles, Inst Neuropsychiat, Dept Child Psychiat, Los Angeles, CA 90095 USA. RP Flanders, SC (reprint author), Ortho McNeil Janssen Sci Affairs LLC, Reg Outcomes Res, 740 Waterford Dr, Grayslake, IL 60030 USA. 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Policy. Ment. Health PD MAY PY 2007 VL 34 IS 3 BP 213 EP 220 DI 10.1007/s10488-006-0098-3 PG 8 WC Health Policy & Services; Public, Environmental & Occupational Health SC Health Care Sciences & Services; Public, Environmental & Occupational Health GA 166MM UT WOS:000246383000003 PM 17082979 ER PT J AU Montes, G Halterman, JS AF Montes, Guillermo Halterman, Jill S. TI Bullying among children with autism and the influence of comorbidity with ADHD: A population-based study SO AMBULATORY PEDIATRICS LA English DT Article DE ADHD; aggression; autism; bullying; child; national surveys; prevalence ID SCHOOL-AGE-CHILDREN; PSYCHOSOCIAL ADJUSTMENT; PREVALENCE; VICTIMIZATION; RISPERIDONE; ADOLESCENTS; CHILDHOOD; BEHAVIORS; DISORDER AB Objective. - Bullying is a significant problem among schoolage children. The prevalence and predictors of bullying among children with autism are not known. The objectives of this population-based study were to: (1) estimate the prevalence of bullying among children with autism in the United States, (2) determine whether the presence of attention-deficit/hyperactivity disorder/attention-deficit disorder (ADHD/ADD) increases prevalence of bullying among children with autism, and (3) determine risk factors of bullying behavior among children with autism. Methods. - The National Survey of Children's Health, 2003 (NSCH), provided nationally representative data for children ages 4 to 17. We used multivariate logistic regression and Wald tests to determine whether children with autism were more likely to bully in the presence of ADHD/ADD. Taylor approximations were used to account for the complex sampling design. Results. - Children with autism had a high prevalence of bullying (44%, 95% confidence interval, 34-55). Parent report of ADHD/ADD appears to moderate the relationship between bullying and autism. Children with autism who did not have ADHD/ ADD were not at greater risk for bullying compared with the general population. Children with autism and ADHD/ADD had increased odds of bullying (odds ratio 4.6, 95% confidence interval 2.4-8.6), even after controlling for household income, age, and gender. In addition to ADHD/ADD, living in a low-income household and younger age were risk factors for bullying among children with autism. Being female, however, did not decrease the risk of bullying in the autistic subpopulation. Conclusions. - Children with autism and ADHD/ADD appear to be at increased risk for bullying behaviors. C1 Univ Rochester, Sch Med & Dent, Childrens Inst, Rochester, NY 14607 USA. Univ Rochester, Sch Med & Dent, Dept Pediat, Strong Childrens Res Ctr, Rochester, NY 14607 USA. RP Montes, G (reprint author), Univ Rochester, Sch Med & Dent, Childrens Inst, 271 Goodman St,Suite D103, Rochester, NY 14607 USA. 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TI Recurrent 10q22-q23 deletions: a genomic disorder on 10q associated with cognitive and behavioral abnormalities SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID RILEY-RUVALCABA-SYNDROME; GENOTYPE-PHENOTYPE CORRELATIONS; SEGMENTAL DUPLICATIONS; COWDEN-SYNDROME; PTEN MUTATION; INTERSTITIAL DELETION; STRUCTURAL VARIATION; JUVENILE POLYPOSIS; DISEASE TRAITS; SCHIZOPHRENIA AB Low-copy repeats (LCRs) are genomic features that affect chromosome stability and can produce disease-associated rearrangements. We describe members of three families with deletions in 10q22.3-q23.31, a region harboring a complex set of LCRs, and demonstrate that rearrangements in this region are associated with behavioral and neurodevelopmental abnormalities, including cognitive impairment, autism, hyperactivity, and possibly psychiatric disease. Fine mapping of the deletions in members of all three families by use of a custom 10q oligonucleotide array-based comparative genomic hybridization (NimbleGen) and polymerase chain reaction - based methods demonstrated a different deletion in each family. In one proband, the deletion breakpoints are associated with DNA fragments containing noncontiguous sequences of chromosome 10, whereas, in the other two families, the breakpoints are within paralogous LCRs, removing similar to 7.2 Mb and 32 genes. Our data provide evidence that the 10q22-q23 genomic region harbors one or more genes important for cognitive and behavioral development and that recurrent deletions affecting this interval define a novel genomic disorder. C1 Univ Minnesota, Dept Genet Cell Biol & Dev, Minneapolis, MN 55455 USA. Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA. Univ Minnesota, Dept Lab Med & Pathol, Minneapolis, MN 55455 USA. Univ Minnesota, Dept Ophthalmol, Minneapolis, MN 55455 USA. 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TI Receptive vocabulary, expressive vocabulary, and speech production of boys with fragile X syndrome in comparison to boys with Down syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID LANGUAGE IMPAIRMENT; CONVERSATIONAL CHARACTERISTICS; DEVELOPMENTAL TRAJECTORIES; AUTISTIC BEHAVIOR; SYNDROME CHILDREN; YOUNG-CHILDREN; MALES; ADOLESCENTS; SKILLS; COMMUNICATION AB Boys with fragile X syndrome with (n = 49) and without (n = 33) characteristics of autism spectrum disorder, boys with Down syndrome (39), and typically developing boys (n = 41) were compared on standardized measures of receptive vocabulary, expressive vocabulary, and speech administered annually over 4 years. Three major findings emerged. Boys with fragile X without autism spectrum disorder did not differ from the younger typically developing boys in receptive and expressive vocabulary and speech production when compared at similar levels of nonverbal cognitive skills. 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PD MAY PY 2007 VL 112 IS 3 BP 177 EP 193 DI 10.1352/0895-8017(2007)112[177:RVEVAS]2.0.CO;2 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 166TU UT WOS:000246404100003 PM 17542655 ER PT J AU Fidler, DJ Hepburn, SL Most, DE Philofsky, A Rogers, SJ AF Fidler, Debbie J. Hepburn, Susan L. Most, David E. Philofsky, Amy Rogers, Sally J. TI Emotional responsivity in young children with Williams syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID TODDLERS; MIND; IMITATION; ATTENTION; LANGUAGE; AUTISM AB The hypothesis that young children with Williams syndrome show higher rates of emotional responsivity relative to other children with developmental disabilities was explored. Performance of 23 young children with Williams syndrome and 30 MA-matched children with developmental disabilities of nonspecific etiologies was compared on an adaptation of Repacholl and Gopnik's (1997) "Yummy-Yucky" task. Results show that children with Williams syndrome were more likely to mimic and/or imitate facial affect and vocalizations than children in the mixed comparison group. Yet, this increased emotional responsivity did not substantially improve decision-making based on the affective display; children with Williams syndrome were more likely to attempt to convince the experimenter that the disliked food was likable. Implications of a social profile that includes enhanced emotional responsivity paired with impaired perspective taking are discussed. C1 Colorado State Univ, Hlth Sci Ctr, Ft Collins, CO 80523 USA. Univ Calif Davis, Med Ctr, Davis, CA 95616 USA. RP Fidler, DJ (reprint author), Colorado State Univ, Hlth Sci Ctr, Ft Collins, CO 80523 USA. EM dfidler@cahs.colostate.edu CR Adamson L. 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PD MAY PY 2007 VL 112 IS 3 BP 194 EP 206 DI 10.1352/0895-8017(2007)112[194:ERIYCW]2.0.CO;2 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 166TU UT WOS:000246404100004 PM 17542656 ER PT J AU Solomon, R Necheles, J Ferch, C Bruckman, D AF Solomon, Richard Necheles, Jonathan Ferch, Courtney Bruckman, David TI Pilot study of a parent training program for young children with autism - The PLAY Project Home Consultation program SO AUTISM LA English DT Article DE autism; DIR model; intervention; parent; training ID BEHAVIORAL TREATMENT; EARLY INTERVENTION; PRESCHOOL-CHILDREN; PREVALENCE; DISORDERS; TRIAL; COMMUNICATION; AGREEMENT; DIAGNOSIS; UK AB The PLAY Project Home Consultation (PPHC) program trains parents of children with autistic spectrum disorders using the DIR/Floortime model of Stanley Greenspan MD. Sixty-eight children completed the 8-12 month program. Parents were encouraged to deliver 15 hours per week of 1: 1 interaction. Pre/post ratings of videotapes by blind raters using the Functional Emotional Assessment Scale (FEAS) showed significant increases (p <= 0.0001) in child subscale scores. Translated clinically, 45.5 percent of children made good to very good functional developmental progress. There were no significant differences between parents in the FEAS subscale scores at either pre-or post-intervention and all parents scored at levels suggesting they would be effective in working with their children. Overall satisfaction with PPHC was 90 percent. Average cost of intervention was $2500/ year. Despite important limitations, this pilot study of The PLAY Project Home Consulting model suggests that the model has potential to be a cost-effective intervention for young children with autism. C1 Northwestern Univ, Feinberg Sch Med, Chicago, IL 60611 USA. Wayne State Univ, Sch Med, Detroit, MI 48202 USA. Dept Publ Hlth, Cleveland, OH USA. Ann Arbor Ctr Dev & Behav Pediat, Ann Arbor, MI USA. 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SO AUTISM LA English DT Article DE assessment; autism; spectrum disorder; autistic; disorder; dyspraxia; gesture; imitation ID ASPERGER-SYNDROME; YOUNG-CHILDREN; DISORDER; IMPAIRMENT; PERFORMANCE; CLUMSINESS; DEFICITS; GESTURE; OBJECT AB This case-control study explores the underlying mechanisms of imitation problems in boys with autism by manipulating imitation task variables and by correlating imitation performance with competence on general motor tests (Movement Assessment Battery for Children and Peabody Developmental Motor Scales). Fifty-five boys participated in this study: eight low-functioning with autism (LFA), 13 with mental retardation (MR), 17 high-functioning with autism (HFA) and 17 typically developing (TD). LFA performed significantly worse than MR on the motor test and on all imitation tasks. HFA performed significantly worse than TD on the motor test, but not on imitation tasks, with the exception of non-meaningful gestures. This study supports the notion that mainly perceptual-motor impairment, and not a cognitive weakness of symbolic representation, causes imitation problems in autism. In addition, in boys with autism, general motor as well as imitation abilities were impaired. We suggest that imitation ability has to be assessed in conjunction with motor competence. C1 Katholieke Univ Leuven, B-3000 Louvain, Belgium. Univ Ghent, B-9000 Ghent, Belgium. Katholieke Univ Leuven, B-3000 Louvain, Belgium. RP Vanvuchelen, M (reprint author), Sterrebos 111, B-3512 Stevoort, Belgium. 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O. Maybery, Murray T. Durkin, Kevin TI Evidence against poor semantic encoding in individuals with autism SO AUTISM LA English DT Article DE autism; memory; phonological encoding; semantic encoding ID HIGH-FUNCTIONING AUTISM; LONG-TERM-MEMORY; ASPERGERS-SYNDROME; SPECTRUM DISORDER; EPISODIC MEMORY; CHILDREN; RECALL; ADULTS; LANGUAGE; CONTEXT AB This article tests the hypothesis that individuals with autism poorly encode verbal information to the semantic level of processing, instead paying greater attention to phonological attributes. Participants undertook a novel explicit verbal recall task. Twenty children with autism were compared with 20 matched typically developing children. On each trial, 20 words were presented individually on a computer screen. Half of the items were related through having either a common semantic theme, or a common phonological feature. Following a filler task, the participants were presented with a cue and asked to recall items consistent with the cue. No differences between the autism and comparison groups were found in either the semantic or the phonological condition. A follow-up comparison revealed that the participants with autism showed comparable levels of recall to an additional group of children matched in chronological age. The findings do not support the-idea of a developmental delay in semantic encoding in children with autism. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. Univ Strathclyde, Glasgow G1 1XQ, Lanark, Scotland. RP Whitehouse, AJO (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. 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The first part of this short article consists of JS's analytical account of his atypical memory abilities, and the strategies he uses for memorizing and learning. JS has also described specific difficulties with creative writing, which are outlined here. The second part of the article consists of an interpretation of the problems JS describes in terms of their implications for understanding the problems of generativity that contribute to the diagnostic impairments of imagination and creativity in autism. C1 Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. RP Boucher, J (reprint author), Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. EM j.boucher@warwick.ac.uk CR Baddeley A, 2000, TRENDS COGN SCI, V4, P417, DOI 10.1016/S1364-6613(00)01538-2 BAUER PJ, 1997, DEV SPANS EVENT COMR Ben Shalom D, 2003, CORTEX, V39, P1129 BOUCHER J, 1976, BRIT J PSYCHOL, V67, P73 Boucher J., 2001, TIME MEMORY, P111 BOUCHER J, 1988, J AUTISM DEV DISORD, V18, P637, DOI 10.1007/BF02211881 BOUCHER J, IN PRESS MEMORY AUTI Bowler DM, 2000, J AUTISM DEV DISORD, V30, P295, DOI 10.1023/A:1005575216176 BRANDT K, 2004, ROLE SUBJECTIVE EXPE Jarrold C, 1996, BRIT J DEV PSYCHOL, V14, P275 LEWIS V, 1991, BRIT J DEV PSYCHOL, V9, P393 LEWIS V, 1995, J AUTISM DEV DISORD, V25, P105, DOI 10.1007/BF02178499 Nelson K., 1986, EVENT KNOWLEDGE STRU Sacks Oliver, 1995, ANTHR MARS SALMOND C, IN PRESS HIGH FUNCTI SCHACTER DL, 1987, PSYCHOBIOLOGY, V15, P21 Tulving Endel, 1985, CANADIAN PSYCHOL, V26, DOI [10.1037/h0080017, DOI 10.1037/H0080017] Turner MA, 1999, J CHILD PSYCHOL PSYC, V40, P189, DOI 10.1017/S0021963098003515 Wheeler MA, 1997, PSYCHOL BULL, V121, P331, DOI 10.1037/0033-2909.121.3.331 YONELINAS AP, 2002, J MEM LANG, V46, P411 Zacks JM, 2001, PSYCHOL BULL, V127, P3, DOI 10.1037//0033-2909.127.1.3 NR 21 TC 11 Z9 11 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAY PY 2007 VL 11 IS 3 BP 255 EP 264 DI 10.1177/1362361307076863 PG 10 WC Psychology, Developmental SC Psychology GA 176EI UT WOS:000247066800005 PM 17478578 ER PT J AU Speer, LL Cook, AE McMahon, WM Clark, E AF Speer, Leslie L. Cook, Anne E. McMahon, William M. Clark, Elaine TI Face processing in children with autism - Effects of stimulus contents and type SO AUTISM LA English DT Article DE autism; eye tracking; face; processing; social; responsiveness ID ASPERGER-SYNDROME; RECOGNITION; INDIVIDUALS; DISORDERS; GAZE AB Recent eye tracking studies of face processing have produced differing accounts of how and whether children with autism differ from their typically developing peers. The two groups' gaze patterns appear to differ for dynamic videos of social scenes, but not for static photos of isolated individuals. The present study replicated and extended previous research by comparing the gaze patterns of individuals with and without autism for four types of stimuli: social dynamic, social static, isolated dynamic, and isolated static. Participants with autism differed from their typically developing peers only for social-dynamic stimuli; fixation durations were decreased for eye regions and increased for body regions. Further, these fixation durations predicted scores on a measure of social responsiveness. These findings reconcile differences in previous reports by identifying the specific social and dynamic task components associated with autism-related face processing impairments. C1 Univ Utah, Dept Educ Psychol, Salt Lake City, UT 84112 USA. RP Cook, AE (reprint author), Univ Utah, Dept Educ Psychol, 1705 Campus Ctr Dr,Room 327, Salt Lake City, UT 84112 USA. EM Anne.Cook@ed.utah.edu CR Adolphs R, 2001, J COGNITIVE NEUROSCI, V13, P232, DOI 10.1162/089892901564289 Baron D, 2002, WIREL NETW, V8, P5, DOI 10.1023/A:1012744023290 BARONCOHEN S, 1989, J AUTISM DEV DISORD, V19, P579, DOI 10.1007/BF02212859 BORMANNKISCHKEL C, 1995, J CHILD PSYCHOL PSYC, V36, P1243, DOI 10.1111/j.1469-7610.1995.tb01368.x BOUCHER J, 1992, J CHILD PSYCHOL PSYC, V33, P843, DOI 10.1111/j.1469-7610.1992.tb01960.x Chawarska K, 2003, CHILD DEV, V74, P1108, DOI 10.1111/1467-8624.00595 Constantino JN, 2005, SOCIAL RESPONSIVENES DiCerbo KE, 2000, J PSYCHOEDUC ASSESS, V18, P344, DOI 10.1177/073428290001800404 Hall GBC, 2003, AM J PSYCHIAT, V160, P1439, DOI 10.1176/appi.ajp.160.8.1439 Hauck M, 1998, CHILD NEUROPSYCHOL, V4, P187, DOI 10.1076/chin.4.3.187.3174 Joseph RM, 2003, J CHILD PSYCHOL PSYC, V44, P529, DOI 10.1111/1469-7610.00142 Klin A, 1999, J AUTISM DEV DISORD, V29, P499, DOI 10.1023/A:1022299920240 Klin A, 2002, ARCH GEN PSYCHIAT, V59, P809, DOI 10.1001/archpsyc.59.9.809 Klin A, 2000, J CHILD PSYCHOL PSYC, V41, P831, DOI 10.1017/S0021963099006101 Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MACDONALD H, 1989, J CHILD PSYCHOL PSYC, V30, P865, DOI 10.1111/j.1469-7610.1989.tb00288.x NICHOLS K, 1998, 30 ANN M NAT ASS SCH Pelphrey KA, 2002, J AUTISM DEV DISORD, V32, P249, DOI 10.1023/A:1016374617369 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 TEUNISSE JP, 1994, INT J NEUROSCI, V77, P1 Trepagnier C, 2002, CYBERPSYCHOL BEHAV, V5, P213, DOI 10.1089/109493102760147204 van der Geest JN, 2002, J CHILD PSYCHOL PSYC, V43, P669, DOI 10.1111/1469-7610.00055 van der Geest JN, 2002, J AUTISM DEV DISORD, V32, P69, DOI 10.1023/A:1014832420206 NR 24 TC 88 Z9 92 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAY PY 2007 VL 11 IS 3 BP 265 EP 277 DI 10.1177/1362361307076925 PG 13 WC Psychology, Developmental SC Psychology GA 176EI UT WOS:000247066800006 PM 17478579 ER PT J AU Goin-Kochel, RP Abbacchi, A Constantino, JN AF Goin-Kochel, Robin P. Abbacchi, Anna Constantino, John N. CA Autism Genetic Resource Exchange C TI Lack of evidence for increased genetic loading for autism among families of affected females - A replication from family history data in two large samples SO AUTISM LA English DT Article DE Asperger's disorder; autism; family history; genetics ID SEX-DIFFERENCES; DIAGNOSTIC INTERVIEW; INFANTILE-AUTISM; INDIVIDUALS; DISORDERS; PHENOTYPE; CHILDREN AB Both the broad and narrow phenotypes of autism have been consistently observed in family members of affected individuals. Additionally, autism spectrum disorders (ASDs) present four times more often in males than in females, for reasons that are currently unknown. In this study, we examined whether there were differences in familial loading of ASD among families of male versus female probands. Analyses were conducted with existing data from two distinct samples. The first sample contained 417 individuals with autism and Asperger's disorder and included information on the ASD diagnoses of their first- and second-degree relatives. The second sample consisted of 405 sibships participating in the Autism Genetic Resource Exchange, of which one or more siblings had an ASD diagnosis. Results from both samples did not suggest significant differences in the prevalence of ASD among relatives of affected males versus females. C1 Baylor Coll Med, Houston, TX 77030 USA. Washington Univ, Sch Med, St Louis, MO 63130 USA. RP Goin-Kochel, RP (reprint author), Texas Childrens Hosp, 6621 Fannin St,CC1560, Houston, TX 77030 USA. EM kochel@bcm.tmc.edu CR Boutin P, 1997, J AUTISM DEV DISORD, V27, P165, DOI 10.1023/A:1025891824269 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P303 Gosling SD, 2004, AM PSYCHOL, V59, P93, DOI 10.1037/0003-066X.59.2.93 Jones MB, 2002, AM J MED GENET, V114, P558, DOI 10.1002/ajmg.10513 LORD C, 1982, J AUTISM DEV DISORD, V12, P317, DOI 10.1007/BF01538320 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LORD C, 1985, J AUTISM DEV DISORD, V15, P185, DOI 10.1007/BF01531604 Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 Pilowsky T, 1998, J AUTISM DEV DISORD, V28, P143, DOI 10.1023/A:1026092632466 Piven J, 1997, AM J PSYCHIAT, V154, P185 PIVEN J, 1990, J AM ACAD CHILD PSY, V29, P177, DOI 10.1097/00004583-199003000-00004 Szatmari P, 2000, AM J PSYCHIAT, V157, P1980, DOI 10.1176/appi.ajp.157.12.1980 SZATMARI P, 1998, AUTISM PERVASIVE DEV, P109 TSAI L, 1981, J AUTISM DEV DISORD, V11, P165, DOI 10.1007/BF01531682 TSAI LY, 1983, BRIT J PSYCHIAT, V142, P373, DOI 10.1192/bjp.142.4.373 Volkmar FR, 2004, J CHILD PSYCHOL PSYC, V45, P1, DOI 10.1046/j.0021-9630.2003.045_1.x WING L, 1981, PSYCHIAT RES, V5, P128 NR 18 TC 21 Z9 21 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAY PY 2007 VL 11 IS 3 BP 279 EP 286 DI 10.1177/1362361307076857 PG 8 WC Psychology, Developmental SC Psychology GA 176EI UT WOS:000247066800007 PM 17478580 ER PT J AU Roylance, C AF Roylance, Carrie TI Encouraging appropriate behavior for children on the autism spectrum: Frequently asked questions SO AUTISM LA English DT Book Review C1 Kennedy Krieger Inst, Baltimore, MD USA. RP Roylance, C (reprint author), Kennedy Krieger Inst, Baltimore, MD USA. CR RICHMAN S, 2006, ENCOURAGING APPROPRI NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAY PY 2007 VL 11 IS 3 BP 287 EP 288 DI 10.1177/1362361307076864 PG 2 WC Psychology, Developmental SC Psychology GA 176EI UT WOS:000247066800008 ER PT J AU Eikeseth, S Smith, T Jahr, E Eldevik, S AF Eikeseth, Svein Smith, Tristram Jahr, Erik Eldevik, Sigmund TI Outcome for children with autism who began intensive behavioral treatment between ages 4 and 7 - A comparison controlled study SO BEHAVIOR MODIFICATION LA English DT Article DE autism; early intervention; behavior modification; behavior analysis ID PERVASIVE DEVELOPMENTAL DISORDER; YOUNG-CHILDREN; INTERVENTION AB This study extends findings on the effects of intensive applied behavior analytic treatment for children with autism who began treatment at a mean age of 5.5 years. The behavioral treatment group (n = 13, 8 boys) was compared to an eclectic treatment group (n = 12, 11 boys). Assignment to groups was made independently based on the availability of qualified supervisors. Both behavioral and eclectic treatment took place in public kindergartens and elementary schools for typically developing children. At a mean age of 8 years, 2 months, the behavioral treatment group showed larger increases in IQ and adaptive functioning than did the eclectic group. The behavioral treatment group also displayed fewer aberrant behaviors and social problems at follow-up. Results suggest that behavioral treatment was effective for children with autism in the study. C1 Univ Rochester, Med Ctr, Rochester, NY 14627 USA. Nordvoll Sch, Ctr Early Intervent, Oslo, Norway. Autism Ctr, Oslo, Norway. CR Achenbach T. M., 1991, MANUAL TEACHERS REPO American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson S. 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I., 1988, ADV CLIN CHILD PSYCH, V11, P285 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 SMITH T, IN PRESS J NORWEGIAN Smith T, 2000, AM J MENT RETARD, V105, P269, DOI 10.1352/0895-8017(2000)105<0269:RTOIEI>2.0.CO;2 Smith T, 1997, AM J MENT RETARD, V102, P238, DOI 10.1352/0895-8017(1997)102<0238:IBTFPW>2.0.CO;2 Sparrow S, 1984, VINELAND ADAPTIVE BE Wechsler D., 1989, WECHSLER PRESCHOOL P Wechsler D, 1974, WECHSLER INTELLIGENC Weiss MJ, 1999, BEHAV INTERVENT, V14, P3, DOI 10.1002/(SICI)1099-078X(199901/03)14:1<3::AID-BIN25>3.0.CO;2-F NR 21 TC 91 Z9 93 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0145-4455 J9 BEHAV MODIF JI Behav. Modificat. PD MAY PY 2007 VL 31 IS 3 BP 264 EP 278 DI 10.1177/0145445506291396 PG 15 WC Psychology, Clinical SC Psychology GA 159VA UT WOS:000245894500002 PM 17438342 ER PT J AU Ducharme, JM Sanjuan, E Drain, T AF Ducharme, Joseph M. Sanjuan, Elena Drain, Tammy TI Errorless compliance training - Success-focused behavioral treatment of children with Asperger syndrome SO BEHAVIOR MODIFICATION LA English DT Article DE Asperger syndrome; noncompliance; parent training; treatment of problem behavior; errorless intervention ID PARENTAL REQUESTS; DISCRIMINATION; DISORDER; AUTISM AB Errorless compliance training is a noncoercive, success-focused approach to treatment of problem behavior in children. The intervention involves graduated exposure of a child to increasingly more challenging requests at a slow enough rate to ensure that noncompliance rarely occurs, providing parents with many opportunities to reinforce cooperative responses and rendering punishment unnecessary. The authors evaluated this approach with three boys with characteristics of Asperger syndrome. Mothers first delivered a range of requests to their children and recorded child responses. For each child, the authors calculated compliance probability for all requests and categorized them into four probability levels, from those yielding high compliance (Level 1) to those that commonly led to opposition (Level 4). Treatment began with delivery of Level I requests. Requests from Levels 2 through 4 were faded in sequentially over several weeks. All three children demonstrated substantial generalized improvement in compliance. C1 Univ Toronto, Dept Human Dev & Appl Psychol, Toronto, ON M5S 1V6, Canada. Autism Partnership, Toronto, ON, Canada. Univ Toronto, Ontario Inst Studies Educ, Toronto, ON M5S 1V6, Canada. RP Ducharme, JM (reprint author), Univ Toronto, Dept Human Dev & Appl Psychol, 252 Bloor St, Toronto, ON M5S 1V6, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H., 1991, AUTISM ASPERGER SYND, P37, DOI 10.1017/CBO9780511526770.002 BARKLEY RA, 1997, DEFIANT CHILDREN CLI BARLOW DH, 1984, SINGLE CASE EXPT DES Bryson S. 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TI Seizures and electroencephalographic findings in CDKL5 mutations: Case report and review SO BRAIN & DEVELOPMENT LA English DT Review DE early-onset seizures Rett syndrome variant; Rett syndrome; autism; CDKL5 ID RETT-SYNDROME; INFANTILE SPASMS; MENTAL-RETARDATION; GENE; EPILEPSY; VARIANT; MECP2 AB Mutations in the X-linked gene cyclin-dependent kinase-like 5 (CDKL5) have been detected in patients presenting with seizures in the first few months of life and Rett syndrome features. Twenty-seven cases have been detected to date. Generalized intractable seizures, as infantile spasms, and generalized tonic-clonic seizures and myoclonic seizures characterize the clinical picture of CDKL5 mutations. Here we report on a patient who presented with sleep-related hyperkinetic seizures. Our observation and review of the literature suggest that a broader polymorphic electroclinical pattern with both generalized and focal seizures may occur in patients with CDKL5 mutations. A screen for CDKL5 mutations is useful in patients, mainly females, with a history of early onset intractable seizures and becomes mandatory when idiopathic infantile spasms and/or atypical Rett syndrome features are also present. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Siena, Santa Maria alle Scotte Hosp, Dept Pediat, Pediat Neurol Sect, I-53100 Siena, Italy. Univ Siena, Dept Med Genet, I-53100 Siena, Italy. RP Grosso, S (reprint author), Univ Siena, Santa Maria alle Scotte Hosp, Dept Pediat, Pediat Neurol Sect, Via Laterina 8, I-53100 Siena, Italy. 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PD MAY PY 2007 VL 29 IS 4 BP 239 EP 242 DI 10.1016/j.braindev.2006.09.001 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 152BV UT WOS:000245336600009 PM 17049193 ER PT J AU Nettle, D AF Nettle, Daniel TI Empathizing and systemizing: What are they, and what do they contribute to our understanding of psychological sex differences? SO BRITISH JOURNAL OF PSYCHOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; PERSONALITY-INVENTORY; ORIENTATION; QUOTIENT; INTERNET; ADULTS; MIND; QUESTIONNAIRE; INTELLIGENCE AB Empathizing and systemizing have recently been put forward as two important individual-difference dimensions, whose different mean levels in men and women are argued to account for many psychological sex differences. This paper presents a series of studies designed to investigate the reliability and validity of the empathizing and systemizing quotients (EQ & SQ), to relate them to existing personality constructs, and to replicate reported sex and sexual orientation-related differences. Correlations with interests and social behaviour suggest the two measures are valid. However, empathizing appears essentially equivalent to agreeableness in the five-factor model of personality. Systemizing cannot be reduced to established personality dimensions, though it is moderately correlated with conscientiousness and openness. Men have higher levels of systemizing than women, and non-heterosexual women higher than heterosexuals. However, no differences were found between heterosexual and non-heterosexual men. Although systemizing and empathizing account for a number of observed sex differences, there are others they do not explain. C1 Univ Newcastle Upon Tyne, Newcastle Upon Tyne NE2 2JS, Tyne & Wear, England. RP Nettle, D (reprint author), Univ Newcastle Upon Tyne, Henry Wellcome Bldg,Framlington Pl, Newcastle Upon Tyne NE2 2JS, Tyne & Wear, England. 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Hippocampal tissue sections from CA1 area of schizophrenic, bipolar, depressed, and controls subjects, matched for age, sex, PMI, drug exposure, and brain pH were prepared for cell size determination using the Stanley Medical Research Foundation postmortem brain collection. 4. Quantification of hippocampal CA1 pyramidal neuron size showed a significant 12% reduction in cell size (p < 0.05) in bipolar subjects vs. controls. There were nonsignificant trends for reduction in cell size in both schizophrenic and depressed subjects vs. controls. 5. These results indicate for the first time that pyramidal cell atrophy is present in hippocampus of subjects with bipolar disorder. C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, MMC 392,420 Delaware St SE, Minneapolis, MN 55455 USA. 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Mol. Neurobiol. PD MAY PY 2007 VL 27 IS 3 BP 351 EP 358 DI 10.1007/s10571-006-9128-7 PG 8 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA 168ZI UT WOS:000246562100008 PM 17235693 ER PT J AU Slaughter, V Peterson, CC Mackintosh, E AF Slaughter, Virginia Peterson, Candida C. Mackintosh, Emily TI Mind what mother says: Narrative input and theory of mind in typical children and those on the autism spectrum SO CHILD DEVELOPMENT LA English DT Article ID MENTAL-STATE LANGUAGE; FALSE BELIEF; INDIVIDUAL-DIFFERENCES; TALK; CONVERSATION; ACQUISITION; PERFORMANCE; MINDEDNESS; DISCOURSE; KNOWLEDGE AB In 2 studies mothers read wordless storybooks to their preschool-aged children; narratives were analyzed for mental state language. Children's theory-of-mind understanding (ToM) was concurrently assessed. In Study 1, children's (N = 30; M age 3 years 9 months) ToM task performance was significantly correlated with mothers' explanatory, causal, and contrastive talk about cognition, but not with mothers' simple mentions of cognition. In Study 2, the same pattern was found in an older sample of typically developing children (N = 24; M age 4 years 7 months), whereas for children on the autism spectrum (N = 24; M age 6 years 7.5 months), ToM task performance was uniquely correlated with mothers' explanatory, causal, and contrastive talk about emotions. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Slaughter, V (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. 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PD MAY-JUN PY 2007 VL 78 IS 3 BP 839 EP 858 DI 10.1111/j.1467-8624.2007.01036.x PG 20 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 176VP UT WOS:000247113300012 PM 17517008 ER PT J AU Mundy, P Block, J Delgado, C Pomares, Y Van Hecke, AV Parlade, MV AF Mundy, Peter Block, Jessica Delgado, Christine Pomares, Yuly Van Hecke, Amy Vaughan Parlade, Meaghan Venezia TI Individual differences and the development of joint attention in infancy SO CHILD DEVELOPMENT LA English DT Article ID AT-RISK CHILDREN; 2ND YEAR; NONVERBAL-COMMUNICATION; YOUNG-CHILDREN; NEUROCOGNITIVE FUNCTION; LANGUAGE-DEVELOPMENT; DOWN-SYNDROME; AUTISM; BEHAVIOR; GAZE AB This study examined the development of joint attention in 95 infants assessed between 9 and 18 months of age. Infants displayed significant test-retest reliability on measures of following gaze and gestures (responding to joint attention, RJA) and in their use of eye contact to establish social attention coordination (initiating joint attention, IJA). Infants displayed a linear, increasing pattern of age-related growth on most joint attention measures. However, IJA was characterized by a significant cubic developmental pattern. Infants with different rates of cognitive development exhibited different frequencies of joint attention acts at each age, but did not exhibit different age-related patterns of development. Finally, 12-month RJA and 18-month IJA predicted 24-month language after controlling for general aspects of cognitive development. C1 Univ Miami, Coral Gables, FL 33146 USA. Univ Illinois, Chicago, IL 60680 USA. Univ Pittsburgh, Pittsburgh, PA 15260 USA. RP Mundy, P (reprint author), Univ Miami, 5665 Ponce De Leon Blvd, Coral Gables, FL 33146 USA. 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PD MAY-JUN PY 2007 VL 78 IS 3 BP 938 EP 954 DI 10.1111/j.1467-8624.2007.01042.x PG 17 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 176VP UT WOS:000247113300018 PM 17517014 ER PT J AU Fanjiang, G Kleinman, RE AF Fanjiang, Gary Kleinman, Ronald E. TI Nutrition and performance in children SO CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE LA English DT Article DE behavior; children; cognition; nutrition; performance; physical activity ID POLYUNSATURATED FATTY-ACIDS; AUTISM SPECTRUM DISORDERS; COGNITIVE-DEVELOPMENT; MENTAL-DEVELOPMENT; PHYSICAL-ACTIVITY; SCHOOL-CHILDREN; YOUNG-CHILDREN; UNITED-STATES; MICRONUTRIENT SUPPLEMENT; DIETARY INTERVENTION AB Purpose of review Malnutrition in late infancy and childhood remains a significant public health issue in developing nations as well as for those in transition to an industrialized economy. In addition, in these settings and particularly in developed nations, overweight is becoming a very serious threat to both the immediate and the long-term health of children. In this review, we present recent studies that have examined relationships between childhood undernutrition and three general areas of performance: physical activity, cognition and behavior. Recent findings Malnourished children have been shown to have decreased physical activity and endurance, and poorer cognitive function and school performance. Multiple single micronutrient deficiencies, including vitamin B12, thiamin, niacin, zinc and iron, have been associated with poorer cognitive performance. Behavioral problems, including attention deficits, have also been associated with food insufficiency and malnutrition. Summary The effects of impaired nutritional status during childhood may have long-standing consequences for the health and performance of children during their adult years. 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TI Investigation of the behavioural phenotype of parents of autistic children through the new FAQ self-report SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE autism; endophenotype; imagination; language; parental; rigidity; self-report; socialization ID RECEPTIVE LANGUAGE DISORDER; SPECTRUM DISORDERS; INFANTILE-AUTISM; PERSONALITY-CHARACTERISTICS; FAMILY HISTORY; INDIVIDUALS; PSYCHIATRY; GENETICS; TWIN AB Introduction - Autism is characterized by impairments in communication and socialization and by the presence of circumscribed and stereotyped interest. Previous studies have shown that genetic mechanisms may enhance the vulnerability to autism. These mechanisms are complex and may involve the combination of several genes, in interaction with the environment. The genetic mechanism involved in the vulnerability to autism may also concern other disorders and some features, with enhanced prevalence in relatives of autistic patients. It has been shown, for example, that the frequency of language disorders or serial difficulties is increased in the siblings of autistic patients. Characterization and taking into account the presence of such phenotypic traits in the relations may help in understanding the results of genetic studies, in particular association studies in sibling pairs or trios. Objective - In this study, we used a new self-reportin order to identify endophenotype traits in socialization, communication, rigidity and imagination in parents of autistic children. This self-report is the French adaptation of the previous self-report created by Baron-Cohen et al., aimed at the identification of Asperger profiles in a population of students studying science. Methodology - Ten autistic children and their parents from a clinical setting were asked to participate in the study. Autistic children were characterized using the ADI-R and various psychometric tests, according to the possibilities of the child (PEP-R, WPPSI-R, WISC3). Twenty parents of normal children were recruited from three different professional settings. There were no differences between the two groups of parents in terms of age or social status. Parents of both groups were asked to fill in the FAQ self-report. Results - We performed a post-hoc analysis comparing the scores of the parents in the two groups. We found a main group, but no sex effect [F (1,37) = 5.46; p < 0.05]. Scores of autistic parents were higher in all domains compared to the control parents (p < 0.05). However, the score on the socialization subscale was the only one that significantly differed from the scores on the imagination, language and rigidity subscales [F (3, 111) = 20.75, p < 0.001]. Conclusion - Our results show significant differences between the two groups of parents in the socialization domain. This is of interest both for the interpretation of the presence of allelic variants in the, genetic association studies, and for the understanding of the interplay between genotype and phenotype in the development of the autistic disorder. C1 [Piana, H.; Fortin, C.; Golse, B.; Robel, L.] Hop Necker Enfants Malad, Serv Psychiat Enfant Adolescent Professeur Bernar, F-75015 Paris, France. [Noulhiane, M.] Hop La Pitie Salpetriere, LENA, F-75013 Paris, France. RP Piana, H (reprint author), Hop Necker Enfants Malad, Serv Psychiat Enfant Adolescent Professeur Bernar, 149 Rue Sevres, F-75015 Paris, France. 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Psychiatr. Clin. Biol. Ther. PD MAY-JUN PY 2007 VL 33 IS 3 BP 285 EP 292 PN 1 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 251WP UT WOS:000252407100008 PM 17675925 ER PT J AU de Wit, TCJ Schlooz, WAJM Hulstijn, W van Lier, R AF de Wit, Tessa C. J. Schlooz, Wim A. J. M. Hulstijn, Wouter van Lier, Rob TI Visual completion and complexity of visual shape in children with pervasive developmental disorder SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autistic spectrum disorder; visual perception; pervasive developmental disorder; visuo-spatial functioning ID PARTLY OCCLUDED OBJECTS; LOCAL COMPLETIONS; AUTISM; PERCEPTION; INDIVIDUALS; OCCLUSION; DEFICIT; MOTION; TASK; INTERPOLATION AB Much evidence has been gathered for differences in visual perceptual processing in individuals with Autistic Spectrum Disorder. The presence of the fundamental process of visual completion was tested in a group of children with Pervasive Developmental Disorder (PDD), as this requires perceptually integrating visual structure into wholes. In Experiment 1, it was investigated whether visual completion is present for simple partly occluded shapes in a group of children with PDD and a typically developing group. In Experiment 2, the presence of contextual influences in visual completion was investigated for the two groups. A total of 19 children with PDD and 28 controls who were matched for chronological age and IQ took part in two primed-matching tasks. For both groups, visual completion was present and for both groups, contextual influences were found to be dominant in this process. However, only for the group with PDD no priming effects (PEs) were found from less regular primes on congruent test pairs. The group with PDD did integrate visual information into wholes and did this in a contextually dependent way. 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We assess which abilities differentiate the disorders. Children aged 3-13 years diagnosed with AD (n = 30), RELD (n = 30), or DCD (n = 22) were tested on measures of language, intelligence, social cognition, motor coordination, and executive functioning. Results indicate that the AD and DCD groups have poorer fine and gross motor coordination and better response inhibition than the RELD group. The AD and DCD groups differ in fine and gross motor coordination, emotion understanding, and theory of mind scores (AD always lower), but discriminant function analysis yielded a non-significant function and more classification errors for these groups. In terms of ability scores, the AD and DCD groups appear to differ more in severity than in kind. C1 Griffith Univ, Sch Psychol, Southport, Qld 9726, Australia. Curtin Univ Technol, Sch Psychol, Bentley, WA 6102, Australia. Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. 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Child Adolesc. Psych. PD MAY PY 2007 VL 16 IS 3 BP 178 EP 186 DI 10.1007/s00787-006-0586-8 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 160UX UT WOS:000245968900004 PM 17136301 ER PT J AU Miller, NL Findling, RL AF Miller, Noah L. Findling, Robert L. TI Is methylphenidate a safe and effective treatment of ADHD-like symptoms in children with pervasive developmental disorders? SO EXPERT OPINION ON PHARMACOTHERAPY LA English DT Review DE ADHD; Asperger's disorder; attention-deficit/hyperactivity disorder; autism; autistic disorder; methylphenidate; pervasive developmental disorder ID HYPERACTIVITY; AUTISM; TRIAL; MTA AB Children with autistic disorder and related pervasive developmental disorders (PDDs) frequently have symptoms of hyperactivity and impulsivity similar to the symptoms of attention-deficit/hyperactivity disorder (ADHD). Clinicians often treat these symptoms with methylphenidate (MPH), but historically there are little available data about the use of MPH in children with PDD. The Research Units on Pediatric Psychopharmacology (RUPP) group set out to determine whether MPH is a safe and effective treatment for the ADHD-like symptoms associated with PDD. MPH was found to be superior to placebo in reducing hyperactivity scores on the Aberrant Behavior Checklist. However there was a lower magnitude of response and a higher incidence of medication discontinuation than previously reported in typically developing children with ADHD. Although MPH seems to be a reasonable choice for the treatment of ADHD-like symptoms in children with PDD, clinicians should consider the findings from the RUPP MPH study before prescribing MPH to children with PDD. C1 Case Western Reserve Univ, Sch Med, Cleveland, OH 44106 USA. RP Miller, NL (reprint author), Case Western Reserve Univ, Sch Med, Univ Hosp, Rainbow Babies & Childrens Hosp, 11100 Euclid Ave, Cleveland, OH 44106 USA. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Greenhill LL, 2001, J AM ACAD CHILD PSY, V40, P180, DOI 10.1097/00004583-200102000-00012 Greenhill LL, 1996, J AM ACAD CHILD PSY, V35, P1304, DOI 10.1097/00004583-199610000-00017 Handen BL, 2000, J AUTISM DEV DISORD, V30, P245, DOI 10.1023/A:1005548619694 Langworthy-Lam KS, 2002, J CHILD ADOL PSYCHOP, V12, P311, DOI 10.1089/104454602762599853 QUINTANA H, 1972, J AUTISM CHILD SCHIZ, V2, P343 Aman MG, 2005, ARCH GEN PSYCHIAT, V62, P1266 SWANSON JM, 1999, PSYCHOL MED, V29, P769 NR 9 TC 1 Z9 1 PU INFORMA HEALTHCARE PI LONDON PA TELEPHONE HOUSE, 69-77 PAUL STREET, LONDON EC2A 4LQ, ENGLAND SN 1465-6566 J9 EXPERT OPIN PHARMACO JI Expert Opin. Pharmacother. PD MAY PY 2007 VL 8 IS 7 BP 1025 EP 1028 DI 10.1517/14656566.8.7.1025 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 161MM UT WOS:000246019400013 PM 17472547 ER PT J AU Sinzig, JK Lehmkuhl, G AF Sinzig, J. K. Lehmkuhl, G. TI Autism and ADHD - Are there common traits? SO FORTSCHRITTE DER NEUROLOGIE PSYCHIATRIE LA German DT Review ID DEFICIT-HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDER; SPECTRUM DISORDERS; SCHIZOPHRENIC CHILDREN; PSYCHIATRIC-DISORDERS; EXECUTIVE FUNCTIONS; SHIFTING ATTENTION; CORPUS-CALLOSUM; GENOMEWIDE SCAN AB Introduction: Genetic, neuropsychological and psychopathological findings refer to a connection of autism and attention deficit/hyperactivity disorder (ADHD). Although the disorders represent different nosological diagnoses they partly include similar symptoms like hyperactivity, impulsivity and attention deficit disorder. Methods: This paper gives an overview of genetic, morphological, neurophysiological and psychological studies concerning ADHD and autism. In addition, results concerning pharmacotherapy and the development of both disorders in adulthood are described. Results: With regard to genetics, common candidate regions are discussed. Under a morphological perspective, results on the one hand point out identical brain regions or functional systems but on the other hand underline that these regions are not equally affected. The morphological results could not be replicated on a neuropsychological basis. So far findings of studies which involved combined ADHD- and autistic samples lead to controversal results. Conclusion: At present, there exist only few studies which include the issue of attention disorders in autism and ADHD in a same sample. With regard to diagnosis and therapeutical interventions, further research concerning the etiology of both disorders is necessary. 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J., 1999, FUNDAMENTALS NEUROSC NR 106 TC 9 Z9 9 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0899-8256 J9 GAME ECON BEHAV JI Games Econ. Behav. PD MAY PY 2007 VL 59 IS 2 BP 316 EP 344 DI 10.1016/j.geb.2006.08.006 PG 29 WC Economics SC Business & Economics GA 179FM UT WOS:000247275100006 ER PT J AU Herman, GE Henninger, N Ratliff-Schaub, K Pastore, M Fitzgerald, S McBride, KL AF Herman, Gail E. Henninger, Nathan Ratliff-Schaub, Karen Pastore, Matthew Fitzgerald, Sara McBride, Kim L. TI Genetic testing in autism: how much is enough? SO GENETICS IN MEDICINE LA English DT Article DE autism; autism spectrum disorder; Rett syndrome; PTEN; genetic testing; array comparative genomic hybridization ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; MENTAL-RETARDATION; RETT-SYNDROME; FRAGILE-X; PHENOTYPE; CHILDREN; CHROMOSOMES; MUTATIONS; YIELD AB Purpose: To evaluate the yield of genetic testing in children with autism spectrum disorders. Methods: We performed a retrospective chart review of 71 unrelated patients with a diagnosis of an isolated autism spectrum disorder seen in a genetics clinic over a period of 14 months. For most, referrals occurred after evaluation by a developmental pediatrician and/or psychologist to establish the diagnosis. Tiered laboratory testing for the majority of the patients followed a guideline that was developed in collaboration with clinicians at The Autism Center at Children's Hospital, Columbus, OH. Results: The patients included 57 males and 14 females; 57 met DSM-IV criteria for autism, with the rest being Asperger or pervasive developmental disorder not otherwise specified. Macrocephaly [head circumference (HC) >= 95%] was present in 19 (27%). Two children had visible chromosome abnormalities (47,XYY; 48,XY + 2mar/49,XY + 3mar). Two patients with autism and macrocephaly had heterozygous mutations in the PTEN tumor suppressor gene. Three females had Rett syndrome, each confirmed by DNA sequencing of the MECP2 gene. Extensive metabolic testing produced no positive results, nor did fragile X DNA testing. Conclusion: The overall diagnostic yield was 10% (7/71). PTEN gene sequencing should be considered in any child with macrocephaly and autism or developmental delay. Metabolic screening may not be warranted in autism spectrum disorders without more specific indications or additional findings. C1 Childrens Res Inst, Ctr Mol & Human Genet, Columbus, OH 43205 USA. 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PD MAY-JUN PY 2007 VL 15 IS 3 BP 93 EP 108 DI 10.1080/10673220701432188 PG 16 WC Psychiatry SC Psychiatry GA 184HZ UT WOS:000247633400001 PM 17510829 ER PT J AU Ingudomnuku, E Baron-Cohen, S Wheelwright, S Knickmeyer, R AF Ingudomnuku, Erin Baron-Cohen, Simon Wheelwright, Sally Knickmeyer, Rebecca TI Elevated rates of testosterone-related disorders in women with autism spectrum conditions SO HORMONES AND BEHAVIOR LA English DT Article DE autism; Asperger syndrome; endocrine disorders; androgens; fetal testosterone; broader autism phenotype ID CONGENITAL ADRENAL-HYPERPLASIA; HIGH-FUNCTIONING AUTISM; POLYCYSTIC-OVARY-SYNDROME; GENDER IDENTITY DISORDER; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME; SYSTEMATIZING QUOTIENT; FETAL TESTOSTERONE; CANCER RISK; PSYCHOSEXUAL DEVELOPMENT AB The androgen theory of autism proposes that autism spectrum conditions (ASC) are in part due to elevated fetal testosterone (FT) levels, which are positively correlated with a number of autistic traits and inversely correlated with social development and empathy. A medical questionnaire was completed by n = 54 women with ASC, n = 74 mothers of children with ASC, and n = 183 mothers of typically developing children to test whether women with ASC have an increased rate of testosterone-related medical conditions, and to see whether mothers of children with ASC show similar abnormalities, as part of the 'broader autism phenotype'. Compared to controls, significantly more women with ASC reported (a) hirsutism, (b) bisexuality or asexuality, (c) irregular menstrual cycle, (d) dysmenorrhea, (c) polycystic ovary syndrome, (f) severe acne, (g) epilepsy, (h) tomboyism, and (i) family history of ovarian, uterine, and prostate cancers, tumors, or growths. Compared to controls, significantly more mothers of ASC children reported (a) severe acne, (b) breast and uterine cancers, tumors, or growths, and (c) family history of ovarian and uterine cancers, tumors, or growths. These results suggest current hormone abnormalities in women with ASC and their mothers. Direct investigations of serum testosterone levels and genetic susceptibility to high testosterone production or sensitivity in women with ASC would illuminate the origin of these conditions. The relationship between FT and current testosterone levels also needs to be clarified. The present results may be relevant to understanding the increased male risk to developing autism. (c) 2007 Elsevier Inc. All rights reserved. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 8AH, England. Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. RP Ingudomnuku, E (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 8AH, England. 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Behav. PD MAY PY 2007 VL 51 IS 5 BP 597 EP 604 DI 10.1016/j.yhbeh.2007.02.001 PG 8 WC Behavioral Sciences; Endocrinology & Metabolism SC Behavioral Sciences; Endocrinology & Metabolism GA 179FT UT WOS:000247275800004 PM 17462645 ER PT J AU Hadjikhani, N Joseph, RM Snyder, J Tager-Flusberg, H AF Hadjikhani, Nouchine Joseph, Robert M. Snyder, Josh Tager-Flusberg, Helen TI Abnormal activation of the social brain during face perception in autism SO HUMAN BRAIN MAPPING LA English DT Article DE autism spectrum disorder; face perception; fusiform gyrus; amygdala; mirror neuron system; social brain; visual processing ID PERVASIVE DEVELOPMENTAL DISORDERS; EMOTIONAL FACIAL EXPRESSIONS; SUPERIOR TEMPORAL SULCUS; HUMAN AMYGDALA; NEURAL BASIS; ASPERGER-SYNDROME; CORTICAL SURFACE; SPECTRUM DISORDER; COORDINATE SYSTEM; FUSIFORM ACTIVITY AB ASD involves a fundamental impairment in processing social-communicative information from faces. Several recent studies have challenged earlier findings that individuals with autism spectrum disorder (ASD) have no activation of the fusiform gyrus (fusiform face area, FFA) when viewing faces. In this study, we examined activation to faces in the broader network of face-processing modules that comprise what is known as the social brain. Using 3T functional resonance imaging, we measured BOLD signal changes in 10 ASD subjects and 7 healthy controls passively viewing nonemotional faces. We replicated our original findings of significant activation of face identity-processing areas (FFA and inferior occipital gyrus, IOG) in ASD. However, in addition, we identified hypoactivation in a more widely distributed network of brain areas involved in face processing [including the right amygdala, inferior frontal cortex (IFC), superior temporal sulcus (STS), and face-related somatosensory and premotor cortex]. In ASD, we found functional correlations between a subgroup of areas in the social brain that belong to the mirror neuron system (IFC, STS) and other face-processing areas. The severity of the social symptoms measured by the Autism Diagnostic Observation Schedule was correlated with the right IFC cortical thickness and with functional activation in that area. When viewing faces, adults with ASD show atypical patterns of activation in regions forming the broader face-processing network and social brain, outside the core FFA and IOG regions. These patterns suggest that areas belonging to the mirror neuron system are involved in the face-processing disturbances in ASD. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Athinoula A Martinos Ctr Biomed Imaging, Charlestown, MA 02129 USA. Harvard Univ, MIT, Div Hlth Sci & Technol, Cambridge, MA 02139 USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Hadjikhani, N (reprint author), Harvard Univ, Massachusetts Gen Hosp, Sch Med, Athinoula A Martinos Ctr Biomed Imaging, Bldg 120,110 6th St,Room 217, Charlestown, MA 02129 USA. 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Menzel, Corinna Erdogan, Fikret Arkesteijn, Ger Ropers, Hans-Hilger Ullmann, Reinhard TI Mutations in autism susceptibility candidate 2 (AUTS2) in patients with mental retardation SO HUMAN GENETICS LA English DT Article ID HUMAN GENOME; TRANSLOCATION BREAKPOINT; DNA MICROARRAYS; GENE; IDENTIFICATION; CHROMOSOMES; DISRUPTION; HAPLOINSUFFICIENCY; CANDIDATE; ENCODES AB We report on three unrelated mentally disabled patients, each carrying a de novo balanced translocation that truncates the autism susceptibility candidate 2 (AUTS2) gene at 7q11.2. One of our patients shows relatively mild mental retardation; the other two display more profound disorders. One patient is also physically disabled, exhibiting urogenital and limb malformations in addition to severe mental retardation. The function of AUTS2 is presently unknown, but it has been shown to be disrupted in monozygotic twins with autism and mental retardation, both carrying a translocation t(7;20)(q11.2;p11.2) (de la Barra et al. in Rev Chil Pediatr 57:549-554, 1986; Sultana et al. in Genomics 80:129-134, 2002). Given the overlap of this autism/mental retardation (MR) phenotype and the MR-associated disorders in our patients, together with the fact that mapping of the additional autosomal breakpoints involved did not disclose obvious candidate disease genes, we ascertain with this study that AUTS2 mutations are clearly linked to autosomal dominant mental retardation. C1 Max Planck Inst Mol Genet, D-14195 Berlin, Germany. Western Gen Hosp, MRC, Dept Clin Genet, Edinburgh EH4 2XU, Midlothian, Scotland. Western Gen Hosp, MRC, Human Genet Unit, Edinburgh EH4 2XU, Midlothian, Scotland. Univ Copenhagen, Panum Inst, Wilhelm Johannsen Ctr Funct Genome Res, DK-2200 Copenhagen, Denmark. Univ Copenhagen, Panum Inst, Dept Med Biochem & Genet, DK-2200 Copenhagen, Denmark. Free Univ Berlin, Inst Human Genet, D-1000 Berlin, Germany. Univ Utrecht, Fac Vet Med, Dept Immunol & Infect Dis, NL-3508 TC Utrecht, Netherlands. RP Kalscheuer, VM (reprint author), Max Planck Inst Mol Genet, Ihnestr 73, D-14195 Berlin, Germany. 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Genet. PD MAY PY 2007 VL 121 IS 3-4 BP 501 EP 509 DI 10.1007/s00439-006-0284-0 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 154GF UT WOS:000245494200021 PM 17211639 ER PT J AU Hobson, RP AF Hobson, R. Peter TI Communicative depth: Soundings from developmental psychopathology SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE autism; identification; intersubjectivity; communication; imitation ID JOINT ATTENTION; AUTISM; CHILDREN; INFANTS; IMITATION; FOUNDATIONS; ORIGINS; PRETEND; SELF AB My aim in this paper is to consider what it means to engage and communicate with another person. I do so by adopting the approach of developmental psychopathology, and compare and contrast the structure of communication that is manifest by typically developing infants on the one hand, and by children and adolescents with autism on the other. I highlight the pivotal significance of human beings' propensity to share or otherwise co-ordinate experiences with others, and analyze the conditions that make sharing and other forms of intersubjective relatedness possible. Often, discussions that oppose cognitive, affective, and motivational accounts of autism are pursued in an inappropriate frame of reference: at root, we need to understand the nature and developmental implications of affected children's difficulties in achieving communicative depth. In the pursuit of such understanding, we may gain insights into typically developing infants' capacities for intersubjective engagement. (c) 2007 Elsevier Inc. All rights reserved. C1 Tavistock Clin, Dev Psychopathol Res Unit, London NW3 5BA, England. UCL, Inst Child Hlth, Behav & Brain Sci Unit, London, England. RP Hobson, RP (reprint author), Tavistock Clin, Dev Psychopathol Res Unit, 120 Belsize Lane, London NW3 5BA, England. 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Dev. PD MAY PY 2007 VL 30 IS 2 BP 267 EP 277 DI 10.1016/j.infbeh.2007.02.006 PG 11 WC Psychology, Developmental SC Psychology GA 162MG UT WOS:000246091100008 PM 17363063 ER PT J AU Legerstee, M Markova, G Fisher, T AF Legerstee, Maria Markova, Gabriela Fisher, Tamara TI The role of maternal affect attunement in dyadic and triadic communication SO INFANT BEHAVIOR & DEVELOPMENT LA English DT Article DE gaze monitoring; coordinated attention; affect attunement; intersubjectivity ID TO-FACE INTERACTION; JOINT ATTENTION; MOTHER-INFANT; NORMAL-CHILDREN; LANGUAGE; IMITATION; AUTISM; PLAY; COMPETENCE; PREDICTORS AB The influence of maternal affect attunement on the relationship between gaze monitoring during dyadic communication at 3 months and coordinated attention during triadic communication at 5, 7 and 10 months was examined in a longitudinal study. 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Dev. PD MAY PY 2007 VL 30 IS 2 BP 296 EP 306 DI 10.1016/j.infbeh.2006.10.003 PG 11 WC Psychology, Developmental SC Psychology GA 162MG UT WOS:000246091100011 PM 17400046 ER PT J AU Berkman, ND Lohr, KN Bulik, CM AF Berkman, Nancy D. Lohr, Kathleen N. Bulik, Cynthia M. TI Outcomes of eating disorders: A systematic review of the literature SO INTERNATIONAL JOURNAL OF EATING DISORDERS LA English DT Review DE outcomes; systematic review; anorexia nervosa; bulimia nervosa; binge eating disorder; eating disorders; binge; purge; cohort study; obsessive-compulsive disorder ID 10-YEAR FOLLOW-UP; ONSET ANOREXIA-NERVOSA; LONG-TERM COURSE; BULIMIA-NERVOSA; SURVIVAL ANALYSIS; 6-YEAR COURSE; PERSONALITY-DISORDERS; PHYSICAL HEALTH; HONG-KONG; MORTALITY AB Objective: The RTI International-University of North Carolina at Chapel Hill Evidence-based Practice Center systematically reviewed evidence on factors associated with outcomes among individuals with anorexia nervosa (AN), bulimia nervosa (BN), and binge eating disorder (BED) and whether outcomes differed by sociodemographic characteristics. Method: We searched electronic databases including MEDLINE and reviewed studies published from 1980 to September, 2005, in all languages against a priori inclusion/exclusion criteria and focused on eating, psychiatric or psychological, or biomarker outcomes. Results: At followup, individuals with AN were more likely than comparisons to be depressed, have Asperger's syndrome and autism spectrum disorders, and suffer from anxiety disorders including obsessive-compulsive disorders. Mortality risk was significantly higher than what would be expected in the population and the risk of suicide was particularly pronounced. The only consistent factor across studies relating to worse BN outcomes was depression. A substantial proportion of individuals continue to suffer from eating disorders over time but BN was not associated with increased mortality risk. Data were insufficient to draw conclusions concerning factors associated with BED outcomes. Across disorders, little to no data were available to compare results based on sociodemographic characteristics. Conclusion: The strength of the bodies of literature was moderate for factors associated with AN and BN outcomes and weak for BED. (c) 2007 by Wiley Periodicals, Inc. C1 Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. RTI Int, Res Triangle Pk, NC USA. Univ N Carolina, Dept Nutr, Chapel Hill, NC 27599 USA. RP Bulik, CM (reprint author), Univ N Carolina, Dept Psychiat, 101 Manning Dr,CB 7160, Chapel Hill, NC 27599 USA. 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J. Eating Disord. PD MAY PY 2007 VL 40 IS 4 BP 293 EP 309 DI 10.1002/eat.20369 PG 17 WC Psychology, Clinical; Nutrition & Dietetics; Psychiatry; Psychology SC Psychology; Nutrition & Dietetics; Psychiatry GA 157KX UT WOS:000245719700002 PM 17370291 ER PT J AU Adreon, D Durocher, JS AF Adreon, Diane Durocher, Jennifer Stella TI Evaluating the college transition needs of individuals with high-functioning autism spectrum disorders SO INTERVENTION IN SCHOOL AND CLINIC LA English DT Article C1 Univ Miami, NSU CARD, Coral Gables, FL 33124 USA. RP Adreon, D (reprint author), Univ Miami, NSU CARD, 5665 Ponce de Leon Blvd,Rm 239, Coral Gables, FL 33124 USA. EM dadreon@miami.edu CR ADREON D, 2004, FLORIDA ASPERGER SYN ADREON D, 2002, FLORIDA ASPERGER SYN American Psychiatric Association, 2000, DIAGN STAT MAN MENT California Department of Developmental Services, 2003, AUT SPECTR DIS CHANG *CDC, 2005, COMM IS AUT SPECTR D Clark C, 2002, J CHILD PSYCHOL PSYC, V43, P785, DOI 10.1111/1469-7610.00084 COULTER J, 2003, LESSONS LEARNED 1 YE HARPER J, 2004, SUCCEEDING COLL ASPE Janiga SJ, 2002, J LEARN DISABIL-US, V35, P462 JEKEL D, 2002, YOU WANT COLL RECOMM Klin A., 1995, ASPERGERS SYNDROME G MAAG JW, 2000, NATL ASS SECONDARY S, V84, P1, DOI 10.1177/019263650008461302 Macintosh KE, 2004, J CHILD PSYCHOL PSYC, V45, P421, DOI 10.1111/j.1469-7610.2004.00234.x MORENO S, 2005, AUTISM SPECTRUM WIN, P16 Myles B., 2001, ASPERGER SYNDROME AD Myles BS, 2005, CHILDREN YOUTH ASPER PERNER L, 2002, AUT SOC AM ANN C IND PERNER L, 2003, AUTISM ASPERGERS DIG, V36, P28 PRINCEHUGHES D, 2002, AQUAMARINE BLUE PERS Prince-Hughes Dawn, 2004, SONGS GORILLA NATION RIETSCHEL L, 2002, COLL BOUND THINGS 2 ROSENWALD L, 2003, CT AUTISM SPECTRUM R Shore S., 2001, WALL PERSONAL EXPERI SHORE SM, 2004, ASK TELL SELF ADVOCA Sitlington P. 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Rendall, Maureen TI An open-label study of risperidone in the improvement of quality of life and treatment of symptoms of violent and self-injurious behaviour in adults with intellectual disability SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE disruptive behaviour disorders; intellectual disability; quality of life; risperidone ID PERVASIVE DEVELOPMENTAL DISORDER; DOUBLE-BLIND; MENTAL-RETARDATION; CHALLENGING BEHAVIORS; ABERRANT BEHAVIOR; SUBAVERAGE IQS; RATING-SCALE; WEIGHT-GAIN; CHILDREN; TRIAL AB Background We examined the benefits of risperidone, including quality of life (QoL), in the treatment of violent and self-injurious behaviour in adults with moderate, severe or profound intellectual disability. Methods Twenty-four participants received open-label, oral, flexible-dose risperidone of 0.5-6 mg/day for 12 weeks. Efficacy was measured primarily using the Aberrant Behaviour Checklist (ABC) and secondarily using validated measures of depression, autism, QoL and global condition. Safety and tolerability were also assessed. Results Total ABC significantly improved from baseline by week 1. This improvement was maintained throughout the study (final visit, P < 0.001). Secondary efficacy measures were also improved with risperidone, including QoL measures (final visit: home life, P < 0.001; activity, P = 0.002; skills, P = 0.014). Risperidone was generally well tolerated, with no unexpected adverse events. Conclusions In this open-label trial, risperidone was efficacious and well tolerated for managing violent and self-injurious behaviour and improving QoL in adults with moderate, severe or profound intellectual disability. C1 Univ Huddersfield, Sch Human & Hlth Sci, Huddersfield HD1 3DH, W Yorkshire, England. RP Read, SG (reprint author), Univ Huddersfield, Sch Human & Hlth Sci, Room 208,Harold Wilson Bldg,Wueensgate, Huddersfield HD1 3DH, W Yorkshire, England. EM s.read@hud.ac.uk CR Allison DB, 1999, AM J PSYCHIAT, V156, P1686 AMAN MG, 1985, AM J MENT DEF, V89, P485 Aman MG, 2002, AM J PSYCHIAT, V159, P1337, DOI 10.1176/appi.ajp.159.8.1337 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Buitelaar JK, 2000, J CHILD ADOL PSYCHOP, V10, P19, DOI 10.1089/cap.2000.10.19 CHOUINARD G, 1980, CAN J NEUROL SCI, V7, P233 Cohen SA, 1998, J AUTISM DEV DISORD, V28, P229, DOI 10.1023/A:1026069421988 Dartnall NA, 1999, J AUTISM DEV DISORD, V29, P87, DOI 10.1023/A:1025926817928 DOSEN A, 1993, J INTELL DISABIL RES, V37, P1 Emerson E, 2001, RES DEV DISABIL, V22, P77, DOI 10.1016/S0891-4222(00)00061-5 Felce D, 1998, J INTELL DISABIL RES, V42, P390, DOI 10.1046/j.1365-2788.1998.00153.x Felce D, 2001, MENT RETARD DEV D R, V7, P75, DOI 10.1002/mrdd.1011 FERNELL E, 1991, ACTA PAEDIATR SCAND, V80, P451, DOI 10.1111/j.1651-2227.1991.tb11881.x Findling RL, 2000, J AM ACAD CHILD PSY, V39, P509, DOI 10.1097/00004583-200004000-00021 Findling RL, 1997, PSYCHOPHARMACOL BULL, V33, P155 Gagiano C, 2005, PSYCHOPHARMACOLOGY, V179, P629, DOI 10.1007/s00213-004-2093-2 Guy W, 1976, ECDEU ASSESSMENT MAN, P217 JANSSEN PAJ, 1988, J PHARMACOL EXP THER, V244, P685 McDougle CJ, 1995, J CHILD ADOL PSYCHOP, V5, P273, DOI 10.1089/cap.1995.5.273 MCDOUGLE CJ, 1997, J AM ACAD CHILD ADOL, V36, P683 Nicolson R, 1998, J AM ACAD CHILD PSY, V37, P372, DOI 10.1097/00004583-199804000-00014 PURDON SE, 1994, CAN J PSYCHIAT, V39, P400 Read S, 1998, BRIT J PSYCHIAT, V172, P381, DOI 10.1192/bjp.172.5.381 Santosh PJ, 1999, LANCET, V354, P233, DOI 10.1016/S0140-6736(98)07059-7 Simon EW, 1996, MENT RETARD, V34, P359 Simonoff E, 2004, BRIT J PSYCHIAT, V184, P118, DOI 10.1192/bjp.184.2.118 SIRELING L, 1986, BRIT J PSYCHIAT, V149, P274, DOI 10.1192/bjp.149.3.274 Snyder R, 2002, J AM ACAD CHILD PSY, V41, P1026, DOI 10.1097/01.CHI.0000020270/43550.CC Spivak B, 2003, J CLIN PSYCHIAT, V64, P755 Suarez GA, 1999, NEUROLOGY, V52, P523 Swann A, 2003, HOSP MED, V64, P4 Symons FJ, 1999, MENT RETARD, V37, P297, DOI 10.1352/0047-6765(1999)037<0297:TOSBAQ>2.0.CO;2 Taylor DM, 2000, ACTA PSYCHIAT SCAND, V101, P416, DOI 10.1034/j.1600-0447.2000.101006416.x Turgay A, 2002, PEDIATRICS, V110, DOI 10.1542/peds.110.3.e34 Van Bellinghen M, 2001, J CHILD ADOL PSYCHOP, V11, P5, DOI 10.1089/104454601750143348 VANDENBORRE R, 1993, ACTA PSYCHIAT SCAND, V87, P167 Zarcone JR, 2001, AM J MENT RETARD, V106, P525, DOI 10.1352/0895-8017(2001)106<0525:EOROAB>2.0.CO;2 NR 37 TC 2 Z9 2 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1360-2322 J9 J APPL RES INTELLECT JI J. Appl. Res. Intellect. Disabil. PD MAY PY 2007 VL 20 IS 3 BP 256 EP 264 DI 10.1111/j.1468-3148.2006.00328.x PG 9 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 160LF UT WOS:000245941400008 ER PT J AU Pisula, E AF Pisula, Ewa TI A comparative study of stress profiles in mothers of children with autism and those of children with Down's syndrome SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE autism; developmental disability; Down's syndrome; parental stress; stress profiles ID MENTAL-RETARDATION; FAMILIES; PARENTS AB Background The purpose of the present study was to determine the stress in mothers whose children have autism and to compare it with the stress in mothers whose children have Down's syndrome. Method Fifty mothers whose children had autism (n = 25) or Down's syndrome (n = 25) completed the Questionnaire on Resources and Stress (QRS) and answered some demographic questions. 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Bennetto, Loisa Yost, Kelley TI Patterns of nonverbal cognitive functioning in young children with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; nonverbal; cognitive functioning; preschool; Leiter-R ID DEVELOPMENTAL PSYCHOPATHOLOGY; COMMUNICATION DEFICITS; EXECUTIVE FUNCTIONS; ASPERGER-SYNDROME; CENTRAL COHERENCE; INFANTILE-AUTISM; LEITER-R; INDIVIDUALS; PERFORMANCE; ATTENTION AB Previous research demonstrates an uneven pattern of cognitive abilities in children with autism spectrum disorders (ASDs). This study examined whether this uneven pattern exists within the nonverbal domain in young children. We hypothesized relative strengths in perceptual abilities and weaknesses in nonverbal conceptual abilities in preschoolers with ASDs compared to groups with non-autism developmental delays and typical development. Profiles were examined using the Leiter International Performance Scale-Revised. The ASD group displayed clear relative strengths in visuospatial disembedding and detail-focused processing, with relative weaknesses in abstraction and concept formation. This contrasted with patterns of roughly equivalent abilities in both comparison groups. These findings have implications for subsequent development and may represent key features of the cognitive profile of autism. C1 Univ Rochester, Dept Clin & Social Sci Psychol, Rochester, NY 14627 USA. Univ Rochester, Sch Med & Dent, Dept Pediat, Rochester, NY 14627 USA. RP Bennetto, L (reprint author), Univ Rochester, Dept Clin & Social Sci Psychol, Box 270266, Rochester, NY 14627 USA. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 795 EP 807 DI 10.1007/s10803-006-0209-8 PG 13 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900001 PM 17004119 ER PT J AU Kroeger, KA Schultz, JR Newsom, C AF Kroeger, K. A. Schultz, Janet R. Newsom, Crighton TI A comparison of two group-delivered social skills programs for young children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; social skills; group interventions; early intervention; empirical design ID BEHAVIORAL TREATMENT; PRESCHOOL-CHILDREN; INTERVENTIONS; INITIATION; VALIDITY; PEERS; MODEL AB A social skills group intervention was developed and evaluated for young children with autism. Twenty-five 4- to 6-year-old (diagnosed) children were assigned to one of two kinds of social skills groups: the direct teaching group or the play activities group. The direct teaching group used a video-modeling format to teach play and social skills over the course of the intervention, while the play activities group engaged in unstructured play during the sessions. Groups met for 5 weeks, three times per week, 1 h each time. Data were derived and coded from videotapes of pre- and post-treatment unstructured play sessions. Findings indicated that while members of both groups increased prosocial behaviors, the direct teaching group made more gains in social skills. C1 Childrens Hosp, Med Ctr, Kelly OLeary Ctr Autism Spectrum Disorders, Cincinnati, OH 45229 USA. Xavier Univ, Cincinnati, OH 45207 USA. SW Ohio Dev Ctr, Batavia, IL USA. RP Kroeger, KA (reprint author), Childrens Hosp, Med Ctr, Kelly OLeary Ctr Autism Spectrum Disorders, MLC 4002,3333 Burnet Ave, Cincinnati, OH 45229 USA. 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W., 1998, ASSESSMENT BASIC LAN Pierce K, 1997, J APPL BEHAV ANAL, V30, P157, DOI 10.1901/jaba.1997.30-157 PIERCE K, 1995, J APPL BEHAV ANAL, V28, P285, DOI 10.1901/jaba.1995.28-285 Pierce K., 1997, FOCUS AUTISM OTHER D, V12, P207 Pollard NL, 1998, CHILD FAM BEHAV THER, V20, P1 Rogers SJ, 2000, J AUTISM DEV DISORD, V30, P399, DOI 10.1023/A:1005543321840 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 TARAS M, 1998, J BEHAV THER EXP PSY, V19, P275 Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 THORP DM, 1995, J AUTISM DEV DISORD, V25, P265, DOI 10.1007/BF02179288 Weiss M. J, 2001, REACHING OUT JOINING WILLIAMS TI, 1989, J AUTISM DEV DISORD, V19, P143, DOI 10.1007/BF02212726 WOLF MM, 1978, J APPL BEHAV ANAL, V11, P203, DOI 10.1901/jaba.1978.11-203 NR 42 TC 36 Z9 36 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 808 EP 817 DI 10.1007/s10803-006-0207-x PG 10 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900002 PM 16927011 ER PT J AU Thomas, KC Morrissey, JP McLaurin, C AF Thomas, Kathleen C. Morrissey, Joseph P. McLaurin, Carolyn TI Use of autism-related services by families and children SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT 4th International Meeting for Autism Research CY MAY 06-07, 2005 CL Boston, MA DE autism; services; treatment approach ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; BEHAVIORAL TREATMENT; SPECTRUM DISORDER; PROGRAM INTERVENTION; PARENTS; DIAGNOSIS; ADULTS; MODEL; NEEDS AB This paper describes approaches to care and associated service use by families with a child with autism. A combined telephone and self-administered survey was completed by 301 families with a child, 8 years old or younger, in North Carolina, during the winter of 2003-2004. Findings indicate that 66% of families used one or more approach to care and there was a significant (p < 0.05) association between approach and the pattern of service use. There appears to be a distinctive set of services associated with each approach to care, but with overlap between them. Speech/language therapy at school was the most frequently used service and also identified as the best service. The majority (81%) of families reported they were satisfied with services. C1 Univ N Carolina, Cecil G Sheps Ctr Hlth Serv Res, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Publ Hlth, Dept Hlth Policy & Adm, Chapel Hill, NC 27599 USA. RP Thomas, KC (reprint author), Univ N Carolina, Cecil G Sheps Ctr Hlth Serv Res, 725 Martin Luther King Jr Blvd,CB 7590, Chapel Hill, NC 27599 USA. EM Kathleen_thomas@unc.edu CR ALLEN SM, 1998, LIVING COMMUNITY DIS, P1 American Academy of Child and Adolescent Psychiatry, 1999, J AM ACAD CHILD PSY, V38, p32S Barry TD, 2003, J AUTISM DEV DISORD, V33, P685, DOI 10.1023/B:JADD.0000006004.86556.e0 Bimbrauer J. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 818 EP 829 DI 10.1007/s10803-006-0208-9 PG 12 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900003 PM 17146709 ER PT J AU Merhar, SL Manning-Courtney, P AF Merhar, S. L. Manning-Courtney, P. TI Two boys with 47, XXY and autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic spectrum disorders; autism; epilepsy; eeg; Klinefelter syndrome ID SPECTRUM DISORDERS; KLINEFELTER-SYNDROME; MENTAL-RETARDATION; SEIZURE DISORDERS; MEDICAL DISORDERS; EPILEPSY; CHILDREN; CHROMOSOME; EEG; ABNORMALITIES AB Two children with autism and Klinefelter syndrome (KS) (47, XXY) are presented. Both qualify for the diagnosis of autism based on DSM-IV with severely delayed and disordered language, difficulties with social interaction, and a restricted range of interests and activities. Both also have abnormal EEGs, and one patient has had what appear to be clinical seizures. Trials of antiepileptic medications have not been beneficial in either patient. We report the clinical and EEG findings of each patient, and discuss the implications of this combination of disorders. C1 Univ Penn, Med Ctr, Philadelphia, PA 19104 USA. Childrens Hosp, Med Ctr, Div Dev Disabil, Cincinnati, OH 45229 USA. RP Merhar, SL (reprint author), Childrens Hosp, Med Ctr, House Staff Dept, 3333 Burnet Ave, Cincinnati, OH 45229 USA. EM stephanie.merhar@cchmc.org CR Auranen M, 2002, AM J HUM GENET, V71, P777, DOI 10.1086/342720 Ballaban-Gil K, 2000, MENT RETARD DEV D R, V6, P300, DOI 10.1002/1098-2779(2000)6:4<300::AID-MRDD9>3.0.CO;2-R BENDER B, 1983, PEDIATRICS, V71, P262 Bojesen A, 2003, J CLIN ENDOCR METAB, V88, P622, DOI 10.1210/jc.2002-021491 BOLTSHAUSER E, 1978, J NEUROL, V219, P253, DOI 10.1007/BF00312978 Cohen D, 2005, J AUTISM DEV DISORD, V35, P103, DOI 10.1007/s10803-004-1038-2 Daoust AM, 2004, CLIN NEUROPHYSIOL, V115, P1368, DOI 10.1016/j.clinph.2004.01.011 ELIA M, 1995, AM J MENT RETARD, V100, P6 ELIA M, 1995, ITAL J NEUROL SCI, V16, P231, DOI 10.1007/BF02282994 FIEDLEROVA D, 1975, Electroencephalography and Clinical Neurophysiology, V39, P439 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Geschwind DH, 2000, MENT RETARD DEV D R, V6, P107, DOI 10.1002/1098-2779(2000)6:2<107::AID-MRDD4>3.0.CO;2-2 Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 Rossi PG, 2000, BRAIN DEV-JPN, V22, P102 GRAHAM JM, 1988, PEDIATRICS, V81, P795 Hollander E, 2001, J CLIN PSYCHIAT, V62, P530 Jamain S, 2003, NAT GENET, V34, P27, DOI 10.1038/ng1136 Kawasaki Y, 1997, J AUTISM DEV DISORD, V27, P605, DOI 10.1023/A:1025886228387 Kielinen M, 2004, AUTISM, V8, P49, DOI 10.1177/1362361304040638 Kobayashi R, 1998, ACTA PSYCHIAT SCAND, V98, P296, DOI 10.1111/j.1600-0447.1998.tb10087.x Konstantareas MM, 1999, J AUTISM DEV DISORD, V29, P275, DOI 10.1023/A:1022155201662 Lanfranco F, 2004, LANCET, V364, P273, DOI 10.1016/S0140-6736(04)16678-6 Laumonnier F, 2004, AM J HUM GENET, V74, P552, DOI 10.1086/382137 Lewine JD, 1999, PEDIATRICS, V104, P405, DOI 10.1542/peds.104.3.405 Mouridsen SE, 1999, DEV MED CHILD NEUROL, V41, P110, DOI 10.1017/S0012162299000213 Muhle R., 2004, PEDIATRICS, V113, P472 NIELSEN J, 1974, BRIT J PSYCHIAT, V125, P236, DOI 10.1192/bjp.125.3.236 OLSSON I, 1988, ARCH NEUROL-CHICAGO, V45, P666 Patwardhan AJ, 2000, NEUROLOGY, V54, P2218 Pavone P, 2004, NEUROPEDIATRICS, V35, P207, DOI 10.1055/s-2004-821079 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 Ratcliffe S, 1999, ARCH DIS CHILD, V80, P192 Robinson A, 1990, Birth Defects Orig Artic Ser, V26, P59 Samaco RC, 2004, HUM MOL GENET, V13, P629, DOI 10.1093/hmg/ddh063 SAMANGOSPROUSE C, 2000, NIH C EXP PHEN ID NE Shinnar S, 2001, PEDIATR NEUROL, V24, P183 Simpson JL, 2003, GENET MED, V5, P460, DOI 10.1097/01.GIM.0000095626.54201.D0 Tatum WO, 1998, PEDIATR NEUROL, V19, P275, DOI 10.1016/S0887-8994(98)00055-1 Temple CA, 2003, NEUROPSYCHOLOGIA, V41, P1547, DOI 10.1016/S0028-3932(03)00061-7 Tuchman R, 2002, LANCET NEUROL, V1, P352, DOI 10.1016/S1474-4422(02)00160-6 Tuchman R, 2000, J AUTISM DEV DISORD, V30, P485, DOI 10.1023/A:1005572128200 TUCHMAN RF, 1991, PEDIATRICS, V88, P1219 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 Vincent JB, 2004, AM J MED GENET B, V129B, P82, DOI 10.1002/ajmg.b.30069 Visootsak J, 2001, CLIN PEDIATR, V40, P639, DOI 10.1177/000992280104001201 VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 Warwick MM, 1999, J NEUROL NEUROSUR PS, V66, P628, DOI 10.1136/jnnp.66.5.628 WONG V, 1993, J CHILD NEUROL, V8, P316 NR 48 TC 11 Z9 11 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 840 EP 846 DI 10.1007/s10803-006-0211-1 PG 7 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900005 PM 16927010 ER PT J AU Thede, LL Coolidge, FL AF Thede, Linda L. Coolidge, Frederick L. TI Psychological and neurobehavioral comparisons of children with Asperger's disorder versus high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger's disorder; high-functioning autism; coolidge personality and neuropsychological inventory; executive functions deficits scale; autism; personality disorders ID PERSONALITY-DISORDER; HERITABILITY; CHILDHOOD; HYPERACTIVITY; EPIDEMIOLOGY; DYSFUNCTION; DEFICITS AB This study investigated personality and neurobehavioral differences between 16 children with Asperger's Disorder, 15 children with High-Functioning Autism (HFA), and 31 controls, all ranging in age from 5-17 years, M age = 10.7 years, SD = 3.0. Parents rated their children's behaviors on a 44-item autistic symptoms survey and on the 200-item Coolidge Personality and Neuropsychological Inventory (Coolidge, Thede, Stewart, & Segal (2002a). The Coolidge Personality and Neuropsychological Inventory for Children (CPNI): Preliminary psychometric characteristics. Behavior Modification, 26, 550-566). The results indicated that the two clinical samples were significantly elevated on the Executive Function Deficits scale and Attention-Deficit/Hyperactivity Disorder (ADHD) scale compared to controls. There were more similarities than differences between the two clinical samples on the personality scales, although the Asperger's group scored significantly on the two scales with anxiety components. C1 Univ Colorado, Dept Psychol, Colorado Springs, CO 80933 USA. RP Coolidge, FL (reprint author), Univ Colorado, Dept Psychol, POB 7150, Colorado Springs, CO 80933 USA. EM fcoolidg@uccs.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Coolidge F. L., 2004, BEHAV GENET, V34, P73 Coolidge F. 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PD MAY PY 2007 VL 37 IS 5 BP 847 EP 854 DI 10.1007/s10803-006-0212-0 PG 8 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900006 PM 16977495 ER PT J AU Lam, KSL Aman, MG AF Lam, Kristen S. L. Aman, Michael G. TI The repetitive behavior scale-revised: Independent validation in individuals with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; repetitive behavior; stereotypies; assessment; rating scale ID PERVASIVE DEVELOPMENTAL DISORDERS; OBSESSIVE-COMPULSIVE SCALE; DIAGNOSTIC INTERVIEW; SELF-STIMULATION; CHILDREN; RELIABILITY; EXPLORATION; PREVALENCE AB A key feature of autism is restricted repetitive behavior (RRB). Despite the significance of RRBs, little is known about their phenomenology, assessment, and treatment. The Repetitive Behavior Scale-Revised (RBS-R) is a recently-developed questionnaire that captures the breadth of RRB in autism. To validate the RBS-R in an independent sample, we conducted a survey within the South Carolina Autism Society. A total of 320 caregivers (32%) responded. Factor analysis produced a five-factor solution that was clinically meaningful and statistically sound. The factors were labeled "Ritualistic/Sameness Behavior," "Stereotypic Behavior," "Self-injurious Behavior," "Compulsive Behavior," and "Restricted Interests." Measures of internal consistency were high for this solution, and interrater reliability data suggested that the RBS-R performs well in outpatient settings. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. Ohio State Univ, Nisonger Ctr, Dept Psychol, Columbus, OH 43210 USA. Ohio State Univ, Nisonger Ctr, Dept Psychiat, Columbus, OH 43210 USA. RP Lam, KSL (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, CB 3367, Chapel Hill, NC 27599 USA. 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PD MAY PY 2007 VL 37 IS 5 BP 855 EP 866 DI 10.1007/s10803-006-0213-z PG 12 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900007 PM 17048092 ER PT J AU Kamio, Y Toichi, M AF Kamio, Yoko Toichi, Motomi TI Memory illusion in high-functioning autism and Asperger's disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high-functioning autism; Asperger's disorder; memory illusion; schema ID FALSE MEMORIES; INFANTILE-AUTISM; WORKING-MEMORY; CHILDREN; INDIVIDUALS; RECALL; TASK; FMRI; RECOGNITION; ASSOCIATION AB In this study, 13 individuals with high-functioning autism (HFA), 15 individuals with Asperger's disorder (AD), and age-, and IQ-matched controls were presented a list of sentences auditorily. Participants then evaluated semantically related but new sentences and reported whether they were old or new. The total rates of false recognition for semantically related sentences were similar among the three groups. Nevertheless, memory illusion on some aspects was reduced in HFA participants. These results suggest that HFA have difficulties in semantic association. Although individuals with AD showed no quantitative abnormalities of memory illusion, some contributing factors were atypical. These findings are discussed in terms of schema theory, enhanced perceptual processing hypothesis, and weak central coherence hypothesis. C1 Natl Ctr Neurol & Psychiat, Natl Inst Mental Hlth, Dept Child & Adolescent Mental Hlth, Kodaira, Tokyo 1878551, Japan. Kyoto Univ, Dept Med, Kyoto, Japan. RP Kamio, Y (reprint author), Natl Ctr Neurol & Psychiat, Natl Inst Mental Hlth, Dept Child & Adolescent Mental Hlth, 4-1-1 Ogawahigashi Cho, Kodaira, Tokyo 1878551, Japan. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 867 EP 876 DI 10.1007/s10803-006-0214-y PG 10 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900008 PM 17031448 ER PT J AU Leekam, SR Nieto, C Libby, SJ Wing, L Gould, J AF Leekam, Susan R. Nieto, Carmen Libby, Sarah J. Wing, Lorna Gould, Judith TI Describing the sensory abnormalities of children and adults with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE sensory abnormalities; Diagnostic Interview for Social and Communication Disorders (DISCO); autism; language impairment; learning disability; typical development ID DIAGNOSTIC INTERVIEW; COMMUNICATION DISORDERS; DEVELOPMENTAL DISORDERS; INDIVIDUALS; PERFORMANCE; SYMPTOMS AB Patterns of sensory abnormalities in children and adults with autism were examined using the Diagnostic Interview for Social and Communication Disorders (DISCO). This interview elicits detailed information about responsiveness to a wide range of sensory stimuli. Study 1 showed that over 90% of children with autism had sensory abnormalities and had sensory symptoms in multiple sensory domains. Group differences between children with autism and clinical comparison children were found in the total number of symptoms and in specific domains of smell/taste and vision. Study 2 confirmed that sensory abnormalities are pervasive and multimodal and persistent across age and ability in children and adults with autism. Age and IQ level affects some sensory symptoms however. Clinical and research implications are discussed. C1 Univ Durham, Sci Labs, Dept Psychol, Durham DH1 3LE, England. Univ Autonoma Madrid, Fac Psicol, Dept Psicol Basica, E-28049 Madrid, Spain. United Bristol Healthcare Trust, Chld & Adolescent Mental Hlth Serv, Bristol, Avon, England. Natl Autist Soc, Ctr Social & Commun Disorders, Bromley, Kent, England. RP Leekam, SR (reprint author), Univ Durham, Sci Labs, Dept Psychol, South Rd, Durham DH1 3LE, England. 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PD MAY PY 2007 VL 37 IS 5 BP 894 EP 910 DI 10.1007/s10803-006-0218-7 PG 17 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900011 PM 17016677 ER PT J AU Guptill, JT Booker, AB Gibbs, TT Kemper, TL Bauman, ML Blatt, GJ AF Guptill, Jeffrey T. Booker, Anne B. Gibbs, Terrell T. Kemper, Thomas L. Bauman, Margaret L. Blatt, Gene J. TI [H-3]-Flunitrazepam-labeled benzodiazepine binding sites in the hippocampal formation in autism: A multiple concentration autoradiographic study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE developmental disorder; autoradiography; hippocampus; GABAergic receptors; hippocampal circuitry ID TEMPORAL-LOBE EPILEPSY; INFANTILE-AUTISM; BRAIN; RECEPTORS; 15Q11-Q13; CHILDREN; SUBTYPES; NEURONS; RAT AB Increasing evidence indicates that the GABAergic system in cerebellar and limbic structures is affected in autism. We extended our previous study that found reduced [H-3]flunitrazepam-labeled benzodiazepine sites in the autistic hippocampus to determine whether this reduction was due to a decrease in binding site number (B-max) or altered affinity (K-d) to bind to the ligand. Quantitation of hippocampal lamina demonstrated a 20% reduction in B-max indicating a trend toward a decreased number of benzodiazepine binding sites in the autistic group but normal K-d values. A reduction in the number of hippocampal benzodiazepine binding sites suggests alterations in the modulation of GABA(A) receptors in the presence of GABA in the autistic brain, possibly resulting in altered inhibitory functioning of hippocampal circuitry. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Boston Univ, Sch Med, Dept Pharmacol & Therapeut, Boston, MA 02118 USA. RP Blatt, GJ (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St,R-1003, Boston, MA 02118 USA. 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Bryant TI Improving the reliability of autism diagnoses: Examining the utility of adaptive behavior SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism diagnosis; diagnostic reliability; autism spectrum disorders; Autism Diagnostic Interview-Revised (ADI-R); Autism Diagnostic Observation Schedule (ADOS); vineland; adaptive functioning ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; MENTAL-RETARDATION; DOWN-SYNDROME; ADI-R; CHILDREN; INTERVIEW; PRESCHOOLERS; ADOLESCENTS; DEFICITS AB The classification agreement of the Autism Diagnostic Interview-Revised (ADI-R) and the Autism Diagnostic Observation Schedule (ADOS) was examined in 129 children and adolescents (aged 7-18 years) who were evaluated for autism. Participants received a diagnosis of autism or non-autism based on the ADI-R. Linear discriminant analysis revealed adequate concordance between the ADI-R and ADOS, with 75% of the participants being correctly classified using the ADOS. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 929 EP 939 DI 10.1007/s10803-006-0232-9 PG 11 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900014 PM 17006775 ER PT J AU Walz, NC AF Walz, Nicolay Chertkoff TI Parent report of stereotyped behaviors, social interaction, and developmental disturbances in individuals with Angelman syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Angelman syndrome; autistic symptoms ID AUTISM; DISORDERS; PHENOTYPES; COMMUNICATION; SPECTRUM; PATTERNS; CHILDREN; UBE3A; GENE AB Research examining autistic symptoms in Angelman syndrome (AS) is limited. The goal of this study was to further characterize the nature of stereotyped behaviors, social interaction deficits, and developmental disturbances in individuals with AS. Parents of 248 individuals between the ages of 3 and 22 completed a survey of autistic symptomatology by mail, the Gilliam Autism Rating Scale. Results confirmed a high degree of developmental delay and limited expressive language skills. In terms of stereotyped behaviors and social interaction, areas of convergence and divergence between AS and behaviors typically associated with autism spectrum disorders are described. The relationship between child characteristics (age, gender, seizure disorder, genetic subtype) and autistic symptomatology are discussed. C1 Childrens Hosp, Med Ctr, Div Behav Med & Clin Psychol, Cincinnati, OH 45229 USA. Univ Cincinnati, Coll Med, Dept Pediat, Cincinnati, OH USA. RP Walz, NC (reprint author), Childrens Hosp, Med Ctr, Div Behav Med & Clin Psychol, 3333 Burnet Ave,MLC 3015, Cincinnati, OH 45229 USA. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 940 EP 947 DI 10.1007/s10803-006-0233-8 PG 8 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900015 PM 17019625 ER PT J AU Freitag, CM Kleser, C Schneider, M von Gontard, A AF Freitag, Christine M. Kleser, Christina Schneider, Marc von Gontard, Alexander TI Quantitative assessment of neuromotor function in adolescents with high functioning autism and Asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high functioning autism; Asperger syndrome; neuromotor function ID DIAGNOSTIC INTERVIEW; SPECTRUM DISORDER; MOTOR IMPAIRMENT; POSTURAL CONTROL; BASAL GANGLIA; GERMAN FORM; CHILDREN; MOVEMENT; BRAIN; PERFORMANCE AB Background: Motor impairment in children with Asperger Syndrome (AS) or High functioning autism (HFA) has been reported previously. This study presents results of a quantitative assessment of neuromotor skills in 14-22 year old HFA/AS. Methods: 16 HFA/AS and 16 IQ-matched controls were assessed by the Zurich Neuromotor Assessment (ZNA). Results: The HFA/AS group showed strongest impairments of dynamic balance skills and diadochokinesis. Motor abilities were associated with degree of social withdrawal in the full sample and severity of current autistic symptoms in the HFA/AS group. Conclusion: Similar motor patterns as in younger children were found in the older adolescents. The association of autistic symptoms with motor performance points towards an essential role of motor impairment in autism spectrum disorders. C1 Saarland Univ Hosp, Dept Child & Adolescent Psychiat, D-66421 Homburg, Saar, Germany. Saarland Univ Hosp, Inst Forens Psychiat, D-66421 Homburg, Saar, Germany. RP Freitag, CM (reprint author), Saarland Univ Hosp, Dept Child & Adolescent Psychiat, D-66421 Homburg, Saar, Germany. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 948 EP 959 DI 10.1007/s10803-006-0235-6 PG 12 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900016 PM 17171541 ER PT J AU Wetherby, AM Watt, N Morgan, L Shumway, S AF Wetherby, Amy M. Watt, Nola Morgan, Lindee Shumway, Stacy TI Social communication profiles of children with autism spectrum disorders late in the second year of life SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; ASD; social communication; early identification; joint attention ID PERVASIVE DEVELOPMENTAL DISORDERS; JOINT ATTENTION; YOUNG-CHILDREN; PREDICTIVE-VALIDITY; EARLY RECOGNITION; HOME VIDEOTAPES; INFANTS; LANGUAGE; AGE; IDENTIFICATION AB This study examined social communication profiles from behavior samples videotaped between 18 and 24 months of age in three groups of children: 50 with autism spectrum disorders (ASD), 23 with developmental delays (DD), and 50 with typical development (TD). The ASD group scored significantly lower than the DD group on 5 social communication measures and the TD group on all 14 measures, indicating distinct profiles late in the second year. Understanding was the strongest predictor of developmental level and behavior regulation and inventory of gestures were the strongest predictors of autism symptoms at 3 years of age. The predictive relations suggest five pivotal skills late in the second year that have a cascading effect on outcomes of children with ASD. C1 Florida State Univ, Dept Commun Disorders, Tallahassee, FL 32306 USA. RP Wetherby, AM (reprint author), Florida State Univ, Dept Commun Disorders, RRC 107, Tallahassee, FL 32306 USA. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 960 EP 975 DI 10.1007/s10803-006-0237-4 PG 16 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900017 PM 17066310 ER PT J AU Baxter, AC Lotspeich, LJ Spiker, D Martin, JL Grether, JK Hallmayer, JF AF Baxter, Alisa C. Lotspeich, Linda J. Spiker, Donna Martin, Jacquelin L. Grether, Judith K. Hallmayer, Joachim F. TI Brief report: Effect of maternal age on severity of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic; autism; maternal age; IQ; social impairments; severity ID PERINATAL RISK-FACTORS; INFANTILE-AUTISM; OBSTETRIC COMPLICATIONS; MULTIPLEX FAMILIES; NEONATAL FACTORS; BIRTH-ORDER; CHILDREN; POPULATION; DISORDER; EPIDEMIOLOGY AB The etiology of autism is complex, consisting of unknown genetic and environmental factors. Previous studies have revealed that maternal age is increased in autism compared to controls, making it a possible risk factor. 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TI Brief report: The impact of subcortical band heterotopia and associated complications on the neuropsychological functioning of a 13-year-old child SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE subcortical band heterotopia; cognitive development; epilepsy; neuropsychological assessment ID DOUBLE CORTEX SYNDROME; MRI; DOUBLECORTIN; MUTATIONS; EEG AB Motor impairment in children with Asperger syndrome (AS) or high functioning autism (HFA) has been reported previously. This study presents results of a quantitative assessment of neuromotor skills in 14-22 year old HFA/AS. Sixteen HFA/AS and 16 IQ-matched controls were assessed by the Zurich Neuromotor Assessment (ZNA). The HFA/AS group showed strongest impairments of dynamic balance skills and diadochokinesis. Motor abilities were associated with degree of social withdrawal in the full sample and severity of current autistic symptoms in the HFA/AS group. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 983 EP 992 DI 10.1007/s10803-006-0236-5 PG 10 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900019 PM 17160462 ER PT J AU McGinnis, WR AF McGinnis, Woody R. TI Could oxidative stress from psychosocial stress affect neurodevelopment in autism? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID CELL-DEATH; BRAIN; GLUCOCORTICOIDS; DAMAGE; DNA C1 Oxidat Stress Autism Study, Ashland, OR 97520 USA. RP McGinnis, WR (reprint author), Oxidat Stress Autism Study, 944 Pinecrest Terrace, Ashland, OR 97520 USA. 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Autism Dev. Disord. PD MAY PY 2007 VL 37 IS 5 BP 993 EP 994 DI 10.1007/s10803-007-0372-6 PG 2 WC Psychology, Developmental SC Psychology GA 169HS UT WOS:000246583900020 PM 17404828 ER PT J AU Sainsbury, W AF Sainsbury, Willow TI Autism, brain, and environment. SO JOURNAL OF BIOSOCIAL SCIENCE LA English DT Book Review C1 Univ Oxford Magdalen Coll, Oxford OX1 4AU, England. RP Sainsbury, W (reprint author), Univ Oxford Magdalen Coll, Oxford OX1 4AU, England. CR Cohen JT, 2005, AM J PREV MED, V29, P366, DOI 10.1016/j.ampere.2005.06.008 Lathe R, 2006, AUTISM BRAIN ENV Reichenberg A, 2006, ARCH GEN PSYCHIAT, V63, P1026, DOI 10.1001/archpsyc.63.9.1026 NR 3 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0021-9320 J9 J BIOSOC SCI JI J. Biosoc. Sci. PD MAY PY 2007 VL 39 IS 3 BP 475 EP 477 DI 10.1017/S0021932007001897 PG 3 WC Demography; Public, Environmental & Occupational Health; Social Sciences, Biomedical SC Demography; Public, Environmental & Occupational Health; Biomedical Social Sciences GA 162KJ UT WOS:000246085700012 ER PT J AU Gutkovich, ZA Carlson, GA Carlson, HE Coffey, B Wieland, N AF Gutkovich, Zinoviy A. Carlson, Gabrielle A. Carlson, Harold E. Coffey, Barbara Wieland, Natalie TI Asperger's disorder and co-morbid bipolar disorder: Diagnostic and treatment challenges SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDER; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; INSULIN-RESISTANCE; WEIGHT-GAIN; CHILDREN; AUTISM; ADOLESCENTS; LITHIUM; ANTIPSYCHOTICS C1 Zucker Hillside Hosp, N Shore Long Isl Jewish Hlth Syst, Dept Psychiat, Div Adolescent & Child Psychiat, Glen Oaks, NY 11004 USA. SUNY Stony Brook, Sch Med, Stony Brook, NY USA. NYU, Ctr Child Study, New York, NY USA. RP Gutkovich, ZA (reprint author), Zucker Hillside Hosp, N Shore Long Isl Jewish Hlth Syst, Dept Psychiat, Div Adolescent & Child Psychiat, Ambulatory Care Pavil,Lower Level 75-59 263rd St, Glen Oaks, NY 11004 USA. 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Child Adolesc. Psychopharmacol. PD MAY PY 2007 VL 17 IS 2 BP 247 EP 255 DI 10.1089/cap.2007.1723 PG 9 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 167XP UT WOS:000246486200012 PM 17489721 ER PT J AU Shulman, C Guberman, A AF Shulman, Cory Guberman, Ainat TI Acquisition of verb meaning through syntactic cues: A comparison of children with autism, children with specific language impairment (SLI) and children with typical language development (TLD) SO JOURNAL OF CHILD LANGUAGE LA English DT Article ID SPECTRUM; DISORDER AB The ability to extract meaning through the use of syntactic cues, adapted from Naigles' (1990) paradigm, was investigated in Hebrew-speaking children with autism, those with specific language impairment (SLI) and those with typical language development (TLD), in an attempt to shed light on similarities and differences between the two diagnostic categories, both defined by primary language deficits. Thirteen children with autism and 13 with SLI were matched on chronological age, level of language functioning and gender, and 13 children with TLD were matched to the children in the two clinical groups according to language level, as measured by the CELF-P. Children with autism and children with TLD learned novel words using the syntactical cues in the sentences in which they were presented, whereas children with SLI experienced more difficulty, learning only that which would be expected from chance according to the binomial test. Only 4 of the 13 children with SLI (31%) learned the new words, whereas 11 children with autism and 10 children with TLD learned the novel verb using syntactical cues from the sentence frame. The results are analyzed in terms of possible underlying mechanisms in language acquisition. Children with autism seem to rely on relatively intact syntactic abilities, while children with SLI seem to have marked impairment in using this mechanism in acquiring word meaning. Implications for future research and intervention with preschool children with primary language disorders are discussed. C1 Hebrew Univ Jerusalem, Sch Social Work, IL-91905 Jerusalem, Israel. RP Shulman, C (reprint author), Hebrew Univ Jerusalem, Sch Social Work, IL-91905 Jerusalem, Israel. EM mscory@msce.huji.ac.il CR *AM PSYCH ASS, 1994, SM IV DIAGN STAT MAN BARTAK L, 1975, BRIT J PSYCHIAT, V126, P127, DOI 10.1192/bjp.126.2.127 Charman T, 2003, J CHILD LANG, V30, P213, DOI 10.1017/S0305000902005482 EYAL S, 1990, TRANSLATION CELF P FERNANDES KJ, 2005, P 29 ANN BOST U C LA, V1, P192 Gleitman Lila, 1990, LANG ACQUIS, V1, P3, DOI DOI 10.1207/S153278171A0101_2 HOWLIN P, 1984, J AUTISM DEV DISORD, V14, P127, DOI 10.1007/BF02409656 Leonard L. 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H., 1992, CELF P CLIN EVALUATI World Health Organisation, 1992, ICD 10 CLASS MENT BE Ziatas K, 2003, DEV PSYCHOPATHOL, V15, P73, DOI 10.1017/S0954579403000051 NR 26 TC 9 Z9 9 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0305-0009 J9 J CHILD LANG JI J. Child Lang. PD MAY PY 2007 VL 34 IS 2 BP 411 EP 423 DI 10.1017/S0305000906007963 PG 13 WC Psychology, Developmental; Linguistics; Psychology, Experimental SC Psychology; Linguistics GA 170NJ UT WOS:000246669900008 PM 17542163 ER PT J AU Chez, MG Burton, Q Dowling, T Chang, MN Khanna, P Kramer, C AF Chez, Michael G. Burton, Quinn Dowling, Timothy Chang, Mina Khanna, Pavan Kramer, Christopher TI Memantine as adjunctive therapy in children diagnosed with autistic spectrum disorders: An observation of initial clinical response and maintenance tolerability SO JOURNAL OF CHILD NEUROLOGY LA English DT Article DE autism treatment; pervasive developmental disorders; memantine ID ABNORMALITIES; BRAIN; TRIALS AB Autism and Pervasive Developmental Disorder Not Otherwise Specified are common developmental problems often seen by child neurologists. There are currently no cures for these lifelong and socially impairing conditions that affect core domains of human behavior such as language, social interaction, and social awareness. The etiology may be multifactorial and may include autoimmune, genetic, neuroanatomic, and possibly excessive glutaminergic mechanisms. Because memantine is a moderate affinity antagonist of the N-methyl-D-aspartic acid (NMDA) glutamate receptor, this drug was hypothesized to potentially modulate learning, block excessive glutamate effects that can include neuroinflammatory activity, and influence neuroglial activity in autism and Pervasive Developmental Disorder Not Otherwise Specified. Open-label add-on therapy was offered to 15 1 patients with prior diagnoses of autism or Pervasive Developmental Disorder Not Otherwise Specified over a 21-month period. To generate a clinician-derived Clinical Global Impression Improvement score for language, behavior, and self-stimulatory behaviors, the primary author observed the subjects and questioned their caretakers within 4 to 8 weeks of the initiation of therapy. Chronic maintenance therapy with the drug was continued if there were no negative side effects. Results showed significant improvements in open-label use for language function, social behavior, and self-stimulatory behaviors, although self-stimulatory behaviors comparatively improved to a lesser degree. Chronic use so far appears to have no serious side effects. C1 Rosalind Franklin Univ, Chicago Med Sch, Dept Neurol, Chicago, IL USA. Illinois State Univ, Normal, IL 61761 USA. RP Chez, MG (reprint author), 2800 L St,Suite 501, Sacramento, CA 95816 USA. EM mchezmd@yahoo.net CR Aman MG, 2004, CNS SPECTRUMS, V9, P36 American Psychiatric Association, 2000, DIAGN STAT MAN MENT BAUMAN M, 1985, NEUROLOGY, V35, P866 Bauman M.L, 1994, NEUROBIOLOGY AUTISM Chez MG, 2004, ANN NEUROL S, V56, P109 Chez MG, 2003, J PEDIAT NEUROL, V1, P83 CHEZ MG, 2004, EPILEPSIA S, V45, P406 Chez MG, 2006, EPILEPSY BEHAV, V8, P267, DOI 10.1016/j.yebeh.2005.11.001 Chez MG, 2004, J CHILD NEUROL, V19, P165 *FOR LAB, 2005, NAM MEM HYDR PRESCR GUY W, 1976, PUBLICATION US DEP H, V76, P218 Hardan AY, 2002, J CHILD ADOL PSYCHOP, V12, P237, DOI 10.1089/104454602760386923 Hollander E, 2004, CNS SPECTRUMS, V9, P49 King BH, 2001, J AM ACAD CHILD PSY, V40, P658, DOI 10.1097/00004583-200106000-00010 Parsons CG, 1999, NEUROPHARMACOLOGY, V38, P735, DOI 10.1016/S0028-3908(99)00019-2 Perry EK, 2001, AM J PSYCHIAT, V158, P1058, DOI 10.1176/appi.ajp.158.7.1058 Posey DJ, 2004, AM J PSYCHIAT, V161, P2115, DOI 10.1176/appi.ajp.161.11.2115 Purcell AE, 2001, NEUROLOGY, V57, P1618 Schieve L. A., 2006, Morbidity and Mortality Weekly Report, V55, P481 Vargas DL, 2005, ANN NEUROL, V57, P67, DOI 10.1002/ana.20315 NR 20 TC 86 Z9 87 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD MAY PY 2007 VL 22 IS 5 BP 574 EP 579 DI 10.1177/0883073807302611 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 179IV UT WOS:000247283900009 PM 17690064 ER PT J AU Brimacombe, M Ming, X Parikh, A AF Brimacombe, Michael Ming, Xue Parikh, Amisha TI Familial risk factors in autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article DE autism; family history; psychiatric disorders; developmental disorders; epidemiology ID SPECTRUM DISORDERS; PRADER-WILLI; HISTORY; TWIN; RELATIVES; HEALTH; PAIRS AB Familial history risk factors in relation to autism were examined in a cohort of 164 autistic children referred to The Autism Center at New Jersey Medical School-University of Medicine and Dentistry of New Jersey, Newark, over a 2-year period (2001-2003). Information related to familial history was obtained from each family and reviewed by a clinician. It is shown that these families carry a higher overall burden of psychiatric and developmental illnesses compared to reported national levels. These families also carry a relatively high incidence of medical disorders, independently of developmental and psychiatric disorders. This work supports the underlying presence of genetic factors in the etiology of autism. C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Prevent Med, Newark, NJ 07101 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurol, Newark, NJ 07103 USA. RP Brimacombe, M (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Prevent Med, 185 S Orange Ave,PO Box 1709, Newark, NJ 07101 USA. EM brimacmb@umdnj.edu CR Bacchelli E, 2006, AM J MED GENET C, V142C, P13, DOI 10.1002/ajmg.c.30078 Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BAILEY A, 1995, PSYCHOL MED, V25, P63 Benayed R, 2005, AM J HUM GENET, V77, P851, DOI 10.1086/497705 Centers for Disease Control and Prevention, 2002, BEH RISK FACT SURV S Chagnon YC, 2005, INT REV NEUROBIOL, V71, P419, DOI 10.1016/S0074-7742(05)71017-5 Comi AM, 1999, J CHILD NEUROL, V14, P388, DOI 10.1177/088307389901400608 Dhossche DM, 2005, INT REV NEUROBIOL, V71, P189, DOI 10.1016/S0074-7742(05)71009-6 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Herbert MR, 2006, NEUROTOXICOLOGY, V27, P671, DOI 10.1016/j.neuro.2006.03.017 Juul-Dam N, 2001, PEDIATRICS, V107, part. no., DOI 10.1542/peds.107.4.e63 Koochek M, 2006, CLIN GENET, V69, P124, DOI 10.1111/j.1399-0004.2005.00560.x Larsson HJ, 2005, AM J EPIDEMIOL, V161, P916, DOI 10.1093/aje/kwi123 LaSalle JM, 2005, INT REV NEUROBIOL, V71, P131, DOI 10.1016/S0074-7742(05)71006-0 MING X, 2006, 10 INT CHILD NEUR C Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 RITVO ER, 1985, AM J PSYCHIAT, V142, P74 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Szatmari P, 2000, J CHILD PSYCHOL PSYC, V41, P579, DOI 10.1017/S0021963099005831 Veltman MWM, 2005, PSYCHIAT GENET, V15, P243, DOI 10.1097/00041444-200512000-00006 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 Ylisaukko-oja T, 2006, ANN NEUROL, V59, P145, DOI 10.1002/ana.20722 Yoon PW, 2002, GENET MED, V4, P304, DOI 10.1097/00125817-200207000-00009 NR 23 TC 6 Z9 6 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0883-0738 J9 J CHILD NEUROL JI J. 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PD MAY PY 2007 VL 22 IS 5 BP 593 EP 597 DI 10.1177/0883073807302609 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 179IV UT WOS:000247283900012 PM 17690067 ER PT J AU Banaschewski, T Brandeis, D AF Banaschewski, Tobias Brandeis, Daniel TI Annotation: What electrical brain activity tells us about brain function that other techniques cannot tell us - a child psychiatric perspective SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE ADHD; anorexia nervosa; anxiety; autism; childhood-onset schizophrenia; depression; developmental dyslexia; EEG; endophenotypes; ERP; fMRI; neuropsychology; obsessive-compulsive disorder; specific language disorder; tic disorder ID EVENT-RELATED POTENTIALS; DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; AUTISM SPECTRUM DISORDER; OBSESSIVE-COMPULSIVE DISORDER; SLOW CORTICAL POTENTIALS; MISMATCH NEGATIVITY MMN; MEDIAL FRONTAL-CORTEX; SELECTIVE-ATTENTION; RESPONSE-INHIBITION AB Background: Monitoring brain processes in real time requires genuine subsecond resolution to follow the typical timing and frequency of neural events. Non-invasive recordings of electric (EEG/ERP) and magnetic (MEG) fields provide this time resolution. They directly measure neural activations associated with a wide variety of brain states and processes, even during sleep or in infants. Mapping and source estimation can localise these time-varying activation patterns inside the brain. Methods: Recent EEG/ERP research on brain functions in the domains of attention and executive functioning, perception, memory, language, emotion and motor processing in ADHD, autism, childhood-onset schizophrenia, Tourette syndrome, specific language disorder and developmental dyslexia, anxiety, obsessive-compulsive disorder, and depression is reviewed. Results: Over the past two decades, electrophysiology has substantially contributed to the understanding of brain functions during normal development, and psychiatric conditions of children and adolescents. 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Child Psychol. Psychiatry PD MAY PY 2007 VL 48 IS 5 BP 415 EP 435 DI 10.1111/j.1469-7610.2006.01681.x PG 21 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 166SE UT WOS:000246399500002 PM 17501723 ER PT J AU Reiersen, AM Constantino, JN Volk, HE Todd, RD AF Reiersen, Angela M. Constantino, John N. Volk, Heather E. Todd, Richard D. TI Autistic traits in a population-based ADHD twin sample SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE ADHD; autism; PDD; Social Responsiveness Scale ID DEFICIT-HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDER; RECIPROCAL SOCIAL-BEHAVIOR; DSM-IV; LATENT CLASS; GENERAL-POPULATION; ADOLESCENT TWINS; SUBTYPES; CHILDREN AB Background: Most diagnostic nomenclatures do not allow for the concurrent diagnosis of autism and attention-deficit/hyperactivity disorder (ADHD). Clinic-based studies suggest autistic symptoms are common in children with ADHD, but such studies are prone to referral bias. This study assesses whether children with ADHD selected from the general twin population have elevated levels of autistic traits. Methods: Nine hundred forty-six twins identified by Missouri birth records were assigned to DSM-IV ADHD diagnoses and seven population-derived ADHD subtypes defined through latent class analysis of DSM-IV ADHD symptoms. The Social Responsiveness Scale (SRS) was used as a quantitative measure of autistic traits. Linear regression was used to evaluate whether mean SRS scores differed between ADHD diagnostic groups. Results: Mean SRS scores for DSM-IV predominantly inattentive subtype and combined subtype ADHD groups were significantly higher than for subjects without DSM-IV ADHD (p < .001, both comparisons). Five of the population-derived ADHD subtypes (talkative-impulsive, mild and severe inattentive, mild and severe combined) had significantly higher mean SRS scores compared to the latent class subtype with few ADHD symptoms (p < .001, all comparisons). DSM-IV combined subtype and the population-derived severe combined subtype had the highest mean total SRS scores and the highest mean scores for each of the three autism symptom domains, with a substantial proportion of individuals scoring in the clinically significant range. Conclusions: This study provides population-based evidence for clinically significant elevations of autistic traits in children meeting diagnostic criteria for ADHD. These results have implications for the design and interpretation of studies of both disorders. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. St Louis Univ, Sch Publ Hlth, Doctoral Program Publ Hlth Studies, St Louis, MO 63103 USA. Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA. RP Reiersen, AM (reprint author), Washington Univ, Sch Med, Dept Psychiat, Box 8134,660 S Euclid Ave, St Louis, MO 63110 USA. EM reiersea@psychiatry.wustl.edu CR Achenbach T. 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Child Psychol. Psychiatry PD MAY PY 2007 VL 48 IS 5 BP 464 EP 472 DI 10.1111/j.1469-7610.2006.01720.x PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 166SE UT WOS:000246399500006 PM 17501727 ER PT J AU Howlin, P Gordon, RK Pasco, G Wade, A Charman, T AF Howlin, Patricia Gordon, R. Kate Pasco, Greg Wade, Angie Charman, Tony TI The effectiveness of Picture Exchange Communication System (PECS) training for teachers of children with autism: a pragmatic, group randomised controlled trial SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE randomised controlled trial; PECS; autism; intervention; communication ID SPECTRUM DISORDERS; YOUNG-CHILDREN; INTERVENTION; SPEECH; CHALLENGES; OUTCOMES AB Background: To assess the effectiveness of expert training and consultancy for teachers of children with autism spectrum disorder in the use of the Picture Exchange Communication System (PECS). Method: Design: Group randomised, controlled trial (3 groups: immediate treatment, delayed treatment, no treatment). Participants: 84 elementary school children, mean age 6.8 years. Treatment: A 2-day PECS workshop for teachers plus 6 half-day, school-based training sessions with expert consultants over 5 months. Outcome measures: Rates of: communicative initiations, use of PECS, and speech in the classroom; Autism Diagnostic Observation Schedule-Generic (ADOS-G) domain scores for Communication and Reciprocal Social Interaction; scores on formal language tests. Results: Controlling for baseline age, developmental quotient (DQ) and language; rates of initiations and PECS usage increased significantly immediately post-treatment (Odds Ratio (OR) of being in a higher ordinal rate category 2.72, 95% confidence interval 1.22-6.09, p < .05 and OR 3.90 (95%CI 1.75-8.68), p < .001, respectively). There were no increases in frequency of speech, or improvements in ADOS-G ratings or language test scores. Conclusions: The results indicate modest effectiveness of PECS teacher training/consultancy. Rates of pupils' initiations and use of symbols in the classroom increased, although there was no evidence of improvement in other areas of communication. Treatment effects were not maintained once active intervention ceased. C1 Kings Coll London, Inst Psychiat, London SE5 8AE, England. Univ London, St Georges Hosp Med Sch, London WC1E 7HU, England. Kings Coll London, Inst Child Hlth, London SE5 8AE, England. RP Howlin, P (reprint author), Kings Coll London, Inst Psychiat, Denmark Hill, London SE5 8AE, England. 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Happe, Francesca TI Eye-witness memory and suggestibility in children with Asperger syndrome SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE Asperger syndrome; autistic disorder; memory; eye-witness; suggestibility; executive function ID AUTISTIC-CHILDREN; FUNCTIONING AUTISM; EPISODIC MEMORY; RECALL; ADULTS; RECOGNITION; ACCOUNT; INTACT; EVENTS AB Background: Individuals with autism spectrum disorders (ASD) present with a particular profile of memory deficits, executive dysfunction and impaired social interaction that may raise concerns about their recall and reliability in forensic and legal contexts. Extant studies of memory shed limited light on this issue as they involved either laboratory-based tasks or protocols that varied between participants. Method: The current study used a live classroom event to investigate eye-witness recall and suggestibility in children with Asperger syndrome (AS group; N = 24) and typically developing children (TD group; N = 27). All participants were aged between 11 and 14 years and were interviewed using a structured protocol. Two measures of executive functioning were also administered. Results: The AS group were found to be no more suggestible and no less accurate than their peers. However, free recall elicited less information, including gist, in the AS group. TD, but not AS, participants tended to focus on the socially salient aspects of the scene in their free recall. Both general and specific questioning elicited similar numbers of new details in both groups. Significant correlations were found between memory recall and executive functioning performance in the AS group only. Conclusions: The present study indicates that children with AS can act as reliable witnesses but they may be more reliant on questioning to facilitate recall. Our findings also provide evidence for poor gist memory. It is speculated that such differences stem from weak central coherence and lead to a reliance on generic cognitive processes, such as executive functions, during recall. Future studies are required to investigate possible differences in compliance, rates of forgetting and false memory. C1 UCL, Anna Freud Ctr, London SW3 5SD, England. Kings Coll London, Dept Psychol, Inst Psychiat, London WC2R 2LS, England. Kings Coll London, Social Genet & Dev Psychiat Ctr, Inst Psychiat, London WC2R 2LS, England. RP McCrory, E (reprint author), UCL, Anna Freud Ctr, 21 Maresfield Gardens, London SW3 5SD, England. 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TI Joint attention and symbolic play in young children with autism: a randomized controlled intervention study (vol 47, pg 611, 2006) SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Correction CR Kasari C, 2006, J CHILD PSYCHOL PSYC, V47, P611, DOI 10.1111/j.1469-7610.2005.01567.x LIFTER K, 1993, J EARLY INTERVENTION, V17, P139 NR 2 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD MAY PY 2007 VL 48 IS 5 BP 523 EP 523 DI 10.1111/j.1469-7610.2007.01768.x PG 1 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 166SE UT WOS:000246399500013 ER PT J AU Macarov, M Zeigler, M Newman, JP Strich, D Sury, V Tennenbaum, A Meiner, V AF Macarov, M. Zeigler, M. Newman, J. P. Strich, D. Sury, V. Tennenbaum, A. Meiner, V. TI Deletions of VCX-A and NLGN4: a variable phenotype including normal intellect SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE contiguous gene syndrome; intellectual disability; NLGN4; VCX-A; Xp22.3 ID X-LINKED ICHTHYOSIS; DISTAL SHORT ARM; MENTAL-RETARDATION; GENE FAMILY; CHROMOSOME; AUTISM; MUTATIONS; BATTERY; MEMBER; XP22.3 AB Background Patients with Xp22.3 interstitial and terminal deletions have been shown to be affected by intellectual disability ( ID) or autism. Previously, VCX-A (variably charged protein X-A), located at Xp22 was introduced as a gene for ID and its presence was suggested to be sufficient to maintain normal mental development. Recent reports suggest that mutations in NLGN(4) ( neuroligin (4)), located at that same region, are involved in autistic disorders and ID. Methods In the current case study, we clinically and molecularly describe a pedigree of three generations affected by contiguous gene syndrome that includes features of X-linked ichthyosis and Kallmann syndrome. Results Molecular analysis revealed the presence of an interstitial deletion spanning approximately 4.5 Mb at Xp22.3 The centromeric breakpoint was localized between markers DXS1467 and DXS8051, proximal to KAL-I. The telomeric breakpoint was localized between markers DXS89 and DXS1060, distal to NLGN(4). The deletion of VCX-A and NLGN(4). in this family prompted us to examine the cognitive functions of our two adult patients using comprehensive intellectual and neurocognitive assessment. Normal intellectual function was found in one patient and mild ID was revealed in the other. Neither patient met any Diagnostic and Statistical Manual of Mental Disorder, Fourth Edition criteria for a pervasive developmental disorder such as autism. Conclusions These findings suggest that deletion of VCX-A and NLGN. can result in variable phenotypic features and that normal mental development can be achieved despite this deletion, emphasizing the importance of environmental factors and possible modifier genes. Conclusions These findings suggest that deletion of VCX-A and NLGN(4). can result in variable phenotypic features and that normal mental development can be achieved despite this deletion, emphasizing the importance of environmental factors and possible modifier genes. C1 Hadassh Univ, Dept Human Genet, Sch Med, Jerusalem, Israel. Hadassah Univ Hosp, IL-91120 Jerusalem, Israel. Hadassh Univ, Dept Neurol, Jerusalem, Israel. Hadassh Univ, Agnes Ginges Human Neurogenet, Jerusalem, Israel. Clait Hlth Serv, Pediat Special Clin Endocrinol & Diabetes, Jerusalem, Israel. Jerusalem Inst Child Dev, Jerusalem, Israel. RP Meiner, V (reprint author), Hadassh Univ, Dept Human Genet, Sch Med, POB 12000, Jerusalem, Israel. EM vmeiner@hadassah.org.il CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Ballabio Andrea, 1992, Human Molecular Genetics, V1, P221, DOI 10.1093/hmg/1.4.221 BALLABIO A, 1989, P NATL ACAD SCI USA, V86, P10001, DOI 10.1073/pnas.86.24.10001 Doherty MJ, 2003, EPILEPSIA, V44, P1529, DOI 10.1111/j.0013-9580.2003.61702.x Dubois B, 2000, NEUROLOGY, V55, P1621 FOLSTEIN MF, 1975, J PSYCHIAT RES, V12, P189, DOI 10.1016/0022-3956(75)90026-6 Fukami M, 2000, AM J HUM GENET, V67, P563, DOI 10.1086/303047 Jamain S, 2003, NAT GENET, V34, P27, DOI 10.1038/ng1136 Lahn BT, 2000, HUM MOL GENET, V9, P311, DOI 10.1093/hmg/9.2.311 Laumonnier F, 2004, AM J HUM GENET, V74, P552, DOI 10.1086/382137 Lesca G, 2005, CLIN GENET, V67, P367, DOI 10.1111/j.1399-0004.2005.00417.x Mathuranath PS, 2000, NEUROLOGY, V55, P1613 SCHAEFER L, 1993, NAT GENET, V4, P272, DOI 10.1038/ng0793-272 Soussi-Yanicostas N, 1998, J CELL SCI, V111, P2953 Tobias ES, 2001, J MED GENET, V38, P466, DOI 10.1136/jmg.38.7.466 Van Esch H, 2005, HUM MOL GENET, V14, P1795, DOI 10.1093/hmg/ddi186 Vincent JB, 2004, AM J MED GENET B, V129B, P82, DOI 10.1002/ajmg.b.30069 Wechsler D, 1981, WECHSLER ADULT INTEL NR 18 TC 34 Z9 34 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD MAY PY 2007 VL 51 BP 329 EP 333 DI 10.1111/j.1365-2788.2006.00880.x PN 5 PG 5 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 149QM UT WOS:000245161700001 PM 17391250 ER PT J AU Jauregi, J Arias, C Vegas, O Alen, F Martinez, S Copet, P Thuilleaux, D AF Jauregi, J. Arias, C. Vegas, O. Alen, F. Martinez, S. Copet, P. Thuilleaux, D. TI A neuropsychological assessment of frontal cognitive functions in Prader-Willi syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE cognitive profile; frontal functions; neuropsychological assessment; Prader-Willi syndrome; social cognition ID OSTERRIETH COMPLEX FIGURE; EXECUTIVE FUNCTION; BIRTH INCIDENCE; AUTISM; DISORDERS; MIND; CHILDREN; LANGUAGE; BEHAVIOR; DELETION AB Background Prader-Willi syndrome (PWS) is associated with a characteristic behavioural phenotype whose main features are, alongside compulsive hyperphagia, deficits in social behaviour: social withdrawal, temper tantrums, perseverative speech and behaviour, mental rigidity, stereotyped behaviour, impulsiveness, etc. Similar symptoms may also be found in autistic spectrum disorders and lesional pathologies of the frontal lobe. In both cases, such symptoms have been related to dysfunctions in frontal cognitive processes such as attention, working memory and executive functions. This study uses standardized neuropsychological instruments to analyse the degree to which these processes are affected in PWS. Methods The sample comprised 16 individuals with a genetically confirmed PWS diagnosis. Subjects' IQ (Wechsler Adult Intelligence Scale), academic level, laterality and body mass index (BMI) were calculated. Attention, memory and executive functions were analysed using standard, widely employed neuropsychological tests. We compared the results of the sample group with the general population. Correlation analyses were carried out with IQ, academic level and BMI. Results In all the neuropsychological measures focusing on attention, executive functions and visuoperceptual organization, the study sample scored significantly lower than the normative reference population. The scores of the tests used for measuring immediate memory were also significantly lower when trials required sequential processing, although not when they required simultaneous processing. In the memorization of a list of words, subjects showed an initial deficit which disappeared with repetition, enabling them to obtain scores similar to the reference population. No significant correlations were found with BMI, and a higher IQ or academic level did not improve scores in the majority of tests. Conclusions The study shows a deficit in elementary frontal cognitive processes in PWS patients. This deficit may be involved in the social behaviour disorders that characterize such patients, as described in other development or frontal syndrome pathologies. However, we cannot affirm that the deficits found are specific to PWS; they could also occur in other causes of intellectual disability. Although in the study sample IQ did not correlate with frontal deficits, further research is needed to establish whether the neuropsychological alterations described form part of a cognitive phenotype for PWS. 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Intell. Disabil. Res. PD MAY PY 2007 VL 51 BP 350 EP 365 DI 10.1111/j.1365-2788.2006.00883.x PN 5 PG 16 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 149QM UT WOS:000245161700003 PM 17391252 ER PT J AU Murphy, MM Abbeduto, L AF Murphy, M. M. Abbeduto, L. TI Gender differences in repetitive language in fragile X syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE communication; fragile X syndrome; gender differences; language; perseveration; self-repetition ID MENTAL-RETARDATION; SAMPLING CONTEXT; MALES; AUTISM; SKILLS; BEHAVIOR; COMMUNICATION; INDIVIDUALS; ADOLESCENTS; AGREEMENT AB Background Verbal perseveration (i.e. excessive self-repetition) is a characteristic of male individuals with fragile X syndrome; however, little is known about its occurrence among females or its underlying causes. This project examined the relationship between perseveration and (1) gender, (2) cognitive and linguistic ability, and (3) language sampling context, among youth with fragile X syndrome. Method Language transcripts were obtained from adolescent male (n = 16) and female participants (n = 8) with fragile X syndrome in two language contexts (i.e. narration and conversation) designed to elicit spontaneous language samples. Transcripts were coded for utterance-level repetition (i.e. repetition of words, phrases, dependent clauses or whole utterances), topic repetition and conversational device repetition (i.e. repetition of rote phrases or expressions). Results Male participants produced more conversational device repetition than did female participants. Gender differences in conversational device repetition were not explained by differences in non-verbal cognitive or expressive language ability. Context influenced the type of repetition observed; for example, more topic repetition occurred in conversation than in narration regardless of gender. Conclusions The observed gender differences in conversational device repetition among adolescents with fragile X syndrome suggest that, relative to females, male participants may rely more heavily on rote phrases or expressions in their expressive language. Further, results suggest that this gender difference is not simply the result of the correlation between gender and cognitive or linguistic ability in fragile X syndrome; rather, gender may make an independent contribution to conversational device repetition. Repetition type also varied as a function of expressive language context, suggesting the importance of assessing language characteristics in multiple contexts. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53706 USA. RP Murphy, MM (reprint author), 3825 Greenspring Ave,Painter Bldg,Top Floor, Baltimore, MD 21211 USA. EM murphym@kennedykrieger.org CR Abbeduto L, 2003, AM J MENT RETARD, V108, P149, DOI 10.1352/0895-8017(2003)108<0149:RLSOAA>2.0.CO;2 Abbeduto L, 1997, MENT RETARD DEV D R, V3, P313, DOI 10.1002/(SICI)1098-2779(1997)3:4<313::AID-MRDD6>3.0.CO;2-O ABBEDUTO L, 1995, MENT RETARD, V33, P279 Belser RC, 1995, DEV BRAIN DYSFUNCT, V8, P270 Bennetto L, 1996, FRAGILE X SYNDROME D, P210 BRINTON B, 1984, J SPEECH HEAR RES, V27, P350 Carrow-Woolfolk E., 1995, ORAL WRITTEN LANGUAG Chapman R., 1990, SYSTEMATIC ANAL LANG COHEN J, 1960, EDUC PSYCHOL MEAS, V20, P37, DOI 10.1177/001316446002000104 Cornish K, 2004, BRAIN COGNITION, V54, P235, DOI 10.1016/j.bandc.2004.02.017 DOLLAGHAN CA, 1990, J SPEECH HEAR DISORD, V55, P582 DORVAL B, 1984, MONOGR SOC RES CHILD, V49, P1, DOI 10.2307/1165872 DYKENS EM, 1994, BEHAV DEV FRAGILE X ELY R, 1997, DEV LANGUAGE, P398 EVANS JL, 1992, J SPEECH HEAR RES, V35, P343 FERRIER LJ, 1991, DEV MED CHILD NEUROL, V33, P776 Hagerman R. 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A., 1998, LATER LANGUAGE DEV S NOLIN SL, 1994, AM J MED GENET, V51, P509, DOI 10.1002/ajmg.1320510444 Ochs Keenan E., 1976, SUBJECT TOPIC, P335 PAUL R, 1987, J AUTISM DEV DISORD, V17, P457, DOI 10.1007/BF01486963 SUDHALTER V, 1991, AM J MED GENET, V38, P493, DOI 10.1002/ajmg.1320380270 SUDHALTER V, 1992, AM J MED GENET, V43, P65, DOI 10.1002/ajmg.1320430110 SUDHALTER V, 1990, AM J MENT RETARD, V94, P431 Tassone F, 1999, AM J MED GENET, V84, P250, DOI 10.1002/(SICI)1096-8628(19990528)84:3<250::AID-AJMG17>3.0.CO;2-4 Thorndike R. L., 1986, STANFORDBINET INTELL VOLKMAR FR, 1988, J AUTISM DEV DISORD, V18, P81, DOI 10.1007/BF02211820 Wilkinson KM, 1999, RES DEV DISABIL, V20, P255, DOI 10.1016/S0891-4222(99)00008-6 WILKINSON KM, 1999, AM J MENT RETARD, V107, P227 YU S, 1991, SCIENCE, V252, P1179, DOI 10.1126/science.252.5009.1179 NR 42 TC 10 Z9 10 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD MAY PY 2007 VL 51 BP 387 EP 400 DI 10.1111/j.1365-2788.2006.00888.x PN 5 PG 14 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 149QM UT WOS:000245161700006 PM 17391255 ER PT J AU Jou, RJ Paterson, SJ Jackowski, AP Jackowski, M Papademetris, X Rajeevan, N Staib, LH Schultz, RT AF Jou, Roger J. Paterson, Sarah J. Jackowski, Andrea P. Jackowski, Marcel Papademetris, Xenophon Rajeevan, Nallakandi Staib, Lawrence H. Schultz, Robert T. TI Abnormalities in white matter structure in autism spectrum disorders detected by diffusion tensor imaging SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Meeting Abstract RI Jackowski, Andrea/D-8616-2012; Jackowski, Marcel/G-7602-2012 OI Jackowski, Andrea/0000-0001-8842-5406; NR 0 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD MAY PY 2007 VL 19 IS 2 BP 220 EP 220 PG 1 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 156RH UT WOS:000245666300053 ER PT J AU Orsati, FT Macedo, EC Schwartzman, SJ Mercadante, TM AF Orsati, Fernanda Tebexreni Macedo, Elizeu Coutinho Schwartzman, Salomao Jose Mercadante, Tomanik Marcos TI The visual scanning pattern of human faces: a precise diagnostic instrument in autism SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD MAY PY 2007 VL 19 IS 2 BP 221 EP 221 PG 1 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 156RH UT WOS:000245666300056 ER PT J AU Mattila, ML Kielinen, M Jussila, K Linna, SL Bloigu, R Ebeling, H Moilanen, I AF Mattila, Marja-Leena Kielinen, Marko Jussila, Katja Linna, Sirkka-Liisa Bloigu, Risto Ebeling, Hanna Moilanen, Irma TI An epidemiological and diagnostic study of Asperger syndrome according to four sets of diagnostic criteria SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE Asperger syndrome; pervasive developmental disorders; prevalence; diagnostics; epidemiology ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM SPECTRUM DISORDERS; HIGH-FUNCTIONING AUTISM; TOTAL POPULATION; SCREENING QUESTIONNAIRE; PRESCHOOL-CHILDREN; PREVALENCE; INTERVIEW; FAMILIES; FEATURES AB Objective: This study evaluated the diagnostic process and prevalence rates of Asperger syndrome (AS) according to the DSM-IV, ICD-10, and criteria developed by Gillberg and Gillberg and by Szatmari and colleagues and clarified confusion about AS. Method: An epidemiological study of 5,484 eight-year-old children in Finland, 4,422 (80.6%) of whom rated on the high-functioning Autism Spectrum Screening Questionnaire by parents and/or teacher, 125 of them screened and 110 examined by using structured interview, semistructured observation, IQ measurement, school day observation, and patient records. Diagnoses were performed by following the DSM-IV, ICD-10, and criteria developed by Gillberg and Gillberg and by Szatmari and colleagues in detail. Results: The prevalence rates per 1,000 were 2.5 according to the DSM-IV, 2.9 to ICD-10, 2.7 to Gillberg and Gillberg's criteria, and 1.6 to the criteria of Szatmari et al. Conclusions: The results emphasize the need to reconsider the diagnostic criteria of AS. The importance of multi-informant sources came up, and the need of several informants was highlighted, especially when diagnosing the broader pervasive developmental disorders. C1 Oulu Univ, Clin Child Psychiat, Oulu, Finland. Univ Hosp Oulu, Oulu, Finland. Oulu Univ, Fac Med, Oulu, Finland. RP Mattila, ML (reprint author), Univ Hosp Oulu, POB 26, FIN-90029 Oys, Finland. EM marja-leena.mattila@fimnet.fi CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Asperger H., 1979, COMMUNICATION, V13, P45 Auranen M, 2003, MOL PSYCHIATR, V8, P879, DOI 10.1038/sj.mp.4001299 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Fombonne E, 2001, J AUTISM DEV DISORD, V31, P363 Frith U, 2004, J CHILD PSYCHOL PSYC, V45, P672, DOI 10.1111/j.1469-7610.2004.00262.x Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 Gillberg C., 1991, AUTISM ASPERGER SYND, P122, DOI 10.1017/CBO9780511526770.004 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Jansson-Verkasalo E, 2005, EUR J NEUROSCI, V22, P986, DOI 10.1111/j.1460-9568.2005.04216.x Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 Kielinen M, 2000, EUR CHILD ADOLES PSY, V9, P162 KORPILAHTI P, 2006, J AUTISM DEV DISORD Lancia R., 2000, ASPERGER SYNDROME, P125 Lesinskiene S., 2000, VILNIAUS MIESTO VAIK LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 LOUKUSA S, 2006, J AUTISM DEV DISORD Paul R, 2005, J AUTISM DEV DISORD, V35, P205, DOI 10.1007/s10803-005-1999-9 Posserud MB, 2006, J CHILD PSYCHOL PSYC, V47, P167, DOI 10.1111/j.1469-7610.2005.01462.x Sponheim E, 1998, J AUTISM DEV DISORD, V28, P217, DOI 10.1023/A:1026017405150 SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WENDT TN, 2005, BMC PSYCHIATRY, V5, P20 WHO, 1993, ICD 10 CLASS MENT BE WING L, 1981, PSYCHOL MED, V11, P115 Woods SE, 2005, ETHNIC HEALTH, V10, P235, DOI 10.1080/13557850500086721 NR 33 TC 46 Z9 48 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 2007 VL 46 IS 5 BP 636 EP 646 DI 10.1097/chi.0b013e318033ff42 PG 11 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 161HQ UT WOS:000246005800012 PM 17450055 ER PT J AU Twoy, R Connolly, PM Novak, JM AF Twoy, Richard Connolly, Phyllis M. Novak, Jean M. TI Coping strategies used by parents of children with autism SO JOURNAL OF THE AMERICAN ACADEMY OF NURSE PRACTITIONERS LA English DT Article DE adaptation; ASD; autism; coping; family stress; resiliency ID SPECTRUM DISORDERS; STRESS; ADAPTATION; FAMILIES; SUPPORT; SYSTEM AB Purpose: The purpose of this research was to determine (a) the level of family adaptation, as measured by the Family Crisis Oriented Personal Evaluation Scales (F-COPESs) instrument, among persons with a child diagnosed with autism spectrum disorder (ASD) aged 12 years and under, (b) if there was a difference in F-COPES scores based on family demographics, and (c) the time lag between parent's suspicion of ASD and the actual professional diagnosis of ASD. Data sources: A descriptive survey was used with a convenience sample derived from ASD treatment agencies and a parental support group in the California Bay Area that supports the children and parents of children with special needs. Conclusions: Overall, the level of adaptation was within the normal limits with coping scores similar to the norm scores of the F-COPES with males scoring slightly higher than females in the coping scale. Subscale scores of the F-COPES indicated that the parents sought encouragement and support from friends, informal support from other families who faced similar problems, and formal support from agencies and programs. Reframing revealed similar results as the norm with less use of spiritual support, and more passive appraisals were noted from the parents of children with ASD. Within internal comparisons, there were no statistical differences among gender and amount of time a member spent in coordination of services. Comparisons in ethnicity for Caucasians and Asian Americans revealed a higher coping score for reframing in Asian Americans and a higher passive appraisal score among Caucasians. Non-English speakers scored higher on spiritual support, while English speakers scored higher in passive appraisals. Because of insufficient statistical power, comparisons in education, income, marital status, and relocation of residence were deferred. The time from parents' suspicions of developmental delays or disability to a professional diagnosis of ASD was at least 6 months or greater. Implications for practice: It is imperative for nurse practitioners (NPs) to provide appropriate professional support and other social support systems to families with children with ASD. Educating parents to sound therapy approaches to provide them with the skills needed to directly address stressful events in order to increase the parent's confidence level as to avoid passive appraisals is also a crucial role of the NP. NPs may want to use the F-COPES as part of the assessment to ascertain the areas of needs of families. This study reveals the resiliency and highly adaptive nature of these parents who are under severe strain and stress of caring for a child with ASD. The effective ways they coped as a family were in the areas of informal and formal social support networks. Participants also used passive appraisal to cope. The study also supports the need for early recognition and diagnoses of ASD and referral for early intervention for better outcomes for the children and families affected by ASD. C1 San Jose State Univ, Sch Nursing, San Jose, CA 95192 USA. San Jose State Univ, Kay Armstead Ctr Commun Disorders, Speech & Hearing Serv, San Jose, CA 95192 USA. RP Twoy, R (reprint author), San Jose State Univ, Sch Nursing, Hlth Bldg 419,1 Washington Sq, San Jose, CA 95192 USA. EM rtwoy@son.sjsu.edu CR *AM AC PED, 2004, AUT ALARM American Psychiatric Association, 2002, DSM 4 TR DIAGN STAT, V4th *AUT SOC AM, 2006, DEF AUT California Department of Developmental Services, 2003, AUT SPECTR DIS CHANG *CDCP, 2004, AUT SPECTR DIS OV Croonenberghs J, 2002, NEUROPSYCHOBIOLOGY, V45, P1, DOI 10.1159/000048665 Dunn ME, 2001, COMMUNITY MENT HLT J, V37, P39, DOI 10.1023/A:1026592305436 Higgins DJ, 2005, AUTISM, V9, P125, DOI 10.1177/1362361305051403 LAVEE Y, 1985, J MARRIAGE FAM, V47, P811, DOI 10.2307/352326 Luther Edith H, 2005, J Sch Nurs, V21, P40, DOI 10.1177/10598405050210010901 McCubbin H. I., 2001, FAMILY MEASURES STRE McGee J. P., 2001, ED CHILDREN AUTISM Olsson MB, 2001, J INTELL DISABIL RES, V45, P535, DOI 10.1046/j.1365-2788.2001.00372.x Page T, 2000, J AUTISM DEV DISORD, V30, P463, DOI 10.1023/A:1005563926383 Patterson J., 1983, STRESS FAMILY, V1 Rivers JW, 2003, J AUTISM DEV DISORD, V33, P383, DOI 10.1023/A:1025006727395 Robinson D L, 1997, J Am Acad Nurse Pract, V9, P17, DOI 10.1111/j.1745-7599.1997.tb01268.x Santangelo SL, 2005, AM J PHARMACOGENOMIC, V5, P71, DOI 10.2165/00129785-200505020-00001 Sarkadi A, 2005, CHILD CARE HLTH DEV, V31, P43 Sharpley CF, 1997, J INTELLECT DEV DIS, V22, P19, DOI 10.1080/13668259700033261 Sivberg B, 2002, AUTISM, V6, P397, DOI 10.1177/1362361302006004006 Strock M., 2004, AUTISM SPECTRUM DISO Svavarsdottir EK, 2005, FAM COMMUNITY HEALTH, V28, P338 NR 23 TC 37 Z9 40 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 1041-2972 J9 J AM ACAD NURSE PRAC JI J. Am. Acad. Nurse Pract. PD MAY PY 2007 VL 19 IS 5 BP 251 EP 260 DI 10.1111/j.1745-7599.2007.00222.x PG 10 WC Health Care Sciences & Services; Nursing SC Health Care Sciences & Services; Nursing GA 163ZM UT WOS:000246202000006 PM 17489958 ER PT J AU Doughty, SS Anderson, CM Doughty, AH Williams, DC Saunders, KJ AF Doughty, Shannon S. Anderson, Cynthia M. Doughty, Adam H. Williams, Dean C. Saunders, Kathryn J. TI Discriminative control of punished stereotyped behavior in humans SO JOURNAL OF THE EXPERIMENTAL ANALYSIS OF BEHAVIOR LA English DT Article; Proceedings Paper CT 30th Annual Meeting of the Association-for-Behavior-Analysis CY MAY, 2004 CL Boston, MA SP Assoc Behav Anal DE autism; punishment; stimulus control; mental retardation; stereotypy; humans ID SELF-STIMULATORY BEHAVIOR; STIMULUS-CONTROL; DEVELOPMENTAL-DISABILITIES; AUTISTIC-CHILDREN; REINFORCEMENT; SCHEDULES AB The purpose of this experiment was to establish discriminative control of responding by an antecedent stimulus using differential punishment because the results of past studies on this topic have been mixed. Three adults with mental retardation who exhibited stereotypy not maintained by social consequences (i.e., automatic reinforcement) participated. For each subject, stereotypy occurred frequently in the presence of a stimulus correlated with nonpunishment of stereotypy and rarely, if ever, in the presence of a stimulus correlated with punishment of stereotypy. Latency measures showed that the antecedent stimulus correlated with punishment served as the discriminative stimulus for the suppression of stereotypy. These results are important insofar as they show that discriminative control by an antecedent stimulus develops with punishment, and because it sometimes may be desirable to establish such control of socially inappropriate behavior. C1 W Virginia Univ, Morgantown, WV 26506 USA. Univ Kansas, Lawrence, KS 66045 USA. RP Doughty, SS (reprint author), Carolina Coast Behav Serv, POB 80901, Charleston, SC 29416 USA. EM deanwms@ku.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron A., 1991, EXPT ANAL BEHAV 1, P173 BIRNBRAU.JS, 1968, J APPL BEHAV ANAL, V1, P201, DOI 10.1901/jaba.1968.1-201 Bodfish J. W., 2002, SELF INJURIOUS BEHAV, P23, DOI 10.1037/10457-002 BOLLES RC, 1980, LEARN MOTIV, V11, P78, DOI 10.1016/0023-9690(80)90022-3 CHARLOP MH, 1990, J APPL BEHAV ANAL, V23, P163, DOI 10.1901/jaba.1990.23-163 Dinsmoor J. A., 1998, LEARNING BEHAV THERA, P188 DOUGHTY AH, IN PRESS MEXICAN J B Garner JP, 2003, BEHAV BRAIN RES, V145, P125, DOI 10.1016/S0166-4328(03)00115-3 HONIG WK, 1964, J EXP ANAL BEHAV, V7, P21, DOI 10.1901/jeab.1964.7-21 IVERSEN IH, 1993, J EXP ANAL BEHAV, V60, P219, DOI 10.1901/jeab.1993.60-219 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Kennedy CH, 2002, SELF INJURIOUS BEHAV, P133, DOI 10.1037/10457-008 Lerman DC, 2002, J APPL BEHAV ANAL, V35, P431, DOI 10.1901/jaba.2002.35-431 LOVAAS OI, 1971, BEHAV RES THER, V9, P39, DOI 10.1016/0005-7967(71)90035-0 Miltenberger R. G., 1997, BEHAV MODIFICATION P O'Donnell J, 2000, J EXP ANAL BEHAV, V73, P261, DOI 10.1901/jeab.2000.73-261 O'Donnell J, 1998, PSYCHOL REC, V48, P211 O'Donnell J, 2001, BEHAV ANALYST, V24, P261 ORMEJOHN.DW, 1974, J EXP ANAL BEHAV, V21, P57, DOI 10.1901/jeab.1974.21-57 RINCOVER A, 1978, J ABNORM CHILD PSYCH, V6, P299, DOI 10.1007/BF00924733 ROLLINGS JP, 1981, AM J MENT DEF, V86, P67 Rovee-Collier C K, 1979, Adv Child Dev Behav, V13, P195, DOI 10.1016/S0065-2407(08)60348-1 Sidman M., 1989, COERCION ITS FALLOUT SILVERMA.PJ, 1971, J EXP ANAL BEHAV, V16, P1, DOI 10.1901/jeab.1971.16-1 VOLLMER TR, 1994, RES DEV DISABIL, V15, P187, DOI 10.1016/0891-4222(94)90011-6 WEISMAN RG, 1975, B PSYCHONOMIC SOC, V5, P427 WILLIAMS DC, 1992, J EXP ANAL BEHAV, V58, P205, DOI 10.1901/jeab.1992.58-205 NR 28 TC 14 Z9 14 PU SOC EXP ANALYSIS BEHAVIOR INC PI BLOOMINGTON PA INDIANA UNIV DEPT PSYCHOLOGY, BLOOMINGTON, IN 47405 USA SN 0022-5002 J9 J EXP ANAL BEHAV JI J. Exp. Anal. Behav. PD MAY PY 2007 VL 87 IS 3 BP 325 EP 336 DI 10.1901/jeab.2007.39-05 PG 12 WC Psychology, Biological; Behavioral Sciences; Psychology, Experimental SC Psychology; Behavioral Sciences GA 171DC UT WOS:000246714100001 PM 17575899 ER PT J AU Geier, DA Geier, MR AF Geier, David A. Geier, Mark R. TI A case series of children with apparent mercury toxic encephalopathies manifesting with clinical symptoms of regressive autistic disorders SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES LA English DT Article ID THIMEROSAL-CONTAINING VACCINES; FOLLOW-UP ANALYSIS; NEURODEVELOPMENTAL DISORDERS; METHYL MERCURY; UNITED-STATES; IN-VITRO; SPECTRUM DISORDERS; SQUIRREL-MONKEYS; OXIDATIVE STRESS; CELL-DEATH AB Impairments in social relatedness and communication, repetitive behaviors, and stereotypic abnormal movement patterns characterize autism spectrum disorders (ASDs). It is clear that while genetic factors are important to the pathogenesis of ASDs, mercury exposure can induce immune, sensory, neurological, motor, and behavioral dysfunctions similar to traits defining or associated with ASDs. The Institutional Review Board of the Institute for Chronic Illnesses (Office for Human Research Protections, U.S. Department of Health and Human Services, IRB number IRB00005375) approved the present study. A case series of nine patients who presented to the Genetic Centers of America for a genetic/developmental evaluation are discussed. Eight of nine patients (one patient was found to have an ASD due to Rett's syndrome) (a) had regressive ASDs; (b) had elevated levels of androgens; (c) excreted significant amounts of mercury post chelation challenge; (d) had biochemical evidence of decreased function in their glutathione pathways; (e) had no known significant mercury exposure except from Thimerosal-containing vaccines/Rho(D)-immune globulin preparations; and (f) had alternate causes for their regressive ASDs ruled out. There was a significant dose-response relationship between the severity of the regressive ASDs observed and the total mercury dose children received from Thimerosal-containing vaccines/Rho (D)immune globulin preparations. Based upon differential diagnoses, 8 of 9 patients examined were exposed to significant mercury from Thimerosal-containing biologic/vaccine preparations during their fetal/infant developmental periods, and subsequently, between 12 and 24 mo of age, these previously normally developing children suffered mercury toxic encephalopathies that manifested with clinical symptoms consistent with regressive ASDs. Evidence for mercury intoxication should be considered in the differential diagnosis as contributing to some regressive ASDs. C1 Inst Chron Illnesses Inc, Silver Spring, MD USA. Genet Ctr Amer, Silver Spring, MD USA. RP Geier, MR (reprint author), 14 Redgate Ct, Silver Spring, MD 20905 USA. 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PD MAY PY 2007 VL 12 IS 5 BP 419 EP 421 DI 10.1038/sj.mp.4001966 PG 3 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 160NA UT WOS:000245947900001 PM 17453057 ER PT J AU Beaudet, AL AF Beaudet, Arthur L. TI Autism: highly heritable but not inherited SO NATURE MEDICINE LA English DT Editorial Material ID CHROMOSOMAL REARRANGEMENTS; SPECTRUM DISORDERS; COPY-NUMBER AB The genetic basis of autism is beginning to come to light. De novo mutations in gene copy number may have a big role. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. RP Beaudet, AL (reprint author), Baylor Coll Med, Dept Mol & Human Genet, 1 Baylor Plaza, Houston, TX 77030 USA. EM abeaudet@bcm.tmc.edu CR CDC (Cent. Dis. 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Med. PD MAY PY 2007 VL 13 IS 5 BP 534 EP 536 DI 10.1038/nm0507-534 PG 3 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 165JW UT WOS:000246302800015 PM 17479094 ER PT J AU [Anonymous] AF [Anonymous] TI Silencing debate over autism SO NATURE NEUROSCIENCE LA English DT Editorial Material NR 0 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 1097-6256 EI 1546-1726 J9 NAT NEUROSCI JI Nat. Neurosci. PD MAY PY 2007 VL 10 IS 5 BP 531 EP 531 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 160NB UT WOS:000245948000001 ER PT J AU Murawski, NJ Brown, KL Chadman, KK Stanton, ME AF Murawski, N. J. Brown, K. L. Chadman, K. K. Stanton, M. E. TI Interstimulus interval discrimination conditioning of the eyeblink reflex in a rodent model of autism SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Meeting Abstract CT 31st Annual Meeting of the Neurobehavioral-Teratology-Society/26th Annual Meeting of the Behavioral-Toxicology-Society/47th Annual Meeting of the Teratology-Society/20th Organization-of-Teratology-Information-Specialists CY JUN 23-27, 2007 CL Pittsburg, PA SP Neurobehav Teratol Soc, Behav Toxicol Soc, Teratol Soc, Org Teratol Informat Specialists C1 Univ Delaware, Dept Psychol, Newark, DE USA. NR 0 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0892-0362 J9 NEUROTOXICOL TERATOL JI Neurotoxicol. Teratol. PD MAY-JUN PY 2007 VL 29 IS 3 BP 404 EP 404 DI 10.1016/j.ntt.2007.03.031 PG 1 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA 185YS UT WOS:000247746900036 ER PT J AU Montes, G Halterman, JS AF Montes, Guillermo Halterman, Jill S. TI Psychological functioning and coping among mothers of children with autism: A population-based study SO PEDIATRICS LA English DT Article DE autism; psychological functioning; health survey; National Survey of Children's Health; resilience; United States ID SCHOOL-AGE-CHILDREN; SPECTRUM DISORDERS; STRESS; PARENTS; STRATEGIES; BEHAVIORS; PRESCHOOL; FAMILIES; FATHERS AB OBJECTIVES. Studies suggest that having a child with autism has a negative impact on maternal psychological functioning, but no large-scale, population-based studies are available. The objectives of this study were to (1) describe the psychological functioning, physical and mental health, family communication, and parenting support of mothers of a child with autism compared with other mothers on a population basis and (2) assess the independent relationship between having a child with autism and these outcomes, controlling for the child's social skills and demographic background. METHODS. Mothers of 61 772 children who were 4 to 17 years of age were surveyed by the National Survey of Children's Health, 2003. Autism was measured from an affirmative maternal response to the question, "Has a doctor or health professional ever told you your child has autism?" There were 364 children with autism in the sample. RESULTS. Mothers of a child with autism were highly stressed and more likely to report poor or fair mental health than mothers in the general population, even after adjustment for the child's social skills and demographic background. However, mothers of a child with autism were more likely to report a close relationship and better coping with parenting tasks and less likely to report being angry with their child after adjustment for the child's social skills and demographic background. Having a child with autism was not associated with lower social support for parenting, an altered manner in which serious disagreements were discussed in the household, or increased violence in the household. CONCLUSION. Mothers of children with autism showed remarkable strengths in the parent-child relationship, social support, and stability of the household in the context of high stress and poorer mental health. C1 Childrens Inst, Rochester, NY 14607 USA. Univ Rochester, Dept Pediat, Sch Med & Dent, Rochester, NY USA. RP Montes, G (reprint author), Childrens Inst, 271 N Goodman St,Suite D103, Rochester, NY 14607 USA. 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PD MAY PY 2007 VL 4 IS 2 BP 119 EP 119 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 178VZ UT WOS:000247249500002 ER PT J AU Parker-Katiraee, L Carson, AR Yamada, T Arnaud, P Feil, R Abu-Amero, SN Moore, GE Kaneda, M Perry, GH Stone, AC Lee, C Meguro-Horike, M Sasaki, H Kobayashi, K Nakabayashi, K Scherer, SW AF Parker-Katiraee, Layla Carson, Andrew R. Yamada, Takahiro Arnaud, Philippe Feil, Robert Abu-Amero, Sayeda N. Moore, Gudrun E. Kaneda, Masahiro Perry, George H. Stone, Anne C. Lee, Charles Meguro-Horike, Makiko Sasaki, Hiroyuki Kobayashi, Keiko Nakabayashi, Kazuhiko Scherer, Stephen W. TI Identification of the imprinted KLF14 transcription factor undergoing human-specific accelerated evolution SO PLOS GENETICS LA English DT Article ID SILVER-RUSSELL-SYNDROME; POSITIVE DARWINIAN SELECTION; HUMAN-CHROMOSOME 7Q32; PROTEIN-CODING GENES; HISTONE METHYLATION; MOLECULAR EVOLUTION; UNIPARENTAL DISOMY; STATISTICAL-METHOD; DNA POLYMORPHISM; CANDIDATE GENES AB Imprinted genes are expressed in a parent- of- origin manner and are located in clusters throughout the genome. Aberrations in the expression of imprinted genes on human Chromosome 7 have been suggested to play a role in the etiologies of Russell- Silver Syndrome and autism. We describe the imprinting of KLF14, an intronless member of the Kru " ppel- like family of transcription factors located at Chromosome 7q32. We show that it has monoallelic maternal expression in all embryonic and extra- embryonic tissues studied, in both human and mouse. We examine epigenetic modifications in the KLF14 CpG island in both species and find this region to be hypomethylated. In addition, we perform chromatin immunoprecipitation and find that the murine Klf14 CpG island lacks allele- specific histone modifications. Despite the absence of these defining features, our analysis of Klf14 in offspring from DNA methyltransferase 3a conditional knockout mice reveals that the gene's expression is dependent upon a maternally methylated region. Due to the intronless nature of Klf14 and its homology to Klf16, we suggest that the gene is an ancient retrotransposed copy of Klf16. By sequence analysis of numerous species, we place the timing of this event after the divergence of Marsupialia, yet prior to the divergence of the Xenarthra superclade. We identify a large number of sequence variants in KLF14 and, using several measures of diversity, we determine that there is greater variability in the human lineage with a significantly increased number of nonsynonymous changes, suggesting humanspecific accelerated evolution. Thus, KLF14 may be the first example of an imprinted transcript undergoing accelerated evolution in the human lineage. C1 Hosp Sick Children, Program Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Hosp Sick Children, Ctr Appl Genom, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Mol & Med Genet, Toronto, ON, Canada. Univ Montpellier 2, Montpellier, France. CNRS, UMR 5535, Inst Genet Mol, Montpellier, France. UCL, Inst Child Hlth, London, England. Res Org Informat & Syst, Natl Inst Genet, Dept Integrated Genet, Div Human Genet, Mishima, Shizuoka, Japan. Arizona State Univ, Sch Human Evolut & Social Change, Tempe, AZ USA. Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA. Grad Univ Adv Studies, Sch Life Sci, Dept Genet, Mishima, Shizuoka, Japan. Kagoshima Univ, Grad Sch Med & Dent Sci, Dept Mol Metab & Biochem Genet, Kagoshima 890, Japan. RP Scherer, SW (reprint author), Hosp Sick Children, Program Genet & Genom Biol, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. 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Benner, Lauren Hopf, Andrea TI A meta-analysis of school-based social skills interventions for children with autism spectrum disorders SO REMEDIAL AND SPECIAL EDUCATION LA English DT Article ID SINGLE-SUBJECT RESEARCH; YOUNG-CHILDREN; STUDENTS; LINKAGES; OUTCOMES AB Social skills deficits are a central feature of autism spectrum disorders (ASD). This meta-analysis of 55 single-subject design studies examined the effectiveness of school-based social skills interventions for children and adolescents with ASD. Intervention, maintenance, and generalization effects were measured by computing the percentage of non-overlapping data points. The results suggest that social skills interventions have been minimally effective for children with ASD. Specific participant, setting, and procedural features that lead to the most effective intervention outcomes are highlighted, and implications for school personnel are discussed. Finally, the results are compared to the outcomes of similar meta-analyses involving social skills interventions with other populations of children. C1 Indiana Resource Ctr Autism, Bloomington, IN 47408 USA. Indiana Univ, Sch Psychol Program, Bloomington, IN 47405 USA. RP Bellini, S (reprint author), Indiana Resource Ctr Autism, 2853 E 10th St, Bloomington, IN 47408 USA. EM sbellini@indiana.edu CR Akullian J., 2007, EXCEPT CHILDREN, V73, P261 Attwood T., 1998, ASPERGERS SYNDROME G Bellini S, 2006, FOCUS AUTISM OTHER D, V21, P138, DOI DOI 10.1177/10883576060210030201 Gresham F. M., 1998, HDB CHILD BEHAV THER, P3, DOI 10.1007/978-1-4615-5323-6_1 Gresham FM, 2001, EXCEPT CHILDREN, V67, P331 HORNER RH, 2005, COUNCIL EXCEPTIONAL, V2, P165 Hume K, 2005, TOP EARLY CHILD SPEC, V25, P195, DOI 10.1177/02711214050250040101 Hwang B, 2000, J AUTISM DEV DISORD, V30, P331, DOI 10.1023/A:1005579317085 La Greca AM, 1998, J ABNORM CHILD PSYCH, V26, P83, DOI 10.1023/A:1022684520514 MASTROPIERI MA, 1985, J SPEC EDUC, V19, P429 Mathur SR, 1998, BEHAV DISORDERS, V23, P193 McConnell SR, 2002, J AUTISM DEV DISORD, V32, P351, DOI 10.1023/A:1020537805154 Myles B. S., 2005, LIFE JOURNEY AUTISM Quinn MM, 1999, J EMOT BEHAV DISORD, V7, P54, DOI 10.1177/106342669900700106 Rogers SJ, 2000, J AUTISM DEV DISORD, V30, P399, DOI 10.1023/A:1005543321840 Scargle J., 2000, J SCI EXPLORATION, V14, P91 Scruggs T. E., 2001, EXCEPTIONALITY, V9, P227, DOI DOI 10.1207/S15327035EX0904_5 Scruggs T. E., 1994, ADV LEARNING BEHAV D, V8, P259 Scruggs TE, 1998, BEHAV MODIF, V22, P221, DOI 10.1177/01454455980223001 Tantam D., 2000, AUTISM INT J RES PRA, V4, P47, DOI DOI 10.1177/1362361300004001004 Welsh M, 2001, J SCHOOL PSYCHOL, V39, P463, DOI 10.1016/S0022-4405(01)00084-X NR 21 TC 102 Z9 104 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0741-9325 J9 REM SPEC EDUC JI Remedial Spec. Educ. PD MAY-JUN PY 2007 VL 28 IS 3 BP 153 EP 162 DI 10.1177/07419325070280030401 PG 10 WC Education, Special SC Education & Educational Research GA 176UT UT WOS:000247111100004 ER PT J AU Campbell, JM AF Campbell, Jonathan M. TI Middle school students' response to the self-introduction of a student with autism - Effects of perceived similarity, prior awareness, and educational message SO REMEDIAL AND SPECIAL EDUCATION LA English DT Article ID MENTALLY-RETARDED PEERS; CHILDRENS ATTITUDES; BEHAVIORAL INTENTIONS AB This study examined the effects of educational messages provided by a student with autism on middle school students' cognitive and conative attitudes. Students (N = 233; M age = 13.07 years) viewed a videotape of an unfamiliar student exhibiting autism-like behaviors and received one of four messages provided by the student via a written pamphlet. Students who were unfamiliar with autism reported more favorable cognitive attitudes when an explanatory message was added to the descriptive information. Explanatory information resulted in more favorable conative attitudes than descriptive information. Female students reported more positive attitudes than male students, regardless of the message; students with prior awareness of autism reported more positive conative attitudes, regardless of the message. Implications of the findings, study limitations, and recommendations for future research are briefly discussed. C1 Univ Georgia, Dept Educ Psychol & Instruct Technol, Athens, GA 30602 USA. RP Campbell, JM (reprint author), Univ Georgia, Dept Educ Psychol & Instruct Technol, 325-J Aderhold Hall, Athens, GA 30602 USA. CR BAK JJ, 1987, AM J MENT RETARD, V91, P524 BENTLER PM, 2005, EQS WINDOWS CAMPBELL JM, 2005, M ORG AUT RES APPL A Campbell JM, 2004, RES DEV DISABIL, V25, P321, DOI 10.1016/j.ridd.2004.01.005 CAMPBELL JM, 2005, UNPUB RELIABILITY VA CAMPBELL JM, 2006, J DEV PHYS DISABILIT Corrigan PW, 2000, CLIN PSYCHOL-SCI PR, V7, P48, DOI 10.1093/clipsy/7.1.48 *GEORG DEP ED, 2006, 2004 2005 GEORG PUBL GOTTLIEB J, 1977, AM J MENT DEF, V82, P65 Harrower JK, 2001, BEHAV MODIF, V25, P762, DOI 10.1177/0145445501255006 Heider F., 1958, PSYCHOL INTERPERSONA *IND RES CTR AUT, 1991, AUT BEING FRIENDS JUVONEN J, 1992, J EDUC PSYCHOL, V84, P314, DOI 10.1037/0022-0663.84.3.314 Lisser M., 2001, OUR JOURNEY HIGH FUN, P133 Magiati I, 2002, J APPL DEV PSYCHOL, V23, P409, DOI 10.1016/S0193-3973(02)00126-0 MORGAN SB, 1996, UNPUB SHARED ACTIVIT MORTON JF, 2007, UNPUB INFORM SOURCE Nabors LA, 2002, J DEV PHYS DISABIL, V14, P403, DOI 10.1023/A:1020339004125 Rose BM, 2004, J DEV BEHAV PEDIATR, V25, P58, DOI 10.1097/00004703-200402000-00013 Rosembaum P. L., 1988, CHILDRENS HLTH CARE, V17, P32, DOI 10.1207/s15326888chc1701_5 Silva A. P. D., 1995, READING UNDERSTANDIN, P277 SIPERSTEIN GN, 1982, AM J MENT DEF, V86, P453 SIPERSTEIN GN, 1977, UNPUB INSTRUMENTS ME Swaim KF, 2001, J AUTISM DEV DISORD, V31, P195, DOI 10.1023/A:1010703316365 Triandis H., 1971, ATTITUDE ATTITUDE CH WEINER B, 1993, AM PSYCHOL, V48, P957, DOI 10.1037//0003-066X.48.9.957 Yarnold P. R., 1995, READING UNDERSTANDIN, P245 NR 27 TC 9 Z9 9 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0741-9325 J9 REM SPEC EDUC JI Remedial Spec. Educ. PD MAY-JUN PY 2007 VL 28 IS 3 BP 163 EP 173 DI 10.1177/07419325070280030501 PG 11 WC Education, Special SC Education & Educational Research GA 176UT UT WOS:000247111100005 ER PT J AU Lacava, PG Golan, O Baron-Cohen, S Myles, BS AF Lacava, Paul G. Golan, Ofer Baron-Cohen, Simon Myles, Brenda Smith TI Using assistive technology to teach emotion recognition to students with Asperger syndrome - A pilot study SO REMEDIAL AND SPECIAL EDUCATION LA English DT Article ID COMPLEX EMOTIONS; AUTISM; CHILDREN; INTERVENTION; ADULTS; MIND AB Many individuals with autism spectrum conditions (ASC) have difficulty recognizing emotions in themselves and others. The present pilot study explored the use of assistive technology to teach emotion recognition (ER) to eight children with ASC. Participants were between the ages of 8 and 11 years and had a diagnosis of Asperger syndrome (AS). ER testing was conducted using a computer at pre- and postintervention. The intervention consisted of 10 weeks of using the computer software Mind Reading: The Interactive Guide to Emotions(TM) in either home or school settings. The results indicated that after intervention, participants improved on face and voice ER for basic and complex emotions that were in the software, as well as for complex voice ER for emotions not included in Mind Reading. The implications of these findings are discussed. C1 Univ Kansas, Dept Special Educ, Lawrence, KS 66045 USA. Bar Ilan Univ, Dept Psychiat, IL-52100 Ramat Gan, Israel. Univ Cambridge, Autism Res Ctr, Cambridge, England. RP Lacava, PG (reprint author), Univ Kansas, Dept Special Educ, Joseph R Pearson Hall,1122 w Campus Rd,Room 521, Lawrence, KS 66045 USA. EM plack@ku.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S., 2001, J DEV LEARNING DISOR, V5, P47 Baron-Cohen S., 2002, HDB COGNITIVE DEV, P491 Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Baron-Cohen S., 2004, MIND READING INTERAC Baron-Cohen S, 1997, HDB AUTISM PERVASIVE, P880 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bauminger N, 2004, DEV PSYCHOPATHOL, V16, P157, DOI 10.1017/S0954579404044451 Bauminger N, 2002, J AUTISM DEV DISORD, V32, P283, DOI 10.1023/A:1016378718278 CAPPS L, 1992, J CHILD PSYCHOL PSYC, V33, P1169, DOI 10.1111/j.1469-7610.1992.tb00936.x Forster KI, 2003, BEHAV RES METH INS C, V35, P116, DOI 10.3758/BF03195503 GOLAN O, 2006, UNPUB TEACHING CHILD GOLAN O, 2006, UNPUB READING MIND F GOLAN O, 2007, WORKING SCH AGE CHIL, P124 Golan O, 2006, DEV PSYCHOPATHOL, V18, P591, DOI 10.1017/S0954579406060305 GOLAN O, 2006, UNPUB CAMBRIDGE MIND GOLAN O, 2006, THESIS U CAMBRIDGE C Gray C., 1994, COMIC STRIP CONVERSA GRAY CA, 2004, SOCIAL STORIES Hadwin J, 1996, DEV PSYCHOPATHOL, V8, P345 Hillier A, 2002, J AUTISM DEV DISORD, V32, P583, DOI 10.1023/A:1021259115185 Horner RH, 2005, EXCEPT CHILDREN, V71, P165 Lawson J, 2004, J AUTISM DEV DISORD, V34, P301, DOI 10.1023/B:JADD.0000029552.42724.1b MYLES BS, 2001, ASPERGER SYNDROME DI MYLES BS, 2000, UNPUB DEMOGRAPHIC PR OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 Silver M, 2001, AUTISM, V5, P299, DOI 10.1177/1362361301005003007 NR 29 TC 27 Z9 27 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0741-9325 J9 REM SPEC EDUC JI Remedial Spec. Educ. PD MAY-JUN PY 2007 VL 28 IS 3 BP 174 EP 181 DI 10.1177/07419325070280030601 PG 8 WC Education, Special SC Education & Educational Research GA 176UT UT WOS:000247111100006 ER PT J AU Quilty, KM AF Quilty, Kimberly Moudry TI Teaching paraprofessionals how to write and implement social stories for students with autism spectrum disorders SO REMEDIAL AND SPECIAL EDUCATION LA English DT Article ID ASPERGER-SYNDROME; CHILDREN; DISABILITIES; ADOLESCENT; ENGAGEMENT; IMPROVE AB A multiple-baseline design across subjects was used to determine if paraprofessionals could be effectively taught to write and implement Social Stories(TM) that shared accurate social information and had a positive impact on the targeted behaviors of students with autism spectrum disorders (ASD). Three paraprofessional-student pairs participated in the study. The data revealed that paraprofessionals could be effectively taught how to write and implement Social Stories. Furthermore, the targeted student behaviors decreased after the implementation of the intervention. Maintenance data showed continued use of the Social Stories intervention and its effectiveness with the students with ASD. RP Quilty, KM (reprint author), 2235 W Lawrence Ave,Unit 2, Chicago, IL 60625 USA. EM kim_moudry@yahoo.com CR Adamian GG, 2004, ACTA PHYS HUNG NS-H, V19, P87, DOI 10.1556/APH.19.2004.1-2.13 American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barry L. M., 2004, FOCUS AUTISM OTHER D, V19, P45, DOI DOI 10.1177/10883576040190010601 Bledsoe R, 2003, AUTISM, V7, P289, DOI 10.1177/1362361303007003005 Brown ML, 2002, COMPUT CARDIOL, V29, P117 Delano M, 2006, J POSIT BEHAV INTERV, V8, P29, DOI 10.1177/10983007060080010501 Giangreco MF, 1997, EXCEPT CHILDREN, V64, P7 Giangreco MF, 2001, J ASSOC PERS SEVERE, V26, P75, DOI 10.2511/rpsd.26.2.75 Gray C., 2000, WRITING SOCIAL STORI Gray C., 1995, TEACHING CHILDREN AU, P219 Gray C. A., 1993, FOCUS AUTISTIC BEHAV, V8, P1, DOI DOI 10.1177/108835769300800101 HALL LJ, 1995, EDUC TRAIN MENT RET, V30, P208 Killoran J., 2001, TEACHING EXCEPTIONAL, V34, P68 Kuoch H., 2003, FOCUS AUTISM OTHER D, V18, P219, DOI DOI 10.1177/10883576030180040301 Kuttler S., 1998, FOCUS AUTISM OTHER D, V13, P176, DOI DOI 10.1177/108835769801300306 LORIMER M, 2002, J POSIT BEHAV INTERV, V4, P53 Causton-Theoharis JN, 2005, EXCEPT CHILDREN, V71, P431 MARTELLA RC, 1995, TEACHING EXCEPTIONAL, V27, P53 Minondo S, 2001, J ASSOC PERS SEVERE, V26, P114, DOI 10.2511/rpsd.26.2.114 Myles B. S., 1999, FOCUS AUTISM OTHER D, V14, P82, DOI 10.1177/108835769901400203 Norris C, 1999, FOCUS AUTISM OTHER D, V14, P180, DOI DOI 10.1177/108835769901400307 Rogers MF, 2001, INTERV SCH CLIN, V36, P310 Rogers SJ, 2000, J AUTISM DEV DISORD, V30, P399, DOI 10.1023/A:1005543321840 Sansosti FJ, 2006, J POSIT BEHAV INTERV, V8, P43, DOI 10.1177/10983007060080010601 Scattone D, 2002, J AUTISM DEV DISORD, V32, P535, DOI 10.1023/A:1021250813367 Storey K., 1993, EXCEPTIONALITY, V4, P1, DOI DOI 10.1207/S15327035EX0401_ Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Tawney J. W., 1984, SINGLE SUBJECT RES S THIEMANN KS, 2001, J APPL BEHAV ANAL, V34, P426 XIN J, 2001, COUNC EXC CHILDR NAT Young B., 1997, FOCUS AUTISM OTHER D, V12, P31 NR 32 TC 13 Z9 13 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 0741-9325 J9 REM SPEC EDUC JI Remedial Spec. Educ. PD MAY-JUN PY 2007 VL 28 IS 3 BP 182 EP 189 PG 8 WC Education, Special SC Education & Educational Research GA 176UT UT WOS:000247111100007 ER PT J AU MacDonald, R Green, G Mansfield, R Geckeler, A Gardenier, N Anderson, J Holcomb, W Sanchez, J AF MacDonald, Rebecca Green, Gina Mansfield, Renee Geckeler, Amy Gardenier, Nicole Anderson, Jennifer Holcomb, William Sanchez, June TI Stereotypy in young children with autism and typically developing children SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article; Proceedings Paper CT 26th Annual Meeting of the Association-for-Behavior-Analysis CY MAY, 2000 CL WASHINGTON, DC SP Assoc Behav Anal DE autism; stereotypy; early intensive behavioral intervention ID SELF-INJURIOUS BEHAVIORS; REPETITIVE BEHAVIOR; MENTAL-RETARDATION; INTERVENTION; STIMULATION; PREVALENCE; DISORDERS; INFANTS; AGE AB Although stereotypy is one of the key diagnostic features of autism, few studies have compared stereotypic behavior in children with autism and typically developing children. The present study employed direct observational measurement methods to assess levels of stereotypic behavior in 2-, 3- and 4-year-old children with autism or pervasive developmental disorder - not otherwise specified (PDD-NOS) and age-matched typically developing peers. Thirty children with autism or PDD-NOS and 30 typically developing children participated. Each child's perfon-nance of several early learning and play skills was assessed using a direct observational assessment protocol developed for children with autism who were entering early intensive behavioral treatment. Duration of episodes of vocal and motor stereotypy was recorded from a videotaped 10 min portion of that assessment session. Results indicated that the 2-year-old children with autism or PDD-NOS had somewhat higher levels of stereotypic behavior than the typically developing 2-year-olds, while the 3- and 4-year-old children with autism or PDD-NOS displayed substantially higher levels stereotypic behavior than their same-age peers. (c) 2006 Elsevier Ltd. All rights reserved. C1 New England Ctr Children, Southborough, MA 01772 USA. RP MacDonald, R (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. EM bmacdonald@necc.org CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERSON J, 2000, ANN M ASS BEH AN WAS Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 Berkson G, 2001, AM J MENT RETARD, V106, P539, DOI 10.1352/0895-8017(2001)106<0539:EDOSAS>2.0.CO;2 Berkson G, 2000, J EARLY INTERVENTION, V23, P1, DOI 10.1177/10538151000230010401 Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 BODFISH JW, 1995, AM J MENT RETARD, V100, P183 DUNLAP G, 1983, AM J MENT DEF, V88, P194 EPSTEIN LH, 1974, J APPL BEHAV ANAL, V7, P385, DOI 10.1901/jaba.1974.7-385 FENSKE EC, 1985, ANAL INTERVEN DEVEL, V5, P49, DOI 10.1016/S0270-4684(85)80005-7 Foster LG, 1998, J AM ACAD CHILD PSY, V37, P711, DOI 10.1097/00004583-199807000-00010 Gardenier NC, 2004, RES DEV DISABIL, V25, P99, DOI 10.1016/j.ridd.2003.05.004 GECKELER A, 1998, ANN M ASS BEH AN ORL Green G, 1996, BEHAV INTERVENTION Y, P29 Hanley GP, 2000, J APPL BEHAV ANAL, V33, P285, DOI 10.1901/jaba.2000.33-285 Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 HAWKINS RP, 1991, J APPL BEHAV ANAL, V24, P205, DOI 10.1901/jaba.1991.24-205 Howard JS, 2005, RES DEV DISABIL, V26, P359, DOI 10.1016/j.ridd.2004.09.005 JONES RSP, 1990, J MENT DEFIC RES, V34, P261 KOEGEL RL, 1972, J APPL BEHAV ANAL, V5, P381, DOI 10.1901/jaba.1972.5-381 LAGROW SJ, 1984, AM J MENT DEF, V88, P595 Lewis MH, 1998, MENT RETARD DEV D R, V4, P80, DOI 10.1002/(SICI)1098-2779(1998)4:2<80::AID-MRDD4>3.0.CO;2-0 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Matson JL, 1997, RES DEV DISABIL, V18, P471, DOI 10.1016/S0891-4222(97)00023-1 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 Miltenberger RG, 1999, J APPL BEHAV ANAL, V32, P119, DOI 10.1901/jaba.1999.32-119 Morrison K, 1997, RES DEV DISABIL, V18, P127, DOI 10.1016/S0891-4222(96)00046-7 MURPHY G, 1980, BEHAV RES THER, V18, P147, DOI 10.1016/0005-7967(80)90109-6 Rojahn J, 2000, RES DEV DISABIL, V21, P437, DOI 10.1016/S0891-4222(00)00057-3 SCHWARTZ SS, 1986, AM J MENT RETARD, V90, P625 Smith EA, 1996, RES DEV DISABIL, V17, P253, DOI 10.1016/0891-4222(96)00007-8 Smith T, 2000, AM J MENT RETARD, V105, P269, DOI 10.1352/0895-8017(2000)105<0269:RTOIEI>2.0.CO;2 THELEN E, 1979, ANIM BEHAV, V27, P699, DOI 10.1016/0003-3472(79)90006-X TROSTER H, 1994, J ABNORM CHILD PSYCH, V22, P79, DOI 10.1007/BF02169257 Weiss MJ, 1999, BEHAV INTERVENT, V14, P3, DOI 10.1002/(SICI)1099-078X(199901/03)14:1<3::AID-BIN25>3.0.CO;2-F WOLERY M, 1985, J AUTISM DEV DISORD, V15, P149, DOI 10.1007/BF01531601 NR 37 TC 64 Z9 64 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD MAY-JUN PY 2007 VL 28 IS 3 BP 266 EP 277 DI 10.1016/j.ridd.2006.01.004 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 152VY UT WOS:000245391300005 PM 16814515 ER PT J AU Ben-Itzchak, E Zachor, DA AF Ben-Itzchak, Esther Zachor, Ditza A. TI The effects of intellectual functioning and autism severity on outcome of early behavioral intervention for children with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE autism; behavioral intervention; predicting variables ID 6-YEAR FOLLOW-UP; YOUNG-CHILDREN; AGE; CLASSIFICATION; PREDICTORS; DISORDERS; SUBTYPES AB This study assessed the relation between pre-intervention variables (cognition, socialization and communication) to outcome in young children with autism. Method: Twenty five children with autism (20-32 months) were enrolled in intensive behavior intervention. The children were divided into groups based on their IQ scores and on the severity of their social interaction and communication deficits [per autism diagnostic observation schedule (ADOS) scores]. Six developmental-behavioral domains including, imitation, receptive language, expressive language, nonverbal communication skills, play skills and stereotyped behaviors were assessed at pre- and post-1 year of intervention times. Results: Significant progress was noted in all the six developmental-behavioral domains after 1 year of intervention. Children with higher initial cognitive levels and children with fewer measured early social interaction deficits showed better acquisition of skills in three developmental areas, receptive language, expressive language and play skills. Both groups showed better progress in Receptive language skills. Better progress in expressive language was associated with the child's social abilities, while more significant progress in play skills was related to pre-intervention cognitive level. Conclusions: These findings emphasize the importance of early intensive intervention in autism and the value of pre-intervention cognitive and social interaction levels for predicting outcome. (c) 2006 Elsevier Ltd. All rights reserved. C1 Bar Ilan Univ, Assaf Harofeh Med Ctr, Sch Educ, Autism Ctr, Ramat Gan, Israel. ALUT Israeli, Natl Alliance Children Autism, Ramat Gan, Israel. Tel Aviv Univ, Assaf Harofeh Med Ctr, Autism Ctr, Sch Med, IL-69978 Tel Aviv, Israel. RP Ben-Itzchak, E (reprint author), Bar Ilan Univ, Assaf Harofeh Med Ctr, Sch Educ, Autism Ctr, Ramat Gan, Israel. EM benitze@mail.biu.ac.il CR Alpern G., 2000, DEV PROFILE, P2 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson S. 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PD MAY-JUN PY 2007 VL 28 IS 3 BP 287 EP 303 DI 10.1016/j.ridd.2006.03.002 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 152VY UT WOS:000245391300007 PM 16730944 ER PT J AU Rua, MO AF Ojea Rua, Manuel TI Autistic spectrum disorders: psychoeducational intervention integrated in the curriculum SO REVISTA ESPANOLA DE PEDAGOGIA LA Spanish DT Article DE augmentative communication; alternative communication; autistic spectrum disorders; psychoeducational programme and autism ID EXCHANGE COMMUNICATION-SYSTEM; ALTERNATIVE COMMUNICATION; CHILDREN; STUDENT; MODEL; SUPPORTS; SKILLS; AAC AB The search for effective learning ways for the education of autistic spectrum students focuses on the development of those basic dimensions which define it. 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Esp. Pedagog. PD MAY-AUG PY 2007 VL 65 IS 237 BP 333 EP 350 PG 18 WC Education & Educational Research SC Education & Educational Research GA 219TV UT WOS:000250112000008 ER PT J AU Hertzog, ZI Hertzog, R Dobrescu, A Burada, F Mixich, V Burada, E AF Hertzog, Zorica-Ileana Hertzog, R. Dobrescu, Amelia Burada, F. Mixich, V. Burada, Emilia TI Numerical and structural chromosomal changes in a case of autism SO ROMANIAN BIOTECHNOLOGICAL LETTERS LA English DT Article DE autism; aneuploidies; chromosomal rearrangements; centromere disfunction ID DISORDER AB Of all the chronic mental disorders the cause of autism is the least understood. Structural and numerical chromosomal aberrations have been seen in many patients with autism. Our paper is meant to present the results of cytogenetic and genealogical investigations in an autism case. Material and methods. Cytogenetic analysis has been performed by standard karyorype and kinetochores were emphasized by modification of fixation stage of chromosomes preparation after the method described by Rooney and Czepulkowski. The information acquired from subject's parents and brother underlie of pedigree construction. Results. Cytogenetic analysis revealed normal and aberrant karyotypes (76% vs. 24%) with affecting chromosomes 2, 3, 14, 15, 17, 20, X and Y We identified trisomy 3, and gonosomal trisomy (XXY), tetrasomy 14 and 15, isochromosome 2q, translocation (17,20) and duplication Yq. Treatment of cells in cultures with bleomicin led to a higher frequency of chromosomal aberrations than in case of patient's parents and brother. Kinetochores analysis exhibits the uni- and bilateral lack of kinetochores on some big and middle chromosomes. Study of pedigree showed that the autism has a multifactor heredity. Conclusions. Reported aneuploidy can be caused by centromere dysfunction raised from mutations of genes involved in structural and functional control of centromeres. C1 [Hertzog, Zorica-Ileana] UMF Craiova, Fac Med Dent, Dept Genet, Craiova, Spain. [Hertzog, R.] Army Ctr Med Res Bucharest, Bucharest, Romania. [Dobrescu, Amelia; Burada, F.; Mixich, V.] UMF Craiova, Fac Med, Dept Med Genet, Craiova, Romania. RP Hertzog, ZI (reprint author), UMF Craiova, Fac Med Dent, Dept Genet, Craiova, Spain. 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PD APR 29 PY 2007 VL 362 IS 1480 BP 679 EP 704 DI 10.1098/rstb.2006.2004 PG 26 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 146QH UT WOS:000244948900015 PM 17301026 ER PT J AU Nishimura, K Nakamura, K Anitha, A Yamada, K Tsujii, M Iwayama, Y Hattori, E Toyota, T Takei, N Miyachi, T Iwata, Y Suzuki, K Matsuzaki, H Kawai, M Sekine, Y Tsuchiya, K Sugihara, G Suda, S Ouchi, Y Sugiyama, T Yoshikawa, T Mori, N AF Nishimura, Katsuhiko Nakamura, Kazuhiko Anitha, A. Yamada, Kazuo Tsujii, Masatsugu Iwayama, Yoshimi Hattori, Eiji Toyota, Tomoko Takei, Nori Miyachi, Taishi Iwata, Yasuhide Suzuki, Katsuaki Matsuzaki, Hideo Kawai, Masayoshi Sekine, Yoshimoto Tsuchiya, Kenji Sugihara, Gen-ichi Suda, Shiro Ouchi, Yasuomi Sugiyama, Toshiro Yoshikawa, Takeo Mori, Norio TI Genetic analyses of the brain-derived neurotrophic factor (BDNF) gene in autism SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE autism; brain-derived neurotrophic factor; serotonin transporter; a trios-based association; peripheral blood lymphocytes ID OBSESSIVE COMPULSIVE SCALE; RAT-BRAIN; SEROTONERGIC AXONS; VAL66MET POLYMORPHISM; MENTAL-RETARDATION; HUMAN-MEMORY; IN-VITRO; CHILDREN; DISORDERS; PROMOTES AB Autism is a severe neurodevelopmental disorder defined by social and communication deficits and ritualistic-repetitive behaviors that are detectable in early childhood. Brain-derived neurotrophic factor (BDNF) plays a critical role in the pathogenesis of autism. In this study, we examined the SNP- and haplotypic-association of BDNF with autism in a trios-based association study (the Autism Genetic Resource Exchange). We also examined the expression of BDNF mRNA in the peripheral blood lymphocytes of drug-naive autism patients and control subjects. In the TDT of autism trios, the SNP haplotype combinations showed significant associations in the autism group. BDNF expression in the drug-naive autistic group was found to be significantly higher than in the control group. We suggest that BDNF has a possible role in the pathogenesis of autism through its neurotrophic effects on the serotonergic system. (c) 2007 Elsevier Inc. All rights reserved. C1 Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 43131, Japan. RIKEN, Brain Sci Inst, Lab Mol Psychiat, Saitama, Japan. Chukyo Univ, Fac Sociol, Toyota, Aichi, Japan. Hamamatsu Univ Sch Med, Osaka Hamamatsu Joint Res Ctr Child Mental Dev, Hamamatsu, Shizuoka 43131, Japan. Osaka Univ, Osaka Hamamatsu Joint Res Ctr Child Mental Dev, Grad Sch Med, Suita, Osaka 565, Japan. Hamamatsu Med Ctr, Positron Med Ctr, Hamamatsu, Shizuoka, Japan. Aichi Childrens Hlth & Med Ctr, Aichi, Japan. RP Nakamura, K (reprint author), Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 43131, Japan. EM nakamura@hama-med.ac.jp CR ALTAR CA, 1994, EXP NEUROL, V130, P31, DOI 10.1006/exnr.1994.1182 American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th ANDERSON GM, 1994, NEUROBIOLOGY AUTISM, P227 Baron-Cohen S, 1999, J AUTISM DEV DISORD, V29, P407, DOI 10.1023/A:1023035012436 BUSS AH, 1992, J PERS SOC PSYCHOL, V63, P452, DOI 10.1037//0022-3514.63.3.452 Carper RA, 2005, BIOL PSYCHIAT, V57, P126, DOI 10.1016/j.biopsych.2004.11.005 Chugani DC, 1997, ANN NEUROL, V42, P666, DOI 10.1002/ana.410420420 Chugani DC, 1999, ANN NEUROL, V45, P287, DOI 10.1002/1531-8249(199903)45:3<287::AID-ANA3>3.0.CO;2-9 CIARANELLO RD, 1982, NEW ENGL J MED, V307, P181, DOI 10.1056/NEJM198207153070310 Connolly AM, 2006, BIOL PSYCHIAT, V59, P354, DOI 10.1016/j.biopsych.2005.07.004 Courchesne E, 2001, NEUROLOGY, V57, P245 Courchesne E, 2003, JAMA-J AM MED ASSOC, V290, P337, DOI 10.1001/jama.290.3.337 Djalali S, 2005, J NEUROCHEM, V92, P616, DOI 10.1111/j.1471-4159.2004.02911.x Egan MF, 2003, CELL, V112, P257, DOI 10.1016/S0092-8674(03)00035-7 Geschwind DH, 2001, AM J HUM GENET, V69, P463, DOI 10.1086/321292 Gladkevich A, 2004, PROG NEURO-PSYCHOPH, V28, P559, DOI 10.1016/j.pnpbo.2004.01.009 Goggi J, 2002, BRAIN RES, V941, P34, DOI 10.1016/S0006-8993(02)02505-2 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1012 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1006 Grider MH, 2005, J NEUROSCI RES, V82, P404, DOI 10.1002/jnr.20635 Hall D, 2003, AM J HUM GENET, V73, P370, DOI 10.1086/377003 HAMILTON M, 1959, BRIT J MED PSYCHOL, V32, P50 HAMILTON M, 1960, J NEUROL NEUROSUR PS, V23, P56, DOI 10.1136/jnnp.23.1.56 HANLEY HG, 1977, ARCH GEN PSYCHIAT, V34, P521 Hariri AR, 2003, J NEUROSCI, V23, P6690 Hashimoto K, 2006, PROG NEURO-PSYCHOPH, V30, P1529, DOI 10.1016/j.pnpbp.2006.06.018 Hazlett HC, 2006, BIOL PSYCHIAT, V59, P1, DOI 10.1016/j.biopsych.2005.06.015 Hollander E, 2005, BIOL PSYCHIAT, V58, P226, DOI 10.1016/j.biopsych.2005.03.040 Kent L, 2005, MOL PSYCHIATR, V10, P939, DOI 10.1038/sj.mp.4001696 Lang UE, 2005, PSYCHOPHARMACOLOGY, V180, P95, DOI 10.1007/s00213-004-2137-7 LEWONTIN RC, 1988, GENETICS, V120, P849 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Mamounas LA, 2000, J NEUROSCI, V20, P771 Mamounas LA, 1995, J NEUROSCI, V15, P7929 MARTINIVERSON MT, 1994, J NEUROSCI, V14, P1262 McDougle CJ, 1996, ARCH GEN PSYCHIAT, V53, P1001 McDougle CJ, 2005, AM J PSYCHIAT, V162, P1142, DOI 10.1176/appi.ajp.162.6.1142 Miyazaki K, 2004, BRAIN DEV-JPN, V26, P292, DOI 10.1016/S0387-7604(03)00168-2 MOSSNER R, 2000, NEUROCHEM INT, V36, P97 Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Perry EK, 2001, AM J PSYCHIAT, V158, P1058, DOI 10.1176/appi.ajp.158.7.1058 Ranade K, 2001, GENOME RES, V11, P1262 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Rumajogee P, 2002, J NEUROCHEM, V83, P1525, DOI 10.1046/j.1471-4159.2002.01264.x Siuciak JA, 1996, BRAIN RES, V710, P11, DOI 10.1016/0006-8993(95)01289-3 Stone VE, 2003, NEUROPSYCHOLOGIA, V41, P209, DOI 10.1016/S0028-3932(02)00151-3 WHITE LA, 1994, J NEUROSCI, V14, P6744 World Health Organziation, 1992, ICD10 CLASS MENT BEH NR 48 TC 42 Z9 44 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0006-291X J9 BIOCHEM BIOPH RES CO JI Biochem. Biophys. Res. Commun. PD APR 27 PY 2007 VL 356 IS 1 BP 200 EP 206 DI 10.1016/j.bbrc.2007.02.135 PG 7 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 153GE UT WOS:000245419300034 PM 17349978 ER PT J AU Mugno, D Ruta, L D'Arrigo, VG Mazzone, L AF Mugno, Diego Ruta, Liliana D'Arrigo, Valentina Genitori Mazzone, Luigi TI Impairment of quality of life in parents of children and adolescents with pervasive developmental disorder SO HEALTH AND QUALITY OF LIFE OUTCOMES LA English DT Article ID WORLD-HEALTH-ORGANIZATION; INCIDENCE AUTISM FAMILIES; SCHOOL-AGE-CHILDREN; PSYCHIATRIC-DISORDERS; MENTAL-RETARDATION; ASSESSMENT WHOQOL; BEHAVIOR PROBLEMS; CEREBRAL-PALSY; SOCIAL SUPPORT; BROAD AUTISM AB Background: Little is known about the Quality of Life (QOL) in parents of children with developmental diseases as compared to other severe neurological or psychiatric disorders. Aims of the present study were: to evaluate QOL in parents of children affected by Pervasive Development Disorder (PDDs), Cerebral Palsy (CP) or Mental Retardation (MR) as compared to a control group (CG); to evaluate QOL of parents of patients with different types of PDDs, namely Autistic Disorder (AD), High Function Autism/Asperger Syndromes (HFA/AS) and Pervasive Developmental Disorder Not Otherwise Specified (PPD-NOS); and to compare the level of impairment in QOL of mothers and fathers within PDDs, CP, MR groups and between AD, HFA/ AS, PDD-NOS sub-groups. Methods: The sample consisted of 212 parents (115 mothers and 97 fathers) of 135 children or adolescents affected by PDDs, MR or CP. An additional sample of 77 parents (42 mothers and 35 fathers) of 48 healthy children was also included and used as a control group. QOL was assessed by the WHOQOL-BREF questionnaire. Results: Compared with parents of healthy children, parents in the PDDs group reported impairment in physical activity (p = 0.0001) and social relationships (p = 0.0001) and worse overall perception of their QOL (p = 0.0001) and health (p = 0.005). Scores in the physical (p = 0.0001), psychological (p = 0.0001) and social relationships domains (p = 0.0001) and in the physical (p = 0.0001) and social relationships (p = 0.0001) domains were lower compared to the MR group CP group respectively. Little differences were observed between MR, CP and control groups. The level of impairment of physical (p = 0.001) and psychological (p = 0.03) well-being were higher in mothers than in fathers in the PDDs and CP groups respectively; in the other groups, and across all the other domains of QQL impairment was similar. There were no statistically significant differences in the scores between the AD, HFA/AS and PDD-NOS sub-groups, but parents in the HFA/AS sub-group seemed to display a lower QOL compared to the AD sub-group. Conclusion: Parents of children with PDDs seem to display a higher burden, probably for a combination of environmental and genetic factors. Within this group of parents also those of HFA or AS people have higher stress. These finding must be taken into account in policy making to provide better and more specific supports and interventions for this group of diseases. C1 Univ Catania, Dept Pediat, Div Child Neurol & Psychiat, I-95100 Catania, Italy. RP Mugno, D (reprint author), Univ Catania, Dept Pediat, Div Child Neurol & Psychiat, Via S Sofia, I-95100 Catania, Italy. 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TI Aristaless-related homeobox gene, the gene responsible for west syndrome and related disorders, is a groucho/transducin-like enhancer of split dependent transcriptional repressor SO NEUROSCIENCE LA English DT Article DE ARX; X-linked mental retardation; transcription repression; polyalanine tract expansion; mutation; MRX ID LINKED MENTAL-RETARDATION; TRACT EXPANSION; ARX; FOREBRAIN; MUTATIONS; DOMAINS; GROUCHO; MOUSE; CELL; ACTIVATOR AB Aristaless-related homeobox gene (ARX) is an important paired-type homeobox gene involved in the development of human brain. The ARX gene mutations are a significant contributor to various forms of X-chromosome-linked mental retardation with and without additional features including epilepsy, lissencephaly with abnormal genitalia, hand dystonia or autism. Here we demonstrate that the human ARX protein is a potent transcriptional repressor, which binds to Groucho/transducin-like enhancer of split (TLE) cofactor proteins and the TLE1 in particular through its octapeptide (Engrailed homology repressor domain (eh-1) homology) domain. We show that the transcription repression activity of ARX is modulated by two strong repression domains, one located within the octapeptide domain and the second in the region of the polyalanine tract 4, and one activator domain, the aristaless domain. Importantly, we show that the transcription repression activity of ARX is affected by various naturally occurring mutations. The introduction of the c.98T > C (p.L33P) mutation results in the lack of binding to TLE1 protein and relaxed transcription repression. The introduction of the two most frequent ARX polyalanine tract expansion mutations increases the repression activity in a manner dependent on the number of extra alanines. Interestingly, deletions of alanine residues within polyalanine tracts I and 2 show low or no effect. In summary we demonstrate that the ARX protein is a strong transcription repressor, we identify novel ARX interacting proteins (TLE) and offer an explanation of a molecular pathogenesis of some APX mutations, including the most frequent ARX mutations, the polyalanine tract expansion mutations, c.304ins(GCG)(7) and c.428_451dup. (c) 2007 IBRO. Published by Elsevier Ltd. All rights reserved. C1 Womens & Childrens Hosp, Dept Med Genet, Adelaide, SA 5006, Australia. DIBIT, Stem Cell Res Inst, Milan, Italy. Univ Adelaide, Dept Paediat, Adelaide, SA, Australia. Univ Adelaide, Dept Mol Biosci, Adelaide, SA, Australia. McGill Univ, Ctr Neuronal Survival, Montreal Neurol Inst, Montreal, PQ H3A 2B4, Canada. RP Gecz, J (reprint author), Womens & Childrens Hosp, Dept Med Genet, 72 King William Rd, Adelaide, SA 5006, Australia. 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Carter, C. S. Leventhal, Bennett L. Lord, Catherine Cook, Edwin H., Jr. TI Association of the oxytocin receptor gene (OXTR) in Caucasian children and adolescents with autism SO NEUROSCIENCE LETTERS LA English DT Article DE oxytocin; OXTR; autism; genetics; linkage disequilibrium; polymorphisms; neuropeptide hormone ID PERVASIVE DEVELOPMENTAL DISORDERS; SOCIAL COGNITION; DISEQUILIBRIUM; VASOPRESSIN; POPULATION; EXPRESSION; SPECTRUM; DEFICITS; HUMANS; REGION AB The oxytocin receptor gene (OXTR) has been studied in autism because of the role of oxytocin (OT) in social cognition. Linkage has also been demonstrated to the region of OXTR in a large sample. Two single nucleotide polymorphisms (SNPs) and a haplotype constructed from them in OXTR have been associated with autism in the Chinese Han population. We tested whether these associations replicated in a Caucasian sample with strictly defined autistic disorder. 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Conrad Ye, Kenny Wigler, Michael TI Strong association of de novo copy number mutations with autism SO SCIENCE LA English DT Article ID COMPARATIVE GENOMIC HYBRIDIZATION; COMMON FRAGILE SITES; SPECTRUM DISORDERS; GENE; DELETIONS; POLYMORPHISM; RETARDATION AB We tested the hypothesis that de novo copy number variation (CNV) is associated with autism spectrum disorders (ASDs). We performed comparative genomic hybridization (CGH) on the genomic DNA of patients and unaffected subjects to detect copy number variants not present in their respective parents. Candidate genomic regions were validated by higher-resolution CGH, paternity testing, cytogenetics, fluorescence in situ hybridization, and microsatellite genotyping. Confirmed de novo CNVs were significantly associated with autism ( P = 0.0005). Such CNVs were identified in 12 out of 118 (10%) of patients with sporadic autism, in 2 out of 77 (3%) of patients with an affected first-degree relative, and in 2 out of 196 (1%) of controls. 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Perez-Sayes, G. Erekatxo-Bilbao, M. Pelegrin-Valero, C. TI What is theory of mind? SO REVISTA DE NEUROLOGIA LA Spanish DT Review DE emotional intelligence; empathy; faux pas; first and second line beliefs; happe stories; prefrontal cortex; social cognition; theory of mind ID BILATERAL AMYGDALA LESIONS; HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; EXECUTIVE FUNCTION; SOCIAL COGNITION; FRONTAL LOBES; FALSE BELIEF; NEUROPSYCHOLOGICAL EVIDENCE; STORY COMPREHENSION; DOMAIN-SPECIFICITY AB Introduction. The brain is, basically speaking, a predictive machine, designed to reduce environmental incertitude. The theory of mind originated from a concept found in the pioneer works of Premack and Woodruf and refers to the ability to understand and predict the behaviour of other people, their knowledge, intentions, emotions and beliefs. This term was initially confined to the study of primatology and aetiology of autism, proposing that the cause of generalised disorders in development was all absence of theory of mind. In recent years however we have observed a great proliferation of studies oil this complex concept and its affectation in various pathologies. Development. This work proposes dividing the concept of theory of mind into different processes and how to evaluate each one. It furthermore aims at establishing the brain structures related with each level of theory of mind. These levels of complexity are: facial recognition of emotions, first and second order beliefs, social usage of language, social behaviour and empathy. Conclusions. 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TI On the selection of patients with developmental delay/mental retardation and autism spectrum disorders for genetic studies SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Editorial Material C1 Inst Child & Adolescent Neuropsychiat, Stella Maris Clin Res Inst, I-56018 Pisa, Italy. Univ Utah, Div Med Genet, Dept Pediat, Salt Lake City, UT USA. RP Battaglia, A (reprint author), Inst Child & Adolescent Neuropsychiat, Stella Maris Clin Res Inst, Via Giacinti 2, I-56018 Pisa, Italy. 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TI Deletion of 7q31-1 supports involvement of FOXP2 in language impairment: Clinical report and review SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Review DE del(7)(q31); FOXP2; WNT2; SPCH1; AUTS1; speech; language; verbal dyspraxia ID INTERSTITIAL DELETION; LONG ARM; AUTISTIC DISORDER; SUSCEPTIBILITY GENE; BRAIN ABNORMALITIES; MENTAL-RETARDATION; SEVERE SPEECH; CHROMOSOME-7; 7Q; DYSPRAXIA AB We report on a young male with moderate mental retardation, dysmorphic features, and language delay who is deleted for 7q31.1-7q31.31. His full karyotype is 46,XY,der(7)del(7)(q31.1-q31.31)ins(10;7)(q24.3;q31.1q31.31)mat. This child had language impairment, including developmental verbal dyspraxia, but did not meet criteria for autism according to standardized ADOS testing. Our patient's deletion, which is the smallest reported deletion including FOXP2, adds to the body of evidence that supports the role of FOXP2 in speech and language impairment, but not in autism. A reported association between autism and deletions of WNT2, a gene also deleted in our patient, is likewise not supported by our case. Previously, fine mapping with rnicrosatellites markers within in a large three-generation family, in which half the members had severe specific language impairment, aided the localization of the SPCH1 locus to 7q31 within markers D7S2459 (107.1 Mb) and D7S643 (120.5 Mb). Additionally, chromosome rearrangement of 7q31 and mutational analyses have supported the growing evidence that FOXP2, a gene within the SPCH1 region, is involved with speech and language development. It is unclear however whether the AUTS1 (autistic spectrum 1) locus, highly linked to 7q31, overlaps with the SPCH1 and FOXP2. (c) 2007 Wiley-Liss, Inc. C1 Baylor Coll Med, Kleberg Cytogenet Lab, Dept Mol & Human Genet, Houston, TX 77030 USA. Illumina Inc, San Diego, CA USA. Texas Childrens Hosp, Houston, TX 77030 USA. RP Cheung, SW (reprint author), Baylor Coll Med, Kleberg Cytogenet Lab, Dept Mol & Human Genet, 1 Baylor Plaza,NAB2015, Houston, TX 77030 USA. 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Yale Univ, Dept Elect Engn, New Haven, CT USA. Yale Univ, Dept Biomed Engn, New Haven, CT USA. RI Jackowski, Andrea/D-8616-2012; Jackowski, Marcel/G-7602-2012 OI Jackowski, Andrea/0000-0001-8842-5406; NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. 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Tel Aviv Univ, Tel Aviv Sourasky Med Ctr, Wohl Inst Adv Imaging, Funct Brain Res Ctr, Tel Aviv, Israel. RI Calhoun, Vince/H-7146-2013 OI Calhoun, Vince/0000-0001-9058-0747 NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2007 VL 61 IS 8 SU S MA 335 BP 104S EP 104S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 157DF UT WOS:000245698100330 ER PT J AU Jou, RJ Paterson, SJ Jackowski, AP Jackowski, M Papademetris, X Rajeevan, N Staib, LH Schultz, RT AF Jou, Roger J. Paterson, Sarah J. Jackowski, Andrea P. Jackowski, Marcel Papademetris, Xenophon Rajeevan, Nallakandi Staib, Lawrence H. Schultz, Robert T. TI Abnormalities in white matter structure in autism spectrum disorders detected by diffusion tensor imaging SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 62nd Annual Scientific Meeting of the Society-of-Biological-Psychiatry CY 2007 CL San Diego, CA SP Soc Biol Psychiat C1 Yale Univ, Dept Psychiat, New Haven, CT 06520 USA. Yale Univ, Investigat Med Program, New Haven, CT USA. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. Univ Fed Sao Paulo, Dept Hlth Sci, Sao Paulo, Brazil. Yale Univ, Dept Diagnost Radiol, New Haven, CT 06510 USA. Yale Univ, Dept Elect Engn, New Haven, CT USA. Yale Univ, Dept Biomed Engn, New Haven, CT USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2007 VL 61 IS 8 SU S MA 702 BP 217S EP 217S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 157DF UT WOS:000245698100697 ER PT J AU Kern, JK Grannemann, BD Trivedi, MH Adams, JB AF Kern, Janet K. Grannemann, Bruce D. Trivedi, Madhukar H. Adams, James B. TI Sulfhydryl-reactive metals in autism SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; FIBRILLARY ACIDIC PROTEIN; MODIFIED CHECKLIST; OXIDATIVE STRESS; MERCURY-VAPOR; CHILDREN; EXPOSURE; BRAIN; HAIR; METHYLMERCURY AB This study examined the difference between sulfhydryl- reactive metals ( mercury, lead, arsenic, and cadmium) in the hair of 45 children with autism ( 1 - 6 yr of age) as compared to 45 gender-, age-, and race- matched typical children. Hair samples were measured with inductively coupled mass spectrometry. Some studies, such as Holmes et al. ( 2003), suggested that children with autism may be poor detoxifiers relative to normally developing children. Metals that are not eliminated sequester in the brain. Our study found that arsenic, cadmium, and lead were significantly lower in the hair of children with autism than in matched controls. Mercury was in the same direction ( lower in autism) following the same pattern, but did not achieve statistical significance. The evidence from our study supports the notion that children with autism may have trouble excreting these metals, resulting in a higher body burden that may contribute to symptoms of autism. C1 Univ Texas, SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA. Arizona State Univ, Tempe, AZ USA. RP Kern, JK (reprint author), Univ Texas, SW Med Ctr Dallas, Dept Psychiat, 6363 Forest Pk Rd,Suite 13-354, Dallas, TX 75390 USA. 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TI Healing the new childhood epidemics: Autism, ADHD, asthma, and allergies; The groundbreaking program for the 4-A disorders. SO LIBRARY JOURNAL LA English DT Book Review C1 Mesa Publ Lib, Los Alamos, NM USA. RP Eastwood, EJ (reprint author), Mesa Publ Lib, Los Alamos, NM USA. CR Stauth Cameron, 2007, HEALING NEW CHILDHOO NR 1 TC 0 Z9 0 PU REED BUSINESS INFORMATION PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD APR 15 PY 2007 VL 132 IS 7 BP 110 EP 110 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 160ID UT WOS:000245933200224 ER PT J AU Safford, E AF Safford, Elizabeth TI Visual supports for people with autism: A guide for parents and professionals. SO LIBRARY JOURNAL LA English DT Book Review C1 Nevins Mem Lib, Methuen, MA USA. RP Safford, E (reprint author), Nevins Mem Lib, Methuen, MA USA. CR Cohen M, 2007, VISUAL SUPPORTS PEOP NR 1 TC 0 Z9 0 PU REED BUSINESS INFORMATION PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD APR 15 PY 2007 VL 132 IS 7 BP 111 EP 111 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 160ID UT WOS:000245933200230 ER PT J AU Dichter, GS Belger, A AF Dichter, Gabriel S. Belger, Aysenil TI Social stimuli interfere with cognitive control in autism SO NEUROIMAGE LA English DT Article DE autism; functional magnetic resonance imaging (fMRI); cognitive control; executive function; attention; social cognition; gaze ID CARD SORTING TEST; POSITRON-EMISSION-TOMOGRAPHY; ANTERIOR CINGULATE CORTEX; ATTENTIONAL NETWORKS; EXECUTIVE FUNCTION; REPETITIVE BEHAVIOR; ASPERGER-SYNDROME; REVISED VERSION; FUNCTIONAL MRI; CHILDREN AB Autism spectrum disorders are characterized by cognitive control deficits as well as impairments in social interactions. However, the brain mechanisms mediating the interactive effects of these deficits have not been addressed. We employed event-related functional magnetic resonance imaging (fMRI) to examine the effects of processing directional information from faces on activity within brain regions mediating cognitive control. High-functioning individuals with autism and age-, gender-, and IQ-matched neurotypical individuals attended to the direction of a centrally-presented arrow or gaze stimulus with similar flanker stimuli oriented in the same ("congruent") or opposite ("incongruent") direction. The incongruent arrow condition was examined to assess functioning of brain regions mediating cognitive control in a context without social-cognitive demands, whereas the incongruent gaze condition assessed functioning of the same brain regions in a social-cognitive context. Consistent with prior studies, the incongruent arrow condition recruited activity in bilateral midfrontal gyrus, right inferior frontal gyrus, bilateral intraparietal sulcus, and the anterior cingulate relative to the congruent arrow condition in neurotypical participants. Notably, there were not diagnostic group differences in patterns of regional fMRI activation in response to the arrow condition. However, while viewing the incongruent gaze stimuli, although neurotypical participants recruited the same brain regions, participants with autism showed marked hypoactivation in these areas. These findings suggest that processing social-cognitive stimuli interferes with functioning of brain regions recruited during cognitive control tasks in autism. Implications for research into cognitive control deficits in autism are discussed. (C)3 2007 Elsevier Inc. All rights reserved. C1 Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA. 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DOI 10.1016/j.neuropsychologia.2005.05.021 NR 88 TC 54 Z9 55 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PD APR 15 PY 2007 VL 35 IS 3 BP 1219 EP 1230 DI 10.1016/j.neuroimage.2006.12.038 PG 12 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 160PZ UT WOS:000245956100022 PM 17321151 ER PT J AU Sadakata, T Washida, M Furuichi, T AF Sadakata, Tetsushi Washida, Miwa Furuichi, Teiichi TI Alternative splicing variations in mouse CAPS2: differential expression and functional properties of splicing variants SO BMC NEUROSCIENCE LA English DT Article ID CA2+-DEPENDENT ACTIVATOR PROTEIN; CORE VESICLE EXOCYTOSIS; NEUROTROPHIN RELEASE; SECRETION; FAMILY; MICE; CALCIUM; MEMBERS; CADPS2; BRAIN AB Background: Ca2+-dependent activator protein 2 (CAPS2/CADPS2) is a secretory vesicle-associated protein involved in the release of neurotrophin. We recently reported that an aberrant, alternatively spliced CAPS2 mRNA that lacks exon 3 (CAPS2 Delta exon3) is detected in some patients with autism. Splicing variations in mouse CAPS2 and their expression and functions remain unclear. Results: In this study, we defined 31 exons in the mouse CAPS2 gene and identified six alternative splicing variants, CAPS2a-f. CAPS2a is an isoform lacking exons 22 and 25, which encode part of the Munc13-1-homologous domain (MHD). CAPS2b lacks exon 25. CAPS2c lacks exons 11 and 22. CAPS2d, 2e, and 2f have C-terminal deletions from exon 14, exon 12, and exon 5, respectively. On the other hand, a mouse counterpart of CAPS2 Delta exon3 was not detected in the mouse tissues tested. CAPS2b was expressed exclusively in the brain, and the other isoforms were highly expressed in the brain, but also in some non-neural tissues. In the brain, all isoforms showed predominant expression patterns in the cerebellum. In the developing cerebellum, CAPS2b showed an up-regulated expression pattern, whereas the other isoforms exhibited transiently peaked expression patterns. CAPS2 proteins were mostly recovered in soluble fractions, but some were present in membrane fractions, except for CAPS2c and 2f, both of which lack the PH domain, suggesting that the PH domain is important for membrane association. In contrast to CAPS2a and 2b, CAPS2c showed slightly decreased BDNF-releasing activity, which is likely due to the C-terminal truncation of the PH domain in CAPS2c. Conclusion: This study indicates that, in mouse, there are six splicing variants of CAPS2 (CAPS2a-f), and that these are subdivided into two groups: a long form containing the C-terminal MHD and a short form lacking the C- terminal MHD. 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PD APR 12 PY 2007 VL 8 AR 25 DI 10.1186/1471-2202-8-25 PG 11 WC Neurosciences SC Neurosciences & Neurology GA 160EU UT WOS:000245924500001 PM 17428348 ER PT J AU Spezio, ML Huang, PYS Castelli, F Adolphs, R AF Spezio, Michael L. Huang, Po-Yin Samuel Castelli, Fulvia Adolphs, Ralph TI Amygdala damage impairs eye contact during conversations with real people SO JOURNAL OF NEUROSCIENCE LA English DT Article DE social cognition; face gaze; lesion; autism; amygdala; eye position; facial ID RHESUS-MONKEYS; GAZE AVERSION; AUTISM; LESIONS; FACES; RESPONSIVITY; INDIVIDUALS; RECOGNITION; ACTIVATION; FIXATION AB The role of the human amygdala in real social interactions remains essentially unknown, although studies in nonhuman primates and studies using photographs and video in humans have shown it to be critical for emotional processing and suggest its importance for social cognition. We show here that complete amygdala lesions result in a severe reduction in direct eye contact during conversations with real people, together with an abnormal increase in gaze to the mouth. These novel findings from real social interactions are consistent with an hypothesized role for the amygdala in autism and the approach taken here opens up new directions for quantifying social behavior in humans. C1 CALTECH, Div Humanities & Social Sci 22877, Pasadena, CA 91125 USA. RP Spezio, ML (reprint author), CALTECH, Div Humanities & Social Sci 22877, Pasadena, CA 91125 USA. 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Neurosci. PD APR 11 PY 2007 VL 27 IS 15 BP 3994 EP 3997 DI 10.1523/JNEUROSCI.3789-06.2007 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 158RB UT WOS:000245810100009 PM 17428974 ER PT J AU Hanson, JE Madison, DV AF Hanson, Jesse E. Madison, Daniel V. TI Presynaptic Fmr1 genotype influences the degree of synaptic connectivity in a mosaic mouse model of fragile X syndrome SO JOURNAL OF NEUROSCIENCE LA English DT Article DE Fmr1; FMRP; mosaic; whole cell; fragile X syndrome; autism; CA3; connectivity; hippocampus; presynaptic ID LONG-TERM POTENTIATION; MENTAL-RETARDATION PROTEIN; KNOCKOUT MICE; EXPRESSION; DROSOPHILA; GENE; AUTISM; MULTICENTER; HIPPOCAMPUS; PLASTICITY AB Almost all female and some male fragile X syndrome (FXS) patients are mosaic for expression of the FMR1 gene, yet all research in models of FXS has been in animals uniformly lacking Fmr1 expression. Therefore, we developed a system allowing neuronal genotype to be visualized in vitro in mouse brain slices mosaic for Fmr1 expression. Whole-cell recordings from individual pairs of presynaptic and postsynaptic neurons in organotypic hippocampal slices were used to probe the cell-autonomous effects of Fmr1 genotype in mosaic networks. These recordings revealed that wild-type presynaptic neurons formed synaptic connections at a greater rate than presynaptic neurons lacking normal Fmr1 function in mosaic networks. At the same time, the postsynaptic Fmr1 genotype did not influence the probability that a neuron received synaptic connections. Asymmetric presynaptic function during development of the brain could result in a decreased participation in network function by the portion of neurons lacking FMR1 expression. C1 Stanford Univ, Sch Med, Dept Cellular & Mol Physiol, Beckman Ctr 003, Stanford, CA 94305 USA. 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TI Gray matter abnormalities in autism spectrum disorder revealed by T2 relaxation - Reply SO NEUROLOGY LA English DT Letter NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR 10 PY 2007 VL 68 IS 15 BP 1237 EP 1238 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 155IC UT WOS:000245570100021 ER PT J AU Loddo, S AF Loddo, Silvio TI Gray matter abnormalities in autism spectrum disorder revealed by T2 relaxation SO NEUROLOGY LA English DT Letter NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR 10 PY 2007 VL 68 IS 15 BP 1237 EP 1237 DI 10.1212/01.wnl.0000261904.82960.bc PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 155IC UT WOS:000245570100020 PM 17420414 ER PT J AU Egan, MM AF Egan, Mary Ellen TI A costly education SO FORBES LA English DT Article AB The recent spike in autism diagnoses has school districts spending ever more time and money fending off special ed disputes. 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Herrup, Karl TI A genetic study of the suppressors of the Engrailed-1 cerebellar phenotype SO BRAIN RESEARCH LA English DT Article DE En1; En2; cerebellum development; genetic background; modifier gene ID GASTROINTESTINAL NEMATODE INFECTIONS; HOMEOBOX-TRANSCRIPTION-FACTOR; AUTISM-SPECTRUM-DISORDER; X-INACTIVATION CENTER; MUTANT MICE; MIDBRAIN DEVELOPMENT; DOSAGE COMPENSATION; INT-1 PROTOONCOGENE; MOUSE GENOME; HINDBRAIN AB The mouse Engrailed genes, En1 and En2, play an important role in the development of the cerebellum from its inception at the mid/hindbrain boundary in early embryonic development through cell type specification events and beyond. In the absence of En1, the cerebellum and caudal midbrain fail to develop normally-a phenotype that we have previously reported to be strain dependent. On the 129/S1 strain background, En1 null alleles lead to mid/hindbrain failure, whereas on the C57BL/6 background, En1 deficiency is compatible with near normal cerebellar development. We have pursued this dramatic effect of genetic background by per-forming a genetic modifier screen through F1 backcross and F1 intercross matings. The backcross has yielded two strong candidate intervals with suggestive linkage to a third region. Moreover, variations in rescue frequency among subgroups within the backcross indicate gender and parent of origin influences on rescue penetrance. The intercross data reveal locus heterogeneity of the En1 modifiers, with more than one compliment of C57BL/6 and 129/S1 alleles capable of mediating the rescue phenotype. These findings highlight the complexity and plasticity of gene networks involved in brain development. (c) 2006 Elsevier B.V. All rights reserved. C1 Case Sch Med, Dept Neurosci, Cleveland, OH 44106 USA. Case Western Reserve Univ, Dept Neurosci, Alzheimers Res Lab, Cleveland, OH 44106 USA. RP Herrup, K (reprint author), Case Sch Med, Dept Neurosci, 10900 Euclid Ave, Cleveland, OH 44106 USA. 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TI Sequence variants within Exon 1 of MECP2 occur in females with mental retardation SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE MECP2; exon 1; autism; mental retardation; polyalanine ID RETT-SYNDROME; HOMEOBOX GENE; MUTATIONS; ARX; PROTEIN; AUTISM; DISORDER; CHANNEL AB A new splice variant of the Rett syndrome gene, MECP2, was recently identified, that includes coding sequence from exon 1, and is the predominant transcript in the central nervous system. This sequence encodes polyalanine and polyglycine stretches within the N-terminal portion of MeCP2, and may confer novel functional properties to the protein. We screened autism, mental retardation (MR), and control populations for sequence variation within this region, and identified variation in similar to 1% of MR cases screened (N = 1,410). No variants were identified in the autism sample (N = 401). Most of these variants occur within a trinucleotide repeat region and result in change in number of alanine or glycine residues within the repeat stretches. We suggest some of these variants may be a relatively frequent cause of non-specific MR or developmental delay. (c) 2006 Wiley-Liss, Inc. C1 Univ Toronto, Ctr Addict & Mental Hlth, Neurogenet Sect, Mol Neuropsychiat & Dev Lab, Toronto, ON M5T 1R8, Canada. Univ Toronto, Dept Psychiat, Toronto, ON M5T 1R8, Canada. Greenwood Genet Ctr, JC Self Res Inst Human Genet, Greenwood, SC 29646 USA. Hosp Sick Children, Program Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Hosp Sick Children, Autism Res Unit, Toronto, ON M5G 1X8, Canada. RP Vincent, JB (reprint author), Univ Toronto, Ctr Addict & Mental Hlth, Neurogenet Sect, Mol Neuropsychiat & Dev Lab, 250 Coll St, Toronto, ON M5T 1R8, Canada. 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TI HOXA1 gene variants influence head growth rates in humans SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; fragile-X syndrome; homeobox; macrocephaly; megalencephaly ID PERVASIVE DEVELOPMENTAL DISORDERS; FRAGILE-X-SYNDROME; AUTISM; CIRCUMFERENCE; HINDBRAIN; HOX-1.6; EAR AB We previously described a significant association between the HOXA1 G218 allele and increased head circumference in autism [Conciatori et al. (2004); Biol Psychiatry 55:413-419]. The present study reveals identical effects also in normal children. HOXA1 A218G alleles and sex explain as much as 10.9 and 6.8% of the variance in head circumference in 142 pediatric controls and in 191 autistic children, aged 3-16 years (F = 6.777,3 and 141 df, P < 0.001 and F = 5.588,3 and 190 df, P < 0.01, respectively). Instead, no association is found in 183 adult controls and in 35 pediatric fragile-X patients. Therefore HOXA1 A218G alleles significantly influence head growth rates, but not final head size, in normal human development. This influence does not differ between normal and autistic children, whereas the lack of FMRP seemingly overwhelms HOXA1 effects in fragile-X patients. (c) 2006 Wiley-Liss, Inc. C1 Lab Mol Psychiat & Neurogenet, I-00155 Rome, Italy. IRCCS Casa Sollievo Sofferenza, Med Genet Serv, Foggia, Italy. IRCCS, Fdn St Lucia, Rome, Italy. II Univ Naples, Dept Child Neuropsychiat, Naples, Italy. Ctr Autism Res & Educ, Phoenix, AZ USA. SW Autism Res & Resource Ctr, Phoenix, AZ USA. IRCCS Oasi Maria SS, Neurol Serv, Enna, Italy. IRCCS Casa Sollieva Sofferenza, Endocrinol Unit, Foggia, Italy. IRCCS Casa Sollieva Sofferenza, Gen Pediat Unit, Foggia, Italy. RP Persico, AM (reprint author), Lab Mol Psychiat & Neurogenet, Univ Campus Biomed,Via Longoni 83, I-00155 Rome, Italy. 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TI Dopamine receptor activation modulates GABA neuron migration from the basal forebrain to the cerebral cortex SO JOURNAL OF NEUROSCIENCE LA English DT Article DE striatum; basal ganglia; ganglionic eminence; dopamine D-1 receptor; dopamine D-2 receptor; tangential neuronal migration ID CAUDAL GANGLIONIC EMINENCE; CORTICAL PRECURSOR CELLS; GABAERGIC INTERNEURONS; PRENATAL EXPOSURE; MESSENGER-RNA; COCAINE; TELENCEPHALON; DYNEIN; CYCLE; BRAIN AB GABA neurons of the cerebral cortex and other telencephalic structures are produced in the basal forebrain and migrate to their final destinations during the embryonic period. The embryonic basal forebrain is enriched in dopamine and its receptors, creating a favorable environment for dopamine to influence GABA neuron migration. However, whether dopamine receptor activation can influence GABA neuron migration is not known. We show that dopamine D-1 receptor activation promotes and D-2 receptor activation decreases GABA neuron migration from the medial and caudal ganglionic eminences to the cerebral cortex in slice preparations of embryonic mouse forebrain. Slice preparations from D1 or D2 receptor knock-out mouse embryos confirm the findings. In addition, D1 receptor electroporation into cells of the basal forebrain and pharmacological activation of the receptor promote migration of the electroporated cells to the cerebral cortex. Analysis of GABA neuron numbers in the cerebral wall of the dopamine receptor knock-out mouse embryos further confirmed the effects of dopamine receptor activation on GABA neuron migration. Finally, dopamine receptor activation mobilizes striatal neuronal cytoskeleton in a manner consistent with the effects on neuronal migration. These data show that impairing the physiological balance between D1 and D2 receptors can alter GABA neuron migration from the basal forebrain to the cerebral cortex. The intimate relationship between dopamine and GABA neuron development revealed here may offer novel insights into developmental disorders such as schizophrenia, attention deficit or autism, and fetal cocaine exposure, all of which are associated with dopamine and GABA imbalance. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Neurol, Cambridge, MA 02139 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Radiol, Cambridge, MA 02139 USA. Univ Massachusetts, Sch Med, Eunice Kennedy Shriver Ctr Mental Retardat Inc, Waltham, MA 02452 USA. RP Bhide, PG (reprint author), Massachusetts Gen Hosp, Dept Neurobiol, 149 13th St, Cambridge, MA 02139 USA. 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The objective of the current article is to review the evidence for the rationale and benefit of LCn-3PUFA in the treatment of common psychiatric disorders in children and adolescents. Methods: A search of Psychlit, PubMed and Cochrane Databases was conducted using the terms child, adolescent, bipolar, depression, psychosis, first-episode psychosis, schizophrenia, attention deficit hyperactivity disorder (ADHD), autism, psychiatric, omega-3, n-3, docosahexaenoic acid and eicosapentaenoic acid. Further studies were identified from the bibliographies of published reviews. Results: One small randomized controlled trial with LCn-3PUFA supplementation in depression in children found a small beneficial effect over placebo. Four placebo-controlled trials showed uncertairi benefit of LCn-3PUFA for ADHD. Single placebo-controlled trials showed no benefit in autism or bipolar disorder. There is an absence of studies examining benefit for first-episode psychosis or schizophrenia in children and adolescents Conclusions: While children and adolescents are receiving LCn-3PUFA for a range of psychiatric indications, there is only evidence of likely benefit for unipolar depression. C1 Hunter New England Area Hlth Serv, Biopolar Program, Newcastle, NSW, Australia. Univ Newcastle, Dept Psychol, Callaghan, NSW 2305, Australia. Univ Sydney, Ctr Clin Sch, Sydney, NSW 2006, Australia. Univ Newcastle, Discipline Psychiat, Sch Med Practice & Populat Hlth, Callaghan, NSW 2305, Australia. 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PD APR PY 2007 VL 19 IS 2 BP 92 EP 103 DI 10.1111/j.1601-5215.2007.00189.x PG 12 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 163MH UT WOS:000246163400004 ER PT J AU Potocki, L Bi, WM Treadwell-Deering, D Carvalho, CMB Eifert, A Friedman, EM Glaze, D Krull, K Lee, JA Lewis, RA Mendoza-Londono, R Robbins-Furman, P Shaw, C Shi, X Weissenberger, G Withers, M Yatsenko, SA Zackai, EH Stankiewicz, P Lupski, JR AF Potocki, Lorraine Bi, Weimin Treadwell-Deering, Diane Carvalho, Claudia M. B. Eifert, Anna Friedman, Ellen M. Glaze, Daniel Krull, Kevin Lee, Jennifer A. Lewis, Richard Alan Mendoza-Londono, Roberto Robbins-Furman, Patricia Shaw, Chad Shi, Xin Weissenberger, George Withers, Marjorie Yatsenko, Svetlana A. Zackai, Elaine H. Stankiewicz, Pawel Lupski, James R. TI Characterization of Potocki-Lupski syndrome (dup(17)(p11.2p11.2)) and delineation of a dosage-sensitive critical interval that can convey an autism phenotype SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID SMITH-MAGENIS-SYNDROME; TOOTH DISEASE TYPE-1A; SUPERNUMERARY MARKER CHROMOSOME; PELIZAEUS-MERZBACHER-DISEASE; GENOME ARCHITECTURE; HOMOLOGOUS RECOMBINATION; PROXIMAL 17P; SEGMENTAL DUPLICATIONS; MOLECULAR-MECHANISM; TANDEM DUPLICATION AB The duplication 17p11.2 syndrome, associated with dup(17)(p11.2p11.2), is a recently recognized syndrome of multiple congenital anomalies and mental retardation and is the first predicted reciprocal microduplication syndrome described the homologous recombination reciprocal of the Smith-Magenis syndrome (SMS) microdeletion (del(17)(p11.2p11.2)). We previously described seven subjects with dup( 17)( p11.2p11.2) and noted their relatively mild phenotype compared with that of individuals with SMS. Here, we molecularly analyzed 28 additional patients, using multiple independent assays, and also report the phenotypic characteristics obtained from extensive multidisciplinary clinical study of a subset of these patients. Whereas the majority of subjects (22 of 35) harbor the homologous recombination reciprocal product of the common SMS microdeletion (similar to 3.7 Mb), 13 subjects (similar to 37%) have nonrecurrent duplications ranging in size from 1.3 to 15.2 Mb. Molecular studies suggest potential mechanistic differences between nonrecurrent duplications and nonrecurrent genomic deletions. Clinical features observed in patients with the common dup( 17)( p11.2p11.2) are distinct from those seen with SMS and include infantile hypotonia, failure to thrive, mental retardation, autistic features, sleep apnea, and structural cardiovascular anomalies. We narrow the critical region to a 1.3-Mb genomic interval that contains the dosage-sensitive RAI1 gene. Our results refine the critical region for Potocki-Lupski syndrome, provide information to assist in clinical diagnosis and management, and lend further support for the concept that genomic architecture incites genomic instability. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Dept Psychiat & Behav Sci, Houston, TX 77030 USA. Baylor Coll Med, Dept Speech Language & Learning, Houston, TX 77030 USA. Baylor Coll Med, Dept Otolaryngol, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. Baylor Coll Med, Dept Ophthalmol, Houston, TX 77030 USA. Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. Baylor Coll Med, Dept Allied Hlth, Houston, TX 77030 USA. Texas Childrens Hosp, Houston, TX 77030 USA. Univ Toronto, Dept Paediat, Div Clin & Metab Genet, Toronto, ON M5S 1A1, Canada. Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA. RP Lupski, JR (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Room 604B,Baylor Plaza 1, Houston, TX 77030 USA. 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Ellison, Jay W. TI Microarray comparative genomic hybridization and FISH studies of an unbalanced cryptic telomeric 2p deletion/16q duplication in a patient with mental retardation and behavioral problems SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE unbalanced translocation; microarray coinparative; genomic hybridization; FISH; 2pter deletion; 16qter duplication ID INDIVIDUALS; AUTISM AB We describe a 7-year-old patient with pervasive developmental disorder and behavioral problems who has a de novo cryptic unbalanced der(2)t(2;16)(p25.3;q24-3) chromosome resulting in deletion of distal 2p and duplication of distal 16q. These segmental aneusomies were detected by microarray comparative genomic hybridization analysis, as was a distal 17p13.3 duplication that was inherited from her father. FISH analysis using bacterial artificial chromosomes confirmed a deletion of approximately 1,700 kbp of DNA from 2pter (containing at least six complete genes or transcription units) and a duplication of similar to 500 kbp from 16qter (including up to ten genes or transcription units). Several genes in these regions tire plausible candidates for contributing to the patient's phenotype. (c) 2007 Wiley-Liss, Inc. C1 Mayo Clin, Dept Med Genet, Rochester, MN 55905 USA. Mayo Clin, Dept Lab Med & Pathol, Cytogenet Lab, Rochester, MN 55905 USA. RP Ellison, JW (reprint author), Mayo Clin, Dept Med Genet, 200 1st St SW, Rochester, MN 55905 USA. 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A PD APR 1 PY 2007 VL 143A IS 7 BP 746 EP 751 DI 10.1002/ajmg.a.31645 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 153QN UT WOS:000245450200016 PM 17345620 ER PT J AU Dager, SR Wang, L Friedman, SD Shaw, DW Constantino, JN Artru, AA Dawson, G Csernansky, JG AF Dager, S. R. Wang, L. Friedman, S. D. Shaw, D. W. Constantino, J. N. Artru, A. A. Dawson, G. Csernansky, J. G. TI Shape mapping of the hippocampus in young children with autism spectrum disorder SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article ID BRAIN; SCHIZOPHRENIA; EPILEPSY; ABNORMALITIES; INDIVIDUALS; ADOLESCENTS; MORPHOMETRY; DIFFERENCE; ASYMMETRY; AMYGDALA AB BACKGROUND AND PURPOSE: We hypothesized the occurrence of characteristic hippocampal-shape alterations in young children with autistic spectrum disorder (ASD) who also exhibit deficits on neuropsychologic tests of medial temporal lobe (MTL) function. MATERIALS AND METHODS: Coronal 3D MR images were acquired from 3- to 4-year-old children with ASD (n = 45) and age-matched children with typical development (n = 13). Children with ASD were further subclassified into those with autism disorder (AD, n = 29) or pervasive developmental disorder-not otherwise specified (PDD-NOS) (n = 16). Variations in hippocampal shape were evaluated by using large-deformation high-dimensional brain mapping. RESULTS: Hippocampal shape measures distinguished children with ASD from those with typical development; within the ASD sample, children with AD were distinguished from those with PDD-NOS. Hippocampal-shape alterations in children with ASD were correlated with degree of mental retardation and performance deficits on tests of MTL function. CONCLUSIONS: Children with ASD exhibited an alteration of hippocampal shape consistent with inward deformation of the subiculum. This pattern of hippocampal-shape deformations in the children with ASD was accentuated in the more severely affected subgroup of children with AD and was associated with deficits on neuropsychologic tests of MTL but not prefrontal function. Hippocampal-shape deformation in the children with ASD was observed to be similar to a pattern of hippocampal shape deformation previously reported in adults with MTL epilepsy. Although the children with ASD, and those with AD in particular, PDD-NOS are at high risk for epilepsy as they enter adolescence, the specificity and causal relationship of this pattern of hippocampal-shape deformation to the development of seizures is not yet known. C1 Univ Washington, Dept Radiol, Seattle, WA 98105 USA. Univ Washington, Dept Psychiat, Seattle, WA 98105 USA. Univ Washington, Dept Bioengn, Seattle, WA 98105 USA. Univ Washington, Dept Anesthesiol, Seattle, WA 98105 USA. Univ Washington, Dept Psychol, Seattle, WA 98105 USA. Washington Univ, Dept Elect Engn, St Louis, MO 63130 USA. Washington Univ, Dept Psychiat, St Louis, MO 63130 USA. Washington Univ, Dept Anat & Neurobiol, St Louis, MO 63130 USA. RP Dager, SR (reprint author), Univ Washington, Dept Radiol, 1100 NE 45th St,Suite 555, Seattle, WA 98105 USA. EM srd@u.washington.edu RI Wang, Lei/I-7552-2013 OI Wang, Lei/0000-0003-3870-3388 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Amundsen LB, 2005, J NEUROSURG ANESTH, V17, P180, DOI 10.1097/01.ana.0000171734.63879.fd Aylward EH, 1999, NEUROLOGY, V53, P2145 BARTH C, 1995, DEV NEUROPSYCHOL, V11, P53 BAUMAN M, 1985, NEUROLOGY, V35, P866 Bauman M.L, 1994, NEUROBIOLOGY AUTISM Christensen G, 1995, TOPOLOGICAL PROPERTI Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Csernansky JG, 2002, AM J PSYCHIAT, V159, P2000, DOI 10.1176/appi.ajp.159.12.2000 Csernansky JG, 2004, NEUROIMAGE, V23, pS56, DOI 10.1016/j.neuroimage.2004.07.025 Csernansky JG, 1998, P NATL ACAD SCI USA, V95, P11406, DOI 10.1073/pnas.95.19.11406 Dawson G, 1998, CHILD DEV, V69, P1276, DOI 10.2307/1132265 Dawson G, 2002, DEV PSYCHOPATHOL, V14, P581, DOI 10.1017/S0954579402003103 Dawson G, 2002, CHILD DEV, V73, P345, DOI 10.1111/1467-8624.00411 Giovanardi Rossi P, 2000, Brain Dev, V22, P102, DOI 10.1016/S0387-7604(99)00124-2 GRENANDER U, 1994, J ROY STAT SOC B MET, V56, P549 Haller JW, 1997, RADIOLOGY, V202, P504 Hogan RE, 2004, BRAIN, V127, P1731, DOI 10.1093/brain/awh197 Hogan RE, 2006, AM J NEURORADIOL, V27, P2149 JOSHI S, 1997, J PATT RECOGN ART IN, V11, P1317 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 MINSHEW NJ, 1994, VIVO NEUROANATOMY AU, P67 Mullen E., 1984, MULLEN SCALES EARLY Piven J, 1998, J AUTISM DEV DISORD, V28, P105, DOI 10.1023/A:1026084430649 Raymond GV, 1996, ACTA NEUROPATHOL, V91, P117 RUMSEY JM, 1996, NEUROIMAGING WINDOW, P119 Saitoh O, 2001, BRAIN, V124, P1317, DOI 10.1093/brain/124.7.1317 SAITOH O, 1995, NEUROLOGY, V45, P317 Schumann CM, 2004, J NEUROSCI, V24, P6392, DOI 10.1523/JNEUROSCI.1297-04.2004 Sparks BF, 2002, NEUROLOGY, V59, P184 Sparrow S, 1984, VINELAND ADAPTIVE BE Tuchman R, 2002, LANCET NEUROL, V1, P352, DOI 10.1016/S1474-4422(02)00160-6 Wang L, 2001, NEUROIMAGE, V14, P531, DOI 10.1006/nimg.2001.0830 ZIPURSKY RB, 1994, BIOL PSYCHIAT, V35, P501, DOI 10.1016/0006-3223(94)90097-3 NR 35 TC 20 Z9 22 PU AMER SOC NEURORADIOLOGY PI OAK BROOK PA 2210 MIDWEST RD, OAK BROOK, IL 60521 USA SN 0195-6108 J9 AM J NEURORADIOL JI Am. J. Neuroradiol. PD APR PY 2007 VL 28 IS 4 BP 672 EP 677 PG 6 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 157NU UT WOS:000245727800018 PM 17416819 ER PT J AU Solomon, M Hessl, D Chiu, SF Hagerman, R Hendren, R AF Solomon, Marjorie Hessl, David Chiu, Sufen Hagerman, Randi Hendren, Robert TI A genetic etiology of pervasive developmental disorder guides treatment SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Editorial Material ID AUTISM SPECTRUM DISORDERS; CHILDREN; POPULATION C1 Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Psychiat & Behav Sci, Davis, CA USA. RP Solomon, M (reprint author), Univ Calif Davis, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. EM marjorie.solomon@ucdmc.ucdavis.edu CR Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Hagerman R. J., 2002, FRAGILE X SYNDROME D Jacquemont S, 2004, JAMA-J AM MED ASSOC, V291, P460, DOI 10.1001/jama.291.4.460 Kaufman A. S., 1983, K ABC KAUFMAN ASSESS Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 *NAT RES COUNC COM, 2001, ED CHILDR AUT 2001 Ozonoff S, 2005, J CLIN CHILD ADOLESC, V34, P523, DOI 10.1207/s15374424jccp3403_8 Posey DJ, 2006, J CHILD ADOL PSYCHOP, V16, P181, DOI 10.1089/cap.2006.16.181 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Rourke B.P., 1995, SYNDROME NONVERBAL L Santosh PJ, 2006, CHILD CARE HLTH DEV, V32, P575, DOI 10.1111/j.1365-2214.2006.00631.x Solomon M, 2004, J AUTISM DEV DISORD, V34, P649, DOI 10.1007/s10803-004-5286-y Sparrow S, 1984, VINELAND ADAPTIVE BE Sporn AL, 2004, BIOL PSYCHIAT, V55, P989, DOI 10.1016/j.biopsych.2004.01.019 Sturm H, 2004, DEV MED CHILD NEUROL, V46, P444, DOI 10.1017/S0012162204000738 Towbin KE, 2005, HDB AUTISM PERVASIVE, P165 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd Woodcock R. W., 2001, WOODCOCKJOHNSON 3 TE NR 20 TC 3 Z9 3 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 2007 VL 164 IS 4 BP 575 EP 580 DI 10.1176/appi.ajp.164.4.575 PG 6 WC Psychiatry SC Psychiatry GA 152ZZ UT WOS:000245402600010 PM 17403969 ER PT J AU Duvall, JA Lu, A Cantor, RM Todd, RD Constantino, JN Geschwind, DH AF Duvall, Jacqueline A. Lu, Ake Cantor, Rita M. Todd, Richard D. Constantino, John N. Geschwind, Daniel H. TI A quantitative trait locus analysis of social responsiveness in multiplex autism families SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID GENOMEWIDE SCREEN; LINKAGE ANALYSIS; GENOMIC SCREEN; SUSCEPTIBILITY LOCI; GENERAL-POPULATION; DISORDER; HETEROGENEITY; TWIN; GENETICS; PAIRS AB Objective: Autism is a complex genetic disorder with a highly heterogeneous phenotype defined by repetitive behaviors, language deficits, and problems with reciprocal social interactions. The authors present the first genome-wide scan for a social endophenotype in autism using the Social Responsiveness Scale, which provides a quantitative measure of autistic-like behavior, primarily focused on social relatedness. Method: A nonparametric quantitative genome scan was performed using the Social Responsiveness Scale in a cohort of about 100 families with two or more autistic probands from the Autism Genetic Resource Exchange to identify autism loci. To determine which additional loci were detected, linkage analysis with the same autism cohort using the qualitative diagnosis of autism was performed. To assess whether there were likely to be sex-specific genetic risk factors, the cohort was stratified by the sex of affected individuals. Results: The quantitative Social Responsiveness Scale genome scan identified two loci on chromosomes 11 and 17, with the highest score on chromosome 11 (z = 3.22). In contrast, no linkage signals reached significance in the Autism Diagnostic Interview-Revised qualitative scan. The Social Responsiveness Scale scan with only male affecteds identified the same signals on chromosomes 11 and 17, as well as three other regions on chromosomes 4, 8, and 10. Conclusions: This study demonstrates the utility of the Social Responsiveness Scale quantitative endophenotype to detect autism-related genetic loci using quantitative behavioral information that may more closely relate to underlying genetic factors. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Univ Calif Los Angeles, David Geffen Sch Med, Semel Inst Neurosci & Human Behav, Ctr Autism Res, Los Angeles, CA USA. Washington Univ, Sch Med, Dept Psychiat, St Louis, MO USA. Washington Univ, Sch Med, Dept Genet, St Louis, MO USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat, 660 S Euclid Ave,Campus Box 8134, St Louis, MO 63110 USA. EM constantino@wustl.edu CR Alarcon M, 2002, AM J HUM GENET, V70, P60, DOI 10.1086/338241 Alarcon M, 2005, MOL PSYCHIATR, V10, P747, DOI 10.1038/sj.mp.4001666 Almasy L, 1998, AM J HUM GENET, V62, P1198, DOI 10.1086/301844 Ashley-Koch A, 1999, GENOMICS, V61, P227, DOI 10.1006/geno.1999.5968 Auranen M, 2002, AM J HUM GENET, V71, P777, DOI 10.1086/342720 BAILEY A, 1995, PSYCHOL MED, V25, P63 Barrett S, 1999, AM J MED GENET, V88, P609 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Boehnke M, 1997, AM J HUM GENET, V61, P423, DOI 10.1086/514862 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Cantor RM, 2005, AM J HUM GENET, V76, P1050, DOI 10.1086/430278 Constantino JN, 2005, BIOL PSYCHIAT, V57, P655, DOI 10.1016/j.biopsych.2004.12.014 Constantino JN, 2004, J CHILD PSYCHOL PSYC, V45, P719, DOI 10.1111/j.1469-7610.2004.00266.x Constantino JN, 2003, J AUTISM DEV DISORD, V33, P427, DOI 10.1023/A:1025014929212 Constantino JN, 2006, AM J PSYCHIAT, V163, P294, DOI 10.1176/appi.ajp.163.2.294 Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Cook EH, 2001, CHILD ADOL PSYCH CL, V10, P333 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Geschwind DH, 2001, AM J HUM GENET, V69, P463, DOI 10.1086/321292 Gottesman II, 2005, ANNU REV PSYCHOL, V56, P263, DOI 10.1146/annurev.psych.56.091103.070208 International Molecular Genetic Study of Autism C., 2001, AM J HUM GENET, V69, P570 Kruglyak L, 1996, AM J HUM GENET, V58, P1347 LANDER E, 1995, NAT GENET, V11, P241, DOI 10.1038/ng1195-241 Liu JJ, 2001, AM J HUM GENET, V69, P327, DOI 10.1086/321980 O'Connell JR, 1998, AM J HUM GENET, V63, P259, DOI 10.1086/301904 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 RISCH N, 1990, GENET EPIDEMIOL, V7, P3, DOI 10.1002/gepi.1370070103 RITVO ER, 1985, AM J PSYCHIAT, V142, P74 Shao YJ, 2002, AM J MED GENET, V114, P99, DOI 10.1002/ajmg.10153 Silverman JM, 2002, AM J MED GENET, V114, P64, DOI 10.1002/ajmg.10048 Stone JL, 2004, AM J HUM GENET, V75, P1117, DOI 10.1086/426034 Sung YJ, 2005, AM J HUM GENET, V76, P68, DOI 10.1086/426951 Sutcliffe JS, 2005, AM J HUM GENET, V77, P265, DOI 10.1086/432648 Szatmari P, 1999, J PSYCHIATR NEUROSCI, V24, P159 Tadevosyan-Leyfer O, 2003, J AM ACAD CHILD PSY, V42, P864, DOI 10.1097/01.CHI.0000046870.56865.90 Yonan AL, 2003, AM J HUM GENET, V73, P886, DOI 10.1086/378778 NR 40 TC 84 Z9 84 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD APR PY 2007 VL 164 IS 4 BP 656 EP 662 DI 10.1176/appi.ajp.164.4.656 PG 7 WC Psychiatry SC Psychiatry GA 152ZZ UT WOS:000245402600021 PM 17403980 ER PT J AU Stachnik, JM Nunn-Thompson, C AF Stachnik, Joan M. Nunn-Thompson, Cheryl TI Use of atypical Antipsychotics in the treatment of autistic disorder SO ANNALS OF PHARMACOTHERAPY LA English DT Article DE aripiprazole; atypical antidepressants; autism; olanzapine; quetiapine; ziprasidone ID PERVASIVE DEVELOPMENTAL DISORDERS; OPEN-LABEL; SPECTRUM DISORDERS; CLINICAL-TRIALS; CASE SERIES; OLANZAPINE TREATMENT; CHILDREN; ADOLESCENTS; RISPERIDONE; QUETIAPINE AB OBJECTIVE: To review clinical trials and reports describing the efficacy and safety of atypical antipsychotics (olanzapine, ziprasidone, quetiapine, aripiprazole) in the treatment of autistic or other pervasive developmental disorders. DATA SOURCES: English-language publications from the MEDLINE database (1966-February 2007) including clinical trials, case reports, and retrospective series were reviewed. STUDY SELECTION AND DATA EXTRACTION: Relevant data were extracted from studies of selected atypical antipsychotics in the treatment of autistic disorder in children, adolescents, and adults. Most literature found was in the form of case reports or case series; however, several open-label and double-blind trials were also identified. DATA SYNTHESIS: Autistic disorder is a chronic neurodevelopmental disorder with limited treatment options. Nonpharmacologic approaches may be the most beneficial, but pharmacologic agents are needed for some patients with significant behavioral manifestations of the disorder. The atypical antipsychotics (olanzapine, ziprasidone, quetiapine, aripiprazole) have shown some efficacy in improving certain behavioral symptoms of autistic disorder- primarily aggressiveness, hyperactivity, and self-injurious behavior. Efficacy was based on observation or changes from baseline in behavioral rating scores. Data appear to be strongest for olanzapine compared with quetiapine, with several open-label trials suggesting its efficacy. Weight gain and sedation were frequently reported adverse events with both agents, Aripiprazole has demonstrated efficacy in limited case series, with minimal adverse effects reported. CONCLUSIONS: Atypical antipsychotics represent a treatment option for symptoms associated with autistic disorder. However, these drugs do not affect the core symptoms of autistic disorder and are associated with potentially significant adverse effects. In addition, there is a lack of randomized controlled trials to determine the true efficacy and long-term safety of these agents in the pediatric population. C1 Univ Illinois, Med Ctr, Coll Pharm, Dept Pharm Practice, Chicago, IL 60612 USA. RP Stachnik, JM (reprint author), Univ Illinois, Med Ctr, Coll Pharm, Dept Pharm Practice, 833 S Wood St M-C 886, Chicago, IL 60612 USA. 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Pharmacother. PD APR PY 2007 VL 41 IS 4 BP 626 EP 634 DI 10.1345/aph.1H527 PG 9 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 158BA UT WOS:000245764700011 PM 17389666 ER PT J AU Hilton, S Hunt, K Petticrew, M AF Hilton, Shona Hunt, Kate Petticrew, Mark TI MMR: marginalised, misrepresented and rejected? Autism: a focus group study SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; RUBELLA VACCINE; MEASLES-VIRUS; NO EVIDENCE; MONONUCLEAR-CELLS; ADVERSE EVENTS; MUMPS; CHILDREN; IMMUNIZATION; POPULATION AB Objective: To explore how the measles, mumps, and rubella ( MMR) vaccine controversy impacted on the lives of parents caring for children with autism. Design: Qualitative focus group study. Setting: United Kingdom. Patients: A purposively selected sample of 38 parents took part in 10 focus group discussions between March 2003 and May 2005. Results: Many parents felt that the MMR vaccine could be too potent for children who are susceptible to developing autism. Of the parents whose children received the MMR vaccine, many felt guilty that they may have caused or contributed to their child's autism. Some parents felt frustrated by health professionals' lack of understanding of the negative impact the MMR controversy has had on them. Some parents were anxious about subsequent MMR decision-making for their children. Conclusions: The controversy has had a negative impact on some parents of children with autism. This has implications for health professionals, who need to be particularly aware of the issues these parents face in future MMR decision-making for their affected child and younger siblings. It is anticipated that these findings will raise awareness among health professionals of the difficulties faced by such parents. More generally, there is a need to promote a greater awareness of the important role health visitors can play in parental decision-making and for research examining whether health professionals feel they receive sufficient training in communication skills. It is also essential that the latest scientific research findings are disseminated quickly to these parents and to those health professionals advising parents on matters of vaccine safety. C1 Univ Glasgow, MRC Social & Publ Hlth Sci Unit, Glasgow G12 8RZ, Lanark, Scotland. RP Hilton, S (reprint author), Univ Glasgow, MRC Social & Publ Hlth Sci Unit, 4 Lilybanck Gardens, Glasgow G12 8RZ, Lanark, Scotland. 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Dis. Child. PD APR PY 2007 VL 92 IS 4 BP 322 EP 327 DI 10.1136/adc.2006.10968 PG 6 WC Pediatrics SC Pediatrics GA 148VD UT WOS:000245103800011 PM 17376937 ER PT J AU Smith, LM AF Smith, Lynne M. TI Autism through my eyes SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Editorial Material C1 Univ Calif Los Angeles, Med Ctr, David Geffen Sch Med, Torrance, CA 90502 USA. RP Smith, LM (reprint author), Univ Calif Los Angeles, Med Ctr, David Geffen Sch Med, 1124 W Carson St,RB-1,Box 446, Torrance, CA 90502 USA. EM smith@labiomed.org NR 0 TC 1 Z9 1 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 324 EP 325 DI 10.1001/archpedi.161.4.324 PG 2 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500002 PM 17404127 ER PT J AU Kolevzon, A Gross, R Reichenberg, A AF Kolevzon, Alexander Gross, Raz Reichenberg, Abraham TI Prenatal and perinatal risk factors for autism - A review and integration of findings SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Review ID LOW-BIRTH-WEIGHT; ADVANCING PATERNAL AGE; REELIN GENE ALLELES; INFANTILE-AUTISM; OBSTETRIC COMPLICATIONS; PARENTAL AGE; MATERNAL AGE; EPIDEMIOLOGIC SURVEY; SPECTRUM DISORDERS; MENTAL-RETARDATION AB Objective: To review the evidence for the presence of prenatal and perinatal factors that affect the risk of autism and autism spectrum disorders. Data Sources: Relevant articles were identified by searching MEDLINE, screening reference lists of original studies, and searching major journals likely to publish epidemiological studies on the topic. Study Selection: For inclusion in this review, studies required (1) a well-defined sample of cases drawn from population-based registers or cohorts; (2) standardized, prospectively collected obstetric information from birth records or registers; (3) comparison subjects drawn from the general population with information on obstetric complications collected from the same source; and (4) a standardized format for presentation of data, allowing for comparisons among studies. Main Exposures: Parental characteristics and obstetric complications. Main Outcome Measures: Rates of autism and autism spectrum disorders. Results: Seven epidemiological studies were identified that fulfilled inclusion criteria. The parental characteristics associated with an increased risk of autism and autism spectrum disorders included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America. The obstetric conditions that emerged as significant fell into 2 categories: (1) birth weight and duration of gestation and (2) intrapartum hypoxia. Conclusions: Evidence to suggest that parental age and obstetric conditions are associated with an increased risk of autism and autism spectrum disorders is accumulating. Although not proven as independent risk factors for autism, these variables should be examined in future studies that use large, population-based birth cohorts with precise assessments of exposures and potential confounders. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Columbia Univ, Dept Epidemiol, Mailman Sch Publ Hlth, New York, NY USA. Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY USA. Gertner Inst Epidemiol & Hlth Policy Res, Unit Mental Hlth Epidemiol, Tel Hashomer, Israel. Kings Coll London, Inst Psychiat, Dept Psychol Med, London WC2R 2LS, England. RP Reichenberg, A (reprint author), Mt Sinai Sch Med, Dept Psychiat, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA. 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P1165, DOI 10.1017/S0033291702006372 Wilcox AJ, 2001, INT J EPIDEMIOL, V30, P1233, DOI 10.1093/ije/30.6.1233 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 Zhang H, 2002, MOL PSYCHIATR, V7, P1012, DOI 10.1038/sj.mp.4001124 ZOMBERG GL, 2000, AM J PSYCHIAT, V157, P196 NR 80 TC 169 Z9 173 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 326 EP 333 DI 10.1001/archpedi.161.4.326 PG 8 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500003 PM 17404128 ER PT J AU Croen, LA Najjar, DV Fireman, B Grether, JK AF Croen, Lisa A. Najjar, Daniel V. Fireman, Bruce Grether, Judith K. TI Maternal and paternal age and risk of autism spectrum disorders SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; PARENTAL AGE; PERINATAL FACTORS; OBSTETRIC COMPLICATIONS; NEONATAL FACTORS; UNITED-STATES; X-CHROMOSOME; SCHIZOPHRENIA; POPULATION AB Objective: To explore the association between maternal and paternal age and risk of autism spectrum disorders (ASDs) in offspring. Design: Historical birth cohort study. Setting: Kaiser Permanente (KP) in Northern California. Participants: All singleton children born at KP from January 1, 1995, to December 31, 1999, were included in the study. We identified 593 children who had ASD diagnoses (International Classification of Diseases, Ninth Revision, Clinical Modification, code 299.0 or 299.8) recorded 2 or more times in KP outpatient databases before May 2005. These children were compared with all 132 251 remaining singleton KP births. Main Exposures: Maternal and paternal age at birth of offspring. Main Outcome Measures: Relative risks (RRs) estimated from proportional hazards regression models. Risk of ASDs evaluated in relation to maternal and paternal age, adjusted for each other and for the sex, birth date, and birth order of the child, maternal and paternal educational level, and maternal and paternal race/ethnicity. Results: Risk of ASDs increased significantly with each 10-year increase in maternal age (adjusted RR, 1.31; 95% confidence interval [CI], 1.07-1.62) and paternal age (RR, 1.28; 95% CI, 1.09-1.51). Adjusted RRs for both maternal and paternal age were elevated for children with autistic disorder (maternal age: RR, 1.18; 95% CI, 0.871.60; paternal age: RR, 1.34; 95% CI, 1.06-1.69) and children with Asperger disorder or pervasive developmental disorder not otherwise specified (maternal age: RR, 1.45; 95% CI, 1.09-1.93; paternal age: RR, 1.24; 95% CI, 0.99-1.55). Associations with parental age were somewhat stronger for girls than for boys, although sex differences were not statistically significant. Conclusion: Advanced maternal and paternal ages are independently associated with ASD risk. C1 Kaiser Permanente, Div Res, Med Care Program No Calif Reg, Oakland, CA 94612 USA. Calif Dept Hlth Serv, Richmond, CA USA. RP Croen, LA (reprint author), Kaiser Permanente, Div Res, Med Care Program No Calif Reg, 2000 Broadway, Oakland, CA 94612 USA. 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Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 334 EP 340 DI 10.1001/archpedi.161.4.334 PG 7 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500004 PM 17404129 ER PT J AU Ganz, ML AF Ganz, Michael L. TI The lifetime distribution of the incremental societal costs of autism SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHOACTIVE MEDICINES; SUPPORTED EMPLOYMENT; ALTERNATIVE MEDICINE; BEHAVIORAL TREATMENT; SPECTRUM DISORDER; UNITED-STATES; CHILDREN; PREVALENCE; PATTERNS AB Objective: To describe the age-specific and lifetime incremental societal costs of autism in the United States. Design: Estimates of use and costs of direct medical and nonmedical care were obtained from a literature review and database analysis. A human capital approach was used to estimate lost productivity. These costs were projected across the life span, and discounted incremental age-specific costs were computed. Setting: United States. Participants: Hypothetical incident autism cohort born in 2000 and diagnosed in 2003. Main Outcome Measures: Discounted per capita incremental societal costs. Results: The lifetime per capita incremental societal cost of autism is $3.2 million. Lost productivity and adult care are the largest components of costs. The distribution of costs over the life span varies by cost category. Conclusions: Although autism is typically thought of as a disorder of childhood, its costs can be felt well into adulthood. The substantial costs resulting from adult care and lost productivity of both individuals with autism and their parents have important implications for those aging members of the baby boom generation approaching retirement, including large financial burdens affecting not only those families but also potentially society in general. 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S., 2000, MICROECONOMICS, V4th Rice D P, 1985, Health Care Financ Rev, V7, P61 Shavelle RM, 2001, J AUTISM DEV DISORD, V31, P569, DOI 10.1023/A:1013247011483 Shavelle R M, 1998, J Insur Med, V30, P220 SKOOG G, 2001, J LEGAL EC, V11, P23 TINES J, 1990, AM J MENT RETARD, V95, P44 United States Census Bureau, 2004, STAT ABSTR US *US BUR CENS, 2004, ANN EST POP SEX 5 YE Walsh KK, 1997, AM J MENT RETARD, V101, P505 WALTZMAN NJ, 1996, COSTS BIRTH DEFECTS Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 Yussman SM, 2004, AMBUL PEDIATR, V4, P429, DOI 10.1367/A03-091R1.1 NR 51 TC 144 Z9 150 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 343 EP E5 DI 10.1001/archpedi.161.4.343 PG 11 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500005 PM 17404130 ER PT J AU Leslie, DL Martin, A AF Leslie, Douglas L. Martin, Andres TI Health care expenditures associated with autism spectrum disorders SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDREN; COSTS; EPIDEMIOLOGY; PREVALENCE AB Objective: To examine the health care expenditures associated with autism spectrum disorders (ASDs) in medical care settings. Design: Retrospective analysis of health insurance claims data. Setting: Administrative claims database for a national sample of privately insured individuals. Participants: Children and adolescents 17 years and younger with a diagnosis of a mental disorder between 2000 and 2004. Main Outcome Measures: Annual inpatient, outpatient, and prescription drug expenditures. Results: Average health care expenditures for individuals with an ASD increased 20.4% from $4965 per patient in 2000 to $5979 per patient in 2004, even after adjustment for inflation. When combined with rising ASD prevalence rates, total expenditures per 10 000 covered lives associated with ASDs increased 142.1% over the 5-year period. Although total expenditures per treated patient were higher for patients with ASDs than for individuals with other mental disorders, ASDs created a smaller burden on health insurers because of their relatively low treated prevalence. Conclusions: In light of anticipated patterns of earlier identification and more proactive treatment of ASDs in the years to come, the burden of autism on the health care system will continue to increase. Efforts should be made to ensure that access to care for this vulnerable population is not compromised. C1 Yale Univ, Sch Med, Dept Psychiat, West Haven, CT 06516 USA. Yale Univ, Sch Med, Dept Epidemiol Publ Hlth, West Haven, CT 06516 USA. Yale Child Study Ctr, Dept Child Psychiat, New Haven, CT USA. Yale Child Study Ctr, Dept Psychiat, New Haven, CT USA. RP Leslie, DL (reprint author), Yale Univ, Sch Med, Dept Psychiat, NEPEC-182,950 Campbell Ave, West Haven, CT 06516 USA. EM douglas.leslie@yale.edu CR Birenbaum A, 1990, Monogr Am Assoc Ment Retard, P1 Curran AL, 2001, DEV MED CHILD NEUROL, V43, P529, DOI 10.1017/S0012162201000962 Fombonne E, 2005, J CLIN PSYCHIAT, V66, P3 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Fombonne E, 2003, JAMA-J AM MED ASSOC, V289, P87, DOI 10.1001/jama.289.1.87 Jacobson J, 1998, BEHAV INTERVENT, V13, P201, DOI DOI 10.1002/(SICI)1099-078X Jarbrink K, 2003, J AUTISM DEV DISORD, V33, P395, DOI 10.1023/A:1025058711465 Jarbrink K, 2001, AUTISM, V5, P7, DOI 10.1177/1362361301005001002 Krauss MW, 2003, MENT RETARD, V41, P329, DOI 10.1352/0047-6765(2003)41<329:ATSMCF>2.0.CO;2 Leslie DL, 2001, HEALTH SERV RES, V36, P113 Mandell DS, 2006, J AUTISM DEV DISORD, V36, P475, DOI 10.1007/s10803-006-0088-z Martin A, 2003, AM J PSYCHIAT, V160, P757, DOI 10.1176/appi.ajp.160.4.757 Peele PB, 2002, PSYCHIATR SERV, V53, P591, DOI 10.1176/appi.ps.53.5.591 Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 YELL M, 2003, FOCUS AUTISM OTHER D, V18, P138, DOI 10.1177/10883576030180030101 NR 16 TC 46 Z9 46 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 350 EP 355 DI 10.1001/archpedi.161.4.350 PG 6 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500006 PM 17404131 ER PT J AU Williams, TA Mars, AE Buyske, SG Stenroos, ES Wang, R Factura-Santiago, MF Lambert, GH Johnson, WG AF Williams, Tanishia A. Mars, Audrey E. Buyske, Steven G. Stenroos, Edward S. Wang, Rong Factura-Santiago, Marivic F. Lambert, George H. Johnson, William G. TI Risk of autistic disorder in affected offspring of mothers with a glutathione S-transferase Pl haplotype SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID POLYCYCLIC AROMATIC-HYDROCARBONS; OXIDATIVE DNA-DAMAGE; DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; LIPID-PEROXIDATION; ANIMAL-MODELS; DIOL EPOXIDES; VALPROIC ACID; SPINA-BIFIDA; STRESS AB Objective: To test whether polymorphisms of the glutathione S-transferase P1 gene (GSTP1) act in the mother during pregnancy to contribute to the phenotype of autistic disorder (AD) in her fetus. Design: Transmission disequilibrium testing (TDT) in case mothers and maternal grandparents. Setting: Autistic disorder may result from multiple genes and environmental factors acting during pregnancy and afterward. Teratogenic alleles act in mothers during pregnancy to contribute to neurodevelopmental disorders in their offspring; however, only a handful have been identified. GSTP1 is a candidate susceptibility gene for AD because of its tissue distribution and its role in oxidative stress, xenobiotic metabolism, and JNK regulation. Participants: We genotyped GSTP1*G313A and GSTP1*C341T polymorphisms in 137 members of 49 families with AD. All probands received a clinical diagnosis of AD by Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule-Generic testing. Main Outcome Measures: Association of haplotypes with AD was tested by the TDT-Phase program, using the expectation-maximization (EM) algorithm for uncertain haplotypes and for incomplete parental genotypes, with standard measures of statistical significance. Results: The GSTP1*A haplotype was overtransmitted to case mothers (P=.01 [P=.03 using permutation testing]; odds ratio, 2.67 [95% confidence interval, 1.39-5.13]). Results of the combined haplotype and genotype analyses suggest that the GSTP1-313 genotype alone determined the observed haplotype effect. Conclusions: Overtransmission of the GSTP1*A haplotype to case mothers suggests that action in the mother during pregnancy likely increases the likelihood of AD in her fetus. If this is confirmed and is a result of a gene-environment interaction occurring during pregnancy, these findings could lead to the design of strategies for prevention or treatment. C1 Rutgers State Univ, Dept Neurol, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA. Rutgers State Univ, Ctr Childhood Neurotoxicol & Exposure Assessment, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Pediat, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Stat, New Brunswick, NJ 08903 USA. Rutgers State Univ, Dept Genet, New Brunswick, NJ 08903 USA. RP Johnson, WG (reprint author), Rutgers State Univ, Dept Neurol, Robert Wood Johnson Med Sch, UBHC Room D-431,671 Hoes Ln, Piscataway, NJ 08854 USA. 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Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 356 EP 361 DI 10.1001/archpedi.161.4.356 PG 6 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500007 PM 17404132 ER PT J AU Hoekstra, RA Bartels, M Verweij, CJH Boomsma, DI AF Hoekstra, Rosa A. Bartels, Meike Verweij, Catharina J. H. Boomsma, Dorret I. TI Heritability of autistic traits in the general population SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; AFFECTED SIBLING PAIRS; SPECTRUM QUOTIENT AQ; INFANTILE-AUTISM; FAMILY HISTORY; TWIN REGISTER; PHENOTYPE; CHILDREN; RISK; PERSONALITY AB Objective: To explore genetic and environmental influences on individual differences in autistic traits in early adulthood and to test if there is assortative mating (non-random partner choice) for autistic traits in the general population. Design: Twin family study using structural equation modeling. Setting: Population-based twin family sample from the Netherlands. Participants: Twins aged 18 years (n=370) and their siblings (n=94); parents of twins (128 couples). Main Outcome Measure: Self-reported Autism-Spectrum Quotient (AQ) scores, a quantitative measure of autistic traits. Results: Autistic traits were continuously distributed in the population. Twins and siblings did not significantly differ in AQ scores; men obtained significantly higher AQ scores than women (in twin-sibling sample, P <.001; twin-parent sample, P=.02). Individual differences in endorsement on autistic traits show substantial heritability (57%). No significant shared environmental influences were detected. The genes affecting autistic traits appear to be the same across the sexes. The correlation in AQ score between spouses was low and not significant (Pearson r=.05; P=.59). Conclusions: Previous general population twin studies reported high heritability for autistic traits in childhood and early adolescence. This study extends these findings to late adolescence and yields no evidence for sex-specific genetic influences on autistic traits in later stages of development. As autistic traits show substantial variation in the general population, future genetic studies may be facilitated by measuring autistic traits on a continuous scale like the AQ. No evidence for assortative mating for autistic traits was found, suggesting that, in the general population, there is no passive or active partner selection for autistic traits. C1 Free Univ Amsterdam, Dept Biol Psychol, NL-1081 BT Amsterdam, Netherlands. RP Hoekstra, RA (reprint author), Free Univ Amsterdam, Dept Biol Psychol, Boechorststr 1, NL-1081 BT Amsterdam, Netherlands. EM ra.hoekstra@psy.vu.nl RI Hoekstra, Rosa/G-2410-2011; Bartels, Meike/D-4492-2014 OI Bartels, Meike/0000-0002-9667-7555 CR ACHENBACH TM, 1987, PSYCHOL BULL, V101, P213, DOI 10.1037/0033-2909.101.2.213 American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BAILEY A, 1995, PSYCHOL MED, V25, P63 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S, 2006, PROG NEURO-PSYCHOPH, V30, P865, DOI 10.1016/j.pnpbp.2006.01.010 Betancur C, 2002, AM J HUM GENET, V70, P1381, DOI 10.1086/340364 Bishop DVM, 2004, J CHILD PSYCHOL PSYC, V45, P1431, DOI 10.1111/j.1469-7610.2004.00325.x BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Boomsma DI, 2002, TWIN RES, V5, P401, DOI 10.1375/136905202320906174 BOOMSMA DI, 1992, BEHAV GENET, V22, P247, DOI 10.1007/BF01067004 Constantino JN, 2005, BIOL PSYCHIAT, V57, P655, DOI 10.1016/j.biopsych.2004.12.014 Constantino JN, 2006, AM J PSYCHIAT, V163, P294, DOI 10.1176/appi.ajp.163.2.294 Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Croen LA, 2002, J AUTISM DEV DISORD, V32, P217, DOI 10.1023/A:1015405914950 FOLSTEIN S, 1977, NATURE, V265, P726, DOI 10.1038/265726a0 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Greenberg DA, 2001, AM J HUM GENET, V69, P1062, DOI 10.1086/324191 Hallmayer J, 2002, AM J HUM GENET, V71, P941, DOI 10.1086/342990 Hultman CM, 2002, EPIDEMIOLOGY, V13, P417, DOI 10.1097/01.EDE.0000016968.14007.E6 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 MASCIETAYLOR CGN, 1988, BEHAV GENET, V18, P339, DOI 10.1007/BF01260934 NEALE MC, 2005, MX STAT MODELING REV PHILLIPS K, 1988, BEHAV GENET, V18, P347, DOI 10.1007/BF01260935 Piven J, 1997, AM J PSYCHIAT, V154, P185 Posserud MB, 2006, J CHILD PSYCHOL PSYC, V47, P167, DOI 10.1111/j.1469-7610.2005.01462.x Posthuma D, 2000, BEHAV GENET, V30, P147, DOI 10.1023/A:1001959306025 Rietveld M J, 2000, Twin Res, V3, P134, DOI 10.1375/136905200320565409 Ronald A, 2005, DEVELOPMENTAL SCI, V8, P444, DOI 10.1111/j.1467-7687.2005.00433.x Ronald A, 2006, J AM ACAD CHILD PSY, V45, P691, DOI 10.1097/01.chi.0000215325.13058.9d Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 Spiker D, 2002, AM J MED GENET, V114, P129, DOI 10.1002/ajmg.10188 Szatmari P, 1998, J AUTISM DEV DISORD, V28, P351, DOI 10.1023/A:1026096203946 VERHULST FC, 1992, J CHILD PSYCHOL PSYC, V33, P1011, DOI 10.1111/j.1469-7610.1992.tb00922.x Wakabayashi A, 2006, J AUTISM DEV DISORD, V36, P263, DOI 10.1007/s10803-005-0061-2 Watson D, 2004, J PERS, V72, P1029, DOI 10.1111/j.0022-3506.2004.00289.x NR 37 TC 109 Z9 109 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 372 EP 377 DI 10.1001/archpedi.161.4.372 PG 6 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500009 PM 17404134 ER PT J AU Nadig, AS Ozonoff, S Young, GS Rozga, A Sigman, M Rogers, SJ AF Nadig, Aparna S. Ozonoff, Sally Young, Gregory S. Rozga, Agata Sigman, Marian Rogers, Sally J. TI A prospective study of response to name in infants at risk for autism SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID FAMILY HOME MOVIES; SPECTRUM DISORDERS; EARLY RECOGNITION; GENETIC DISORDER; CHILDREN; AGE; 1ST; VIDEOTAPES; LIFE; REGRESSION AB Objective: To assess the sensitivity and specificity of decreased response to name at age 12 months as a screen for autism spectrum disorders (ASD) and other developmental delays. Design: Prospective, longitudinal design studying infants at risk for ASD. Setting: Research laboratory at university medical center. Participants: Infants at risk for autism (55 six-month-olds, 101 twelve-month-olds) and a control group at no known risk (43 six-month-olds, 46 twelve-montholds). To date, 46 at-risk infants and 25 control infants have been followed up to 24 months. Intervention: Experimental task eliciting response-to-name behavior. Main Outcome Measures: Autism Diagnostic Observation Schedule, Mullen Scales of Early Learning. Results: At age 6 months, there was a nonsignificant trend for control infants to require a fewer number of calls to respond to name than infants at risk for autism. At age 12 months, 100% of infants in the control group "passed," responding on the first or second name call, while 86% in the at-risk group did. Three fourths of children who failed the task were identified with developmental problems at age 24 months. Specificity of failing to respond to name was 0.89 for ASD and 0.94 for any developmental delay. Sensitivity was 0.50 for ASD and 0.39 for any developmental delay. Conclusions: Failure to respond to name by age 12 months is highly suggestive of developmental abnormality but does not identify all children at risk for developmental problems. Lack of responding to name is not universal among infants later diagnosed with ASD and/or other developmental delays. Poor response to name may be a trait of the broader autism phenotype in infancy. C1 Univ Calif Davis, Med Ctr, MIND Inst, Off 1262, Sacramento, CA 95817 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. RP Nadig, AS (reprint author), Univ Calif Davis, Med Ctr, MIND Inst, Off 1262, 2825 50th St, Sacramento, CA 95817 USA. EM aparna.nadig@ucdmc.ucdavis.edu CR ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BAILEY A, 1995, PSYCHOL MED, V25, P63 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 FENSKE EC, 1985, ANAL INTERVEN DEVEL, V5, P49, DOI 10.1016/S0270-4684(85)80005-7 Gottesman II, 2003, AM J PSYCHIAT, V160, P636, DOI 10.1176/appi.ajp.160.4.636 Harrington JW, 2006, J DEV BEHAV PEDIATR, V27, pS156, DOI 10.1097/00004703-200604002-00014 Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 Landa R, 2006, J CHILD PSYCHOL PSYC, V47, P629, DOI 10.1111/j.1469-7610.2006.01531.x LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 Lord C, 2004, J CHILD PSYCHOL PSYC, V45, P936, DOI 10.1111/j.1469-7610.2004.t01-1-00287.x Maestro S, 2002, J AM ACAD CHILD PSY, V41, P1239, DOI 10.1097/01.CHI.0000020277.43550.02 Maestro S, 2001, PSYCHOPATHOLOGY, V34, P147, DOI 10.1159/000049298 Mandell DS, 2005, PSYCHIAT SERV, V56, P56, DOI 10.1176/appi.ps.56.1.56 MERIN NM, 2006, J AUTISM DEV DI 1227 Mullen E, 1995, MULLEN SCALES EARLY OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Osterling JA, 2002, DEV PSYCHOPATHOL, V14, P239 Palomo R, 2006, J DEV BEHAV PEDIATR, V27, pS59, DOI 10.1097/00004703-200604002-00003 Rutter M., 2003, SOCIAL COMMUNICATION Veenstra-VanderWeele J, 2004, ANNU REV GENOM HUM G, V5, P379, DOI 10.1146/annurev.genom5.061903.180050 Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 Werner E, 2005, ARCH GEN PSYCHIAT, V62, P889, DOI 10.1001/archpsyc.62.8.889 Wetherby AM, 2004, J AUTISM DEV DISORD, V34, P473, DOI 10.1007/s10803-004-2544-y Wiggins LD, 2006, J DEV BEHAV PEDIATR, V27, pS79, DOI 10.1097/00004703-200604002-00005 Yirmiya N, 2006, J CHILD PSYCHOL PSYC, V47, P511, DOI 10.1111/j.1469-7610.2005.01528.x Zwaigenbaum L, 2005, INT J DEV NEUROSCI, V23, P143, DOI 10.1016/j.ijdevneu.2004.05.001 NR 28 TC 77 Z9 79 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610-0946 USA SN 1072-4710 J9 ARCH PEDIAT ADOL MED JI Arch. Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 378 EP 383 DI 10.1001/archpedi.161.4.378 PG 6 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500010 PM 17404135 ER PT J AU Stone, WL McMahon, CR Yoder, PJ Walden, TA AF Stone, Wendy L. McMahon, Caitlin R. Yoder, Paul J. Walden, Tedra A. TI Early social-communicative and cognitive development of younger siblings of children with autism spectrum disorders SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID JOINT ATTENTION; FAMILY-HISTORY; INFANTS; LANGUAGE; PHENOTYPE; BEHAVIORS; RELATIVES; SYMPTOMS; BRAIN; STAT AB Objective: To compare the early social-communicative development of younger siblings of children with autism spectrum disorders (ASDs) with that of younger siblings of children with typical development, using parental report and child-based measures. Design: Group comparison. Setting: Vanderbilt University, between July 1, 2003, and July 31, 2006. Participants: Younger siblings of children with ASD (n=64) and younger siblings of children with typical development (n=42) between the ages of 12 and 23 months ( mean, 16 months). Main Exposure: Having a sibling with an ASD. Outcome Measures: Child-based measures included a cognitive assessment; an interactive screening tool assessing play, imitation, and communication; and a rating of autism symptoms. Parental report measures were an interview of social-communicative interactions and a questionnaire assessing language and communication skills. Results: Younger siblings of children with ASD demonstrated weaker performance in nonverbal problem solving (mean difference [MD], 5.91; 95% confidence interval [CI], 2.48-9.34), directing attention (MD, 0.52; 95% CI, 0.07-0.97), understanding words (MD, 33.30; 95% CI, 3.11-63.48), understanding phrases (MD, 4.56; 95% CI, 1.85-7.27), gesture use (MD, 1.49; 95% CI, 0.51-2.47), and social-communicative interactions with parents (MD, 1.32; 95% CI, 0.27-2.37), and had increased autism symptoms (MD, 2.54; 95% CI, 1.05-4.03), relative to control siblings. A substantial minority of the ASD sibling group exhibited lower performance relative to controls. Significant correlations between child-based measures and parental reports assessing similar constructs were found (r=-0.74 to 0.53; P range,.000-.002). Conclusion: The weaker performance found for children in the ASD sibling group may represent early-emerging features of the broader autism phenotype, thus highlighting the importance of developmental surveillance for younger siblings. C1 Vanderbilt Univ, Kennedy Ctr, Nashville, TN 37203 USA. Vanderbilt Univ, Dept Pediat, Nashville, TN 37203 USA. Vanderbilt Univ, Dept Psychol & Human Dev, Nashville, TN 37203 USA. Vanderbilt Univ, Dept Special Educ, Nashville, TN 37203 USA. RP Stone, WL (reprint author), Vanderbilt Univ, Kennedy Ctr, Peabody Box 74,230 Appleton Pl, Nashville, TN 37203 USA. 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Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 384 EP 390 DI 10.1001/archpedi.161.4.384 PG 7 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500011 PM 17404136 ER PT J AU Silverman, C Brosco, JP AF Silverman, Chloe Brosco, Jeffrey P. TI Understanding autism - Parents and pediatricians in historical perspective SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID SPECTRUM DISORDERS; CHILDREN; PREVALENCE; INTERVENTIONS; THIMEROSAL; REGRESSION; PHENOTYPE; EPIDEMIC; HOME AB Both primary care providers and subspecialists in pediatrics encounter families who are actively involved in the diagnosis and treatment of their children. Parents of children with an autism spectrum disorder in particular are often aware of scientific issues, and their expertise and desire for a medical cure for autism sometimes put them at odds with the medical team. We investigated the role of parents and advocates in autism research and treatment over the last 50 years. Our review of scientific publications and archival sources documents how parents and advocacy groups have done the following: (1) organized research funding; (2) constructed clinical research networks; (3) suggested new avenues for research; (4) popularized empirically based therapies; and (5) anticipated paradigmatic shifts in the understanding of autism. We believe that this historical account will help pediatricians and researchers recognize that families can contribute to expert understanding of complex medical conditions such as autism and that the existence of partnerships with families of children with autism is a critical component of future research and treatment programs. C1 Penn State Univ, Dept Sci Technol & Soc, University Pk, PA 16802 USA. Univ Miami, Dept Pediat, Miller Sch Med, Miami, FL 33152 USA. RP Silverman, C (reprint author), Penn State Univ, Dept Sci Technol & Soc, 102 Old Bot, University Pk, PA 16802 USA. 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Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 392 EP 398 DI 10.1001/archpedi.161.4.392 PG 7 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500012 PM 17404137 ER PT J AU Brachlow, AE Ness, KK McPheeters, ML Gurney, JG AF Brachlow, Allison E. Ness, Kirsten K. McPheeters, Melissa L. Gurney, James G. TI Comparison of indicators for a primary care medical home between children with autism or asthma and other special health care needs - National survey of children's health SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID ALTERNATIVE MEDICINE; SPECTRUM DISORDERS; PREVALENCE; COMPLEMENTARY; EPILEPSY; PHYSICIANS; EQUIPMENT; ACCESS AB Objective: To assess the extent to which parents of children with autism compared with parents of children with asthma or other special health care needs report receiving primary care for their child consistent with the American Academy of Pediatrics medical home model. Design: Population-based cross-sectional study. Setting: National Survey for Children's Health 20032004 telephone interview. Participants: Parents of 495 children with autism, parents of 6716 children with asthma, and parents of 11403 children with other special health care needs without asthma. Main Exposures: Autism and other special health care needs including asthma. Main Outcome Measures: Medical home score and components of care, as follows: personal provider and preventive; family-centered, compassionate, and culturally appropriate; accessible; comprehensive; and coordinated. Results: The odds of parents reporting care consistent with that in a medical home were less likely for children with autism (odds ratio, 0.45; 95% confidence interval, 0.30-0.66) and more likely for children with asthma (odds ratio, 1.17; 95% confidence interval, 1.06-1.30) compared with children with other special health care needs (1 [reference]). These differences persisted even after controlling for condition severity, personal characteristics, and insurance status. Specific components of a medical home less prevalent among children with autism than among children with other special health care needs included family-centered, comprehensive, and coordinated care. Conclusion: Although we could not evaluate the reasons why, a large percentage of children with autism do not receive primary care consistent with that in a medical home. C1 Univ Minnesota, Dept Pediat, Minneapolis, MN 55455 USA. St Jude Childrens Res Hosp, Dept Epidemiol & Canc Control, Memphis, TN 38105 USA. Univ Michigan, Dept Pediat, Ann Arbor, MI 48109 USA. RP Brachlow, AE (reprint author), Univ Minnesota, Dept Pediat, McNamara Alumni Bldg,200 Oak St SE,Suite 260, Minneapolis, MN 55455 USA. 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Pediatr. Adolesc. Med. PD APR PY 2007 VL 161 IS 4 BP 399 EP 405 DI 10.1001/archpedi.161.4.399 PG 7 WC Pediatrics SC Pediatrics GA 152OY UT WOS:000245372500013 PM 17404138 ER PT J AU Caronna, EB Augustyn, M Zuckerman, B AF Caronna, Elizabeth B. Augustyn, Marilyn Zuckerman, Barry TI Revisiting parental concerns in the age of autism spectrum disorders - The need to help parents in the face of uncertainty SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Editorial Material ID CHILDREN; DIAGNOSIS C1 Boston Med Ctr, Div Dev & Behav Pediat, Boston, MA 02118 USA. RP Caronna, EB (reprint author), Boston Med Ctr, Div Dev & Behav Pediat, Matern 5,91 E Concord St, Boston, MA 02118 USA. 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PD APR PY 2007 VL 30 IS 2 BP 214 EP + DI 10.1017/S0140525X07001537 PG 12 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 286LO UT WOS:000254847600036 ER PT J AU O'Reilly, M Edrisinha, C Sigafoos, J Lancioni, G Cannella, H Machalicek, W Langthorne, P AF O'Reilly, Mark Edrisinha, Chaturi Sigafoos, Jeff Lancioni, Giulio Cannella, Helen Machalicek, Wendy Langthorne, Paul TI Manipulating the evocative and abative effects of an establishing operation: Influences on challenging behavior during classroom instruction SO BEHAVIORAL INTERVENTIONS LA English DT Article ID REFINEMENTS; AGGRESSION AB In this study we examined the evocative and abative effects of an establishing operation on challenging behavior during classroom instruction for a student with severe disabilities including autism. A prior functional analysis indicated that his challenging behavior was maintained by access to preferred snack items. During classroom instructional sessions these snack items were visible but not available to the student. In other words challenging behavior was placed on extinction during instruction. Immediately prior to instructional sessions the student received either access to snack items or did not receive access to snacks. Access versus no access to snacks prior to instruction was systematically controlled using a multi-element design. Results demonstrated higher levels of challenging behavior during instruction when the student did not have access to snacks prior to instruction. Very little challenging behavior occurred during instructional sessions when the student had prior access to snacks. Implications for considering the evocative and abative effects of establishing operations when implementing operant extinction in applied settings are discussed. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Univ Texas, Dept Special Educ, Austin, TX 78712 USA. 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