FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Klauck, SM AF Klauck, S. M. TI Autism and ADHD - is there a least common multiple of genetic predisposition loci SO JOURNAL OF NEURAL TRANSMISSION LA English DT Meeting Abstract CT 39th International Danube Symposium for Neurological Science and Continuing Education/1st International Congress on ADHD, from Childhood t Adult Disease CY JUN 02-05, 2007 CL Wuzburg, GERMANY NR 0 TC 0 Z9 0 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 2007 VL 114 IS 7 BP LI EP LII PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 189PU UT WOS:000248001800043 ER PT J AU Poustka, F Holtmann, M AF Poustka, F. Holtmann, M. TI Autism-specific impairment and co-morbidity in autism with ADHS SO JOURNAL OF NEURAL TRANSMISSION LA English DT Meeting Abstract CT 39th International Danube Symposium for Neurological Science and Continuing Education/1st International Congress on ADHD, from Childhood t Adult Disease CY JUN 02-05, 2007 CL Wuzburg, GERMANY NR 0 TC 0 Z9 0 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 2007 VL 114 IS 7 BP LI EP LI PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 189PU UT WOS:000248001800041 ER PT J AU Sinzig, J AF Sinzig, J. TI Mentalizing in autism with and without ADRD SO JOURNAL OF NEURAL TRANSMISSION LA English DT Meeting Abstract CT 39th International Danube Symposium for Neurological Science and Continuing Education/1st International Congress on ADHD, from Childhood t Adult Disease CY JUN 02-05, 2007 CL Wuzburg, GERMANY NR 0 TC 0 Z9 0 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 2007 VL 114 IS 7 BP LI EP LI PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 189PU UT WOS:000248001800042 ER PT J AU Huennerkopf, R Grassi, J Dudley, E Jans, T Guderian, E Mehler-Wex, C Warnke, A Gerlach, M Thome, J AF Huennerkopf, R. Grassi, J. Dudley, E. Jans, T. Guderian, E. Mehler-Wex, C. Warnke, A. Gerlach, M. Thome, J. TI Proteonaic technologies in autism and adult attention-deficit hyperactivity disorder (ADHD) research SO JOURNAL OF NEURAL TRANSMISSION LA English DT Meeting Abstract CT 39th International Danube Symposium for Neurological Science and Continuing Education/1st International Congress on ADHD, from Childhood t Adult Disease CY JUN 02-05, 2007 CL Wuzburg, GERMANY NR 0 TC 0 Z9 0 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 2007 VL 114 IS 7 BP LXIX EP LXIX PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 189PU UT WOS:000248001800117 ER PT J AU Johnson, K Robertson, I Kelly, S Barry, E Watchorn, A Keavey, M Gallagher, L Gill, M Bellgrove, M AF Johnson, K. Robertson, I. Kelly, S. Barry, E. Watchorn, A. Keavey, M. Gallagher, L. Gill, M. Bellgrove, M. TI Dissociation in performance of children with ADHD and high-functioning autism on a task of sustained attention SO JOURNAL OF NEURAL TRANSMISSION LA English DT Meeting Abstract CT 39th International Danube Symposium for Neurological Science and Continuing Education/1st International Congress on ADHD, from Childhood t Adult Disease CY JUN 02-05, 2007 CL Wuzburg, GERMANY NR 0 TC 0 Z9 0 PU SPRINGER WIEN PI WIEN PA SACHSENPLATZ 4-6, PO BOX 89, A-1201 WIEN, AUSTRIA SN 0300-9564 J9 J NEURAL TRANSM JI J. Neural Transm. PY 2007 VL 114 IS 7 BP LXXVII EP LXXVII PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 189PU UT WOS:000248001800146 ER PT J AU Patterson, PH AF Patterson, Paul H. TI Activating the maternal immune system causes changes in the offspring resembling those in Schizophrenia and autism SO JOURNAL OF NEUROVIROLOGY LA English DT Meeting Abstract CT 8th International Symposium on Neurovirology CY OCT 30-NOV 02, 2007 CL San Diego, CA SP NIMH, NINDS, NIDA, Biogen Idec, Dept Microbiol & Immunol, Drexel Univ Coll Med, Inst Mol Med & Infect Dis, Temple Univ Sch Med, Dept Neurosci, Sbarro Inst Canc Res & Mol Med, Journal NeuroVirol C1 [Patterson, Paul H.] CALTECH, Pasadena, CA 91125 USA. NR 0 TC 0 Z9 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1355-0284 J9 J NEUROVIROL JI J. Neurovirol. PY 2007 VL 13 SU 1 BP 20 EP 20 PG 1 WC Neurosciences; Virology SC Neurosciences & Neurology; Virology GA 228SX UT WOS:000250754000034 ER PT J AU Libbey, JE Coon, HH Kirkman, NJ Sweeten, TL Miller, JN Lainhart, JE McMahon, WM Fujinami, RS AF Libbey, Jane E. Coon, Hilary H. Kirkman, Nikki J. Sweeten, Thayne L. Miller, Judith N. Lainhart, Janet E. McMahon, William M. Fujinami, Robert S. TI Are there altered antibody responses to measles, mumps, or rubella viruses in autism? SO JOURNAL OF NEUROVIROLOGY LA English DT Article DE autism; immunoglobulin; Tourette's syndrome ID PERVASIVE DEVELOPMENTAL DISORDERS; LYMPHOID-NODULAR HYPERPLASIA; INFLAMMATORY-BOWEL-DISEASE; MYELIN BASIC-PROTEIN; SCLEROSING PANENCEPHALITIS; CONGENITAL-RUBELLA; MULTIPLE-SCLEROSIS; CAUSAL ASSOCIATION; SPECTRUM DISORDER; MMR VACCINATION AB The role that virus infections play in autism is not known. Others have reported that antibodies against measles virus are higher in the sera/plasma of children with autism versus controls. The authors investigated antibody titers to measles, mumps, and rubella viruses and diphtheria toxoid in children with autism, both classic onset (33) and regressive onset (26) forms, controls (25, healthy age- and gender-matched) and individuals with Tourette's syndrome (24) via enzyme-linked immunosorbent assays. No significant differences in antibody titers to measles, mumps, and rubella viruses and diphtheria toxoid were found among the four groups. Additionally, there were no significant differences between the four groups for total immunoglobulin (Ig) G or IgM. Interestingly, the authors did find a significant number (15/59) of autism subjects (classic and regressive onset combined) who had a very low or no antibody titer against rubella virus, compared to a combine control/Tourette's group (2/49). C1 Univ Utah, Dept Neurol, Salt Lake City, UT 84132 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT USA. RP Fujinami, RS (reprint author), Univ Utah, Dept Neurol, 30 N 1900 E,3R330 SOM, Salt Lake City, UT 84132 USA. 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Neurovirol. PY 2007 VL 13 IS 3 BP 252 EP 259 DI 10.1080/13550280701278462 PG 8 WC Neurosciences; Virology SC Neurosciences & Neurology; Virology GA 186KZ UT WOS:000247778900008 PM 17613715 ER PT J AU Kujala, T AF Kujala, Teija TI The role of early auditory discrimination deficits in language disorders SO JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Article DE mismatch negativity; event-related potentials; language impairments; dyslexia; aphasia; autism spectrum ID MISMATCH NEGATIVITY MMN; HIGH-FUNCTIONING AUTISM; COCHLEAR-IMPLANT USERS; NON-SPEECH SOUNDS; ASPERGER-SYNDROME; BRAIN RESPONSES; DYSLEXIC ADULTS; SENSORY MEMORY; ELECTROPHYSIOLOGICAL EVIDENCE; FREQUENCY DISCRIMINATION AB Language impairments can have a devastating effect on the individual's life. Brain damage such as stroke may cause varying degrees of impaired language. Even milder language problems, such as developmental dyslexia or specific language impairment, can have long-lasting detrimental effects on the individual's life, affecting both success at school as well as motivation and even self-esteem. In recent years, the mismatch negativity (MMN) has been intensively applied to study the neural basis of language impairments. These studies have shown that the MMN, which reflects the early stages of cortical sound discrimination, is abnormal in a large variety of language impairments. Furthermore, a close relationship between the MMN and some language disorders is suggested by significant correlations between the MMN and language test results. Further support is provided by follow-up studies suggesting that the MMN parameters may predict future language problems in children and by investigations indicating that intervention programs with an ameliorating effect also concurrently change the MMN. However, when interpreting the implications of MMN results it is important to acknowledge that this response specifically reflects early stages of auditory discrimination and should, therefore, be combined with measures probing the further steps of auditory processing for a more complete picture of the underlying deficits of language. The current review addresses how the MMN can be used in determining auditory impairments in language disorders such as aphasia, dyslexia, autism spectrum, and specific language impairment. C1 Univ Helsinki, Dept Psychol, Cognit Brain Res Unit, FIN-00014 Helsinki, Finland. RP Kujala, T (reprint author), Univ Helsinki, Dept Psychol, Cognit Brain Res Unit, POB 9,Siltavuorenpenger 20D, FIN-00014 Helsinki, Finland. 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Psychophysiol. PY 2007 VL 21 IS 3-4 BP 239 EP 250 DI 10.1027/0269-8803.21.34.239 PG 12 WC Psychology, Biological; Neurosciences SC Psychology; Neurosciences & Neurology GA 282OO UT WOS:000254577300012 ER PT J AU Lane, D AF Lane, David TI Autism, brain, and environment SO JOURNAL OF THE ROYAL SOCIETY FOR THE PROMOTION OF HEALTH LA English DT Book Review C1 Middlesex Univ, Prof Dev Fdn, London N17 8HR, England. RP Lane, D (reprint author), Middlesex Univ, Prof Dev Fdn, London N17 8HR, England. CR Lathe R, 2006, AUTISM BRAIN ENV NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1466-4240 J9 J R SOC PROMO HEALTH JI J. R. Soc. Promot. Health PD JAN PY 2007 VL 127 IS 1 BP 47 EP 47 DI 10.1177/146642400712700110 PG 1 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 130TV UT WOS:000243822800011 ER PT J AU Adams, JB Romdalvik, J Ramanujam, VMS Legator, MS AF Adams, James B. Romdalvik, Jane Ramanujam, V. M. Sadagopa Legator, Marvin S. TI Mercury, lead, and zinc in baby teeth of children with autism versus controls SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES LA English DT Article ID THIMEROSAL-CONTAINING VACCINES; BILIARY-SECRETION; EXPOSURE; ASSOCIATION; DISORDERS; HEALTH; METHYLMERCURY; METHYLATION; GLUTATHIONE; CHLORIDE AB This study determined the level of mercury, lead, and zinc in baby teeth of children with autism spectrum disorder (n = 15, age 6.1 +/- 2.2 yr) and typically developing children (n = 11, age = 7 1.7 yr). Children with autism had significantly (2.1-fold) higher levels of mercury but similar levels of lead and similar levels of zinc. Children with autism also had significantly higher usage of oral antibiotics during their first 12 mo of life, and possibly higher usage of oral antibiotics during their first 36 mo of life. Baby teeth are a good measure of cumulative exposure to toxic metals during fetal development and early infancy, so this study suggests that children with autism had a higher body burden of mercury during fetal/infant development. Antibiotic use is known to almost completely inhibit excretion of mercury in rats due to alteration of gut flora. Thus, higher use of oral antiobiotics in the children with autism may have reduced their ability to excrete mercury, and hence may partially explain the higher level in baby teeth. Higher usage of oral antibiotics in infancy may also partially explain the high incidence of chronic gastrointestinal problems in individuals with autism. C1 Arizona State Univ, Tempe, AZ 85287 USA. Univ Texas, Med Branch, Dept Prevent Med & Community Hlth, Galveston, TX 77555 USA. RP Adams, JB (reprint author), Arizona State Univ, POB 876006, Tempe, AZ 85287 USA. 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Toxicol. Env. Health Part A PY 2007 VL 70 IS 11-12 BP 1046 EP 1051 DI 10.1080/15287390601172080 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 169GG UT WOS:000246580100023 PM 17497416 ER PT J AU Geier, DA Geier, MR AF Geier, David A. Geier, Mark R. TI A prospective study of mercury toxicity biomarkers in autistic spectrum disorders SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES LA English DT Article ID URINARY PORPHYRIN PROFILES; OXIDATIVE STRESS; COPROPORPHYRINOGEN OXIDASE; CHILDREN; THIMEROSAL; EXPOSURE; POLYMORPHISMS; ASSOCIATION; METABOLISM; CHALLENGE AB Porphyrins are derivatives formed in the heme synthesis pathway and porphyrins afford a measure of xenobiotic exposure. The steps in the heme pathway most vulnerable to heavy metal inhibition are uroporphyrin decarboxylase (UROD) and coproporphyrinogen oxidase (CPOX) reactions. Mercury toxicity was associated with elevations in urinary coproporphyrin (cP), pentacarboxyporphyrin (5cxP), and precoproporphyrin (prcP) (also known as keto-isocoproporphyrin) levels. Two cohorts of autistic patients in the United States and France had urine porphyrin levels associated with mercury toxicity. A prospective study of urinary porphyrin testing at LabCorp (United States) and the Laboratoire Philippe Auguste (France) involving 71 autism spectrum disorder (ASD) patients, neurotypical sibling controls, and general population controls was undertaken. ASD patients had significant elevations in urinary levels of cP, 5cxP, and prcP relative to controls, and > 50% of ASD patients had urinary cP levels more than 2 standard deviations above the mean values for neurotypical sibling controls. Significant reductions in urinary 5cxP and cP levels were observed in ASD patients following chelation. A significant correlation was found between urinary porphyrins measured at LabCorp and those measured at the Laboratoire Philippe Auguste on individual ASD patients. The established developmental neurotoxicity attributed to mercury and biochemical/genomic evidence for mercury susceptibility/toxicity in ASDs indicates a causal role for mercury. Urinary porphyrin testing is clinically available, relatively inexpensive, and noninvasive. Porphyrins need to be routinely measured in ASDs to establish if mercury toxicity is a causative factor and to evaluate the effectiveness of chelation therapy. C1 Genet Ctr Amer, Silver Spring, MD 20905 USA. Inst Chron Illnesses, Silver Spring, MD USA. RP Geier, MR (reprint author), Genet Ctr Amer, 14 Redgate Ct, Silver Spring, MD 20905 USA. 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Toxicol. Env. Health Part A PY 2007 VL 70 IS 20 BP 1723 EP 1730 DI 10.1080/15287390701457712 PG 8 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 215CI UT WOS:000249785500003 PM 17885929 ER PT J AU Park, EK Mak, SK Kultz, D Hammock, BD AF Park, Eun-Kee Mak, Sally K. Kueltz, Dietmar Hammock, Bruce D. TI Evaluation of cytotoxicity attributed to thimerosal on murine and human kidney cells SO JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES LA English DT Article ID OSMOTIC-STRESS; TOXICITY; APOPTOSIS; OXIDATION; VACCINES; MERCURY; NEURONS; PATHWAY; AUTISM; MICE AB Renal inner medullary collecting duct cells ( mIMCD3) and human embryonic kidney cells ( HEK293) were used for cytoscreening of thimerosal and mercury chloride ( HgCl2). Thimerosal and HgCl2 acted in a concentration-dependent manner. In mIMCD3 cells the 24-h LC50 values for thimerosal, thiosalicylic acid, 2,2-dithiosalicylic acid, and 2-sulfobenzoic acid were 2.9, 2200, >1000, and >10,000 mu M, respectively. The 24-h LC50 value for HgCl2 in mIMCD3 cells was 40 mu M. In HEK293 ells, the 24-h LC50 value for thimerosal was 9.5 mu M. These data demonstrate that the higher cytotoxicity produced by thimerosal on renal cells with respect to similar compounds without Hg may be related to this metal content. The present study also establishes mIMCD3 cells as a valuable model for evaluation of cytotoxicity of nephrotoxic compounds. C1 Workers Compensat Dust Dis Board NSW, Res & Educ Unit, Sydney, NSW 2000, Australia. Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA. Univ Calif Davis, Canc Res Ctr, Davis, CA 95616 USA. Univ Calif Davis, Dept Anim Sci, Physiol Genom Grp, Davis, CA 95616 USA. RP Park, EK (reprint author), Workers Compensat Dust Dis Board NSW, Res & Educ Unit, Level 2,82 Elizabeth St, Sydney, NSW 2000, Australia. 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Hagerman, Paul J. Leehey, Maureen A. TI Fragile-X syndrome and fragile X-associated tremor/ataxia syndrome: two faces of FMR1 SO LANCET NEUROLOGY LA English DT Review ID PREMATURE OVARIAN FAILURE; MENTAL-RETARDATION PROTEIN; MULTIPLE SYSTEM ATROPHY; INTERMEDIATE ALLELES; SYNDROME FXTAS; MOUSE MODEL; CGG REPEAT; PREMUTATION CARRIERS; MESSENGER-RNA; INTRANUCLEAR INCLUSIONS AB Recent advances in our understanding of the clinical and molecular features of the fragile-X mental-retardation 1 gene, FMR1, highlight the importance of single-gene disorders. 15 years after its discovery, FMR1 continues to reveal new and unexpected clinical presentations and molecular mechanisms. Loss of function of FMR1 is a model for neurodevelopmental and behavioural disorders, including mental retardation, autism, anxiety, and mood instability. In addition, overexpression and CNS toxicity of FMR1 mRNA causes a late-onset neurodegenerative disorder, the fragile-X-associated tremor/ataxia syndrome (FXTAS). 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We present findings from three experiments probing sensitivity to lexical stress and to affective prosodic cues considered at several processing levels. Adolescents and adults with WS were compared with age, IQ and receptive vocabulary-matched participants with learning or intellectual disabilities (LID), and with age-matched normal controls (NC). The WS group performed significantly better than the LID group only in recognising emotional tone of voice in filtered speech. Results reflect a relative sensitivity in the WS group to affective prosody, while the ability to use linguistic prosodic cues for semantic interpretation remains constrained by perceptual and cognitive limitations, suggesting a possible dissociation in sensitivity to different types of prosody in this population. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. SUNY Binghamton, New York, NY 13902 USA. Univ Connecticut, Storrs, CT 06269 USA. Univ Washington, Seattle, WA 98195 USA. RP Skwerer, DP (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 albany St,L-814, Boston, MA 02118 USA. 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Cogn. Process. PY 2007 VL 22 IS 2 BP 247 EP 271 DI 10.1080/01690960600632671 PG 25 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 151GA UT WOS:000245276700004 ER PT J AU Billington, J Baron-Cohen, S Wheelwright, S AF Billington, Jac Baron-Cohen, Simon Wheelwright, Sally TI Cognitive style predicts entry into physical sciences and humanities: Questionnaire and performance tests of empathy and systemizing SO LEARNING AND INDIVIDUAL DIFFERENCES LA English DT Article DE sex differences; cognitive style; science ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME; MATHEMATICS ACHIEVEMENT; COLLEGE-STUDENTS; SPATIAL ABILITY; ADULTS; QUOTIENT; MIND AB It is often questioned as to why fewer women enter science. This study assesses whether a cognitive style characterized by systemizing being at a higher level than empathizing (S > E) is better than sex in predicating entry into the physical sciences compared to humanities. 415 students in both types of discipline (203 males, 212 females) were given questionnaire and performance measures of systemizing and empathy. 59.1% of the science students were male and 70.1% of the humanities students were female. There were significant sex differences on the Empathy Quotient (EQ) (females on average scoring higher) and on the Systerruzing Quotient (SQ) (males on average scoring higher), confirming earlier studies. Scientists also scored higher on the SQ, and scored lower on the EQ, compared to those in the humanities. Thus, independent of sex, SQ was a significant predictor of entry into the physical sciences. Results from questionnaire data and performance data indicate an S > E profile for physical science students as a group, and an E > S profile for humanities students as a group, regardless of sex. We interpret this as evidence that whilst on average males show stronger systemizing and females show stronger empathizing, individuals with a strong systemizing drive are more likely to enter the physical sciences, irrespective of their sex. (c) 2007 Elsevier Inc. All rights reserved. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 8AH, England. RP Billington, J (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 8AH, England. 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CR Grinker Roy Richard, 2007, UNSTRANGE MINDS REMA 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 JAN PY 2007 VL 132 IS 1 BP 128 EP 128 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 126YK UT WOS:000243551300280 ER PT J AU Helland, WA Heimann, M AF Helland, Wenche Andersen Heimann, Mikael TI Assessment of pragmatic language impairment in children referred to psychiatric services: A pilot study of the Children's Communication Checklist in a Norwegian sample SO LOGOPEDICS PHONIATRICS VOCOLOGY LA English DT Article; Proceedings Paper CT 12th Congress of the European-Society-of-Child-and-Adolescent-Psychiatry CY OCT 01, 2003 CL Paris, FRANCE SP European Soc Child & Adolescent Psychiat DE child psychiatry; Children's Communication Checklist; pragmatic language impairment ID DEFICIT HYPERACTIVITY DISORDER; BEHAVIORAL-CHARACTERISTICS; DISTURBED-CHILDREN; PREVALENCE; AUTISM; ADHD AB The aim of the present pilot study was to explore whether pragmatic language impairments are more prevalent among children referred to child psychiatric services (n = 21) than among a comparison group of typically developing children (n = 29) in the age range 8-10 years. A second and minor aim was also to assess the usability of a Norwegian translation of the Children's Communication Checklist (CCC). Communication disorders defined as a pragmatic score equal to or below 140 on the CCC were identified in a majority (0.57) of the children in the clinical group; the corresponding proportion for the typically developing comparison group was only 0.10. Thus, the Norwegian version of the CCC distinguishes between children with symptoms of pragmatic language impairments and those with no symptoms, as does the English version. C1 [Helland, Wenche Andersen; Heimann, Mikael] Univ Bergen, N-5020 Bergen, Norway. RP Heimann, M (reprint author), Ctr Child & Adolescent Mental Hlth, POB 7800, N-5020 Bergen, Norway. EM Mikael.Heimann@rbup.uib.no CR ANDERSON K, 2002, CCC CHILDRENS COMMUN BAKER L, 1987, J AUTISM DEV DISORD, V17, P499, DOI 10.1007/BF01486966 Beitchman J. 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Phoniatr. Vocology. PY 2007 VL 32 IS 1 BP 23 EP 30 DI 10.1080/14015430600712056 PG 8 WC Audiology & Speech-Language Pathology; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Otorhinolaryngology GA 275SW UT WOS:000254092900005 PM 17454657 ER PT J AU Brimacombe, M Ming, X Lamendola, M AF Brimacombe, M. Ming, X. Lamendola, M. TI Prenatal and birth complications in autism SO MATERNAL AND CHILD HEALTH JOURNAL LA English DT Article DE prenatal history; autism; risk factors; epidemiology ID PERINATAL FACTORS; RISK-FACTORS; CHILDREN; POPULATION; ACTIVATION; DISORDERS; PREGNANCY; ETIOLOGY; TWINS AB Objectives: Prenatal and birth history as potential sources of risk factors in relation to the onset of autism were examined. Methods: A cohort of 164 families of autistic children referred to The Autism Center at New Jersey Medical School-UMDNJ, Newark, New Jersey, over a two-year period was studied. Intake prenatal and birth history information was obtained from each family and reviewed by a clinician. Results: Prevalence rates in this cohort for vaginal bleeding, prolonged labor and prematurity were higher than comparable rates reported nationally and in New Jersey. Clustering of multiple prenatal risk factors was observed. This clustering was associated with the age of the mother, but uncorrelated with birth order. Conclusions: These findings support the general hypothesis that systemic problems at the prenatal stage may form a distinct dimension of risk associated with autism. C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Prevent Med, Newark, NJ 07103 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, Newark, NJ 07103 USA. 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Child Health J. PD JAN PY 2007 VL 11 IS 1 BP 73 EP 79 DI 10.1007/s10995-006-0142-7 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 128GG UT WOS:000243645600010 PM 17053965 ER PT J AU Dochniak, MJ AF Dochniak, Michael J. TI Autism spectrum disorders - Exogenous protein insult SO MEDICAL HYPOTHESES LA English DT Article ID HEVEA-BRASILIENSIS LATEX; CROSS-REACTIVE ALLERGEN; EXPRESSION; CHITINASE; IDENTIFICATION; PURIFICATION; PROFILIN; EPITOPES; ANTIBODY; ENOLASE AB The immune-response perspective described herein is intended to explore how certain environmental proteins may affect neuro-cognitive development in children. Specifically, proteins inherent in natural rubber latex are known to cause severe and pervasive immune responses. More specifically, the Hevea Brasiliensis proteins in natural rubber latex may trigger immunoglobulin-E mediated reaction antibodies and influence cross-react immune responses to other exogenous/endogenous proteins. In adults, repeated exposure to the Hevea Brasiliensis proteins has been shown to cause an increased incidence of sensitization, adverse allergic reactions, and even death through anaphylactic shock. Natural rubber latex has seen a dramatic increase in usage over the last 30-years (e.g., health care industry, consumer products). The timing, frequency, intensity, and type of exposure to such proteins may influence the incidence, degree of atypicality, and prevalence of autism spectrum disorders. Therefore, research efforts should be directed at exploring how immune responses to such proteins affect lymphocyte sensitivity, enzyme regulation, and neural formation during prenatal/neonatal development. (c) 2007 Elsevier Ltd. All rights reserved. RP Dochniak, MJ (reprint author), POB 296, Hugo, MN 55038 USA. 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Hypotheses PY 2007 VL 69 IS 3 BP 545 EP 549 DI 10.1016/j.mehy.2007.01.060 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 201VT UT WOS:000248861400015 PM 17374559 ER PT J AU Boorom, KF AF Boorom, Kenneth Fiske TI Is this recently characterized gastrointestinal pathogen responsible for rising rates of inflammatory bowel disease (IBD) and IBD associated autism in Europe and the United States in the 1990s? SO MEDICAL HYPOTHESES LA English DT Article ID BLASTOCYSTIS-HOMINIS; ENTAMOEBA-HISTOLYTICA; CROHNS-DISEASE; IMMUNE-RESPONSES; CHILDREN; SEROTONIN; DIAGNOSIS; COLITIS; CELLS; FIBROMYALGIA AB In 2006, a pathogenic variant of the common intestinal organism Blastocystis was discovered in patients who were experiencing chronic gastrointestinal symptoms. Most species of Blastocystis inhabit humans with no symptoms. The discovery of a pathogenic variant of Blastocystis is significant, because Blastocystis is related to Entamoeba, a similar organism with pathogenic variants that kill over 100,000 people each year. Recent research has shown that Blastocystis infections may be undetectable using existing clinical methods. Medical case reports from the Middle East, Europe, and United States suggest that infection with this variant may already be widespread and misdiagnosed as one of several functional disorders. Hypothesis: A more virulent or transmissible type of Blastocystis emerged in the Middle East in the 1980's, and was transmitted to Europe and the United States by military and more significantly vacation and business travel. The lack of adequate tests made it impossible to detect the infection. Transmission to the larger population resulted in rising inflammatory bowel disease (IBD) rates in Europe in the 1990's. The relationship between IBD and autism is explored, along with the possibility that the same pathogen causes both conditions. Supporting data: Serological and epidemiological findings are presented supporting the hypothesis. Blastocystis survives sewage treatment, shows low host specificity, and can be spread by many animals. Several communities which have been studied due to high autism rates are located close to rivers which receive large quantities of sewage effluent, such as South Thames (England), Olmsted County (Minnesota, USA) and many communities in Oregon (USA). Conclusions: Scientists from other countries represent the first line of defense against emerging infectious diseases, but their publications on Blastocystis are not well known in the United States and Europe. With the publication of corroborating research by Western scientists in core scientific journals, it is hoped that an appropriate response from the public health system will, be forthcoming. 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Hypotheses PY 2007 VL 69 IS 3 BP 652 EP 659 DI 10.1016/j.mehy.2007.01.027 PG 8 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 201VT UT WOS:000248861400034 PM 17382484 ER PT J AU Chen, F Planche, P Lemonnier, E AF Chen, Fei Planche, Pascale Lemonnier, Eric TI How could language interact with visuo-spatial performance in autism? SO MEDICAL HYPOTHESES LA English DT Letter ID COGNITION; SUPERIOR C1 Hop Bohars, CHU Brest, Serv Pedopsychiat, F-29820 Bohars, France. Univ Bretagne Occidentale, Fac Lettres & Sci Sociales, Dept Psychol, F-29200 Brest, France. RP Chen, F (reprint author), Hop Bohars, CHU Brest, Serv Pedopsychiat, BP17, F-29820 Bohars, France. 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TI Autism, asthma, inflammation, and the hygiene hypothesis SO MEDICAL HYPOTHESES LA English DT Editorial Material ID PERVASIVE DEVELOPMENTAL DISORDERS; SINGLE-NUCLEOTIDE POLYMORPHISMS; HEPATOCYTE GROWTH-FACTOR; SPECTRUM DISORDERS; HEAD CIRCUMFERENCE; CHILDHOOD ASTHMA; RISING INCIDENCE; SIBSHIP SIZE; RISK-FACTORS; BIRTH-ORDER AB Inflammation and the genes, molecules, and biological pathways that lead to inflammatory processes influence many important and disparate biological processes and disease states that are quite often not generally considered classical inflammatory or autoimmune disorders. These include development, reproduction, aging, tumor development and tumor rejection, cardiovascular pathologies, metabolic disorders, as well as neurological and psychiatric disorders. This paper compares parallel aspects of autism and inflammatory disorders with an emphasis on asthma. 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Because a variety of epigenetic influences, particularly those occurring during the prenatal period, can override or masquerade as genetic influences, these should be considered as prime contributors to the recent increase of autism. Prenatal influences on dopamine activity are especially well-documented, including the effects of maternal psychosocial stress, maternal fever, maternal genetic and hormonal status, use of certain medications, urban birth, and fetal hypoxia. All of these factors have been implicated in the genesis of autism, which is characterized by a "hyperdopaminergic" state based on evidence from monkey and human behavioral studies, pharmacological studies in humans, and a left-hemispheric predominance of both dopamine and autistic-like symptoms. 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Hypotheses PY 2007 VL 68 IS 1 BP 46 EP 60 DI 10.1016/j.mehy.2006.06.041 PG 15 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 114GH UT WOS:000242654200008 PM 16959433 ER PT J AU Ijichi, S Ijichi, N AF Ijichi, Shinji Ijichi, Naomi TI Computerized lifelong mentoring support using robot for autistic individuals SO MEDICAL HYPOTHESES LA English DT Article ID QUANTITATIVE TRAIT LOCUS; SUBSTANTIAL GENETIC INFLUENCE; GENOME SCAN; BEHAVIORS; DISORDER; CHILDREN; ETIOLOGY; SPECTRUM; DEFICIT; BRAIN AB Developmental diversity in childhood is transformed into personality variation in adulthood. This view is now revalued through an ongoing paradigm shift in the field of developmental conditions, the transition from the qualitative dichotomy perspective to the quantitative concept. In the quantitative concept, autism is not a disease nor a developmental qualitative disorder, but a behavioral extreme in individual variation. Although the traditional qualitative view cannot interpret the recent worldwide prevalence of autism, the increase in the reported number of cases with autism and border cases can be easily explained by a dimensional exploration in which the primary autistic phenotype is regarded as an evolutional superiority. Therefore, the only suitable intervention is mentoring which provides a powerful lifelong support for higher social achievement in individuals with autism. Here, we hypothesize the coming mentoring circumstances for autistic individuals in the near future. Ongoing progress in robot and computer technology might allow the guardians to leave the major part of mentoring support to an individualized robot, and the 'folk physics' tendency in individuals with autism could facilitate the spread of the mentoring support system. The development of the robot mentor software may be simple because of the uniformity and stereotypy of the behavior patterns in individuals with autism. With the help of the robot mentor and under its guidance, autistic people might enjoy their social life and contribute to the prosperity of the human society to the maximum degree. Because the future population ratio of autistics/non-autistics might be reversed according to the current trend of the prevalence, mentoring robot programs for autistic individuals should be developed without delay as a novel preliminary activity in the Jiminy Cricket movement, which is a campaign to reverse the estrangement of the present majority from autism and to increase the number of mentors for autistic individuals. In this article, prerequisites for the mentoring program of the robot mentor are expected and discussed. (c) 2006 Published by Elsevier Ltd. C1 EGT, Kagoshima 8910144, Japan. Kagoshima Univ, Hlth Serv Ctr, Kagoshima 8908580, Japan. RP Ijichi, S (reprint author), EGT, 7421-1 Shimofukumoto Cho, Kagoshima 8910144, Japan. 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Hypotheses PY 2007 VL 68 IS 3 BP 493 EP 498 DI 10.1016/j.mehy.2006.08.016 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 136NX UT WOS:000244232500005 PM 17023117 ER PT J AU Vakalopoulos, C AF Vakalopoulos, C. TI Unilateral neglect: A theory of proprioceptive space of a stimulus as determined by the cerebellar component of motor efference copy (and is autism a special case of neglect) SO MEDICAL HYPOTHESES LA English DT Article ID SUPERIOR TEMPORAL SULCUS; LINE BISECTION JUDGMENTS; RIGHT HEMISPHERE LESIONS; SPATIAL WORKING-MEMORY; VISUAL NEGLECT; VISUOSPATIAL NEGLECT; PARIETAL CORTEX; VESTIBULAR STIMULATION; CORTICAL CONNECTIONS; HEMISPATIAL NEGLECT AB Unilateral neglect is a devastating condition, which manifests as a loss of a person's spatial awareness opposite the damaged side of the brain. It challenges our conception of the seat of the soul and its explanation is at the heart of the mind-body problem. A heuristic definition of the dorsal stream of a modality is here based on the categorization of parietal networks by the cerebellar component of motor efference copy. Taking this premise, the proprioceptive space of a stimulus is established as a concept in this paper. It is proposed that unilateral neglect is typically a dysfunction of proprioceptive space of a stimulus associated with lesions of the dorsal stream. Furthermore, most experimental findings of unilateral visual neglect (and by extrapolation, other sensory modalities), can be explained by two developmental mechanisms by which the proprioceptive space of a stimulus is encoded in the parietal cortex. Its right and Left hemisphere representation can be dissociated from the hemifield of presentation of perceptual information, such that the left hemifield can have a left hemisphere representation through callosal connections and likewise, the right hemifield can have a right hemifield representation. The processing of a sensory stimulus in either parietal hemisphere is dynamically determined as shown by experimental modulation of performance. A theory of historical precedence will provide a developmental background to the organization of proprioceptive space and will invoke separate models according to specified terms of engagement. A model based on the expansion and contraction of the proprioceptive space of a stimulus as a gradient across both hemispheres and modulated by concurrent proprioceptive state will be differentiated from a model that is non-graduating but competitive and lacks such modulation. In other words, the dorsal representation of a sensory stimulus in the former case is shared to a varying degree by the two parietal hemispheres, whereas in the tatter case the representation of Left and right aspects of the same object stimulus is strictly divided between the two hemispheres. A further hypothesis of a dorsoventral gradient of the peripheral and foveal components of proprioceptive space characterizing dorsal stream networks will predict the double dissociation revealed by experimental paradigms. It will explain why some patients show neglect only in foveal while others only in peripheral vision. The paper proposes to unify neglect, extinction and optic ataxia on the one hand, and spatial and object-based neglect on the other hand, under a singularly proficient paradigmatic structure. A binding model as described is a component theory that acknowledges how the involved pathways or transitional zones in a pathway may contribute to a differential clinical picture as one progresses from posterior to anterior parietal cortex. Finally, a brief discussion is given on how autistic subjects neglect spatial cues and the inability of a spatial cognitive transformation underlies the impairments postulated for 'a theory of mind'. (c) 2006 Published by Elsevier Ltd. RP Vakalopoulos, C (reprint author), 171 McKean St, Melbourne, Vic 3068, Australia. 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Hypotheses PY 2007 VL 68 IS 3 BP 574 EP 600 DI 10.1016/j.mehy.2006.08.013 PG 27 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 136NX UT WOS:000244232500021 PM 17070652 ER PT J AU Bradstreet, JJ Smith, S Granpeesheh, D El-Dahr, JM Rossignol, D AF Bradstreet, James Jeffrey Smith, Scott Granpeesheh, Doreen El-Dahr, Jane M. Rossignol, Daniel TI Spironolactone might be a desirable immunologic and hormonal intervention in autism spectrum disorders SO MEDICAL HYPOTHESES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDER; GASTROINTESTINAL SYMPTOMS; IMMUNE-RESPONSES; OXIDATIVE STRESS; T-CELLS; CHILDREN; BRAIN; AUTOANTIBODIES; SERUM; ABNORMALITIES AB Multiple studies now demonstrate that autism is medically characterized, in part, by immune system dysregulation, including evidence of neuroglial activation and gastrointestinal inflammation. This neuroglial process has further been characterized as neuroinflammation. In addition, a subset of autistic children exhibit higher than average levels of androgens. Spironolactone is an aldosterone antagonist and potassium-sparing diuretic with a desirable safety profile. It possesses potent anti-inflammatory and immune modifying properties that might make it an excellent medical intervention for autism spectrum disorders. Furthermore, spironolactone demonstrates substantial anti-androgen properties that might further enhance its appeal in autism, particularly in a definable subset of hyperandrogenic autistic children. One case report is briefly reviewed demonstrating objective clinical improvements in an autistic child after spironolactone administration. Additional research in controlled trials is now needed to further define the risks and benefits of spironolactone use in children with autism. (c) 2006 Elsevier Ltd. All rights reserved. C1 Melbourne & Florida Hosp, Int Child Dev Resource Ctr, Melbourne, FL 32901 USA. Ctr Autism Related Disorders, Tarzana, CA USA. Tulane Univ, Hlth Sci Ctr, Dept Pediat, New Orleans, LA 70118 USA. Tulane Univ, Dept Med, Sect Pediat Allergy Immunol & Rheumatol, New Orleans, LA 70118 USA. Univ Virginia, Dept Family Med, Charlottesville, VA USA. RP Bradstreet, JJ (reprint author), Melbourne & Florida Hosp, Int Child Dev Resource Ctr, 1688 W Hibiscus Blvd, Melbourne, FL 32901 USA. 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Hypotheses PY 2007 VL 68 IS 5 BP 979 EP 987 DI 10.1016/j.mehy.2006.10.015 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 157EL UT WOS:000245701300009 PM 17150311 ER PT J AU Cortesi, M Alfei, E Barale, F Fusar-Poli, P AF Cortesi, Mariachiara Alfei, Enrico Barale, Francesco Fusar-Poli, Paolo TI Linking autism, regression and Landau-Kieffner syndrome: Integrative role of nerve growth factor SO MEDICAL HYPOTHESES LA English DT Letter ID SPECTRUM DISORDERS; CHILDREN; EPILEPSY C1 Univ Pavia, Dept Child Neurol & Psychiat, I-27100 Pavia, Italy. Univ Pavia, Dept Psychobehav Hlth Sci, I-27100 Pavia, Italy. RP Fusar-Poli, P (reprint author), Univ Pavia, Dept Appl & Psychobehav Sci, Via Bassi 21, I-27100 Pavia, Italy. EM p.fusar@libero.it RI Fusar-Poli, Paolo/D-8605-2011 CR Chavko M, 2002, NEUROCHEM RES, V27, P1649, DOI 10.1023/A:1021687011281 Connolly AM, 2006, BIOL PSYCHIAT, V59, P354, DOI 10.1016/j.biopsych.2005.07.004 ECHENNE B, 1992, BRAIN DEV-JPN, V14, P216 Klyushnik T P, 2001, Neurosci Behav Physiol, V31, P165, DOI 10.1023/A:1005208206719 Lewine JD, 1999, PEDIATRICS, V104, P405, DOI 10.1542/peds.104.3.405 MARIEN P, 1993, ACTA NEUROL BELG, V93, P183 Nass R, 1998, DEV MED CHILD NEUROL, V40, P453 Nelson KB, 2001, ANN NEUROL, V49, P597, DOI 10.1002/ana.1024 Tuchman R, 2002, LANCET NEUROL, V1, P352, DOI 10.1016/S1474-4422(02)00160-6 NR 9 TC 3 Z9 3 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PY 2007 VL 68 IS 5 BP 1178 EP 1179 DI 10.1016/j.mehy.2006.10.029 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 157EL UT WOS:000245701300049 PM 17157996 ER PT J AU Rossignol, DA AF Rossignol, Daniel A. TI Hyperbaric oxygen therapy might improve certain pathophysiological findings in autism SO MEDICAL HYPOTHESES LA English DT Review ID CEREBRAL-BLOOD-FLOW; PERVASIVE DEVELOPMENTAL DISORDERS; SYSTEMIC-LUPUS-ERYTHEMATOSUS; INCREASED OXIDATIVE STRESS; FIBRILLARY ACIDIC PROTEIN; PERIANAL CROHNS-DISEASE; CARRIER SLC25A12 GENE; ECD BRAIN SPECT; CHILDHOOD AUTISM; MITOCHONDRIAL DYSFUNCTION AB Autism is a neurodevelopmental disorder currently affecting as many as 1 out of 166 children in the United States. Numerous studies of autistic individuals have revealed evidence of cerebral hypoperfusion, neuroinflammation and gastrointestinal inflammation, immune dysregutation, oxidative stress, relative mitochondriat dysfunction, neurotransmitter abnormalities, impaired detoxification of toxins, dysbiosis, and impaired production of porphyrins. Many of these findings have been correlated with core autistic symptoms. For example, cerebral hypoperfusion in autistic children has been correlated with repetitive, self-stimulatory and stereotypical behaviors, and impairments in communication, sensory perception, and social interaction. Hyperbaric oxygen therapy (HBOT) might be able to improve each of these problems in autistic individuals. Specifically, HBOT has been used with clinical success in several cerebral hypoperfusion conditions and can compensate for decreased blood flow by increasing the oxygen content of plasma and body tissues. HBOT has been reported to possess strong anti-inflammatory properties and has been shown to improve immune function. There is evidence that oxidative stress can be reduced with HBOT through the upregulation of antioxidant enzymes. HBOT can also increase the function and production of mitochondria and improve neurotransmitter abnormalities. In addition, HBOT upregulates enzymes that can help with detoxification problems specifically found in autistic children. Dysbiosis is common in autistic children and HBOT can improve this. Impaired production of porphyrins in autistic children might affect the production of heme, and HBOT might help overcome the effects of this problem. Finally, HBOT has been shown to mobilize stem cells from the bone marrow to the systemic circulation. Recent studies in humans have shown that stem cells can enter the brain and form new neurons, astrocytes, and microglia. It is expected that amelioration of these underlying pathophysiotogicat problems through the use of HBOT will lead to improvements in autistic symptoms. Several studies on the use of HBOT in autistic children are currently underway and early results are promising. (C) 2006 Elsevier Ltd. All rights reserved. C1 Univ Virginia, Dept Family Med, Charlottesville, VA 22908 USA. RP Rossignol, DA (reprint author), Univ Virginia, Dept Family Med, POB 800729, Charlottesville, VA 22908 USA. 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Hypotheses PY 2007 VL 68 IS 6 BP 1208 EP 1227 DI 10.1016/j.mehy.2006.09.064 PG 20 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 168QV UT WOS:000246540000004 PM 17141962 ER PT J AU Campos-Castello, J Fernaindez-Mayoralas, DM Munoz-Jareno, N Antonio-Arce, VS AF Campos-Castello, Jaime Fernaindez-Mayoralas, Daniel M. Munoz-Jareno, Nuria Antonio-Arce, Victoria San TI Rett syndrome: 50 years' history of a still not well known condition SO MEDICINA-BUENOS AIRES LA Spanish DT Article DE rett syndrome; diagnostic criteria; genetics; molecular diagnosis; pathogenesis; neuropathology ID X-CHROMOSOME INACTIVATION; BINDING PROTEIN MECP2; NEURODEVELOPMENTAL DISORDER; MENTAL-RETARDATION; SYNDROME PHENOTYPE; MOUSE MODEL; EXPRESSION; MUTATION; BRAIN; AUTISM AB Since it was first described by Andrea Rett 50 years ago, Rett syndrome (RS) has been the subject of further investigations, nonetheless it continues to be a not well known condition. Our own experience and an updated literature review on RS is presented. RS is a severe dominant X chromosome-linked neurodevelopmental disorder with a characteristic clinical picture that mostly occurs in girls, most of the cases are sporadic and genetically determined. The diagnosis of RS is made based on observation and clinical assessment. Main clinical features are mental retardation, behavioural changes, stereotypes, loss of speech and hand skills, gait apraxia, irregular breathing with hyperventilation while awake, and frequent seizures. The internationally established criteria are reviewed. RS is caused by mutations in MECP2 in the majority of cases, but a proportion of atypical cases may result from mutations in CDKL5. particularly the early onset seizure variant. However, the molecular pathogenesis of this disorder remains unclear, as well as the relation between the mutations in MECP2 and other neurodevelopmental disorders. 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Clinical and genetics aspects SO MEDICINA-BUENOS AIRES LA Spanish DT Article DE autism; Asperger syndrome; Rett syndrome; childhood desintegrative disorder ID AUTISM-SPECTRUM DISORDER; UTAH EPIDEMIOLOGIC SURVEY; FRAGILE-X PREMUTATION; RETT-SYNDROME; ASPERGER-SYNDROME; TUBEROUS SCLEROSIS; SUSCEPTIBILITY GENES; COGNITIVE PHENOTYPE; INFANTILE-AUTISM; MECP2 MUTATIONS AB Pervasive developmental disorders (PDD) encompass a heterogeneous group of children with deficits of verbal and non-verbal language, social communication, and with a restricted repertoire of activities or repetitive behaviours. The frequency in general population is considered 27.5/10,000. In this study, we analyzed the clinical and genetic aspects of Autism, Asperger Syndrome, PDD Not Otherwise Specified, Rett Syndrome and Childhood Disintegrative Disorder. We analyzed clinical, behavioural and neuropsychological features. We revised different medical genetics associated conditions and divided the genetics aspects of pervasive developmental disorders into two groups: Syndromic forms (around 20%) and non syndromic forms (currently proposed to be 80%). The early recognition of pervasive developmental disorders and the diagnosis of specific associated syndromes allow early therapy, correct genetic counselling, and follow up anticipating possible complications related to the entity. Finally, although the genetic bases of autism have not yet been identified, the following candidate genes have been proposed: 15q, 2q, 17q, 7q, 12q, and X related genes, among others; which are analyzed in this study and will allow a better understanding of these disorders in the future. C1 [Ruggieri, Victor] Hosp Pediat Juan P Garrahan, Serv Neurol, Buenos Aires, DF, Argentina. [Arberas, Claudia] Hosp Ninos Dr Ricardo Gutierrez, Secc Genet, Buenos Aires, DF, Argentina. 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To assess parental attitudes and knowledge about children's vaccination. Methods. In this study, 20 day-care centers, 25 schools, and 6 health centers were randomly selected in Vilnius, and an anonymous survey of 2743 parents was conducted. Females made up 85.2% of all respondents, males -14.8%; the mean age was 35.7 years. Results. Two-thirds of respondents (66.7%) agreed that vaccines for children's immunization are safe; 80.7% stated that vaccination is more beneficial than harmful. Only 16.9% of parents indicated that vaccines cause adverse events more frequently than other medical treatment, 62.7% that vaccines are amongst the most effective and least costly forms of medical treatment, and 35.9% that vaccines always warrant protection. Majority of parents agreed that children's vaccination is essential (89.0%), and children should be vaccinated regularly according schedule (88.6%). Only 30.1% of respondents agreed with the idea of taking a newly developed vaccine even if it has been carefully tested for safety; 42.3% of respondents could afford to pay for nonreimbursed vaccines. On an average, 38.0% of respondents know that they should be revaccinated every 10 years against diphtheria and tetanus, 61.3% have never been vaccinated against influenza. The main sources of information on vaccination are medical institutions (92.2%), print media (38.1%), and broadcast media (38.2%). Conclusions. While most of respondents can be characterized as having a positive opinion about vaccination, 20-40% of respondents indicated insufficient knowledge on this issue. For implementing the new vaccines, communication efforts should focus on clarifying correct parental beliefs about immunization. Vaccines for child should be reimbursed on the same basis as other medical treatment. Vaccination of adult and risk groups should be emphasized in the national vaccination program. 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The focus of this paper is on the early development of communication in autism, and early intervention for impairments in communication associated with this disorder. An overview of components of communication is provided. Communication characteristics that are diagnostic of autism are summarized, with consideration of the overlap between social and communication impairment, particularly for children with autism functioning at the prelinguistic level. Early communication development and predictors of communication functioning in autism are examined, based on a review of prospective and retrospective studies. The focus of the discussion then turns to intervention. Consideration is given to the rationale for beginning intervention as early in life as possible for children with autism. Implications of motor, imitation, and play deficits for communication-based intervention are examined. 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Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 1 BP 16 EP 25 DI 10.1002/mrdd.20134 PG 10 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 141OC UT WOS:000244587200003 PM 17326115 ER PT J AU Abbeduto, L Brady, N Kover, ST AF Abbeduto, Leonard Brady, Nancy Kover, Sara T. TI Language development and fragile X syndrome: Profiles, syndrome-specificity, and within-syndrome differences SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE fragile X syndrome; language; communication; autism; mental retardation ID NONSPECIFIC MENTAL-RETARDATION; DOWN-SYNDROME; YOUNG-CHILDREN; FMR1 GENE; NEUROBEHAVIORAL PHENOTYPE; JOINT ATTENTION; NEUROCOGNITIVE PHENOTYPE; PREMUTATION CARRIERS; INTERMEDIATE ALLELES; FAMILY EXPERIENCES AB Fragile X syndrome (FXS) is the leading inherited cause of mental retardation. In this article, we review what is known about the language and related problems of individuals with FXS. In doing so, we focus on the syndrome-specific features of the language phenotype and on the organismic (i.e., genetic and individual neurocognitive and behavioral) and environmental factors associated with within-syndrome variation in the phenotype. We also briefly review those aspects of the behavioral phenotype of FXS that are relevant for understanding syndrome-specific features of, and within-syndrome variability in, language. The review includes summaries of research on the pre-linguistic foundations for language development and on each of the major components of language (i.e., vocabulary, morphosyntax, and pragmatics). Throughout the review, we point out implications of existing research for intervention as well as directions for future research. (C) 2007 Wiley-Liss, Inc. MRDD Research Reviews 2007,13:36-46. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 1 BP 36 EP 46 DI 10.1002/mrdd.20142 PG 11 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 141OC UT WOS:000244587200005 PM 17326110 ER PT J AU Muller, RA AF Mueller, Ralph-Axel TI The study of autism as a distributed disorder SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; brain imaging; connectivity; functional networks ID HIGH-FUNCTIONING AUTISM; DEVELOPMENTAL LANGUAGE DISORDER; MEDIAL TEMPORAL-LOBE; FRAGILE-X-SYNDROME; ASPERGER-SYNDROME; WHITE-MATTER; MAGNETIC-RESONANCE; SPECTRUM DISORDER; YOUNG-CHILDREN; SENTENCE COMPREHENSION AB Past autism research has often been dedicated to tracing the causes of the disorder to a localized neurological abnormality, a single functional network, or a single cognitive-behavioral domain. In this review, I argue that autism is a "distributed disorder" on various levels of study (genetic, neuroanatomical, neurofunctional, behavioral). "Localizing" models are therefore not promising. The large array of potential genetic risk factors suggests that multiple (or all) emerging functional brain networks are affected during early development. This is supported by widespread growth abnormalities throughout the brain. Interactions during development between affected functional networks and atypical experiential effects (associated with atypical behavior) in children with autism further complicate the neurological bases of the disorder, resulting in an "exponentially distributed" profile. Promising approaches to a better characterization of neural endophenotypes in autism are provided by techniques investigating white matter and connectivity, such as MR spectroscopy, diffusion-tensor imaging (DTI), and functional connectivity MRI. According to a recent hypothesis, the autistic brain is generally characterized by "underconnectivity." However, not all findings are consistent with this view. The concepts and methodology of functional connectivity need to be refined and results need to be corroborated by anatomical studies (such as DTI tractography) before definitive conclusions can be drawn. (C) 2007 Wiley-Liss, Inc. C1 San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, San Diego, CA 92120 USA. Univ Calif San Diego, Dept Cognit Sci, San Diego, CA 92103 USA. RP Muller, RA (reprint author), San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, 6363 Alvarado Ct,225 E, San Diego, CA 92120 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 1 BP 85 EP 95 DI 10.1002/mrdd.20141 PG 11 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 141OC UT WOS:000244587200010 PM 17326118 ER PT J AU Smith, SD AF Smith, Shelley D. TI Genes, language development, and language disorders SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE behavior genetics; neurodevelopmental genetics; language disorders; language impairment; dyslexia; reading disability ID QUANTITATIVE-TRAIT LOCUS; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DYSLEXIA SUSCEPTIBILITY LOCUS; PHONOLOGICAL CODING DYSLEXIA; SPEECH-SOUND DISORDER; MICROTUBULE-ASSOCIATED PROTEIN; FAMILY-BASED ASSOCIATION; COMPLEX COGNITIVE TRAIT; GENOME-WIDE SCAN; READING-DISABILITY AB Genetic factors are important contributors to language and learning disorders, and discovery of the underlying genes can help delineate the basic neurological pathways that are involved. This information, in turn, can help define disorders and their perceptual and processing deficits. Initial molecular genetic studies of dyslexia, for example, appear to converge on defects in neuronal and axonal migration. Further study of individuals with abnormalities of these genes may lead to the recognition of characteristic cognitive deficits attributable to the neurological dysfunction. Such abnormalities may affect other disorders as well, and studies of co-morbidity of dyslexia with attention deficit disorder and speech sound disorder are helping to define the scope of these genes and show the etiological and cognitive commonalities between these conditions. The genetic contributions to specific language impairment (SLI) are not as well defined at this time, but similar molecular approaches are being applied to identify genes that influence SLI and comorbid disorders. While there is co-morbidity of SLI with dyslexia, it appears that most of the common genetic effects may be with the language characteristics of autism spectrum disorders rather than with dyslexia and related disorders. Identification of these genes and their neurological and cognitive effects should lay out a functional network of interacting genes and pathways that subserve language development. Understanding these processes can form the basis for refined procedures for diagnosis and treatment. (C) 2007 Wiley-Liss, Inc. MRDD Research Reviews 2007; 13:96-105. C1 Univ Nebraska, Med Ctr, Dept Pediat, Omaha, NE 68198 USA. RP Smith, SD (reprint author), Univ Nebraska, Med Ctr, Dept Pediat, 985456 Nebraska Med Ctr, Omaha, NE 68198 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 1 BP 96 EP 105 DI 10.1002/mrdd.20135 PG 10 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 141OC UT WOS:000244587200011 PM 17326114 ER PT J AU Shattuck, PT Grosse, SD AF Shattuck, Paul T. Grosse, Scott D. TI Issues related to the diagnosis and treatment of autism spectrum disorders SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; policy; developmental screening; special education; early intervention ID PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIORAL TREATMENT; UNITED-STATES; CHILDREN; PREVALENCE; MEDICAID; AGE AB This paper explores issues and implications for diagnosis and treatment, stemming from the growing number of children identified with autism spectrum disorders (ASDs). Recent developments and innovations in special education and Medicaid programs are emphasized. Eligibility determination policies, innovations in diagnostic practices, the cost and financing of assessment, variability among programs in diagnostic criteria, and racial/ethnic disparities in the timing of diagnosis all influence the capacity of service systems to provide diagnoses in a timely, coordinated, accurate, economical, and equitable manner. There are several barriers to the more widespread provision of intensive intervention for children with ASDs, including lack of strong evidence of effectiveness in scaled-up public programs, uncertainty about the extent of obligations to provide services under the Individuals with Disabilities Education Act, high cost of intervention, and variability among states in their willingness to fund intensive intervention via Medicaid. Innovative policy experiments with respect to financing intensive intervention through schools and Medicaid are being conducted in a number of states. (C) 2007 Wiley-Liss, Inc. C1 Univ Wisconsin, Waisman Ctr 533, Madison, WI 53705 USA. Ctr Dis Control & Prevent, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA USA. RP Shattuck, PT (reprint author), Univ Wisconsin, Waisman Ctr 533, 1500 Highland Ave, Madison, WI 53705 USA. EM shattuck@waisman.wisc.edu CR *AM AC PED, 2005, DEV SCREEN TEST COD American Psychiatric Association (APA), 1980, DIAGN STAT MAN MENT Atkins D, 2005, HEALTH AFFAIR, V24, P102, DOI 10.1377/hlthaff.24.1.102 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 BHASIN TK, IN PRESS J AUTISM DE CAMPBELL KP, 2006, PURCHASERS GUIDE CLI *CDCP, 2006, LEARN SIGNS ACT EARL Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 Chambers J, 2003, TOTAL EXPENDITURES S Sandler AD, 2001, PEDIATRICS, V107, P1221 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Crowley J. 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PY 2007 VL 13 IS 2 BP 129 EP 135 DI 10.1002/mrdd.20143 PG 7 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 189SW UT WOS:000248009800005 PM 17563895 ER PT J AU Muller, RA AF Muller, R-A TI Atypical activity seen in adolescents or adults, who have lived with autism for many years, may reflect the brain's normal plasticity in response to atypical perceptual input. (vol 13, pg 85, 2007) SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Correction CR Muller RA, 2007, MENT RETARD DEV D R, V13, P85, DOI 10.1002/mrdd.20141 NR 1 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1080-4013 J9 MENT RETARD DEV D R JI Ment. Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 2 BP 195 EP 195 DI 10.1002/mrdd.20154 PG 1 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 189SW UT WOS:000248009800013 ER PT J AU Dykens, EM AF Dykens, Elisabeth M. TI Psychiatric and behavioral disorders in persons with Down syndrome SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE psychopathology; behavioral problem; psychiatric illness; risk and protective factors; Down syndrome ID AUTISTIC-SPECTRUM DISORDERS; MENTAL-RETARDATION; ALZHEIMERS-DISEASE; INTELLECTUAL DISABILITY; LEARNING-DISABILITIES; MALADAPTIVE BEHAVIOR; MATERNAL STRESS; CHILDREN; ADULTS; PREVALENCE AB Similar to the state of the broader intellectual disabilities field, many gaps exist in the research and treatment of mental health concerns in people with Down syndrome. This review summarizes key findings on the type and prevalence of behavior and emotional problems in children, adolescents, and adults with Down syndrome. Such findings include relatively low rates of severe problems in children, and well-documented risks of depression and Alzheimer's disease in older adults. The review also considers emerging data on autism, and the paucity of studies on adolescents. Three next steps for research are highlighted, including a need to: (1) connect research on psychiatric status and diagnoses across developmental periods, including adolescence, and to examine such associated processes as sociability, anxiety and attention; (2) unravel complicated bopsycho-social risk and protective factors that serve to increase or diminish psychopathology; and (3) identify evidence-based treatments that both reduce distressful symptoms and enhance well-being in individuals with Down syndrome. (C) 2007 Wiley-Liss, Inc. 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TI Sociocultural studies of families of children with intellectual disabilities SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE family studies; mixed methods; meaning; cultural context; family ecology; qualitative methods ID HIGH-FUNCTIONING AUTISM; DEVELOPMENTAL DELAYS; MENTAL-RETARDATION; PROBLEM BEHAVIOR; POOR FAMILIES; PARENTS; LIFE; PERSPECTIVES; IMPAIRMENT; CHILDHOOD AB This article reviews recent sociocultural studies of families of children with intellectual disabilities to introduce the range of research conducted from this perspective and to highlight the methodological, conceptual, and theoretical contributions of this approach to the study of mental retardation. Sociocultural studies examine families within their cultural, historical, and sociopolitical contexts. This type of research is comparative across different cultural groups, but is not limited to such comparisons. Sociocultural studies use varied theories and methods, but they share a focus on families' coproduction of meanings and practices related to intellectual disability; families' responses and adaptations to disability; and how their understandings and experiences are shaped within larger social institutions and inequities. Sociocultural approaches take into account community contexts that matter to families with members with mental retardation or developmental delay, and they examine the broader systems that define and position individuals with disabilities and their families. As a whole, these studies provide a more experiential and holistic view of families' beliefs and adaptations within sociopolitical worlds, and offer new tools by which to study the families of children with developmental delays within and across different cultural groups. (c) 2007 Wiley-Liss, Inc. C1 Univ N Carolina, FPG Child Dev Inst, Chapel Hill, NC 27599 USA. Univ Calif Los Angeles, Ctr Culture & Hlth, NPI Semel Inst Neurosci, Dept Psychiat, Los Angeles, CA 90024 USA. RP Skinner, D (reprint author), Univ N Carolina, FPG Child Dev Inst, 105 smith Level Rd, Chapel Hill, NC 27599 USA. EM skinner@tnail.fpg.unc.edu CR Albrecht G. 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S., 2005, DISCOVERING SUCCESSF Weisner T. S., 2005, LEARNING CULTURAL CO, P47 Weisner TS, 1996, MAC FDN MEN, P305 Weisner TS, 2002, HUM DEV, V45, P275, DOI 10.1159/000064989 WEISNER TS, 1991, AM J MENT RETARD, V95, P647 WEISNER TS, 1996, PARENTS CULTURE BELI Weisner TS, 1997, ETHOS, V25, P177, DOI 10.1525/eth.1997.25.2.177 Weiss M, 1997, TRANSCULT PSYCHIATRY, V34, P235, DOI [10.1177/136346159703400204, DOI 10.1177/136346159703400204] Whitmarsh I, 2007, SOC SCI MED, V65, P1082, DOI 10.1016/j.socscimed.2007.04.034 Whyte S. R., 1995, DISABILITY CULTURE, P3 NR 91 TC 21 Z9 21 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1080-4013 J9 MENT RETARD DEV D R JI Ment. Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 4 BP 302 EP 312 DI 10.1002/mrdd.20170 PG 11 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 232GB UT WOS:000251005300003 PM 17979204 ER PT J AU Orsmond, GI Seltzer, MM AF Orsmond, Gael I. Seltzer, Marsha Mailick TI Siblings of individuals withautism spectrum disorders across the life course SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE siblings; lifespan; sibling relationship; well-being ID MENTAL-RETARDATION; BEHAVIORAL-ADJUSTMENT; FAMILY HISTORY; DEVELOPMENTAL-DISABILITIES; RELATIONSHIP QUALITY; ASPERGERS-SYNDROME; EARLY ADOLESCENCE; AUTISM PHENOTYPE; ADULT SIBLINGS; SOCIAL SUPPORT AB In this article, we review the literature on siblings of individuals with autism spectrum disorders (ASD) from a lifespan developmental perspective, from infancy through adulthood, focusing on the sibling relationship and sibling well-being. We situate this review within the larger body of research on siblings of individuals with developmental disabilities (DD) across the lifespan. We then consider the genetic aspects of ASDS and their implications for siblings. We conclude that there is an evidence of atypical social and communication development in some siblings of children with an ASD during infancy. During childhood and adolescence, siblings describe both positive and negative aspects of their sibling relationship and there is some evidence that siblings of children with an ASD may be at heightened risk for social and behavioral adjustment problems. The limited research on adulthood suggests that lack of closeness in the sibling relationship and social and emotional difficulties may continue. We encourage more attention focused on developmental issues, specifically with respect to samples in narrower age groups and in longitudinal research. Finally, we note the variability in sibling outcomes, and suggest further examination of potential moderating and mediating factors, including genetic predispositions. (c) 2007 Wiley-Liss, Inc. C1 Boston Univ, Dept Occupat Therapy & Rehabil Counseling, Boston, MA 02215 USA. Univ Wisconsin, Waisman Ctr, Madison, WI 53706 USA. RP Orsmond, GI (reprint author), Boston Univ, Dept Occupat Therapy & Rehabil Counseling, 635 Commonwealth Ave, Boston, MA 02215 USA. EM gorsmond@bu.edn CR Achenbach TM, 2001, MANUAL ASEBA SCH AGE Akiyama H., 1996, J GERONTOL B-PSYCHOL, V51B, P374 American Psychiatric Association, 2000, DIAGN STAT MAN MENT BAGENHOLM A, 1991, J MENT DEFIC RES, V35, P291 BAILEY A, 1995, PSYCHOL MED, V25, P63 Bauminger N, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P61 Brody GH, 1998, ANNU REV PSYCHOL, V49, P1, DOI 10.1146/annurev.psych.49.1.1 Brody GH, 2004, CURR DIR PSYCHOL SCI, V13, P124, DOI 10.1111/j.0963-7214.2004.00289.x Cicirelli V. 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Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 4 BP 313 EP 320 DI 10.1002/mrdd.20171 PG 8 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 232GB UT WOS:000251005300004 PM 17979200 ER PT J AU Hastings, RP Lloyd, T AF Hastings, Richard P. Lloyd, Tracey TI Expressed emotion in famities of childrien and adutls with intellectual disabrities SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE expressed emotion; criticism; emotional over-involvement; families; intellectual disability; autism ID 5-MINUTE SPEECH SAMPLE; BEHAVIOR PROBLEMS; LEARNING-DISABILITIES; RELATIONSHIP QUALITY; PSYCHIATRIC-ILLNESS; SPECTRUM DISORDERS; PARENTING STRESS; YOUNG-CHILDREN; MOTHERS; FAMILY AB Expressed emotion (EE) is a measure of the affective relationship between two people characterized by criticism, hostility, and emotionally over-involved attitudes. Outside of the field of intellectual disabilities, there has been considerable interest in EE as an environmental marker that explains variance in the severity and/or course of a number of psychiatric disorders. Researchers have also studied EE in parents and found strong associations with children's behavior problems. In this review, we focus on the data from I I published studies of EE in families of children and adults with intellectual disabilities. We conclude that there is evidence for the presence of high EE in some families, and that this alone should concern researchers and clinicians and set an agenda for considerable future rE search effort. We also note a lack of attention to the measurement of EE in intellectual disability. In terms of the existing evidence base, we suggest that there is support for the hypothesis that behavior problems in children and adults with intellectual disabilities may be related to high EE in parents, and a small amount of data predicting over time support the putative causal effect of high EE on maintaining or exacerbating behavior problems. Given that EE is perhaps best conceptualized as the result of an interaction between caregivers and those cared for, there is a need to explore interventions that may help to remediate high EE within families. It is also important to understand from this position that EE may be a normative part of the experience of caring for someone under very stressful circumstances and not something for which families are blamed. Other future research priorities and some implications for practice are also discussed. (c) 2007 Wiley-Liss, Inc. C1 Bangor Univ, Sch Psychol, Bangor LL57 2AS, Gwynedd, Wales. 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Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 4 BP 339 EP 345 DI 10.1002/mrdd.20173 PG 7 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 232GB UT WOS:000251005300007 PM 17979206 ER PT J AU Turnbull, AP Summers, JA Lee, SH Kyzar, K AF Turnbull, Ann P. Summers, Jean Ann Lee, Suk-Hyang Kyzar, Kathleen TI Conceptualization and measurement of family outcomes associated with families of individuals with intiellectual disabilities SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE family well-being; family adaptation; family functioning; family quality of life; parenting capabilities; mental retardation; intellectual disability; autism; developmental disabilities; family support ID QUALITY-OF-LIFE; EARLY INTERVENTION PROGRAMS; DEVELOPMENTAL-DISABILITIES; INTELLECTUAL DISABILITIES; MENTAL-RETARDATION; REARING CHILDREN; EARLY-CHILDHOOD; YOUNG-CHILDREN; MOTHERS; ADAPTATION AB The purpose of this review is to (a) document the current status of conceptualizing and measuring family outcomes related to having a member with an intellectual disability and (b) determine the extent to which family research focuses on internal family characteristics as contrasted to external family support. The reviewers collected 28 articles using the terms well-being, adaptation, family functioning, or family quality of life in the title. Results of our analyses are presented as a comparison between well-being, adaptation, and family functioning articles in one group and family quality of life articles in a second group. Both groups lacked explicit conceptual definitions, theory, and random/representative samples. The articles placed an undue emphasis on maternal participation, and tended to report a single family member score as representative of the whole family. Two major differences between the groups was a tendency for family quality of life studies to be grounded in conceptual frameworks and focus on new instrument development. Recommendations for future research directions are included. (c) 2007 Wiley-Liss, Inc. C1 Univ Kansas, Beach Ctr Disabil, Lawrence, KS 66045 USA. 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E., 2000, EARLY EDUC DEV, V11, P499 Warfield ME, 1999, J DEV BEHAV PEDIATR, V20, P9, DOI 10.1097/00004703-199902000-00002 NR 58 TC 24 Z9 24 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1080-4013 J9 MENT RETARD DEV D R JI Ment. Retard. Dev. Disabil. Res. Rev. PY 2007 VL 13 IS 4 BP 346 EP 356 DI 10.1002/mrdd.20174 PG 11 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 232GB UT WOS:000251005300008 PM 17979209 ER PT J AU Singer, GHS Ethridge, BL Aldana, SI AF Singer, George H. S. Ethridge, Brandy L. Aldana, Sandra I. TI Primary and secondary effects of parenting and stress management interventions for parents of children with developmental disabilities: A meta-analysis SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE rneta-analysis; developmental disability; treatment efficacy; parent training; stress management; evidence-based treatment ID SKILLS TRAINING-PROGRAM; MENTAL-RETARDATION; BEHAVIOR PROBLEMS; INTELLECTUAL DISABILITIES; PRESCHOOL-CHILDREN; AUTISM; DEPRESSION; FAMILIES; MOTHERS; ADJUSTMENT AB A meta-analysis of the group intervention research for parents of children with developmental disabilities was conducted in order to characterize the efficacy of treatments in reducing depressive symptoms and other forms of psychological distress associated with stress in parents of children with developmental disabilities. An extensive search led to the identification of 17 studies which were divided into three categories for comparative purposes: parenting education studies usually based on behavioral parent training, coping skills education studies based primarily on cognitive behavioral training, and studies that combined these methods along with other support services. Studies were rated for the quality of the research designs and of the reports. Consistent positive benefits were found in the form of reductions in parents' distress, and these effects were comparable to those reported in other syntheses of parenting interventions for parents of children without disabilities. The studies were evaluated in order to assess whether or not they met standards for established evidence-based practices. On the basis of the quality and number of the randomized trials, we present evidence to support the claim that there are established evidence-based interventions for reducing psychological distress at least in middle-class mothers in the short term. The interventions for fathers are promising as are the data on somewhat longer-term effects. The need for replications with a more diverse group of parents and longer-term follow-up were discussed. Multiple component interventions addressing both parent well-being and behavioral parent training were significantly more effective than either behavioral parent training or cognitive behavioral training along. (c) 2007 Wiley-Liss, Inc. C1 Univ Calif Santa Barbara, Gevirtz Grad Sch Educ, Dept Educ, Santa Barbara, CA 93106 USA. RP Singer, GHS (reprint author), Univ Calif Santa Barbara, Gevirtz Grad Sch Educ, Dept Educ, Santa Barbara, CA 93106 USA. 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Disabil. Res. Rev. PY 2007 VL 13 IS 4 BP 357 EP 369 DI 10.1002/mrdd.20175 PG 13 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 232GB UT WOS:000251005300009 PM 17979202 ER PT J AU Petek, E Schwarzbraun, T Noor, A Patel, M Nakabayashi, K Choufani, S Windpassinger, C Stamenkovic, M Robertson, MM Aschauer, HN Gurling, HMD Kroisel, PM Wagner, K Scherer, SW Vincent, JB AF Petek, Erwin Schwarzbraun, Thomas Noor, Abdul Patel, Megha Nakabayashi, Kazuhiko Choufani, Sanaa Windpassinger, Christian Stamenkovic, Mara Robertson, Mary M. Aschauer, Harald N. Gurling, Hugh M. D. Kroisel, Peter M. Wagner, Klaus Scherer, Stephen W. Vincent, John B. TI Molecular and genomic studies of IMMP2L and mutation screening in autism and Tourette syndrome SO MOLECULAR GENETICS AND GENOMICS LA English DT Article DE autism; Tourette; chromosome 7; inner mitochondrial peptidase 2-like ID MITOCHONDRIAL INNER MEMBRANE; NUCLEOTIDE; ASSOCIATION; PROTEASE; 7Q31; BREAKPOINT; COMPLEX; REGION; ARRAYS AB We recently reported the disruption of the inner mitochondrial membrane peptidase 2-like (IMMP2L) gene by a chromosomal breakpoint in a patient with Gilles de la Tourette syndrome (GTS). In the present study we sought to identify genetic variation in IMMP2L, which, through alteration of protein function or level of expression might contribute to the manifestation of GTS. We screened 39 GTS patients, and, due to the localization of IMMP2L in the critical region for the autistic disorder (AD) locus on chromosome 7q (AUTS1), 95 multiplex AD families; however, no coding mutations were found in either GTS or AD patients. In addition, no parental-specific expression of IMMP2L was detected in somatic cell hybrids containing human chromosome 7 and human cell lines carrying a maternal uniparental disomy for chromosome 7 (mUPD7). Despite the fact that no deleterious mutations in IMMPL2 (other than the inverted duplication identified previously) were identified in either GTS or AD, this gene cannot be excluded as a possible rare cause of either disorder. C1 Ctr Addict & Mental Hlth, Neurogenet Sect, Toronto, ON M5T 1R8, Canada. Med Univ Graz, Inst Med Biol & Human Genet, A-8010 Graz, Austria. Univ Toronto, Hosp Sick Children, Program Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Univ Vienna, Hosp Psychiat, Dept Gen Psychiat, Vienna, Austria. UCL Royal Free & UCL Med Sch, Windeyer Inst Med Sci, Dept Psychiat & Behav Sci, Mol Psychiat Lab, London, England. RP Vincent, JB (reprint author), Ctr Addict & Mental Hlth, Neurogenet Sect, 250 Coll St, Toronto, ON M5T 1R8, Canada. 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Lee, Jee Eun Lazar, Mariana Boudos, Rebecca DuBray, Molly B. Oakes, Terrence R. Miller, Judith N. Lu, Jeffrey Jeong, Eun-Kee McMahon, William M. Bigler, Erin D. Lainhart, Janet E. TI Diffusion tensor imaging of the corpus callosum in Autism SO NEUROIMAGE LA English DT Article DE Autism; diffusion tensor imaging; corpus callosum; radial diffusivity; performance IQ ID HIGH-FUNCTIONING AUTISM; WHITE-MATTER; MAGNETIC-RESONANCE; WORKING-MEMORY; QUANTITATIVE INTERPRETATION; CSF-SUPPRESSION; RESPONSE-TIME; HUMAN BRAIN; MRI; ANISOTROPY AB The corpus callosum is the largest commissural white matter pathway that connects the hemispheres of the human brain. In this study, diffusion tensor imaging (DTI) was performed on subject groups with high-functioning autism and controls matched for age, handedness, IQ, and head size. DTI and volumetric measurements of the total corpus callosum and subregions (genu, body and splenium) were made and compared between groups. The results showed that there were significant differences in volume, fractional anisotropy, mean diffusivity, and radial diffusivity between groups. These group differences appeared to be driven by a subgroup of the autism group that had small corpus callosum volumes, high mean diffusivity, low anisotropy, and increased radial diffusivity. This subgroup had significantly lower performance IQ measures than either the other individuals with autism or the control subjects. Measurements of radial diffusivity also appeared to be correlated with processing speed measured during the performance IQ tests. The subgroup of autism subjects with high mean diffusivity and low fractional anisotropy appeared to cluster with the highest radial diffusivities and slowest processing speeds. These results suggest that the microstructure of the corpus callosum is affected in autism, which may be related to nonverbal cognitive performance. (c) 2006 Elsevier Inc. All rights reserved. C1 Waisman Ctr Mental Retardat & Human Dev, Waisman Lab Brain Imaging & Behav, Madison, WI 53705 USA. Univ Wisconsin, Dept Med Phys, Madison, WI 53706 USA. Univ Wisconsin, Dept Psychiat, Madison, WI 53706 USA. Dept Psychiat, Salt Lake City, UT USA. Dept Radiol, Salt Lake City, UT USA. Dept Anesthesiol, Salt Lake City, UT USA. Dept Neurosci Program, Salt Lake City, UT USA. Univ Utah, Brain Inst, Salt Lake City, UT USA. Utah Ctr Adv Imaging Res, Salt Lake City, UT USA. Brigham Young Univ, Dept Psychol, Provo, UT 84602 USA. RP Alexander, AL (reprint author), Waisman Ctr Mental Retardat & Human Dev, Waisman Lab Brain Imaging & Behav, 1500 Highland Ave, Madison, WI 53705 USA. 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Bonanni, L. Onofrj, M. TI Symptomatic REM sleep behaviour disorder SO NEUROLOGICAL SCIENCES LA English DT Article; Proceedings Paper CT Meeting on Dopamine - Sleep, Wakefulness and Movements CY MAY 06, 2006 CL Milan, ITALY DE symptomatic REM sleep behaviour disorder; neurodegenerative disorders; synucleinopathy; tauopathy; drug-induced RBD; therapy ID EYE-MOVEMENT SLEEP; MACHADO-JOSEPH-DISEASE; MULTIPLE SYSTEM ATROPHY; GUILLAIN-BARRE-SYNDROME; LEWY BODY DEMENTIA; PROGRESSIVE SUPRANUCLEAR PALSY; POSTTRAUMATIC-STRESS-DISORDER; OBSESSIVE-COMPULSIVE DISORDER; PURE AUTONOMIC FAILURE; PARKINSONS-DISEASE AB Rapid eye movement (REM) sleep behaviour disorder (RBD) precedes or accompanies many neurodegenerative disorders. In synucleinopathies, including dementia with Lewy bodies, Parkinson's disease and multiple system atrophy, the prevalence of RBD varies from 19% to almost 77% in different reports. 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Sci. PD JAN PY 2007 VL 28 SU 1 BP S21 EP S36 DI 10.1007/s10072-007-0735-y PG 16 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 123XS UT WOS:000243331000005 PM 17235429 ER PT J AU Dogangun, B Guzeltas, A Emul, M Demir, T Karacetin, G Oztunc, F Kayaalp, L AF Dogangun, Burak Guzeltas, Alper Emul, Murat Demir, Tevfik Karacetin, Gul Oztunc, Funda Kayaalp, Levent TI Assessment of P wave dispersion in children treated with risperidone SO NEUROLOGY PSYCHIATRY AND BRAIN RESEARCH LA English DT Article DE risperidone; child psychiatry; ECG; p wave dispersion ID PAROXYSMAL ATRIAL-FIBRILLATION; YOUNG-CHILDREN; QTC; DISORDER; INTERVAL; AUTISM AB Objective: Risperidone, which is an atypical antipsychotic, is widely used in treating children and adolescents with many psychiatric disorders. Despite widespread clinical use, the safety of risperidone is a matter of concern for child psychiatrists. The aim of this study is to explore the supraventricular cardiac effects of risperidone. Methods: 34 patients who were diagnosed as mental retardation, attention deficit hyperactivity disorder or pervasive developmental disorder according to the DSM-IV criteria were included in this study. Risperidone treatment was initiated for the behavioral problems. Baseline biochemical parameters were assessed. The ECG records were obtained while patients were drug naive and two weeks after 0.25-1.0 mg/day risperidone intake. Measurement of P wave duration was carried out manually using a caliper. The difference between the P maximum (P-max) and P minimum (P-min) wave duration was calculated from the 12-lead ECG and was defined as the PWD. The data was analyzed using SPSS for Windows version 13.0. Results: Of 34 patients, aged 4-14 years, 6 were female and 28 were male. The weight of the patients was between 12-42 kg. The received dose of risperidone was between 0.25-1 mg/day. After treatment with risperidone for two weeks, ECGs of patients were compared with baseline ECGs. The differences between baseline and after risperidone therapy among PWD, P-max, P-min were statistically insignificant (p>0.05). The ECG variables in patients and healthy group were compared. In addition, there were no significant correlations between age, weight, received dose of risperidone and ECG variables in both patients and controls (p>0.05). Conclusion: Our study shows that risperidone may not influence atrial myocardial conduction in children with various psychiatric disorders at least in doses between 0.25-1.0 mg/day. Although the clinical importance of P wave measurements is unclear, our study is important that is investigating the influences of risperidone on atrial conduction. Further studies with larger sample size and higher doses of risperidone or comparing other atypical antipsychotic drugs with risperidone would be more explanatory. C1 [Dogangun, Burak; Karacetin, Gul; Kayaalp, Levent] Istanbul Univ, Cerrahpasa Med Fac, Dept Child & Adolscent Psychiat, TR-34098 Istanbul, Turkey. [Guzeltas, Alper; Oztunc, Funda] Istanbul Univ, Cerrahpasa Med Fac, Dept Pediat Cardiol, TR-34098 Istanbul, Turkey. [Emul, Murat; Demir, Tevfik] Afyon Kocatepe Univ, Fac Med, Dept Psychiat & Pediat, Afyon, Turkey. RP Dogangun, B (reprint author), Istanbul Univ, Cerrahpasa Med Fac, Dept Child & Adolscent Psychiat, TR-34098 Istanbul, Turkey. 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Adolphs, Ralph Hurley, Robert S. E. Piven, Joseph TI Analysis of face gaze in autism using "Bubbles" SO NEUROPSYCHOLOGIA LA English DT Article DE social cognition; emotion; autism; HFA; eyetracking; facial information ID FACIAL EXPRESSIONS; SOCIAL-BEHAVIOR; PSYCHOPHYSICS TOOLBOX; NORMAL-CHILDREN; EYE-MOVEMENT; RECOGNITION; FIXATION; DISORDER; INDIVIDUALS; INFORMATION AB One of the components of abnormal social functioning in autism is an impaired ability to direct eye gaze onto other people's faces in social situations. Here, we investigated the relationship between gaze onto the eye and mouth regions of faces, and the visual information that was present within those regions. We used the "Bubbles" method to vary the facial information available on any given trial by revealing only small parts of the face, and measured the eye movements made as participants viewed these stimuli. Compared to ten TQ- and age-matched healthy controls, eight participants with autism showed less fixation specificity to the eyes and mouth, a greater tendency to saccade away from the eyes when information was present in those regions, and abnormal directionality of saccades. The findings provide novel detail to the abnormal way in which people with autism look at faces, an impairment that likely influences all subsequent face processing. (c) 2006 Elsevier Ltd. All rights reserved. C1 CALTECH, Div Humanities & Social Sci, Pasadena, CA 91125 USA. Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. RP Spezio, ML (reprint author), CALTECH, Div Humanities & Social Sci, HSS 228-77, Pasadena, CA 91125 USA. 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To evaluate these alternatives, we adopted a fine-grained analysis of facial expression processing in autism. Specifically, we used the 'facial expression megamix' paradigm [Young, A. W., Rowland, D., Calder, A. J, Etcoff, N. L., Seth, A., & Perrett, D. I. (1997). Facial expression megamix: Tests of dimensional and category accounts of emotion recognition Cognition and Emotion, 14, 39-60] in which adults with autism and a typically developing comparison group performed a six alternative forced-choice response to morphs of all possible combinations of the six basic expressions identified by Ekman [Ekman, P. (1972). Universals and cultural differences in facial expressions of emotion. In J. K. Cole (Ed.), Nebraska symposium on motivation: vol. 1971, (pp. 207-283). Lincoln, Nebraska: University of Nebraska Press] (happiness, sadness, disgust, anger, fear and surprise). Clear differences were evident between the two groups, most obviously in the recognition of fear, but also in the recognition of disgust and happiness. A second experiment demonstrated that individuals with autism are able to discriminate between different emotional images and suggests that low-level perceptual difficulties do not underlie the difficulties with emotion recognition. (c) 2006 Elsevier Ltd. All rights reserved. C1 Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Psychiat & Neurol, Pittsburgh, PA USA. RP Humphreys, K (reprint author), Carnegie Mellon Univ, Dept Psychol, Baker Hall,5000 Forbes Ave, Pittsburgh, PA 15213 USA. 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Three different encoding strategies were provided in order to vary the level of consciousness involved in verbal information processing. A shallow (alphabetic), a deep (semantic) and a very deep (contextual) encoding instruction related to visual word presentation were given to all study participants. After the encoding of pronoun-noun pairs, recognition performances of nouns only were tested. The number of correctly recognized nouns previously associated with "sein" was significantly lower than the number of correctly recognized nouns previously associated with "ein" in the shallow encoding condition. The same trend was found for "mein" associated nouns which were also less accurately recognized compared to "ein" associated nouns. Magnetic field distributions recorded during the encoding phases revealed two significant effects, one between about 200 and 400 ms after stimulus onset and the other between about 500 and 800 ms. The earlier effect was found over occipito-parietal sensors, whereas the later effect occurred over left frontal sensors. Within both time ranges, brain activation varied significantly as a function of associated pronoun independent of depth of word processing. In the respective areas of both time ranges, conditions including personal pronouns ("mein" and "sein") showed higher magnetic field components compared to the control condition of no personal pronouns ("ein"). Evidence is shown that early stage processing is able to distinguish between no personal and personal information, whereas later stage processing is able to distinguish between information related to oneself and to another person (self and non-self). Along with other previous reports our MEG findings support the notion that particular human brain functions involved in processing neurophysiological correlates of self and non-self can be identified. (c) 2006 Elsevier Ltd. All rights reserved. C1 Med Univ Vienna, ENT Clin, Dept Clin Neurol, Ludwig Boltzmann Inst Funct Brain Topog, A-1090 Vienna, Austria. Med Univ Vienna, ENT, Complex Syst Res Grp, A-1090 Vienna, Austria. Univ Vienna, Fac Psychol, Biol Psychol Unit, A-1010 Vienna, Austria. Appl Neurosci Inst, A-1150 Vienna, Austria. RP Walla, P (reprint author), Med Univ Vienna, ENT Clin, Dept Clin Neurol, Ludwig Boltzmann Inst Funct Brain Topog, Waehringer Guertel 18-20, A-1090 Vienna, Austria. 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TI Integrity of lateral and feedbackward connections in visual processing in children with pervasive developmental disorder SO NEUROPSYCHOLOGIA LA English DT Article DE pervasive developmental disorders; autistic disorder; event-related potentials; visual integration ID FIGURE-GROUND SEGREGATION; TEXTURE SEGREGATION; ASPERGER-SYNDROME; AUTISM; MOTION; CORTEX; INDIVIDUALS; PERCEPTION; RECOGNITION; FEEDFORWARD AB Enhanced visual detail processing in subjects with pervasive developmental disorder (PDD) has been related to impairments in feature integration. The functional integrity of two types of neuronal connections involved in visual feature integration, namely horizontal and feedbackward connections, were tested. Sixteen children with PDD and 17 age- and IQ-matched control children (mean age 13.3 years) were included. In a texture segregation task the difference in ERP response to homogeneous and checkered visual stimuli was determined. Additionally, in a contour integration task subjects had to point out a contour consisting of colinearly aligned Gabor signals in backgrounds increasing in noise. Children with PDD showed a normal performance on the contour integration task, suggesting that neurons in the primary visual cortex of children with PDD can effectively integrate the activity of local detectors that process different aspects of the same object information by making use of long-range lateral connections. The amplitude of ERP activity related to texture segregation was also not different between the PDD and control groups, indicating functional visual feedback mechanisms between V I and higher order areas in subjects with PDD. However, a difference in latency of texture-segmentation related activity between the groups was noted. This effect did not reach significance, which could be due to the small N of the study. Therefore, the data need replication in a study with larger samples before more definitive conclusions can be drawn. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, NL-3514 CX Utrecht, Netherlands. Rudolf Magnus Inst Neurosci, NL-3508 TA Utrecht, Netherlands. Maastricht Univ, Fac Psychol, Dept Neurocognit, Maastricht, Netherlands. Univ Amsterdam, Dept Psychol, Amsterdam, Netherlands. Netherlands Ophthalm Res Inst, NL-1100 AC Amsterdam, Netherlands. Budapest Univ Technol & Econ, Fac Econ & Social Sci, Dept Cognit Sci, Budapest, Hungary. RP Kemner, C (reprint author), Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, B01-324,Heidelberglaan 100, NL-3514 CX Utrecht, Netherlands. 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We compared emotion recognition ability using a novel test involving computerised animations, and a more conventional emotion recognition test using facial expressions. Adults with autism and normal controls, matched for age and verbal IQ, participated in two experiments. First, participants viewed a series of short (5s) animations. These featured an 'emotional' triangle, interacting with a circle. They were designed to evoke an attribution of emotion to the triangle, which was rated both in terms of anger, happiness, sadness or fear from its pattern of movement, and how animate ("living") it appeared to be. Second, emotion recognition was tested from standardised photographs of facial expressions. In both experiments, adults with autism were significantly impaired relative to comparisons in their perception of sadness. This is the first demonstration that, in autism, individuals can have difficulties both in the interpretation of facial expressions and in the recognition of equivalent emotions based on the movement of abstract stimuli. Poor performance in the animations task was significantly correlated with the degree of impairment in reciprocal social interaction, assessed by the Autism Diagnostic Observation Schedule. Our findings point to a deficit in emotion recognition in autism, extending beyond the recognition of facial expressions, which is associated with a functional impairment in social interaction skills. Our results are discussed in the context of the results of neuroimaging studies that have used animated stimuli and images of faces. (c) 2006 Elsevier Ltd. All rights reserved. C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. UCL, Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 3AR, England. RP Blakemore, SJ (reprint author), UCL, Inst Cognit Neurosci, London WC1N 3AR, England. 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Kleinhans, Natalia M. Haist, Frank Akshoomoff, Natacha Campbell, Ashley Courchesne, Eric Mueller, Ralph-Axel TI A typical participation of visual cortex during word processing in autism: An fMRI study of semantic decision SO NEUROPSYCHOLOGIA LA English DT Article DE autism; language delay; functional MRI; lexical; semantic categorization; visual perception ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; LANGUAGE-ASSOCIATION CORTEX; LONG-TERM-MEMORY; JOINT ATTENTION; SENTENCE COMPREHENSION; MAGNETIC-RESONANCE; MENTAL-IMAGERY; LEXICAL RETRIEVAL; EPISODIC MEMORY AB Language delay and impairment are salient features of autism. More specifically, there is evidence of atypical semantic organization in autism, but the functional brain correlates are not well understood. The current study used functional MRI to examine activation associated with semantic category decision. Ten high-functioning men with autism spectrum disorder and 10 healthy control subjects matched for gender, handedness, age, and nonverbal IQ were studied. Participants indicated via button press response whether visually presented words belonged to a target category (tools, colors, feelings). The control condition required target letter detection in unpronounceable letter strings. Significant activation for semantic decision in the left inferior frontal gyrus (Brodmann areas 44 and 45) was found in the control group. Corresponding activation in the autism group was more limited, with smaller clusters in left inferior frontal areas 45 and 47. Autistic participants, however, showed significantly greater activation compared to controls in extrastriate visual cortex bilaterally (areas 18 and 19), which correlated with greater number of errors on the semantic task. Our findings suggest an important role of perceptual components (possibly visual imagery) during semantic decision, consistent with previous evidence of atypical lexicosemantic performance in autism. In the context of similar findings from younger typically developing children, our results suggest an immature pattern associated with inefficient processing, presumably due to atypical experiential embedding of word acquisition in autism. (c) 2007 Elsevier Ltd. All rights reserved. C1 San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, San Diego, CA 92120 USA. Univ Wisconsin, Dept Psychol, Milwaukee, WI 53211 USA. San Diego State Univ, Joint Doctoral Program Clin Psychol, San Diego, CA 92182 USA. Univ Calif San Diego, San Diego, CA 92103 USA. Univ Washington, Dept Radiol, Seattle, WA 98195 USA. Univ Calif San Diego, Dept Psychiat, 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. 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cingulated cortex ID MEDIAL-FRONTAL-CORTEX; ANTERIOR CINGULATE CORTEX; EVENT-RELATED FMRI; EXECUTIVE DYSFUNCTION; ASPERGER-SYNDROME; STROOP TASK; PERFORMANCE; DISORDER; SPECTRUM; SYSTEM AB Deficits in executive function (EF), i.e. function of the prefrontal cortex, may be central in the etiology of autism. One of the various aspects of EF is error detection and adjusting behavior after an error. In cognitive tests, adults normally slow down their responding on the next trial after making an error, a compensatory mechanism geared toward improving performance on subsequent trials, and a faculty critically associated with activity in the anterior cingulate cortex (ACC). The current study evaluated post-error slowing in people with high functioning autism (HFA) (n = 36), taking symptom severity into account, compared to the performance of a normal control group (n = 32). Symptom severity in the HFA group was defined in terms of level of adaptation: living independently (outpatients; n = 12) and living residentially (inpatients; n = 24). Half the group of inpatients was on medication; the results of their performance were analyzed separately. A computerized version of a memory search task was used with two response probability conditions. The subjects in the control group adjusted their reaction time (RT) substantially after an error, while the group of participants with HFA appeared to be overall slow, with no significant adjustment of RT after an error. This finding remained significant if the medication factor was taken into account, and was independent of the degree of severity of the autistic disorder, as defined by the dichotomy 'inpatient versus outpatient'. Possible causes and implications of the finding are discussed. (c) 2007 Elsevier Ltd. All rights reserved. C1 GGZ Midden Overijssel, Dept Child & Adolescent Psychiat, NL-7400 GC Deventer, Netherlands. Univ Groningen, Lab Expt Clin Psychol, Groningen, Netherlands. Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, Utrecht, Netherlands. RP Bogte, H (reprint author), GGZ Midden Overijssel, Dept Child & Adolescent Psychiat, POB 5003, NL-7400 GC Deventer, Netherlands. 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Brindley, Rachel M. Frith, Uta TI Imitation and action understanding in autistic spectrum disorders: How valid is the hypothesis of a deficit in the mirror neuron system? SO NEUROPSYCHOLOGIA LA English DT Article DE autism; imitation; mirror neuron system; goal; action; social cognition ID CHILDREN; MOTOR; GESTURES; MIND; RECOGNITION; EMPATHY; HUMANS; OBJECT; OTHERS; REPRESENTATIONS AB The motor mirror neuron system supports imitation and goal understanding in typical adults. Recently, it has been proposed that a deficit in this mirror neuron system might contribute to poor imitation performance in children with autistic spectrum disorders (ASD) and might be a cause of poor social abilities in these children. We aimed to test this hypothesis by examining the performance of 25 children with ASD and 31 typical children of the same verbal mental age on four action representation tasks and a theory of mind battery. Both typical and autistic children had the same tendency to imitate an adult's goals, to imitate in a mirror fashion and to imitate grasps in a motor planning task. Children with ASD showed superior performance on a gesture recognition task. These imitation and gesture recognition tasks all rely on the mirror neuron system in typical adults, but performance was not impaired in children with ASD. In contrast, the ASD group were impaired on the theory of mind tasks. These results provide clear evidence against a general imitation impairment and a global mirror neuron system deficit in children with autism. We suggest this data can best be understood in terms of multiple brain systems for different types of imitation and action understanding, and that the ability to understand and imitate the goals of hand actions is intact in children with ASD. (c) 2006 Elsevier Ltd. All rights reserved. C1 Dartmouth Coll, Dept Psychol & Brain Sci, Hanover, NH 03755 USA. UCL, Inst Cognit Neurosci, London, England. RP Hamilton, AFD (reprint author), Dartmouth Coll, Dept Psychol & Brain Sci, Hanover, NH 03755 USA. 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Bowler, Dermot M. TI Differential fear conditioning in Asperger's syndrome: Implications for an amygdala theory of autism SO NEUROPSYCHOLOGIA LA English DT Article DE autism spectrum disorder; cortico-amygdala connectivity; emotional processes; psychophysiological reactivity ID HIGH-FUNCTIONING AUTISM; SKIN-CONDUCTANCE RESPONSES; MEDIAL PREFRONTAL CORTEX; CHILDS APPRAISAL; NEURAL RESPONSES; BRAIN; EMOTION; EXTINCTION; FMRI; EXPRESSIONS AB Since the first descriptions of individuals with autism spectrum disorders (ASD), abnormalities in socio-emotional behaviours have been described as amongst the most characteristic clinical features of this condition. Current evidence in this area suggests that individuals with ASD experience difficulties in the perception and expression of emotions within the social domain. The causes for these emotional difficulties are, however, still poorly understood. At the developmental level, it is unclear whether emotional disturbances constitute a primary feature of the clinical presentation of ASD or whether they are secondary to abnormalities in other areas of cognition. At the neurobiological level, it is still debated to what extent abnormalities of the limbic system, in particular the amygdala, may be responsible for the emotional disturbances characterising ASD. Here we show that a group of individuals with Asperger's syndrome exhibit a pattern of abnormality in differentially acquiring fear, which suggests that their fear responses are atypically modulated by conditioned and non-conditioned stimuli. On the basis of these results and the existing literature we suggest that ASD may be characterised by atypicalities in the integration of physiological and cognitive aspects of emotional experiences which we argue arise because of poor connectivity between the amygdala and functionally associated cortical areas. (c) 2007 Elsevier Ltd. 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Robertson, Ian H. Kelly, Simon P. Silk, Timothy J. Barry, Edwina Daibhis, Aoife Watchorn, Amy Keavey, Michelle Fitzgerald, Michael Gallagher, Louise Gill, Michael Bellgrove, Mark A. TI Dissociation in performance of children with ADHD and high-functioning autism on a task of sustained attention SO NEUROPSYCHOLOGIA LA English DT Review DE response time; fast Fourier transform; variability; arousal; response inhibition; executive function ID DEFICIT-HYPERACTIVITY-DISORDER; POSITRON-EMISSION-TOMOGRAPHY; ANTERIOR CINGULATE CORTEX; DEFICIT/HYPERACTIVITY DISORDER; SPECTRUM DISORDERS; EXECUTIVE FUNCTION; RESPONSE VARIABILITY; INTRAINDIVIDUAL VARIABILITY; DIAGNOSTIC INTERVIEW; DOPAMINE-TRANSPORTER AB Attention deficit hyperactivity disorder (ADHD) and autism are two neurodevelopmental disorders associated with prominent executive dysfunction, which may be underpinned by disruption within fronto-striatal and fronto-parietal circuits. We probed executive function in these disorders using a sustained attention task with a validated brain-behaviour basis. Twenty-three children with ADHD, 21 children with high-functioning autism (HFA) and 18 control children were tested on the Sustained Attention to Response Task (SART). In a fixed sequence version of the task, children were required to withhold their response to a predictably occurring no-go target (3) in a 1-9 digit sequence; in the random version the sequence was unpredictable. The ADHD group showed clear deficits in response inhibition and sustained attention, through higher errors of commission and omission on both SART versions. The HFA group showed no sustained attention deficits, through a normal number of omission errors on both SART versions. The HFA group showed dissociation in response inhibition performance, as indexed by commission errors. On the Fixed SART, a normal number of errors was made, however when the stimuli were randomised, the HFA group made as many commission errors as the ADHD group. Greater slow-frequency variability in response time and a slowing in mean response time by the ADHD group suggested impaired arousal processes. The ADHD group showed greater fast-frequency variability in response time, indicative of impaired top-down control, relative to the HFA and control groups. These data imply involvement of fronto-parietal attentional networks and sub-cortical arousal systems in the pathology of ADHD and prefromal cortex dysfunction in children with HFA. (c) 2007 Elsevier Ltd. All rights reserved. C1 Univ Dublin Trinity Coll, Sch Psychol, Dublin 2, Ireland. Univ Dublin Trinity Coll, Trinity Coll Inst Neurosci, Dublin 2, Ireland. Univ Dublin Trinity Coll, Sch Med & Hlth Sci, Dublin 2, Ireland. Nathan S Kline Inst Psychiat Res, Cognit Neurophysiol Lab, Orangeburg, NY 10962 USA. Univ Melbourne, Howard Florey Inst Expt Physiol & Med, Parkville, Vic 3052, Australia. Univ Melbourne, Ctr Neurosci, Parkville, Vic 3052, Australia. Univ Melbourne, Dept Pediat, Acad Child Psychiat Unit, Parkville, Vic 3052, Australia. Monash Univ, Dept Psychol, Clayton, Vic 3168, Australia. Univ Queensland, Sch Psychol, Cognit Neurosci Lab, Brisbane, Qld 4067, Australia. Univ Queensland, Queensland Brain Inst, Brisbane, Qld 4067, Australia. RP Johnson, KA (reprint author), Univ Dublin Trinity Coll, Sch Psychol, Dublin 2, Ireland. 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Penn, David L. Adolphs, Ralph Piven, Joseph TI Orienting to social stimuli differentiates social cognitive impairment in autism and schizophrenia SO NEUROPSYCHOLOGIA LA English DT Article DE autism; schizophrenia; eyetracking; social cognition; emotion; perception ID FUSIFORM FACE AREA; ASPERGER-SYNDROME; FACIAL EXPRESSIONS; EMOTION RECOGNITION; AMYGDALA DAMAGE; FUNCTIONAL MRI; MIND ABILITIES; NORMAL ADULTS; BRAIN; INDIVIDUALS AB Both autism and schizophrenia feature deficits in aspects of social cognition that may be related to amygdala, dysfunction, but it is unclear whether these are similar or different patterns of impairment. We compared the visual scanning patterns and emotion judgments of individuals with autism, individuals with schizophrenia and controls on a task well characterized with respect to amygdala functioning. On this task, eye movements of participants are recorded as they assess emotional content within a series of complex social scenes where faces are either included or digitally erased. Results indicated marked abnormalities in visual scanning for both disorders. Controls increased their gaze on face regions when faces were present to a significantly greater degree than both the autism or schizophrenia groups. While the control and the schizophrenia groups oriented to face regions faster when faces were present compared to when they were absent, the autism group oriented at the same rate in both conditions. The schizophrenia group, meanwhile, exhibited a delay in orienting to face regions across both conditions, although whether antipsychotic medication contributed to this effect is unclear. These findings suggest that while processing emotional information in social scenes, both individuals with autism and individuals with schizophrenia fixate faces less than controls, although only those with autism fail to orient to faces more rapidly based on the presence of facial information. Autism and schizophrenia may therefore share an abnormality in utilizing facial information for assessing emotional content in social scenes, but differ in the ability to seek out socially relevant cues from complex stimuli. Impairments in social orienting are discussed within the context of evidence suggesting the role of the amygdala in orienting to emotionally meaningful information. (c) 2007 Elsevier Ltd. All rights reserved. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. CALTECH, Div Humanities & Social Sci, Pasadena, CA 91125 USA. Univ N Carolina, Dept Psychol, Chapel Hill, NC 27515 USA. RP Sasson, N (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, CB 3367, Chapel Hill, NC 27599 USA. 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Kleinhans, Natalia M. Haist, Frank Akshoomoff, Natacha Campbell, Ashley Courchesne, Eric Mueller, Ralph-Axel TI Atypical participation of visual cortex during word processing in autism: An fMRI study of semantic decision (vol 45, pg 1672, 2007) SO NEUROPSYCHOLOGIA LA English DT Correction C1 San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, San Diego, CA 92120 USA. Univ Wisconsin, Dept Psychol, Milwaukee, WI 53211 USA. San Diego State Univ, Joint Doctoral Program Clin Psychol, San Diego, CA USA. Univ Calif San Diego, San Diego, CA USA. Univ Washington, Dept Radiol, Seattle, WA 98195 USA. Univ Calif San Diego, Dept Psychiat, San Diego, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, San Diego, CA 92093 USA. Univ Calif San Diego, Dept Cognit Sci, San Diego, CA 92093 USA. RP Muller, RA (reprint author), San Diego State Univ, Dept Psychol, Brain Dev Imaging Lab, San Diego, CA 92120 USA. EM amueller@sciences.sdsu.edu RI Haist, Frank/C-3177-2013 OI Haist, Frank/0000-0002-7254-6083 CR Gaffrey MS, 2007, NEUROPSYCHOLOGIA, V45, P1672, DOI 10.1016/j.neuropsychologia.2007.01.008 NR 1 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PY 2007 VL 45 IS 11 BP 2644 EP 2644 DI 10.1016/j.neuropsychologia.2007.04.014 PG 1 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 187RL UT WOS:000247865800027 ER PT J AU Shamay-Tsoory, SG Aharon-Peretz, J AF Shamay-Tsoory, Simone G. Aharon-Peretz, Judith TI Dissociable prefrontal networks for cognitive and affective theory of mind: A lesion study SO NEUROPSYCHOLOGIA LA English DT Article DE affective processing; theory of mind; ventromedial prefrontal cortex ID FRONTAL-LOBE; PERSPECTIVE-TAKING; ASPERGER-SYNDROME; EMPATHY DEFICITS; AUTISM; BRAIN; DAMAGE; SELF; REPRESENTATION; COMPREHENSION AB The underlying mechanisms and neuroanatomical correlates of theory of mind (ToM), the ability to make inferences on others' mental states, remain largely unknown. While numerous studies have implicated the ventromedial (VM) frontal lobes in ToM, recent findings have questioned the role of the prefrontal cortex. We designed two novel tasks that examined the hypothesis that affective ToM processing is distinct from that related to cognitive ToM and depends in part on separate anatomical substrates. The performance of patients with localized lesions in the VM was compared to responses of patients with dorsolateral lesions, mixed prefrontal lesions, and posterior lesions and with healthy control subjects. While controls made fewer errors on affective as compared to cognitive ToM conditions in both tasks, patients with VM damage showed a different trend. Furthermore, while affective ToM was mostly impaired by VM damage, cognitive ToM was mostly impaired by extensive prefrontal damage, suggesting that cognitive and affective mentalizing abilities are partly dissociable. By introducing the concept of 'affective ToM' to the study of social cognition, these results offer new insights into the mediating role of the VM in the affective facets of social behavior that may underlie the behavioral disturbances observed in these patients. (C) 2007 Elsevier Ltd. All rights reserved. C1 Univ Haifa, Dept Psychol, IL-31905 Haifa, Israel. Univ Haifa, Brain & Behav Ctr, IL-31905 Haifa, Israel. 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V. Kemner, C. de Haan, E. H. Coppens, J. E. van den Berg, T. J. T. P. van Engeland, H. TI Visual information processing in high-functioning individuals with autism spectrum disorders and their parents SO NEUROPSYCHOLOGY LA English DT Article DE autism spectrum disorders; contrast sensitivity; motion perception; parents; visual ID DIAGNOSTIC OBSERVATION SCHEDULE; WEAK CENTRAL COHERENCE; MOTION PERCEPTION; ENHANCED DISCRIMINATION; COGNITIVE PHENOTYPE; ASPERGER-SYNDROME; INFANTILE-AUTISM; 2ND-ORDER MOTION; FAMILY HISTORY; CHILDREN AB The authors assessed visual information processing in high-functioning individuals with pervasive developmental disorders (PDD) and their parents. The authors used tasks for contrast sensitivity, motion, and form perception to test visual processing occurring relatively early and late in the magnocellular-dorsal and parvocellular-ventral pathways. No deficits were found in contrast sensitivity for low or high spatial frequencies or for motion or form perception between individuals with PDD in comparison with a matched control group. Individuals with PDD performed equally with or better than controls on motion detection tasks. In addition, the authors did not find differences on any of the tasks between parents of the PDD group and matched control parents. These results indicate that high-functioning individuals with PDD and their parents are able to process visual stimuli that rely on early or late processing in the magnocellular-dorsal and parvocellular-ventral pathways as well as controls. C1 Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, NL-3508 GA Utrecht, Netherlands. Maastricht Univ, Maastricht, Netherlands. Univ Utrecht, Helmholtz Res Inst, Psychol Lab, NL-3508 TC Utrecht, Netherlands. Roayl Netherlands Acad Arts & Sci, Netherlands Ophthalm Res Inst, Amsterdam, Netherlands. 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Dissanayake, Cheryl Clifford, Sally Gould, Emma Bulhak-Paterson, Danuta Tassone, Flora Taylor, Annette K. Hessl, David Hagerman, Randi Huggins, Richard M. TI Molecular and cognitive predictors of the continuum of autistic behaviours in fragile X SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE fragile X; autism spectrum; ADOS-G; cognitive impairments; FMRP; predictors of autism behaviours ID MENTAL-RETARDATION PROTEIN; PERVASIVE DEVELOPMENTAL DISORDERS; ROBUST PEDIGREE ANALYSIS; POSTERIOR-FOSSA; TUBEROUS SCLEROSIS; CLINICAL-FEATURES; SPECTRUM DISORDER; WILLIAMS-SYNDROME; STATUS CATEGORIES; ASPERGER-SYNDROME AB The distributions of scores for autistic behaviours obtained from the Autism Diagnostic Observation Scale-Generic (ADOS-G) were investigated in 147 males and females affected with the full mutation in the fragile X mental retardation 1 (FMR1) gene, in 59 individuals with the premutation, and in 42 non-fragile X relatives, aged 4 70 years. The scores representing communication and social interaction were continuously distributed across the two fragile X groups, and they were significantly elevated compared with the non-fragile X controls. Strong relationships were found between both these scores and FMRP deficits, but they became insignificant for social interaction, and the sum of social interaction and communication scores, when FSIQ was included as another predictor of autism scores. Other significant predictors of these scores in both sexes were those executive skills which related to verbal fluency, and to the regulation and control of motor behaviour. Overall, our data have shown that cognitive impairment, especially of verbal skills, best explains the comorbidity of autism and fragile X. This implies some more fundamental perturbations of specific neural connections which are essential for both specific behaviours and cognition. We also emphasize that FXS offers a unique molecular model for autism since FMRP regulates the translation of many other genes involved in synaptic formation and plasticity which should be natural targets for further exploration. (c) 2006 Elsevier Ltd. All rights reserved. C1 La Trobe Univ, Sch Psychol Sci, Melbourne, Vic, Australia. Univ Melbourne, Dept Math & Stat, Melbourne, Vic, Australia. Univ Calif Davis, Dept Biol Chem, Sch Med, Sacramento, CA 95817 USA. Kimball Genet Inc, Denver, CO USA. Univ Calif Davis, Dept Psychiat & Behav Sci, Sch Med, Sacramento, CA 95817 USA. Univ Calif Davis, MIND Inst, Sch Med, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Pediat, Sch Med, Sacramento, CA 95817 USA. RP Loesch, DZ (reprint author), La Trobe Univ, Dept Psychol Sci, Bundoora, Vic 3086, Australia. 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Biobehav. Rev. PY 2007 VL 31 IS 3 BP 315 EP 326 DI 10.1016/j.neubiorev.2006.09.007 PG 12 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 165OZ UT WOS:000246316100002 PM 17097142 ER PT J AU Laycock, R Crewther, SG Crewther, DP AF Laycock, R. Crewther, S. G. Crewther, D. P. TI A role for the 'magnocellular advantage' in visual impairments in neuro developmental and psychiatric disorders SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE magnocellular; attention; primary visual cortex; feedback; dorsal stream; ventral stream; neurodevelopmental and psychiatric disorder ID LATERAL GENICULATE-NUCLEUS; TRANSCRANIAL MAGNETIC STIMULATION; FIGURE-GROUND SEGREGATION; FRAGILE-X-SYNDROME; MACAQUE MONKEY; AREA MT; MOTION PERCEPTION; PARVOCELLULAR CONTRIBUTIONS; CONTRAST SENSITIVITY; STRIATE CORTEX AB Evidence exists implicating abnormal visual information processing and visually driven attention in a number of neurodevelopmental and psychiatric disorders, suggesting that research into such disorders may benefit from a better understanding of more recent advances in visual system processing. A new integrated model of visual processing based on primate single cell and human electrophysiology may provide a framework, to understand how the visual system is involved, by implicating the magnocellular pathway's role in driving attentional mechanisms in higher-order cortical regions, what we term the 'magnocellular advantage'. Evidence is also presented demonstrating visual processing occurs considerably faster than previously assumed, and emphasising the importance of top-down feedback signals into primary visual cortex, as well as considering the possibility of lateral connections from dorsal to ventral visual areas. Such organisation is argued to be important for future research highlighting visual aspects of impairment in disorders as diverse as schizophrenia and autism. (c) 2006 Elsevier Ltd. All rights reserved. C1 La Trobe Univ, Sch Psychol Sci, Bundoora, Vic 3086, Australia. Swinburne Univ, Brain Sci Inst, Hawthorn, Vic 3122, Australia. 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Biobehav. Rev. PY 2007 VL 31 IS 3 BP 363 EP 376 DI 10.1016/j.neubiorev.2006.10.003 PG 14 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 165OZ UT WOS:000246316100005 PM 17141311 ER PT J AU Hashimoto, T AF Hashimoto, Toshiaki TI Clinical syndromes as models of autism SO NEUROSCIENCE RESEARCH LA English DT Meeting Abstract C1 Naruto Univ Educ, Dept Educ Disabled, Naruto 772, Japan. NR 0 TC 0 Z9 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0168-0102 J9 NEUROSCI RES JI Neurosci. Res. PY 2007 VL 58 SU 1 BP S27 EP S27 DI 10.1016/j.neures.2007.06.159 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 207TA UT WOS:000249272800156 ER PT J AU Inagaki, M Kaga, M AF Inagaki, Masumi Kaga, Makiko TI Autism: Clinical medicine to neuroscience SO NEUROSCIENCE RESEARCH LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0168-0102 J9 NEUROSCI RES JI Neurosci. Res. PY 2007 VL 58 SU 1 BP S27 EP S27 DI 10.1016/j.neures.2007.06.157 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 207TA UT WOS:000249272800154 ER PT J AU Jou, RJ Paterson, SJ Papademetris, X Staib, LH Schultz, RT AF Jou, Roger J. Paterson, Sarah J. Papademetris, Xenophon Staib, Lawrence H. Schultz, Robert T. TI Abnormalities in white matter structure in autism spectrum disorders detected by diffusion tensor imaging SO NEUROSCIENCE RESEARCH LA English DT Meeting Abstract C1 Yale Univ, Dept Psychiat, New Haven, CT 06520 USA. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. Yale Univ, Dept Diagnost Radiol, New Haven, CT 06510 USA. NR 0 TC 0 Z9 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0168-0102 J9 NEUROSCI RES JI Neurosci. Res. PY 2007 VL 58 SU 1 BP S62 EP S62 DI 10.1016/j.neures.2007.06.367 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 207TA UT WOS:000249272800364 ER PT J AU Kasai, K Kawakubo, Y Kuwabara, H Yamasue, H AF Kasai, Kiyoto Kawakubo, Yuki Kuwabara, Hitoshi Yamasue, Hidenori TI Neuroimaging in autism spectrum disorders SO NEUROSCIENCE RESEARCH LA English DT Meeting Abstract C1 Univ Tokyo, Dept Neuropsychiat, Tokyo, Japan. NR 0 TC 0 Z9 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0168-0102 J9 NEUROSCI RES JI Neurosci. Res. PY 2007 VL 58 SU 1 BP S27 EP S27 DI 10.1016/j.neures.2007.06.158 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 207TA UT WOS:000249272800155 ER PT J AU Narita, M AF Narita, Masaaki TI Experimental animals as models of autism SO NEUROSCIENCE RESEARCH LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0168-0102 J9 NEUROSCI RES JI Neurosci. Res. PY 2007 VL 58 SU 1 BP S28 EP S28 DI 10.1016/j.neures.2007.06.161 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 207TA UT WOS:000249272800158 ER PT J AU Takahashi, H Omori, T Murohashi, H Kamio, Y AF Takahashi, Hideyuki Omori, Takashi Murohashi, Harumitu Kamio, Yoko TI Dysfunction of dynamical modulation of decision-making process depending on social context in autism spectrum disorder SO NEUROSCIENCE RESEARCH LA English DT Meeting Abstract C1 Hokkaido Univ, Grad Sch Informat Sci & Technol, Sapporo, Hokkaido 060, Japan. Tamagawa Univ, Res Inst, Tokyo, Japan. Hokkaido Univ, Grad Sch Educ, Sapporo, Hokkaido 060, Japan. NIMH, Tokyo, Japan. RI Murohashi, Harumitsu/G-8896-2011 NR 0 TC 0 Z9 0 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0168-0102 J9 NEUROSCI RES JI Neurosci. Res. PY 2007 VL 58 SU 1 BP S64 EP S64 DI 10.1016/j.neures.2007.06.379 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 207TA UT WOS:000249272800376 ER PT J AU Wagner, GC Reuhl, KR Ming, X Halladay, AK AF Wagner, George C. Reuhl, Kenneth R. Ming, Xue Halladay, Alycia K. TI Behavioral and neurochemical sensitization to amphetamine following early postnatal administration of methylmercury (MeHg) SO NEUROTOXICOLOGY LA English DT Article DE methylmercury; amphetamine; self-injurious behavior ID SELF-INJURIOUS-BEHAVIOR; STRIATAL DOPAMINE RELEASE; METHYL MERCURY EXPOSURE; NEUROBEHAVIORAL CHANGES; PRENATAL METHYLMERCURY; RATS; AUTISM; MICE; CHILDREN; NEUROTOXICITY AB Perinatal exposure to methylmercury (MeHg) in rodents has been linked to changes in sensitivity to dopaminergic agents later in life. In an effort to determine the behavioral and neurochemical response to the indirect dopaminergic and serotonergic agonist amphetamine following neonatal exposure to MeHg, male BALB/c mice were administered MeHg during critical periods of neural development and challenged with amphetamine as adults. Mice were observed 15, 30 and 60 min after a single amphetamine injection (7.5 mg/kg i.p.) for presence of stereotypic and self-injurious behaviors, abnormal posture, and hyperthermia. Mice treated with 2 or 4 mg/kg MeHg on alternate days 3-15 of life demonstrated an increase in body temperature and the appearance of stereotypic and self-injurious behaviors not observed when amphetamine was administered to either vehicle-exposed mice or those treated with an equivalent total amount of MeHg administered on postnatal days 13 and 15. Neurochemical analysis of MeHg- and vehicle-exposed mice challenged with amphetamine or saline revealed alterations in dopaminergic and serotonergic activity which corresponded to the sensitized behavioral response to amphetamine. These observations demonstrate a critical window for MeHg exposure affecting the later appearance of amphetamine-induced self-injurious behavior and support the hypothesis that early exposure to environmental neurotoxicants may predispose individuals to engage in aberrant, intrusive behaviors later in life. (c) 2006 Elsevier Inc. All rights reserved. C1 Rutgers State Univ, Dept Psychol, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Toxicol, Piscataway, NJ 08854 USA. Rutgers State Univ, Ctr Child Neurotoxicol & Exposure Assessment, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Dept Neurosci, Newark, NJ 07101 USA. RP Wagner, GC (reprint author), Rutgers State Univ, Dept Psychol, 152 Frelinghuysen Rd, Piscataway, NJ 08854 USA. 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Miller TI Toll-like receptor ligands and CD154 stimulate microglia to produce a factor(s) that promotes excess cholinergic differentiation in the developing rat basal forebrain: Implications for neurodevelopmental disorders SO PEDIATRIC RESEARCH LA English DT Article ID CENTRAL-NERVOUS-SYSTEM; ADAPTIVE IMMUNE-RESPONSES; IN-VITRO; MATERNAL INFECTION; CONDITIONED MEDIUM; CEREBRAL-CORTEX; FETAL BRAIN; CELL-DEATH; AUTISM; MACROPHAGES AB Maternal inflammation plays a role in the etiology of certain neurodevelopmental disorders including autism and schizophrenia. Because maternal inflammation can lead to activation of fetal microglia, we have examined effects of inflamed microglia on cultured neural progenitors from rat embryonic septal region and basal forebrain. These cells give rise to cholinergic neurons projecting to cortex and hippocampus. Microglia stimulated with lipopolysaccharide (LPS), peptidoglycan, Poly I:C and CD154 produce conditioned media (CM) that promotes excessive numbers of cholinergic neurons and levels of choline acetyltransferase (ChAT) activity 6-8 times that of untreated cultures. Expression of the neural-specific transcription factor MATH1 increases substantially within 1 h of plating in LPS-CM. Untreated cultures do not attain equivalent levels until 6 h. By contrast, expression of glial-related transcription factors in LPS-CM-treated cultures never attains the elevated levels of untreated cultures. LPS-CM-treated clones derived from individual progenitors labeled with a LacZ-expressing retrovirus showed > 2.5-fold increase in the percentage of cholinergic cells compared with untreated clones. 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Res. PD JAN PY 2007 VL 61 IS 1 BP 15 EP 20 DI 10.1203/01.pdr.0000249981.70618.18 PG 6 WC Pediatrics SC Pediatrics GA 119WS UT WOS:000243045700004 PM 17211134 ER PT J AU Gupta, VB Hyman, SL Johnson, CP Bryant, J Byers, B Kallen, R Levy, SE Myers, SM Rosenblatt, AI Yeargin-Allsopp, M AF Gupta, Vidya Bhushan Hyman, Susan L. Johnson, Chris Plauche Bryant, James Byers, Barbara Kallen, Ronald Levy, Susan E. Myers, Scott M. Rosenblatt, Alan I. Yeargin-Allsopp, Marshalyn TI Identifying children with autism early? SO PEDIATRICS LA English DT Editorial Material ID SPECTRUM DISORDERS; YOUNG-CHILDREN; DIAGNOSIS; FAMILIES; AGE C1 New York Med Coll, Valhalla, NY 10595 USA. Univ Rochester, Sch Med & Dent, Rochester, NY USA. Univ Texas, Hlth Sci Ctr, San Antonio, TX 78285 USA. Ohio Bur Children Med Handicaps, Columbus, OH USA. Ann Arbor Families Autist Childrens Educ & Suppor, Ann Arbor, MI USA. Northwestern Univ, Childrens Mem Hosp, Feinberg Sch Med, Chicago, IL 60611 USA. 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EM bhushan07627@yahoo.com CR Bailey DB, 2005, PEDIATRICS, V116, P1346, DOI 10.1542/peds.2004-1239 Coonrod EE, 2004, INFANT YOUNG CHILD, V17, P258 Guralnick MJ., 1997, EFFECTIVENESS EARLY Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Luyster R, 2005, DEV NEUROPSYCHOL, V27, P311, DOI 10.1207/s15326942dn2703_2 Mandell DS, 2002, J AM ACAD CHILD PSY, V41, P1447, DOI 10.1097/01.CHI.0000024863.60748.53 *NRC COMM INT CHIL, 2001, ED CHILDR AUT Robins DL, 2006, J DEV BEHAV PEDIATR, V27, pS111, DOI 10.1097/00004703-200604002-00009 Smith CG, 2006, PEDIATRICS, V118, P1, DOI 10.1542/peds.2005-1879 Williams J, 2006, AUTISM, V10, P11, DOI 10.1177/13623613060S7876 NR 12 TC 19 Z9 19 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 JAN PY 2007 VL 119 IS 1 BP 152 EP 153 DI 10.1542/peds.2006-2026 PG 2 WC Pediatrics SC Pediatrics GA 121YB UT WOS:000243191800058 PM 17200280 ER PT J AU Rosen, NJ Yoshida, CK Croen, LA AF Rosen, Nila J. Yoshida, Cathleen K. Croen, Lisa A. TI Infection in the first 2 years of life and autism spectrum disorders SO PEDIATRICS LA English DT Article DE autism; autistic disorder; infant; newborn infant; infection; epidemiology ID CONGENITAL CYTOMEGALOVIRUS-INFECTION; HERPES-SIMPLEX ENCEPHALITIS; NERVOUS-SYSTEM INFECTIONS; URINARY-TRACT INFECTIONS; PRENATAL VIRAL-INFECTION; INFANTILE-AUTISM; RISK-FACTORS; FOLLOW-UP; CHILDREN; SCHIZOPHRENIA AB OBJECTIVE. The purpose of this work was to investigate the association between infections in the first 2 years and subsequent diagnosis of autism spectrum disorders. METHODS. We conducted a case-control study among children born at Kaiser Permanente Northern California from 1995 to 1999. Case subjects (n = 403) were children with an autism diagnosis recorded in Kaiser Permanente databases. Control subjects (n = 2100) were randomly sampled from the remaining children without autism and frequency matched to case subjects on gender, birth year, and birth hospital. Information on infections and covariates were obtained from Kaiser Permanente and birth certificate databases. RESULTS. Overall, infection diagnoses in the first 2 years of life were recorded slightly less often for children with autism than control children (95.0% vs 97.5%). Among specific diagnoses, upper respiratory infections were significantly less frequently diagnosed and genitourinary infections more frequently diagnosed in children with autism. In the first 30 days of life, the frequency of having an infection was slightly higher among children with autism (22.6% vs 18.7%). CONCLUSIONS. Children with subsequent diagnoses of autism do not have more overall infections in the first 2 years of life than children without autism. Data suggest that children with autism may have modestly elevated rates of infection in the first 30 days and that, during the first 2 years, children with autism may be at higher risk for certain types of infections and lower risk for others. Additional studies that explore the associations between prenatal and early childhood infections and autism may help clarify the role of infection and the immune system in the etiology of autism spectrum disorder. C1 Kaiser Permanente, Div Res, Oakland, CA USA. RP Rosen, NJ (reprint author), Calif Dept Hlth Serv, 850 Marina Bay Pkwy,Bldg P, Richmond, CA 94804 USA. 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R. Mckay, L. McAleer, P. Toal, E. Robertson, A. Pollick, F. E. TI Neural noise and autism spectrum disorders SO PERCEPTION LA English DT Meeting Abstract C1 [Simmons, D. R.; Mckay, L.; McAleer, P.; Toal, E.; Robertson, A.; Pollick, F. E.] Univ Glasgow, Dept Psychol, Glasgow, Lanark, Scotland. EM david@psy.gla.ac.uk RI McAleer, Phil/A-8178-2011; Pollick, Frank/B-1971-2010; Simmons, David/A-4916-2012 OI McAleer, Phil/0000-0002-4523-2097; NR 0 TC 2 Z9 2 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2007 VL 36 SU S BP 119 EP 120 PG 2 WC Psychology; Psychology, Experimental SC Psychology GA 226NA UT WOS:000250594600426 ER PT J AU Congiu, S Schlottmann, A AF Congiu, S. Schlottmann, A. TI The perception of social and physical causality in high-functioning children with autism SO PERCEPTION LA English DT Meeting Abstract C1 Univ Siena, Dipartimento Filosofia & Sci Social, I-53100 Siena, Italy. [Schlottmann, A.] UCL, London, England. EM congiu@media.unisi.it NR 0 TC 0 Z9 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2007 VL 36 SU S BP 139 EP 139 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA 226NA UT WOS:000250594600497 ER PT J AU Falter, CM Plaisted, K Davis, G AF Falter, C. M. Plaisted, K. Davis, G. TI Competition between perceptual grouping principles reveals latent selective grouping abnormalities in autism SO PERCEPTION LA English DT Meeting Abstract C1 [Falter, C. M.; Plaisted, K.; Davis, G.] Univ Cambridge, Dept Expt Psychol, Cambridge CB2 1TN, England. EM cmf42@cam.ac.uk RI Davis, Gregory/G-9954-2012 NR 0 TC 0 Z9 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2007 VL 36 SU S BP 139 EP 139 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA 226NA UT WOS:000250594600500 ER PT J AU Rhodes, GI Pellicano, L Jeffery, L Burr, D AF Rhodes, G. I. Pellicano, L. Jeffery, L. Burr, D. TI Abnormal adaptive face-coding mechanisms in autism SO PERCEPTION LA English DT Meeting Abstract C1 [Rhodes, G. I.; Jeffery, L.] Univ Western Australia, Dept Psychol, Perth, WA 6009, Australia. [Pellicano, L.] Univ Bristol, Bristol, Avon, England. [Burr, D.] Univ Florence, Florence, Italy. EM gill@psy.uwa.edu.au NR 0 TC 0 Z9 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2007 VL 36 SU S BP 152 EP 152 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA 226NA UT WOS:000250594600545 ER PT J AU Gowen, E Miall, RC AF Gowen, E. Miall, R. C. TI Perceiving and drawing ambiguous figures in autism spectrum disorder SO PERCEPTION LA English DT Meeting Abstract C1 [Gowen, E.] Univ Manchester, Fac Life Sci, Manchester M13 9PL, Lancs, England. [Miall, R. C.] Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England. EM emma.gowen@manchester.ac.uk NR 0 TC 0 Z9 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2007 VL 36 IS 9 MA 20 BP 1406 EP 1406 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA 251CH UT WOS:000252347700032 ER PT J AU Wiefel, A Titze, K Kuntze, L Winter, M Seither, C Witte, B Lenz, K Gruters, A Lehmkuhl, U AF Wiefel, Andreas Titze, Karl Kuntze, Lena Winter, Mirja Seither, Corinna Witte, Ben Lenz, Klaus Grueters, Annette Lehmkuhl, Ulrike TI Diagnostic classification of mental disorders in infants and toddlers age 0 to 5 SO PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE LA German DT Review DE diagnostic classification 0-3 (DC : 0-3R); infant psychiatry; parent-infant-interaction-practise parameters; Research Diagnostic Criteria Preschool Age (RDC-PA) ID PSYCHOPATHOLOGY; CHALLENGES; RISK; PSYCHIATRY; BEHAVIOR; AUTISM; CHILD AB The Article is working on developmental psychopathology, diagnosis, and treatment of behavioral problems in infants and toddlers age 0 to 5. An overview of the literature about the international discussion is given. In particular diagnostic classification is elaborated by mentioning the revision of,Diagnostic Classification 0-3 (DC: 0-3R)" and "Research Diagnostic Criteria-Preschool Age (RDC-PA)". State of the art and clinical implication is reported on the basis of principal considerations on infant psychiatry. The american practice parameters become adapted and a working title for diagnostic formulation is given. More research should be done against the background of the introduced standards. C1 Otto Heubner Ctr Kinder & Jugendmed, Charite, Sozialpadiatr Zentrum Chron Kranke Kinder, D-13353 Berlin, Germany. RP Wiefel, A (reprint author), Otto Heubner Ctr Kinder & Jugendmed, Charite, Sozialpadiatr Zentrum Chron Kranke Kinder, Augustenburger Pl 1, D-13353 Berlin, Germany. 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This review summarizes some of the features of the human brain that differentiate it from the brains of other animals, some of the methods used in cognitive neuroscience, and concludes with an example of research from the author's own lab that implicates the amygdala in emotion recognition, social judgment, and autism. C1 CALTECH, Pasadena, CA 91125 USA. RP Adolphs, R (reprint author), CALTECH, Pasadena, CA 91125 USA. 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PY 2007 VL 17 SI SI BP 99 EP 105 PG 7 WC Materials Science, Multidisciplinary; Multidisciplinary Sciences SC Materials Science; Science & Technology - Other Topics GA 225IJ UT WOS:000250510000016 ER PT J AU Passerino, LM Santarosa, LCM AF Passerino, Liliana Maria Santarosa, Lucila Costi M. TI Social interaction in austim in learning virtual environment SO PSICOLOGIA-REFLEXAO E CRITICA LA Portuguese DT Article DE autism; social interaction; virtual learning environment AB The goal of this, paper is to discuss the development of social interactions ill virtual environments, specially considering the autism. The literature review is based oil Sociohistorical Theory and main theoretical works about this condition, We start from a wide discussion about social interaction, its development and relation to autism characteristics, considering that the concept of intentional communication is fundamental to the analysis of social interaction of autistic subjects in virtual environments. Furthermore, , We present and discuss the data obtained from a case of study carried out with four subjects that suffer from different levels of autism. The study was developed as a two years of research applying several virtual environments. We also discuss the main results of this research. C1 [Passerino, Liliana Maria; Santarosa, Lucila Costi M.] Univ Fed Rio Grande do Sul, Porto Alegre, RS, Brazil. RP Passerino, LM (reprint author), Av Paulo Gama,110 Predio 12105-3 Andar Sala 334, BR-90040060 Porto Alegre, RS, Brazil. EM liliana@pgie.ufrgs.br; lucila.santarosa@ufrgs.br CR Baron-Cohen S., 1990, REV PORTUGUESA PEDAG, V24, P407 BARTH C, 2004, 7 C IB INF ED MONT M Bosa Cleonice, 2002, Psicol. Reflex. 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PD JAN-APR PY 2007 VL 20 IS 1 BP 54 EP 64 DI 10.1590/S0102-79722007000100008 PG 11 WC Psychology, Multidisciplinary SC Psychology GA 338RG UT WOS:000258525300008 ER PT J AU Schmidt, C Dell'Aglio, DD Bosa, CA AF Schmidt, Carlo Dell'Aglio, Debora Dalbosco Bosa, Cleonice Alves TI Coping strategies of mothers of autistic children: Dealing with behavioral problems and emotions SO PSICOLOGIA-REFLEXAO E CRITICA LA Spanish DT Article DE autism; maternal stress; coping strategies ID PERVASIVE DEVELOPMENTAL DISORDERS; HANDICAPPED-CHILDREN; FAMILY STRESS; PARENTS; SATISFACTION; CHILDHOOD; IMPACT; CARE AB Many studies have shown evidence of high levels of stress in families with autistic children. Concerning this process, it is important to consider the coping strategies of mothers when dealing with their autistic children, as well as how they deal with their own emotions unleashed by the stress. Thirty mothers, between 30 and 56 years old participated in the study. Their children have met the criteria for autism and attended special education schools. The coping strategies were investigated using a semi-structured interview, which was transcribed and analysed by content analysis. The main difficulties refer to the child's behavior. In relation to these difficulties, the strategy used by the mothers was predominantly direct action and acceptance. Concerning the strategies to deal with their own emotions, the most frequent categories were distraction, reaching out for social/religious support, lack of action and avoidance. Results are discussed in terms of stress and maternal adaptation model. C1 [Dell'Aglio, Debora Dalbosco] Univ Fed Rio Grande do Sul, Inst Psicol, BR-90035003 Porto Alegre, RS, Brazil. RP Dell'Aglio, DD (reprint author), Univ Fed Rio Grande do Sul, Inst Psicol, Ramiro Barcelos 2600, BR-90035003 Porto Alegre, RS, Brazil. 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Crit. PD JAN-APR PY 2007 VL 20 IS 1 BP 124 EP 131 DI 10.1590/S0102-79722007000100016 PG 8 WC Psychology, Multidisciplinary SC Psychology GA 338RG UT WOS:000258525300016 ER PT J AU Lebedeva, EI AF Lebedeva, E. I. TI Understanding of intentions in situation of deception by children with typical development and autistic children SO PSIKHOLOGICHESKII ZHURNAL LA Russian DT Article DE "model of psychic"; understanding of intentions; understanding of lie and "harmless lie"; children with typical development and with autistic disorders of different spectrum ID YOUNG-CHILDREN; ADULTS; MIND AB The results of comparative study of understanding of intentions in the situation of deception by normal children and by autistic ones as the phenomenon of cognitive representations about other people inner world are presented. 92 children with typical development (age from 3 to 6) and 44 children with autistic disorders of different spectrum (age from 5 to 11) took part in this study. Age dynamics of intentions' understanding in the situation of deception is determined by the degree of development of "model of psychic". At the age of four children begin to discern the lie and understand the intentions of the other person in the situation of the simple deception. From five years they understand "harmless lie" in situation when intentions to deceive are implicit. Lack of understanding of lie by children with autism is accounted for the deficiency of "model of psychic" development. The decrease in the level of mentality in preschool ages has an influence on formation of other people inner world understanding. C1 RAS, Psychol Inst, Moscow, Russia. RP Lebedeva, EI (reprint author), RAS, Psychol Inst, Moscow, Russia. 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Ann. PD JAN PY 2007 VL 37 IS 1 BP 19 EP 26 PG 8 WC Psychiatry SC Psychiatry GA 130OZ UT WOS:000243810200008 ER PT J AU Golse, B Eliez, S AF Golse, Bernard Eliez, Stephan TI Regarding autism and pervasive developmental disorders. From the "autisticizing process" to scanner autism ... SO PSYCHIATRIE DE L ENFANT LA French DT Article; Proceedings Paper CT Symposium on Infant and Adolescent Psychiatry CY NOV 27, 2004 CL Geneva, SWITZERLAND ID CHILDREN; LIFE; INDIVIDUALS; CEREBELLUM; PATTERNS; MRI AB The first part of the text is devoted to the early detection of infantile autism when it is viewed using Hochman's concept of the "autisticizing process" and the notion of the initial plasticity of the troubles. Then, the article centers itself on the perspective of autism as a major failure of the processes of access to intersubjectivity, using both the recent data from cerebral neuro-imagery concerning the superior temporal lobe (M Zilbovicius, N. Boddaert...) and the PILE research program (International Program for the Language of the Child) (IPLC), introduced at Necker Hospital, Paris, by B. Golse and V. Desjardins. The final part of this work offers S. Eliez the chance to re-discuss and comment upon the material so as to re-situate the concept of sensorial co-modalization which is at the core of current neurodevelopmental research. C1 [Golse, Bernard] Hop Necker Enfants Malad, Serv Pedopsychiat, F-75015 Paris, France. [Golse, Bernard] Univ Paris 05, F-75270 Paris 06, France. [Eliez, Stephan] Univ Geneva, Fac Med, Serv Medicopedag, CH-1211 Geneva, Switzerland. RP Golse, B (reprint author), Hop Necker Enfants Malad, Serv Pedopsychiat, 149 Rue Sevres, F-75015 Paris, France. EM bernard.golse@nck.ap-hop-paris.fr; stephan.eliez@medecine.unige.ch CR Andreasen NC, 1998, SCHIZOPHRENIA BULL, V24, P203 Barnea-Goraly N, 2004, BIOL PSYCHIAT, V55, P323, DOI 10.1016/j.biopsych.2003.10.022 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BELMONTE, 2004, CHACUN CERVEAU PLAST BELMONTE MK, 2004, J NEUROSCI, V24, P228 Bion W., 1974, ATTENTION INTERPRETA Bion W. 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Enfant PY 2007 VL 50 IS 1 BP 29 EP 60 PG 32 WC Psychiatry SC Psychiatry GA 318XT UT WOS:000257126800002 ER PT J AU Springer, S Schnobel-Muller, E Kluger, G Noterdaeme, M AF Springer, Stephan Schnoebel-Mueller, Elisabeth Kluger, Gerhard Noterdaeme, Michele TI Importance of structured cooperation between child and adolescent psychiatry and neuropediatrics SO PSYCHIATRISCHE PRAXIS LA German DT Article; Proceedings Paper CT Regional Research Conference of the Psychiatric and Neurological Special Clinics of Bavaria ` CY OCT 12-14, 2005 CL Bavaria, GERMANY SP Educ Inst Assoc Bavarian Sectors HO Educ Inst Kloster Irsee DE neuropediatric; child and adolescent psychiatry; comorbidity epilepsy cognition AB Neuropediatric-psychiatric comorbidity is a frequent phenomenon typically described in the clinical entity autism and epilepsy. The obvious influence of the level of intelligence on the type of the psychiatric diagnosis is also described. The data of 176 commonly patients attended patients illustrate complex diagnosis spectra other than the above-mentioned combination, e.g. the association not only of epilepsy but of structural brain damage or cerebral palsy with conduct disorders. The therapeutic consequences with respect to drug and patient management are discussed. The intelligence level is of considerable importance for the planning of interventions because of its association with impulse control disorders. The results show that attention disorders and conduct disorders play a major role in neuropediatric patients. An early and common patient management within a structured cooperation should be the consequence of these results. C1 Heckscher Klin, D-81539 Munich, Germany. Bezirksklinikum Regensburg, Regensburg, Germany. RP Springer, S (reprint author), Heckscher Klin, Deisenhofener Str 28, D-81539 Munich, Germany. EM stephan.springer@heckscher-klinik.de NR 0 TC 0 Z9 0 PU GEORG THIEME VERLAG KG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0303-4259 J9 PSYCHIAT PRAX JI Psychiatr. Prax. PD JAN PY 2007 VL 34 SU 1 BP S64 EP S65 DI 10.1055/s-2006-940190 PG 2 WC Psychiatry SC Psychiatry GA 151HE UT WOS:000245280300028 ER PT J AU Wiberg, A Heidenreich, E Springer, S Noterdaeme, M AF Wiberg, Anja Heidenreich, Evelyn Springer, Stephan Noterdaeme, Michele TI Analysis of stress and needs in children with pervasive developmental disorders SO PSYCHIATRISCHE PRAXIS LA German DT Article; Proceedings Paper CT Regional Research Conference of the Psychiatric and Neurological Special Clinics of Bavaria ` CY OCT 12-14, 2005 CL Bavaria, GERMANY SP Educ Inst Assoc Bavarian Sectors HO Educ Inst Kloster Irsee DE autism; parental stress; needs ID YOUNG-CHILDREN; MOTHERS; AUTISM AB Objective The assessment of stress factors and needs of families living with a child with a pervasive developmental disorder. Methods 260 families were recruited to participate the study. All families had been seen at our special clinic for developmental disorders. We used standardized questionnaires to measure stress and needs in families (Parental Stress Index, Needs of parents, Child behavior Checklist). Results Stress was high in most families. Parents feel high demands with respect to their child and feel incompetent. Most families report they need better professional advice in the care of their child. Conclusions More extensive services should be provided for families with children having a pervasive developmental disorder. C1 Heckscher Klin Kinder & Jugenspsychiat & Psychoth, D-81539 Munich, Germany. RP Wiberg, A (reprint author), Heckscher Klin Kinder & Jugenspsychiat & Psychoth, Deisenhofenerstr 28, D-81539 Munich, Germany. EM anja.wiberg@heckscher-klinik.de CR Abbeduto L, 2004, AM J MENT RETARD, V109, P237, DOI 10.1352/0895-8017(2004)109<237:PWACIM>2.0.CO;2 Abidin R, 1990, PARENTING STRESS IND BAILEY DB, 1988, J SPEC EDUC, V22, P117 BAILEY DB, 1992, AM J MENT RETARD, V97, P1 Kasari C, 1997, J AUTISM DEV DISORD, V27, P39, DOI 10.1023/A:1025869105208 Weiss MJ, 2002, AUTISM, V6, P115, DOI 10.1177/1362361302006001009 1999, ARBEITSGRUPPE DTSCH NR 7 TC 2 Z9 2 PU GEORG THIEME VERLAG KG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0303-4259 J9 PSYCHIAT PRAX JI Psychiatr. Prax. PD JAN PY 2007 VL 34 SU 1 BP S66 EP S68 DI 10.1055/s-2006-940191 PG 3 WC Psychiatry SC Psychiatry GA 151HE UT WOS:000245280300029 ER PT J AU Steege, MW Mace, FC Perry, L Longenecker, H AF Steege, Mark W. Mace, F. Charles Perry, Lora Longenecker, Harold TI Applied behavior analysis: Beyond discrete trial teaching SO PSYCHOLOGY IN THE SCHOOLS LA English DT Article ID CHILDREN AB We discuss the problem of autism-specific special education programs representing themselves as Applied Behavior Analysis (ABA) programs when the only ABA intervention employed is Discrete Trial Teaching (DTT), and often for limited portions of the school day. Although DTT has many advantages to recommend its use, it is not well suited to teach the full range of cognitive, social, academic, leisure, and functional living skills children with autism and related disorders need to develop and generalize to varied natural environments. DTT also does not address the treatment of behaviors that can interfere with instruction and the acquisition, generalization, and maintenance of skills many children with autism bring to instructional situations. We describe a comprehensive program of ABA services for children with autism and briefly discuss the various interventions and their applications and combinations to achieve broad improvement in many different skill areas. In our view, "true" ABA programs are comprised of multiple assessment and intervention methods used individually and dynamically to achieve the best results. (c) 2007 Wiley Periodicals, Inc. C1 Univ So Maine, Gorham, ME 04038 USA. RP Steege, MW (reprint author), Univ So Maine, 400 Bailey Hall, Gorham, ME 04038 USA. EM msteege@usm.maine.edu CR Anderson S. R., 1996, BEHAV INTERVENTION Y, P181 BAER DM, 2005, FOCUS BEHAV ANAL ED, P3 BAER DM, 1968, J APPL BEHAV ANAL, V1, P91, DOI 10.1901/jaba.1968.1-91 Brown-Chidsey R., 2004, ENCY SCH PSYCHOL, P96 Brown-Chidsey R., 2005, RESPONSE INTERVENTIO Charlop-Christy M. H., 2000, J POSIT BEHAV INTERV, V2, P98, DOI DOI 10.1177/109830070000200203 Deno S. L., 2005, ASSESSMENT INTERVENT, P10 Foxx R., 1982, INCREASING BEHAV SEV Green G, 1996, BEHAV INTERVENTION Y, P29 HART B, 1975, J APPL BEHAV ANAL, V8, P411, DOI 10.1901/jaba.1975.8-411 Hart B. M., 1982, USE INCIDENTAL TEACH HORNER RH, 1978, J APPL BEHAV ANAL, V8, P301 Howard JS, 2005, RES DEV DISABIL, V26, P359, DOI 10.1016/j.ridd.2004.09.005 Kazdin A. E., 2003, EVIDENCE BASED PSYCH KOEGEL RL, 1977, J APPL BEHAV ANAL, V10, P197, DOI 10.1901/jaba.1977.10-197 MAURICE C, 2005, FOCUS BEHAV ANAL ED, P31 McDonough K. A., 1996, BEHAV INTERVENTION Y, P63 Miltenberger R.G., 2004, BEHAV MODIFICATION P *NAT RES COUNC, 2001, DIV BEH SOC SCI ED PAGE TJ, 1976, J APPL BEHAV ANAL, V9, P433, DOI 10.1901/jaba.1976.9-433 STEEGE M, 2005, ASSESSMENT INTERVENT, P131 STEEGE MW, 1987, J APPL BEHAV ANAL, V20, P293, DOI 10.1901/jaba.1987.20-293 Sundberg M. L., 1998, TEACHING LANGUAGE CH WACKER DP, 1990, J APPL BEHAV ANAL, V23, P417, DOI 10.1901/jaba.1990.23-417 Watson T. S., 2003, CONDUCTING SCH BASED WILCZYNSKI SM, 2003, PROVEN PRACTICE PREV, V5, P23 NR 26 TC 17 Z9 17 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0033-3085 J9 PSYCHOL SCHOOLS JI Psychol. Schools PD JAN PY 2007 VL 44 IS 1 BP 91 EP 99 DI 10.1002/pits.20208 PG 9 WC Psychology, Educational SC Psychology GA 121TS UT WOS:000243180500009 ER PT J AU Mouridsen, SE Rich, B Isager, T Nedergaard, NJ AF Mouridsen, Svend Erik Rich, Bente Isager, Torben Nedergaard, Niels Jorgen TI Psychiatric disorders in the parents of individuals with infantile autism: A case-control study SO PSYCHOPATHOLOGY LA English DT Article DE infantile autism; psychiatric disorders, relatives ID PERSONALITY-CHARACTERISTICS; CASE REGISTER; FAMILIES; CHILDREN; PHENOTYPE; RELATIVES; LIABILITY; DENMARK; MOTHERS; TRAITS AB Background: The rates and types of psychiatric disorders were studied in the parents of individuals with infantile autism ( IA). Sampling and Methods: To estimate the prevalence and types of psychiatric disorders, the parents of 115 individuals with IA and the parents of 330 controls from the general population were screened through the nationwide Danish Psychiatric Central Register covering a period of 33 years. The IA individuals had been seen as in- patients at two university clinics of child psychiatry during a 25- year period and had been referred from the entire country of Denmark. Results: Psychiatric disorders were found in 15.7% of mothers with autistic children, which was significantly higher than the 8.2% found in the control group. The only diagnostic category in which a statistically significant overrepresentation could be found was that of personality disorder. A personality disorder diagnosis was found in 7.8% of mothers with autistic children in comparison to 2.1% of mothers in the control group. Conclusion: The findings so far suggest that in future studies it is important to pay attention to issues such as relatives examined, control groups and methods of data collection. Copyright (c) 2007 S. Karger AG, Basel. C1 Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. Glostrup Cty Hosp, Ctr Child & Adolescent Psychiat, Glostrup, Denmark. Aarhus Univ Hosp, Psychiat Hosp Children & Adolescents, Risskov, Denmark. RP Mouridsen, SE (reprint author), Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. EM sem01@bbh.hosp.dk CR ABRAMSON RK, 1992, J AM ACAD CHILD PSY, V31, P370, DOI 10.1097/00004583-199203000-00030 Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BOLTON PF, 1998, PSYCHOL MED, V28, P395 DELONG R, 1994, DEV MED CHILD NEUROL, V36, P441 Dumas J. 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The aim of the present study was to examine the impact of inattention, hyperactivity and impulsivity on the clinical phenotype of children and adolescents with PDD. Sampling and Methods: A total of 182 subjects ( 41 females) diagnosed as having PDD were split into a high ( PDD +) and a lower ( PDD) attention problem group using the median of the Child Behavior Checklist ( CBCL) syndrome scale 'attention problems' ( median T score = 75). The groups were compared with regard to the degree of coexisting psychopathology, as measured by the remaining 7 CBCL subscales, and autistic core features assessed by the Autism Diagnostic Interview- Revised ( ADI- R) and the Autism Diagnostic Observation Schedule using a multivariate analysis of covariance adjusted for age, IQ and socioeconomic status. Results: The PDD+ subjects exhibited a significantly higher degree of general psychopathology than the subjects in the PDD subgroup, regarding both internalizing and externalizing symptoms. In addition, the PDD+ subgroup tended to exhibit more impairments on the social interaction scale of the ADI- R. Conclusions: Clinicians should adjust treatment plans to ensure comprehensive and effective treatment for both PDD and associated ADHD. A dual diagnosis may be essential to the implementation of effective treatments. Copyright (c) 2007 S. Karger AG, Basel. C1 Univ Frankfurt, Dept Child & Adolescent Psychiat & Psychotherapy, DE-60528 Frankfurt, Germany. RP Holtmann, M (reprint author), Univ Frankfurt, Dept Child & Adolescent Psychiat & Psychotherapy, Deutschordenstr 50, DE-60528 Frankfurt, Germany. 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Lehmkuhl, G. TI What do we know about the serotonergic genetic heterogeneity in attention-deficit/hyperactivity and autistic disorders? SO PSYCHOPATHOLOGY LA English DT Article DE attention-deficit/hyperactivity disorder; autism; pharmacogenetics; serotonin ID DEFICIT-HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; WHOLE-BLOOD SEROTONIN; TRANSPORTER GENE; PROMOTER VARIANTS; REGION POLYMORPHISM; REGULATORY REGION; ASPERGER-SYNDROME; ANOREXIA-NERVOSA; GENOMEWIDE SCAN AB Background: Shared candidate gene regions point to a link between autistic disorders and attention-deficit/hyperactivity disorder (ADHD). Although they represent nosologically different diagnoses, the disorders do show some shared symptoms, above all inattention. For both disorders, the association with the serotonergic system is a focus of current research. Sampling and Methods: The current work provides an overview of serotonergic mechanisms in ADHD and autistic disorders as well as the resulting pharmacogenetic approaches. Results: No uniform picture emerges either for ADHD or for autistic disorders. In pharmacogenetic terms, there are some isolated studies on associations between serotonergic mechanisms and pharmacotherapy. For the area of autism, such studies are still lacking. Conclusions: The presented serotonergic mechanisms show relationships of this polymorphism to ADHD and autistic disorders, but they do not result in a uniform picture. The overlaps can best be explained by a dimensional classification approach. As yet, only a small number of studies on attentional disorders in autism and ADHD using shared samples have been carried out. With regard to diagnostics and therapy, analyses on the etiology of the attentional disorder of ADHD and autism are required. 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Benevides, Teal TI Sensory processing, physiological reactivity and adaptive behavior in children with autism and sensory modulation dysfunction SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 47th Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 16-21, 2007 CL Savannah, GA NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PY 2007 VL 44 SU 1 BP S85 EP S85 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 203VK UT WOS:000249001900388 ER PT J AU Delano, ME AF Delano, Monica E. TI Video modeling interventions for individuals with autism SO REMEDIAL AND SPECIAL EDUCATION LA English DT Article ID TEACH PERSPECTIVE-TAKING; CLASSROOM-BEHAVIOR; PURCHASING SKILLS; CHILDREN; SELF; PLAY; SETTINGS; MIND AB Video modeling interventions involve a child watching videotapes of positive examples of adults, peers, or him- or herself engaging in a behavior that is being taught. The purpose of this review was to examine empirical studies in which video modeling interventions were applied to individuals with autism, Nineteen studies published between 1985 and 2005 met the inclusion criteria for this review. The findings suggest that video modeling interventions are effective in teaching a variety of skills to children with autism. Descriptive summaries are provided for each study. Directions for future research and implications for practitioners are provided. 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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Educ. PD JAN-FEB PY 2007 VL 28 IS 1 BP 33 EP 42 DI 10.1177/07419325070280010401 PG 10 WC Education, Special SC Education & Educational Research GA 131JF UT WOS:000243864400004 ER PT J AU Goldsmith, TR LeBlanc, LA Sautter, RA AF Goldsmith, Tina R. LeBlanc, Linda A. Sautter, Rachael A. TI Teaching intraverbal behavior to children with autism SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Language intervention; Categories; Intraverbal; Skinner; Questions AB Skinner's conceptual analysis of language has influenced one model of early and intensive behavioral intervention with children, which incorporates verbal operants including mands, facts, intraverbals, etc. Many Studies have examined the mand and tact relations, with little focus on teaching intraverbal behavior. 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PD JAN-MAR PY 2007 VL 1 IS 1 BP 1 EP 13 DI 10.1016/j.rasd.2006.07.001 PG 13 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400001 ER PT J AU Herrington, JD Baron-Cohen, S Wheelwright, SJ Singh, KD Bullmore, ET Brammer, M Williams, SCR AF Herrington, John D. Baron-Cohen, Simon Wheelwright, Sally J. Singh, Krishna D. Bullmore, Edward T. Brammer, Michael Williams, Steve C. R. TI The role of MT+/V5 during biological motion perception in Asperger Syndrome: An fMRI study SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Asperger Syndrome; Autism; fMRI Motion perception; MT+/V5; Temporal lobe AB Asperger Syndrome (AS), a condition on the autistic spectrum, is characterized by deficits in the ability to use social cues to infer mental state information. Few studies have examined whether these deficits might be understood in terms of differences in visual information processing. The present study employed functional magnetic resonance imaging to examine differences in brain activity among individuals with AS while performing a task that typically leads to the automatic interpretation of human movement. Despite similar behavioural performance, significantly less activity was found for the AS group (relative to a control group) in inferior, middle and superior temporal regions, including the human analogue of MT+/V5. These data suggest that AS is associated with unique patterns of brain activity during the perception of visually presented social cues. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Herrington, John D.; Baron-Cohen, Simon; Wheelwright, Sally J.] Univ Cambridge, Dept Psychol, Autism Res Ctr, Cambridge CB2 1TN, England. 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Autism Spectr. Disord. PD JAN-MAR PY 2007 VL 1 IS 1 BP 14 EP 27 DI 10.1016/j.rasd.2006.07.002 PG 14 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400002 ER PT J AU Matson, JL Wilkins, J AF Matson, Johnny L. Wilkins, Jonathan TI A critical review of assessment targets and methods for social skills excesses and deficits for children with autism spectrum disorders SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Social skills; Autism spectrum disorders; Assessment AB A substantial research literature is beginning to develop regarding social skills excesses and deficits for children with autism spectrum disorders. These developments are likely to continue given the increasing recognition that these behaviors are among the most critical core symptoms of these disorders. A review is provided of developments in the field with respect to the social excesses and deficits that are most critical for this population of children. A discussion of direct observation and scaling methods used to do these evaluations along with a discussion of strengths and weaknesses of these methods is provided. A discussion of the current status and potential future developments of the area is also covered. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Matson, Johnny L.; Wilkins, Jonathan] 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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Autism Spectr. Disord. PD JAN-MAR PY 2007 VL 1 IS 1 BP 28 EP 37 DI 10.1016/j.rasd.2006.07.003 PG 10 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400003 ER PT J AU Matson, JL Nebel-Schwalm, M Matson, ML AF Matson, Johnny L. Nebel-Schwalm, Marie Matson, Michael L. TI A review of methodological issues in the differential diagnosis of autism spectrum disorders in children SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Methodology; Differential diagnosis; Autism ID PERVASIVE DEVELOPMENTAL DISORDERS; RECEPTIVE LANGUAGE DISORDER; PDD BEHAVIOR INVENTORY; RATING-SCALE; CHILDHOOD AUTISM; OBSERVATION SCHEDULE; EARLY INTERVENTION; INFANTILE-AUTISM; YOUNG-CHILDREN; ADI-R AB The development of standardized tests to assess autism, particularly in young children, is a topic of considerable interest in the research Community. Recent years have seen an exponential growth in scales for differential diagnosis. Particular emphasis has been placed on defining and better delineating the symptoms of the disorder relative to other forms of autism spectrum disorder (ASD) and intellectual disability (ID), and identifying the condition at the earliest possible age. The general consensus is that scaling methods are the core means of establishing a diagnosis. Thus, analyzing the research activity in the area for strengths and weaknesses in methodology would appear to be in order. A critical overview of existing psychometric properties of these tests is presented with suggestions for future research on the topic. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Matson, Johnny L.; Nebel-Schwalm, Marie; Matson, Michael L.] 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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PD JAN-MAR PY 2007 VL 1 IS 1 BP 38 EP 54 DI 10.1016/j.rasd.2006.07.004 PG 17 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400004 ER PT J AU Pituch, KA Green, VA Sigafoos, J Itchon, J O'Reilly, M Lancioni, GE Didden, R AF Pituch, Keenan A. Green, Vanessa A. Sigafoos, Jeff Itchon, Jonathan O'Reilly, Mark Lancioni, Giulio E. Didden, Robert TI Factor structure of the Behavior Flexibility Rating Scale (BFRS) SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Asperger's syndrome; Down syndrome; Behavior flexibility rating scale; Insistence on sameness; Factor structure AB The Behavior Flexibility Rating Scale (BFRS) is designed to assess insistence on sameness or lack of behavioral flexibility, which is often associated with autism and other developmental disabilities. This study was designed to assess the factor structure of this scale for a sample of 968 individuals with autism, Asperger's syndrome, and Down syndrome. To establish factorial validity, an exploratory factor analysis (EFA) was conducted with half of the sample, with a confirmatory factor analysis (CFA) conducted with the remaining cases to cross-validate the mode obtained with the EFA. The factor analyses supported the presence of two factors Interruption/Disruption and Position/Location. However, further analysis suggested the presence of a third factor, Interpersonal Mishaps, for the Asperger's syndrome group. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Green, Vanessa A.; Sigafoos, Jeff] Univ Tasmania, Sch Educ, Hobart, Tas 7001, Australia. [Pituch, Keenan A.; Itchon, Jonathan; O'Reilly, Mark] Univ Texas Austin, Coll Educ, Austin, TX 78712 USA. [Lancioni, Giulio E.] Univ Bari, Dept Psychol, Bari, Italy. [Didden, Robert] Radboud Univ Nijmegen, Dept Special Educ, Nijmegen, Netherlands. RP Sigafoos, J (reprint author), Univ Tasmania, Sch Educ, Private Bag 66, Hobart, Tas 7001, Australia. EM Jeff.Sigafoos@utas.edu.au CR Boudrias JS, 2004, EDUC PSYCHOL MEAS, V64, P861, DOI 10.1177/0013164404264840 Byrne B.M., 1998, STRUCTURAL EQUATION de Vet HCW, 2005, QUAL LIFE RES, V14, P1203, DOI 10.1007/s11136-004-5742-3 FORD JK, 1986, PERS PSYCHOL, V39, P291, DOI 10.1111/j.1744-6570.1986.tb00583.x Gerbing DW, 1996, STRUCT EQU MODELING, V3, P62, DOI 10.1080/10705519609540030 GREEN VA, FOCUS AUTIS IN PRESS Green VA, 2006, RES DEV DISABIL, V27, P70, DOI 10.1016/j.ridd.2004.12.002 Kanner L, 1943, NERV CHILD, V2, P217 Keith T. Z., 2006, MULTIPLE REGRESSION Kline R. B., 2005, PRINCIPLES PRACTICE, V2nd 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 Matson JL, 1994, AUTISM CHILDREN ADUL PRIOR M, 1973, J AUTISM CHILD SCHIZ, V3, P154, DOI 10.1007/BF01537990 RIMLAND B, 1971, J AUTISM CHILD SCHIZ, V1, P161, DOI 10.1007/BF01537955 Rutter M., 1978, AUTISM REAPPRAISAL C, P1 Rutter M., 1978, AUTISM REAPPRAISAL C Turner M, 1999, J CHILD PSYCHOL PSYC, V40, P839, DOI 10.1017/S0021963099004278 WAHLBERG T, 2001, AUTISTIC SPECTRUM DI, V14, P53, DOI 10.1016/S0270-4013(01)80007-6 NR 18 TC 11 Z9 11 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 JAN-MAR PY 2007 VL 1 IS 1 BP 55 EP 66 DI 10.1016/j.rasd.2006.07.005 PG 12 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400005 ER PT J AU Kern, JK Garver, CR Grannemann, BD Trivedi, MH Carmody, T Andrews, AA Mehta, JA AF Kern, Janet K. Garver, Carolyn R. Grannemann, Bruce D. Trivedi, Madhukar H. Carmody, Thomas Andrews, Alonzo A. Mehta, Jyutika A. TI Response to vestibular sensory events in autism SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism; Sensory processing; Vestibular; Thresholds AB The purpose of this study was to examine the response to vestibular sensory events in persons with autism. The data for this study was collected is part of a cross-sectional study that examined sensory processing (using the Sensory Profile) in 103 pet-sons with autism, 3 43 years of age, compared to, age- and gender-matched community controls. The Vestibular Processing section of the Sensory Profile was used. The results showed that Vestibular Processing (both high and low threshold processing) on the Sensory Profile was significantly different in persons with autism as compared to community controls, with persons with autism engaging in the behaviors more frequently than the controls. Vestibular processing differences Could explain certain problems in autism. It is important to try 10 understand sensory problems in autism because it can enable us to better understand the needs of persons with autism, and in turn, influence treatment protocols. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Kern, Janet K.; Grannemann, Bruce D.; Trivedi, Madhukar H.; Carmody, Thomas] Univ Texas SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA. [Garver, Carolyn R.] Autism Treatment Ctr, Dallas, TX USA. [Andrews, Alonzo A.] Autism Treatment Ctr, San Antonio, TX USA. [Mehta, Jyutika A.] Univ Texas Dallas, Dallas, TX 75230 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. EM janet.kern@UTSouthwestern.edu CR Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 Coster W., 1998, SCH FUNCTION ASSESSM COURCHESNE E, 1991, PEDIATRICS, V87, P781 COURCHESNE E, 1995, J AUTISM DEV DISORD, V25, P19, DOI 10.1007/BF02178164 CRISPINO L, 1984, P NATL ACAD SCI-BIOL, V81, P2917, DOI 10.1073/pnas.81.9.2917 Dunn W., 1999, SENSORY PROFILE Elia M, 2000, BRAIN DEV-JPN, V22, P88, DOI 10.1016/S0387-7604(99)00119-9 FRITH U, 1997, AUTISM EXPLOITING EN HORAK FB, 1988, DEV MED CHILD NEUROL, V30, P64 Kandel E. R., 1991, PRINCIPLES NEURAL SC KEMPER TL, 1993, NEUROL CLIN, V11, P175 Kern JK, 2001, J CHILD NEUROL, V16, P169, DOI 10.1177/088307380101600303 Kern JK, 2002, MED HYPOTHESES, V59, P255, DOI 10.1016/S0306-9877(02)00212-8 Kern JK, 2006, AUTISM, V10, P480, DOI 10.1177/1362361306066564 MAURER RG, 1979, DEV MED CHILD NEUROL, V21, P656 Minshew NJ, 2004, NEUROLOGY, V63, P2056 Molloy CA, 2003, J AUTISM DEV DISORD, V33, P643, DOI 10.1023/B:JADD.0000006001.00667.4c Njardvik U, 1999, J AUTISM DEV DISORD, V29, P287, DOI 10.1023/A:1022107318500 RITVO ER, 1986, AM J PSYCHIAT, V143, P862 Schopler E, 1994, CHILDHOOD AUTISM RAT, P90025 Takarae Y, 2004, J NEUROL NEUROSUR PS, V75, P1359, DOI 10.1136/jnnp.2003.022491 Vernazza-Martin S, 2005, J AUTISM DEV DISORD, V35, P91, DOI 10.1007/s10803-004-1037-3 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 JAN-MAR PY 2007 VL 1 IS 1 BP 67 EP 74 DI 10.1016/j.rasd.2006.07.006 PG 8 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400006 ER PT J AU Matson, JL Boisjoli, JA AF Matson, Johnny L. Boisjoli, Jessica A. TI Differential diagnosis of PDDNOS in children SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE PDDNOS; Children; Differential diagnosis ID PERVASIVE DEVELOPMENTAL DISORDER; AUTISM SPECTRUM DISORDERS; DEFICIT-HYPERACTIVITY DISORDER; BEHAVIORAL OBSERVATION; CLUSTER-ANALYSIS; RATING-SCALE; DSM-IV; SUBTYPES; EPIDEMIOLOGY; BORDERLANDS AB PDDNOS is a particularly important form of autism spectrum disorder (ASD) due to the frequency with which it is diagnosed. Having said that, it is often diagnosed by what it is not (not autism) as opposed to what it is. And, while PDDNOS is likely to be more common than autism, studies on PDDNOS are much less frequent. Perhaps with the exception of childhood degenerative disorder, PDDNOS has less diagnostic research on it than any other ASD. The purpose of the present paper was to review the available research on the definition and diagnosis of PDDNOS. The data are analyzed and future goals for conceptual and diagnostic research are discussed with the idea of further enhancing a neglected diagnostic category. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Matson, Johnny L.] 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. EM Johnmatson@aol.com CR Barrett S, 2004, AUTISM, V8, P61, DOI 10.1177/1362361304040640 Bishop DVM, 2002, J CHILD PSYCHOL PSYC, V43, P917, DOI 10.1111/1469-7610.00114 Bradley EA, 2004, J AUTISM DEV DISORD, V34, P151, DOI 10.1023/B:JADD.0000022606.97580.19 Bryson SE, 1998, MENT RETARD DEV D R, V4, P97, DOI 10.1002/(SICI)1098-2779(1998)4:2<97::AID-MRDD6>3.0.CO;2-U Buitelaar JK, 1998, J CHILD PSYCHOL PSYC, V39, P911, DOI 10.1017/S0021963098002820 Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 Charman T, 2002, EUR CHILD ADOLES PSY, V11, P249, DOI 10.1007/s00787-002-0297-8 Charman T., 2006, SOCIAL COMMUNICATION Clark T, 1999, EUR CHILD ADOLES PSY, V8, P50 COHEN D, 1987, J AM ACAD CHILD ADOL, V25, P213 Cohen IL, 2003, J AUTISM DEV DISORD, V33, P31, DOI 10.1023/A:1022226403878 EAVES LC, 1994, J AUTISM DEV DISORD, V24, P3, DOI 10.1007/BF02172209 Eaves RC, 2000, PSYCHOL SCHOOLS, V37, P311, DOI 10.1002/1520-6807(200007)37:4<323::AID-PITS2>3.0.CO;2-S Fein D, 1999, CHILD NEUROPSYCHOL, V5, P1, DOI 10.1076/chin.5.1.1.7075 FOLSTEIN S, 2000, ASPERGER SYNDROME, P159 Frazier J. 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PD JAN-MAR PY 2007 VL 1 IS 1 BP 75 EP 84 DI 10.1016/j.rasd.2006.09.001 PG 10 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400007 ER PT J AU Lewis, FM Murdoch, BE Woodyatt, GC AF Lewis, Fiona M. Murdoch, Bruce E. Woodyatt, Gail C. TI Linguistic abilities in children with autism spectrum disorder SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Article DE Autism spectrum disorder; Clinical Evaluation of Language Fundamentals-Fourth Edition; DSM-IV; Developmental language history AB Background: Two broad approaches have been used to examine linguistic skills in Asperger syndrome (AS) and high functioning autism (HFA). One approach has aimed at determining the external validity of each diagnosis by investigating whether developmental language history, which differentiates AS from HFA, is relevant in long-term linguistic outcomes. Ail alternative approach, viewing AS and HFA as presentations on an autism spectrum (ASD), has investigated Subgroups within the spectrum based on linguistic performance. Neither approach, however, has provided an in-depth description of the linguistic difficulties experienced in ASD necessary for therapy planning. Purpose: To provide clinically applicable research findings to extend the clinical understanding of the linguistic difficulties in ASD by: (I) comparing the linguistic skills in ASD with those of normally developing controls (2) comparing the linguistic skills of children with ASD re-classified as AS and HFA using DSM-IV language criterion; (3) documenting the heterogeneity within a group of children with ASD by investigating within-group differences. Methods and procedures: Twenty children (aged 9; 0-17; 1 years) with a diagnosis of ASD were assessed using the Clinical Evaluation of Language Fundamentals-Fourth Edition (CELF-4) and the Test of Nonverbal Intelligence Second Edition (TONI-2). Performance by ASD participants was compared to typically developing peers. Re-classification of individuals with ASD its AS or HFA was undertaken using DSM-IV language criterion to determine between-group differences on linguistic measures. Hiearchical cluster analysis was undertaken using the ASD performance oil the CELF-4 to examine within-group differences based oil linguistic abilities. Outcomes and results: There were significant differences between the ASD children and normally developing peers oil a range of linguistic measures. There were no significant differences between the children re-classified as AS and HFA on the comprehensive linguistic assessment. Subgroups within ASD, based oil linguistic performance, could be identified. Conclusions and implications: Collectively, the children with ASD in the study had a range of compromised linguistic skills relative to their peers. Children re-classified as AS could not be differentiated from children re-classified as HFA on current linguistic performance. An examination Of Subgroups of ASD participants revealed the heterogeneous nature of the linguistic skills associated with ASD, where linguistic proficiency ranged from above average performance to severe difficulties. The results of the study are discussed in terms of the clinical applicability of the findings. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Lewis, Fiona M.] Univ Queensland, Div Speech Pathol, Sch Hlth & Rehabil Sci, Brisbane, Qld 4072, Australia. RP Lewis, FM (reprint author), Univ Queensland, Div Speech Pathol, Sch Hlth & Rehabil Sci, Brisbane, Qld 4072, Australia. 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Autism Spectr. Disord. PD JAN-MAR PY 2007 VL 1 IS 1 BP 85 EP 100 DI 10.1016/j.rasd.2006.08.001 PG 16 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400008 ER PT J AU Accordino, R Comer, R Heller, WB AF Accordino, Robert Comer, Ronald Heller, Wendy B. TI Searching for music's potential: A critical examination of research on music therapy with individuals with autism SO RESEARCH IN AUTISM SPECTRUM DISORDERS LA English DT Review DE Autism; Music therapy; Musical ability ID CHILDREN; METAANALYSIS; ADOLESCENTS AB The authors conducted it literature review on music therapy for individuals with autism because of the frequent use of music therapy for those with autism and recent research on the musical abilities of this Population. To accomplish this narrative review, articles were searched from relevant databases, reference lists from articles, and book chapters to provide a thorough critique of past research, which was categorized according to the area of symptomology the therapy intended to treat (social, communicative, behavioral). Music therapists and researchers have carried out mostly case studies and it Surprisingly limited number of empirical investigations. Although these reports provide limited empirical support of the therapy with this population, they have utilized a wide array of creative techniques and varying types of music therapy worthy of discussion. The qualities of necessary future empirical investigations are explored. (C) 2006 Elsevier Ltd. All rights reserved. C1 [Accordino, Robert] Univ Oxford, Dept Expt Psychol, Oxford OX1 2JD, England. [Accordino, Robert; Comer, Ronald; Heller, Wendy B.] Princeton Univ, Princeton, NJ 08544 USA. RP Accordino, R (reprint author), Mt Sinai Sch Med, 50 E 98th St,Unit 2E, New York, NY 10029 USA. EM robert.accordino@psy.ox.ac.uk CR ALVIN J, 1991, MUSIC THERAPY AUTIST APPLEBAUM E, 1979, J AUTISM DEV DISORD, V9, P279, DOI 10.1007/BF01531742 Berger D. S., 2002, MUSIC THERAPY SENSOR Bettison S, 1996, J AUTISM DEV DISORD, V26, P361, DOI 10.1007/BF02172480 Bonnel A, 2003, J COGNITIVE NEUROSCI, V15, P226, DOI 10.1162/089892903321208169 BROWNELL M, 2002, J MUSIC THER, V34, P117 DILEO C, 2000, MUSIC THERAPY ENCY P, V5, P366 Edelson SM, 1999, FOCUS AUTISM OTHER D, V14, P73, DOI 10.1177/108835769901400202 EDGERTON CL, 1994, J MUSIC THER, V31, P31 Evers S, 1992, Acta Paedopsychiatr, V55, P157 Foxton JM, 2003, BRAIN, V126, P2703, DOI 10.1093/brain/awg274 Gillberg C., 1997, AUTISM, V1, P97, DOI 10.1177/1362361397011009 Gold C, 2004, J CHILD PSYCHOL PSYC, V45, P1054, DOI 10.1111/j.1469-7610.2004.t01-1-00298.x Gold C, 2006, COCHRANE DB SYST REV, DOI 10.1002/14651858.CD004381.pub2 Griggs-Drane E. 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Autism Spectr. Disord. PD JAN-MAR PY 2007 VL 1 IS 1 BP 101 EP 115 DI 10.1016/j.rasd.2006.08.002 PG 15 WC Education, Special; Psychology, Developmental; Psychiatry; Rehabilitation SC Education & Educational Research; Psychology; Psychiatry; Rehabilitation GA V89GO UT WOS:000206033400009 ER PT J AU Siklos, S Kerns, KA AF Siklos, Susan Kerns, Kimberly A. TI Assessing the diagnostic experiences of a small sample of parents of children with autism spectrum disorders SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE pervasive developmental disorders; autism spectrum disorders; autism; diagnosis; symptomatology ID SCREENING QUESTIONNAIRE; EARLY RECOGNITION; ASPERGER-SYNDROME; FAMILIES; 1ST; DISTURBANCES; SERVICES; CARE; AGE AB Although no Canadian studies have been conducted, studies suggest parents of children with autism experience difficulties obtaining a diagnosis for their child. Fifty-six parents of children with autism completed three questionnaires providing information on the families' demographics, parents' experiences throughout the diagnostic process, and their child's autistic symptornatology. These parents experienced significant difficulties obtaining a diagnosis for their child. Parents saw an average of 4.5 professionals, and waited almost 3 years to receive a diagnosis following their first visit to a professional regarding their child's development. The impact of autistic symptomatology on the diagnostic process is discussed. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Victoria, Dept Psychol, Victoria, BC V8W 3P5, Canada. RP Kerns, KA (reprint author), Univ Victoria, Dept Psychol, POB 3050, Victoria, BC V8W 3P5, Canada. EM kkerns@uvic.ca CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Baghdadli A, 2003, EUR CHILD ADOLES PSY, V12, P122, DOI 10.1007/s00787-003-0314-6 BENTOVIM A, 1972, BRIT MED J, V3, P579 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Charvin G, 2002, SINGLE MOL, V3, P43, DOI 10.1002/1438-5171(200204)3:1<43::AID-SIMO43>3.3.CO;2-J CHUNG M, 1995, ED CHILD PSYCHOL, V12, P31 COTTRELL DJ, 1990, CHILD CARE HLTH DEV, V16, P211, DOI 10.1111/j.1365-2214.1990.tb00655.x Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 ERWIN WJ, 2002, J MENTAL HLTH COUNSE, V24, P247 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Gillberg C, 1996, EUR CHILD ADOLES PSY, V5, P67 HO HH, 2001, BC MED J, V43, P272 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Kabot S, 2003, PROF PSYCHOL-RES PR, V34, P26, DOI 10.1037/0735-7028.34.1.26 Kanner L, 1943, NERV CHILD, V2, P217 KONSTANTAREAS MM, 1989, CAN J PSYCHIAT, V34, P549 KONSTANTAREAS MM, 1990, J MARITAL FAM THER, V16, P59, DOI 10.1111/j.1752-0606.1990.tb00045.x KOPE TM, 2001, BC MED J, V43, P266 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x Leff P. T., 1992, FAMILY SYSTEMS MED, V10, P147, DOI 10.1037/h0089203 Nissenbaum M. S., 2002, FOCUS AUTISM OTHER D, V17, P30, DOI [10.1177/108835760201700103, DOI 10.1177/108835760201700103] OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Osterling JA, 2002, DEV PSYCHOPATHOL, V14, P239 Phillips KM, 2004, PROF PSYCHOL-RES PR, V35, P281, DOI 10.1037/0735-7028.35.3.281 QUINE L, 1986, SOC SCI MED, V22, P53, DOI 10.1016/0277-9536(86)90308-4 Selfe L, 2002, ED PSYCHOL PRACTICE, V18, P335, DOI 10.1080/0266736022000022039 Siegel B., 1996, WORLD AUTISTIC CHILD SMITH B, 1994, J AUTISM DEV DISORD, V24, P551, DOI 10.1007/BF02172137 STALLARD P, 1992, CHILD CARE HLTH DEV, V18, P197, DOI 10.1111/j.1365-2214.1992.tb00354.x White C, 2002, DRUG-EDUC PREV POLIC, V9, P305, DOI 10.1080/09687630110116470 Wing L, 1988, DIAGNOSIS ASSESSMENT WOOLLEY H, 1989, BRIT MED J, V298, P1623 NR 33 TC 53 Z9 54 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 JAN-FEB PY 2007 VL 28 IS 1 BP 9 EP 22 DI 10.1016/j.ridd.2005.09.003 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 134MN UT WOS:000244087600002 PM 16442261 ER PT J AU Crockett, JL Fleming, RK Doepke, KJ Stevens, JS AF Crockett, Jennifer L. Fleming, Richard K. Doepke, Karla J. Stevens, Jenny S. TI Parent training: Acquisition and generalization of discrete trials teaching skills with parents of children with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE parent training; discrete trials teaching; autism ID FUTURE-RESEARCH; YOUNG-CHILDREN; INTERVENTION AB This study examined the effects of an intensive parent training program on the acquisition and generalization of discrete trial teaching (DTT) procedures with two parents of children with autism. Over the course of the program, parents applied the DTT procedures to teach four different functional skills to their children, which allowed for an assessment of "free" and programmed generalization across stimulus exemplars. Parent training was conducted by the first author utilizing instructions, demonstrations, roleplay, and practice with feedback. Parents' use of DTT skills and children's correct and incorrect responding were measured. A within-subject multiple-baseline across stimulus exemplars (functional skills taught) design was employed both to demonstrate control of the training program over parents' correct use of DTT, and to allow a preliminary investigation of the generalized effects of training to multiple stimulus exemplars. Results demonstrate initial control of the training program over parent responding, and the extent to which each parent extended her use of DTT procedures across untrained and topographically different child skills. The potential for designing more generalizable and thus more cost-effective parent training programs is discussed. (c) 2005 Elsevier Ltd. All rights reserved. C1 Auburn Univ, Auburn, AL 36849 USA. RP Crockett, JL (reprint author), Auburn Univ, Auburn, AL 36849 USA. EM crockettj@kennedykrieger.org CR Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 Baker B. L., 1989, PARENT TRAINING DEV BALDWIN TT, 1988, PERS PSYCHOL, V41, P63, DOI 10.1111/j.1744-6570.1988.tb00632.x BRUDER MB, 1985, J DIVISION EARLY CHI, V9, P136 Dawson G., 1997, EFFECTIVENESS EARLY HARRIS SL, 1983, FAMILIES DEV DISABLE KAISER AP, 1986, FAMILIES HANDICAPPED, P219 KOEGEL RL, 1977, J APPL BEHAV ANAL, V10, P197, DOI 10.1901/jaba.1977.10-197 KOEGEL RL, 1978, J APPL BEHAV ANAL, V11, P95, DOI 10.1901/jaba.1978.11-95 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 LOVAAS OI, 1973, J APPL BEHAV ANAL, V6, P131, DOI 10.1901/jaba.1973.6-131 McConnell SR, 2002, J AUTISM DEV DISORD, V32, P351, DOI 10.1023/A:1020537805154 MILAN MA, 1990, INT HDB BEAHV MODIFI, P67 Moes DR, 2002, J AUTISM DEV DISORD, V32, P519, DOI 10.1023/A:1021298729297 *NAT RES COUNC, 2001, DIV BEHAV SOC SCI ED NEEF NA, 1995, J APPL BEHAV ANAL, V28, P333, DOI 10.1901/jaba.1995.28-333 Oliver J. R., 1997, INT J TRAINING DEV, V1, P173, DOI 10.1111/1468-2419.00017 Reid D. H., 1995, MOTIVATING HUMAN SER Smith T., 2001, PRESCHOOL ED PROGRAM, P29 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 STOKES TF, 1974, J APPL BEHAV ANAL, V7, P599, DOI 10.1901/jaba.1974.7-599 Wolery M, 2002, J AUTISM DEV DISORD, V32, P463, DOI 10.1023/A:1020598023809 NR 23 TC 29 Z9 30 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 JAN-FEB PY 2007 VL 28 IS 1 BP 23 EP 36 DI 10.1016/j.ridd.2005.10.003 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 134MN UT WOS:000244087600003 PM 16338118 ER PT J AU Sigafoos, J Ganz, JB O'Reilly, M Lancioni, GE Schlosser, RW AF Sigafoos, Jeff Ganz, Jennifer B. O'Reilly, Mark Lancioni, Giulio E. Schlosser, Ralf W. TI Assessing correspondence following acquisition of an exchange-based communication system SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE exchange-based communication; requesting; acquisition; correspondence ID YOUNG-CHILDREN; AUTISM; DISABILITIES; INDIVIDUALS; STUDENT; SPEECH; PECS AB Two students with developmental disabilities were taught to request six snack items. Requesting involved giving a graphic symbol to the trainer in exchange for the matching snack item. Following acquisition, we assessed the correspondence between requests and subsequent item selections by requiring the student to select the previously requested snack item from an array containing all six items. The effects of acquisition training were evaluated in a multiple-probe across subjects design. Acquisition was achieved in from 9 to 29 trials per item. Following acquisition, Jason showed a high level of correspondence between requesting and selecting, but Ryan required additional training to achieve correspondence. These data support the use of exchange-based communication systems, but suggest that some students may require explicit correspondence training. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ Texas San Antonio, Dept Special Educ, Austin, TX 78712 USA. Univ Tasmania, Hobart, Tas 7001, Australia. Univ Texas San Antonio, San Antonio, TX 78285 USA. Univ Bari, I-70121 Bari, Italy. RP O'Reilly, M (reprint author), Univ Texas San Antonio, Dept Special Educ, 1 Univ Stn,D5300, Austin, TX 78712 USA. EM markoreilly@mail.utexas.edu CR American Association on Mental Retardation, 1992, MENT RET DEF CLASS S American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bondy A, 2001, BEHAV MODIF, V25, P725, DOI 10.1177/0145445501255004 Bondy A, 2004, BEHAV ANALYST, V27, P247 Carroll MD, 1983, VITAL HLTH STAT, V11, P1 Charlop-Christy MH, 2002, J APPL BEHAV ANAL, V35, P213, DOI 10.1901/jaba.2002.35-213 DUKER P, 1994, J INTELL DISABIL RES, V38, P177 DUKER PC, 1993, RES DEV DISABIL, V14, P39, DOI 10.1016/0891-4222(93)90004-4 Ganz JB, 2004, J AUTISM DEV DISORD, V34, P395, DOI 10.1023/B:JADD.0000037416.59095.d7 Kennedy C, 2005, SINGLE CASE DESIGNS Kravits TR, 2002, J AUTISM DEV DISORD, V32, P225, DOI 10.1023/A:1015457931788 Magiati I, 2003, AUTISM, V7, P297, DOI 10.1177/1362361303007003006 *MAY JOHNS CO, 1998, PICT COMM SYMB COMB Reichle J., 1991, IMPLEMENTING AUGMENT Reichle J., 2002, EXEMPLARY PRACTICES REICHLE J, 1989, J ASSOC PERS SEVERE, V14, P75 REICHLE J, 1986, J ASSOC PERS SEVERE, V11, P68 Rodi MS, 2000, J ASSOC PERS SEVERE, V25, P175, DOI 10.2511/rpsd.25.3.175 Schepis MM, 1998, J APPL BEHAV ANAL, V31, P561, DOI 10.1901/jaba.1998.31-561 Schwartz IS, 1998, TOP EARLY CHILD SPEC, V18, P144 Sigafoos J, 2003, AUGMENTATIVE ALTERNA, V19, P37, DOI 10.1080/0743461032000056487 Sigafoos J., 1992, DEV DISABILITIES B, V20, P1 SIGAFOOS J, 1999, AUGMENTATIVE ALTERNA, V15, P135, DOI 10.1080/07434619912331278635 SUNDBERG ML, 1981, DISS ABSTR INT, V41, P3922 Tincani M., 2004, FOCUS AUTISM OTHER D, V19, P152, DOI DOI 10.1177/10883576040190030301 YAMAMOTO J, 1988, J APPL BEHAV ANAL, V21, P57, DOI 10.1901/jaba.1988.21-57 NR 26 TC 14 Z9 14 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 JAN-FEB PY 2007 VL 28 IS 1 BP 71 EP 83 DI 10.1016/j.ridd.2005.12.002 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 134MN UT WOS:000244087600008 PM 16546350 ER PT J AU Jarbrink, K McCrone, P Fornbonne, E Zanden, H Knapp, M AF Jarbrink, Krister McCrone, Paul Fornbonne, Eric Zanden, Hakan Knapp, Martin TI Cost-impact of young adults with high-functioning autistic spectrum disorder SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE cost analysis; supported employment; autism; Asperger syndrome ID ASPERGERS SYNDROME; PROGRAM; MEN AB There is a general lack of information about the economic impact of autistic spectrum disorder (ASD), particularly regarding adults and those with high-functioning ASD. In this study, the societal economic consequences of ASD were investigated using a sample of young high-functioning adults in need of employment support. A methodology for the collection of cost information was developed and information about how to avoid obstacles in the collection process was obtained. Today, many people with ASD who would be able to function in open employment do not get this opportunity. This study demonstrated that ASD results in high costs and indicates that a lack of supported employment programmes for people with ASD may have negative resource consequences for the economy. The study also contributes towards a methodology of economically evaluating supported employment programs as well as other interventions for people with high-functioning ASD. (c) 2006 Elsevier Ltd. All rights reserved. C1 Inst Psychiat, Hlth Serv Res Dept, Ctr Econ Mental Hlth, London SE5 8AF, England. McGill Univ, Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3A 2T5, Canada. Natl Autism Soc, RFA, Stockholm, Sweden. RP Jarbrink, K (reprint author), Inst Psychiat, Hlth Serv Res Dept, Ctr Econ Mental Hlth, De Crespigny Pk, London SE5 8AF, England. EM k.jarbrink@iop.kcl.ac.uk RI McCrone, Paul/D-1793-2010 CR Alcock J., 2003, EVALUATION PROSPECTS Beecham J, 2001, MEASURING MENTAL HLT, V2nd, P200 Beecham J, 1992, MEASURING MENTAL HLT, P203 Cimera RE, 1998, MENT RETARD, V36, P280, DOI 10.1352/0047-6765(1998)036<0280:AIWSMR>2.0.CO;2 FERRIE JE, 1995, BRIT MED J, V311, P1264 Henriksson F, 2001, EUR J NEUROL, V8, P27, DOI 10.1046/j.1468-1331.2001.00169.x HOWLIN P, 1999, AUTISM, P229 Jarbrink K, 2003, J AUTISM DEV DISORD, V33, P395, DOI 10.1023/A:1025058711465 JOHANNESSON M, 1995, J INTERN MED, V237, P19 JOHANNESSON M, 1992, J HYPERTENS, V10, P1063 Keel JH, 1997, J AUTISM DEV DISORD, V27, P3, DOI 10.1023/A:1025813020229 Tantam D, 2003, CHILD ADOL PSYCH CL, V12, P143, DOI 10.1016/S1056-4993(02)00053-6 TANTAM D, 1988, J CHILD PSYCHOL PSYC, V29, P245, DOI 10.1111/j.1469-7610.1988.tb00713.x WING L, 1981, PSYCHOL MED, V11, P115 NR 14 TC 21 Z9 21 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 JAN-FEB PY 2007 VL 28 IS 1 BP 94 EP 104 DI 10.1016/j.ridd.2005.11.002 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 134MN UT WOS:000244087600010 PM 16551499 ER PT J AU Bellini, S Akullian, J Hopf, A AF Bellini, Scott Akullian, Jennifer Hopf, Andrea TI Increasing social engagement in young children with autism spectrum disorders using video self-modeling SO SCHOOL PSYCHOLOGY REVIEW LA English DT Article ID SINGLE-SUBJECT RESEARCH; INTERVENTION; INITIATIONS; STUDENTS; OUTCOMES; SKILLS AB An emerging body of research demonstrates the effectiveness of video self-modeling (VSM) in addressing social, communication, and behavioral functioning of children with autism spectrum disorders. The primary purpose of this study was to examine the benefits of a VSM intervention in increasing the social engagement of young children with autism spectrum disorders. The study expands previous research on VSM by measuring social interactions with same-aged peers in a natural setting rather than with adults in a controlled clinical setting. Intervention and maintenance effects were measured in addition to the social validity of the VSM procedure. The results of the VSM intervention are provided, and implications for practice and future research are discussed. C1 [Bellini, Scott; Akullian, Jennifer; Hopf, Andrea] Indiana Univ, Indiana Resource Ctr Autism, Indiana Inst Disabil & Community, Bloomington, IN 47408 USA. RP Bellini, S (reprint author), Indiana Univ, Indiana Resource Ctr Autism, Indiana Inst Disabil & Community, 2853 East 10th St, Bloomington, IN 47408 USA. EM sbellini@indiana.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT BELLINI S, IN PRESS EXCEPTIONAL Bellini S., 2004, FOCUS AUTISM OTHER D, V19, P78, DOI DOI 10.1177/10883576040190020201 Busk PL, 1992, SINGLE CASE RES DESI, P187 Charlop-Christy MH, 2000, J AUTISM DEV DISORD, V30, P537, DOI 10.1023/A:1005635326276 Dowrick PW, 1999, APPL PREV PSYCHOL, V8, P23, DOI 10.1016/S0962-1849(99)80009-2 Gresham FM, 2001, EXCEPT CHILDREN, V67, P331 Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hitchcock CH, 2003, REM SPEC EDUC, V24, P36, DOI 10.1177/074193250302400104 Hume K, 2005, TOP EARLY CHILD SPEC, V25, P195, DOI 10.1177/02711214050250040101 Kazdin A. E., 1982, SINGLE CASE RES DESI Kehle TJ, 2002, PSYCHOL SCHOOLS, V39, P203, DOI 10.1002/pits.10031 McConnell SR, 2002, J AUTISM DEV DISORD, V32, P351, DOI 10.1023/A:1020537805154 National Research Council, 2001, ED CHILDR AUT Nikopoulos CK, 2004, J APPL BEHAV ANAL, V37, P93, DOI 10.1901/jaba.2004.37-93 Rogers SJ, 2000, J AUTISM DEV DISORD, V30, P399, DOI 10.1023/A:1005543321840 RUBIN KH, 2001, DEV PSYCHOPATHOL, P435 SCHWARTZ IS, 1991, J APPL BEHAV ANAL, V24, P189, DOI 10.1901/jaba.1991.24-189 Scruggs TE, 1998, BEHAV MODIF, V22, P221, DOI 10.1177/01454455980223001 SCRUGGS TE, 1987, REM SPEC EDUC, V8, P24 Shattuck PT, 2006, PEDIATRICS, V117, P1028, DOI 10.1542/peds.2005-1516 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 Tantam D., 2000, AUTISM INT J RES PRA, V4, P47, DOI DOI 10.1177/1362361300004001004 Ysseldyke J., 1997, SCH PSYCHOL BLUEPRIN NR 24 TC 35 Z9 35 PU NATL ASSOC SCHOOL PSYCHOLOGISTS PI BETHESDA PA 4340 EAST WEST HWY, STE 402, BETHESDA, MD 20814 USA SN 0279-6015 J9 SCHOOL PSYCHOL REV JI Sch. Psychol. Rev. PY 2007 VL 36 IS 1 BP 80 EP 90 PG 11 WC Psychology, Educational SC Psychology GA 299DU UT WOS:000255736800005 ER PT J AU Adkins, K Goldman, S Crowe, C Malow, B AF Adkins, K. Goldman, S. Crowe, C. Malow, B. TI Practical tips for conducting successful actigraphy research in children with autism spectrum disorders SO SLEEP LA English DT Meeting Abstract CT 21st Annual Meeting of the Association-Professional-Sleep-Societies CY JUN 09-14, 2007 CL Minneapolis, MN C1 Vanderbilt Univ, Nashville, TN USA. NR 0 TC 0 Z9 0 PU AMER ACADEMY SLEEP MEDICINE PI WESTCHESTER PA ONE WESTBROOK CORPORATE CENTER STE 920, WESTCHESTER, IL 60154 USA SN 0161-8105 J9 SLEEP JI Sleep PY 2007 VL 30 SU S MA 230 BP A79 EP A80 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 164HR UT WOS:000246224900232 ER PT J AU Cruz, M Kaleyias, J Adams, R Legido, A Kothare, S AF Cruz, M. Kaleyias, J. Adams, R. Legido, A. Kothare, S. TI Insomnia as a presenting manifestation of autism in children SO SLEEP LA English DT Meeting Abstract CT 21st Annual Meeting of the Association-Professional-Sleep-Societies CY JUN 09-14, 2007 CL Minneapolis, MN C1 St Christophers Hosp Children, Philadelphia, PA 19133 USA. NR 0 TC 0 Z9 0 PU AMER ACADEMY SLEEP MEDICINE PI WESTCHESTER PA ONE WESTBROOK CORPORATE CENTER STE 920, WESTCHESTER, IL 60154 USA SN 0161-8105 J9 SLEEP JI Sleep PY 2007 VL 30 SU S MA 675 BP A229 EP A229 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 164HR UT WOS:000246224900676 ER PT J AU Meltzer, L Leas, C Reamy, A AF Meltzer, L. Leas, C. Reamy, A. TI Sleep and daytime functioning in children with autism spectrum disorders and their parents SO SLEEP LA English DT Meeting Abstract CT 21st Annual Meeting of the Association-Professional-Sleep-Societies CY JUN 09-14, 2007 CL Minneapolis, MN C1 Childrens Hosp Philadelphia, Philadelphia, PA 19104 USA. St Josephs Univ, Philadelphia, PA 19131 USA. NR 0 TC 0 Z9 0 PU AMER ACADEMY SLEEP MEDICINE PI WESTCHESTER PA ONE WESTBROOK CORPORATE CENTER STE 920, WESTCHESTER, IL 60154 USA SN 0161-8105 J9 SLEEP JI Sleep PY 2007 VL 30 SU S MA 285 BP A98 EP A98 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 164HR UT WOS:000246224900287 ER PT J AU Artar, M AF Artar, Muege TI Adolescent egocentrism and theory of mind: In the context of family relations SO SOCIAL BEHAVIOR AND PERSONALITY LA English DT Article; Proceedings Paper CT 9th Conference of the European-Association-for-Research-on-Adolescence CY MAY, 2004 CL Oporto, PORTUGAL SP European Assoc Res Adolescence DE theory of mind; egocentricism; family relations; adolescent ID NORMAL ADULTS; ASPERGER-SYNDROME; AUTISM; PREADOLESCENCE; CHILDREN; BELIEFS; EMOTION; EYES AB While dealing with the issues of theory of mind (ToM) and false belief, the author realized that adolescents have similar false beliefs to those of children, but in a more complex manner. These false beliefs seem to be related to a typical developmental issue called "egocentrism." Participants in this study were 11 adolescents (ages 16-18) and their families from a middle SES high school. ToM stories and new imaginary audience and personal fable categories were examined. Every adolescent was interviewed about his or her family relationships. To observe them all together, the author wanted to analyze adolescents' most sophisticated relations: family relations. The results seemed to indicate that in the context of their family, adolescents have more emotional inference than social inference or intentions - that is, they have more thoughts about their parents' feelings. If they have to describe their parents' relations, they seem to have more ToM (overall inference). C1 Ankara Univ, Fac Educ Sci, TR-06100 Ankara, Turkey. RP Artar, M (reprint author), Ankara Univ, Fac Educ Sci, TR-06100 Ankara, Turkey. 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Behav. Pers. PY 2007 VL 35 IS 9 BP 1211 EP 1220 PG 10 WC Psychology, Social SC Psychology GA 257RO UT WOS:000252816400006 ER PT J AU Downs, A Strand, P Cerna, S AF Downs, Andrew Strand, Paul Cerna, Sandra TI Emotion understanding in English- and Spanish-speaking preschoolers enrolled in head start SO SOCIAL DEVELOPMENT LA English DT Article DE reliability; validity; emotion understanding; theory of mind ID INDIVIDUAL-DIFFERENCES; FALSE-BELIEF; CULTURAL-DIFFERENCES; FACIAL EXPRESSIONS; SOCIAL COGNITION; YOUNG-CHILDREN; AUTISM; UNIVERSALS; LANGUAGE; BEHAVIOR AB Research assessing children's emotion understanding has increased over the past several years. Despite the proliferation of research, there have been few studies conducted examining the development of emotion understanding in children from diverse backgrounds. Further, there has been no research conducted examining the psychometric properties of emotion understanding measures when used with children from diverse backgrounds. 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PY 2007 VL 16 IS 3 BP 410 EP 439 DI 10.1111/j.1467-9507.2007.00391.x PG 30 WC Psychology, Developmental SC Psychology GA 204NR UT WOS:000249051800002 ER PT J AU Baker, DL AF Baker, Dana Lee TI Defining autism in Canada: Unfolding the public aspects of neurological disability SO SOCIAL SCIENCE JOURNAL LA English DT Article ID POLICY; HISTORY; LEVEL AB Modern disability policy seeks a balance between individual and social responsibility for disability. Striking this balance involves redefining issues related to disability. This article presents an analysis of the issue definition process on autism in Canada. The findings suggest although autism became an increasingly present issue in public discourse in Canada during the last 20 years, no specific aspect of the autism experience became defined as an urgent public problem. Furthermore, public discourse surrounding autism focuses on health care, challenging ongoing development of rights-based disability policy. (C) 2007 Elsevier Inc. All rights reserved. C1 Washington State Univ, Dept Polit Sci & Criminal Justice, Vancouver, WA 98686 USA. RP Baker, DL (reprint author), Washington State Univ, Dept Polit Sci & Criminal Justice, Vancouver, WA 98686 USA. 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PY 2007 VL 44 IS 4 BP 687 EP 697 DI 10.1016/j.soscij.2007.10.010 PG 11 WC Social Sciences, Interdisciplinary SC Social Sciences - Other Topics GA 250UV UT WOS:000252327700008 ER PT J AU Guclu, B Tanidir, C Mukaddes, NM Unal, F AF Guclu, Burak Tanidir, Canan Mukaddes, Nahit Motavalli Unal, Fatih TI Tactile sensitivity of normal and autistic children SO SOMATOSENSORY AND MOTOR RESEARCH LA English DT Article DE somatosensation; Pacinian channel; non-Pacinian I channel; hyper-sensitivity; hypo-sensitivity; pervasive developmental disorder ID INFORMATION-PROCESSING CHANNELS; DEFICIT-HYPERACTIVITY DISORDER; SENSORY PROFILE; VIBROTACTILE THRESHOLDS; INFANTILE-AUTISM; RESPONSES; TOUCH; DEFENSIVENESS; DISABILITIES; DYSFUNCTION AB Many children with autistic spectrum disorders have unusual reactions to certain sensory stimuli. These reactions vary along a hyper- to hypo-responsivity continuum. For example, some children overreact to weak sensory input, but others do not respond negatively to even strong stimuli. It is typically assumed that this deviant responsivity is linked to sensitivity, although the particular stage of sensory processing affected is not known. Psychophysical vibrotactile thresholds of six male children (age: 8-12) who were diagnosed to have autistic spectrum disorders and six normal male children ( age: 7-11) were measured by using a two-alternative forced-choice task. The tactile stimuli were sinusoidal displacements and they were applied on the terminal phalanx of the left middle finger of each subject. By using a forward-masking paradigm, 40-and 250-Hz thresholds of the Pacinian tactile channel and 40-Hz threshold of the Non-Pacinian I tactile channel were determined. There was no significant difference between the thresholds of autistic and normal children, and the autistic children had the same detection and masking mechanisms as the normal children. The sensory responsivity of each subject was tested by clinical questionnaires, which showed again no difference between the two subject groups. Furthermore, no significant correlations could be found between the questionnaire data and the psychophysical thresholds. However, there was a high correlation between the data from the tactile and emotional subsets of the questionnaires. These results support the hypothesis that the hyper-and hypo-responsivity to touch, which is sometimes observed in autistic spectrum disorders, is not a perceptual sensory problem, but may probably be emotional in origin. C1 Bogazici Univ, Inst Biomed Engn, TR-34342 Istanbul, Turkey. Istanbul Univ, Istanbul Med Sch, Autism Clin, Child & Adolescent Psychiat Dept, Istanbul, Turkey. 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Coll. Rec. PY 2007 VL 109 IS 12 BP 2579 EP 2600 PG 22 WC Education & Educational Research SC Education & Educational Research GA 273PH UT WOS:000253943700001 ER PT J AU Ventegodt, S Kandel, I Merrick, J AF Ventegodt, Soren Kandel, Isack Merrick, Joav TI Clinical holistic medicine (mindful short-term psychodynamic psychotherapy complimented with bodywork) in the treatment of schizophrenia (ICD10-F20/DSM-IV code 295) and other psychotic mental diseases SO THESCIENTIFICWORLDJOURNAL LA English DT Review DE mental health; psychiatry; holistic health and medicine ID HIPPOCRATIC PELVIC MASSAGE; CHILDHOOD SEXUAL-ABUSE; QUALITY-OF-LIFE; SCALE SOC-II; PHYSICAL HEALTH; BIOLOGICAL INFORMATION; CASE STORY; ANTONOVSKYS SENSE; CHRONIC PAIN; FOLLOW-UP AB Clinical holistic medicine (CHM) has developed into a system that can also be helpful with mentally ill patients. CHM therapy supports the patient through a series of emotionally challenging, existential, and healing crises. The patient's sense of coherence and mental health can be recovered through the process of feeling old repressed emotions, understanding life and self, and finally letting go of negative beliefs and delusions. The Bleuler's triple condition of autism, disturbed thoughts, and disturbed emotions that characterizes the schizophrenic patient can be understood as arising from the early defense of splitting, caused by negative learning from painful childhood traumas that made the patient lose sense of coherence and withdraw from social contact. Self-insight gained through the therapy can allow the patients to take their bodily, mental, and spiritual talents into use. At the end of therapy, the patients are once again living a life of quality centered on their life mission and they relate to other people in a way that systematically creates value. There are a number of challenges meeting the therapist who works with schizophrenic and psychotic patients, from the potential risk of experiencing a patient's violence, to the obligation to contain the most difficult and embarrassing of feelings when the emotional and often also sexual content of the patient's unconsciousness becomes explicit. There is a long, well-established tradition for treating schizophrenia with psychodynamic therapy, and we have found that the combination of bodywork and psychotherapy can enhance and accelerate the therapy and might improve the treatment rate further. C1 [Ventegodt, Soren] Qual Life Res Ctr, DK-1452 Copenhagen K, Denmark. [Ventegodt, Soren] Res Clin Holist Med, Copenhagen, Denmark. [Ventegodt, Soren] Nord Sch Holist Med, Copenhagen, Denmark. [Ventegodt, Soren] Scandinavian Fdn Holist Med, Sandvika, Norway. [Ventegodt, Soren] Interuniv Coll, Graz, Austria. [Kandel, Isack] Ariel Univ Ctr, Fac Social Sci, Dept Behav Sci, Samaria, Ariel, Israel. 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Multidisciplinary Sciences SC Environmental Sciences & Ecology; Science & Technology - Other Topics GA 288KD UT WOS:000254984400027 PM 18167614 ER PT J AU Coelho, CB Sanchez, TG Tyler, RS AF Coelho, Claudia Barros Sanchez, Tanit Ganz Tyler, Richard S. BE Langguth, B Hajak, G Kleinjung, T Cacace, A Moller, AR TI Hyperacusis, sound annoyance, and loudness hypersensitivity in children SO TINNITUS: PATHOPHYSIOLOGY AND TREATMENT SE Progress in Brain Research LA English DT Review; Book Chapter DE hyperacusis; tinnitus; loudness annoyance; children; cross-over study ID WILLIAMS-SYNDROME; INDIVIDUALS; AUTISM AB The objective of the present study was to estimate the prevalence of hyperacusis among school-aged children. We define hyperacusis as lowered loudness discomfort levels (LDL) associated with an abnormal annoyance to sounds. We used questionnaires, interviews, and estimates of LDL in a study of 506 children from 5 to 12 years of age from 15 different schools. Participants with LDL in the lowest 5th percentile were classified as having loudness hypersensitivity; an abnormal annoyance to sounds if they responded "yes" to the question "Are you bothered by any kind of sounds or noise?" could describe the sound, and were able to identify at least 10 sounds from a list of 20 as being annoying. Phonophobia was defined as a fear of sound. Children with LDL in the lowest 5th percentile typically had LDLs lower than 90 dB HL; 42% of the participants in this group were bothered by sounds and 3.2% had hyperacusis. Fifty percent of the participants with hyperacusis had tinnitus and mild hearing loss in the left ear was an associated risk factor. Phonophobia was experienced by 9% of the children. It is concluded that hyperacusis in children is prevalent, and should be considered in clinical examinations. C1 [Coelho, Claudia Barros; Sanchez, Tanit Ganz] Univ Sao Paulo, Sch Med, Dept Otolaryngol, Sao Paulo, Brazil. 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PY 2007 VL 26 IS 1 BP 97 EP 114 DI 10.1007/s11245-006-9012-6 PG 18 WC Philosophy SC Philosophy GA 176NT UT WOS:000247092800008 ER PT J AU Mukaddes, NM Herguner, S AF Mukaddes, Nahit Motavalli Herguner, Sabri TI Autistic disorder and 22q11.2 duplication SO WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY LA English DT Article DE 22q11.2 duplication; autistic disorder; chromosome 22; interphase FISH; velocardiofacial syndrome ID DELETION SYNDROME; CHROMOSOME 22Q11; MICRODUPLICATION AB Although several reports have described the co-occurrence of autism in subjects with chromosome 22 abnormalities including trisomy 22, translocation 20/22, 22q11.2 deletion, ring chromosome 22, and 22q13.3 deletion, there is no report with 22q11.2 duplication. We report a 9-year-old girl, referred to our department for her behavioural problems and language delay. She was diagnosed with autistic disorder according to DSM-IV criteria. Because of her dysmorphic characteristics comprising narrow face, narrow forehead, mandibular prognathism, synophrys, and operated cleft palate and cardiac problems, she had gone under cytogenetic analysis. Although she was ascertained as suspected velocardiofacial syndrome (VCFS), the duplication of 22q11.2 was detected by interphase fluorescence in situ hybridization. Previous reports on the psychiatric aspects of 22q11.2 duplication have shown the existence of hyperactivity, learning disability, speech problems, and aggressive behaviours but not autism. Moreover, the lack of reports of co-occurrence of autism and 22q11.2 duplication may be related to paucity as a result of technical problems. C1 Istanbul Univ, Istanbul Fac Med, Dept Child & Adolescent Psychiat, Istanbul, Turkey. RP Mukaddes, NM (reprint author), Sezai Selek Sok,Sevim Ap 7,D4, TR-80200 Istanbul, Turkey. EM nmotavalli@yahoo.com CR ALPAS B, 2002, THESIS ANKARA American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAIRAGHI S, 2004, AM J HUM GENET S, V75, P138 Carratala F, 1998, DEV MED CHILD NEUROL, V40, P492 Edelmann L, 1999, HUM MOL GENET, V8, P1157, DOI 10.1093/hmg/8.7.1157 Ensenauer RE, 2003, AM J HUM GENET, V73, P1027, DOI 10.1086/378818 Fine SE, 2005, J AUTISM DEV DISORD, V35, P461, DOI 10.1007/s10803-005-5036-9 GURKAN A, 2004, 2 IST AUT S ABSTR BO, V38 Hassed S, 2004, AM J HUM GENET S, V75, P151 Hassed SJ, 2004, CLIN GENET, V65, P400, DOI 10.1111/j.1399-0004.2004.00212.x Kozma C, 1998, AM J MED GENET, V81, P269, DOI 10.1002/(SICI)1096-8628(19980508)81:3<269::AID-AJMG12>3.0.CO;2-D LAMB A, 2004, AM J HUM GENET S, V75, P191 MacLean JE, 2000, AM J MED GENET, V90, P382, DOI 10.1002/(SICI)1096-8628(20000228)90:5<382::AID-AJMG7>3.0.CO;2-T Niklasson L, 2002, DEV MED CHILD NEUROL, V44, P44, DOI 10.1017/S0012162201001645 Portnoi MF, 2005, AM J MED GENET A, V137A, P47, DOI 10.1002/ajmg.a.30847 Prasad C, 2000, CLIN GENET, V57, P103, DOI 10.1034/j.1399-0004.2000.570203.x SOMERVILLE MJ, 2004, AM J HUM GENET S, V75, P55 Sparkes R, 2005, CARDIOL YOUNG, V15, P229, DOI 10.1017/S1047951105000466 SUCUOGLU B, 1996, PSIKIYATRI PSIKOLOJI, V4, P116 TURNER FW, 1962, CANCER RES, V22, P49 Vorstman JAS, 2006, MOL PSYCHIATR, V11, P18, DOI 10.1038/sj.mp.4001757 Yobb TM, 2005, AM J HUM GENET, V76, P865, DOI 10.1086/429841 NR 22 TC 36 Z9 36 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1562-2975 J9 WORLD J BIOL PSYCHIA JI World J. Biol. Psychiatry PY 2007 VL 8 IS 2 BP 127 EP 130 DI 10.1080/15622970601026701 PG 4 WC Psychiatry SC Psychiatry GA 171JO UT WOS:000246732300006 PM 17455106 ER PT J AU Kerbeshian, J Burd, L Tait, A AF Kerbeshian, Jacob Burd, Larry Tait, Alison TI Chain reaction or time bomb: A neuropsychiatric-developmental/neurodevelopmental formulation of tourettisms, pervasive developmental disorder, and schizophreniform symptomatology associated with PANDAS SO WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY LA English DT Article DE tourette's syndrome; pervasive developmental disorders; children; neuropsychiatric; PANDAS ID POSTSTREPTOCOCCAL AUTOIMMUNE DISORDERS; STREPTOCOCCAL INFECTION PANDAS; BASAL GANGLIA ANTIBODIES; CENTRAL-NERVOUS-SYSTEM; PSYCHIATRIC-DISORDERS; MONOCLONAL-ANTIBODY; RHEUMATIC-FEVER; TIC DISORDER; CHILDREN; AUTISM AB We present the case of a boy who over time sequentially exhibited symptoms consistent with a pervasive developmental disorder, schizophreniform symptornatology, multiple motor and vocal tics, and myoclonus. During this period he experienced multiple episodes of group A beta-haemolytic streptococcal (strep) infection confirmed by culture and serological studies. We speculate that paediatric autoimmune neuropsychiatric disorder associated with strep (PANDAS) may have served as an element in a complex chain of causation influencing the expression of his symptoms. Our main emphasis is to utilize our case study as an example of the application in case formulation of the neuropsychiatric developmental model and of the neurodevelopmental model on symptom ontogenesis and clinical outcome. C1 Univ N Dakota, Sch Med & Hlth Sci, Dept Pediat, Grand Forks, ND 58202 USA. Univ N Dakota, Sch Med & Hlth Sci, Dept Pediat, Grand Forks, ND 58202 USA. Lipp Carlson Lommen & Witucki Ltd, Grand Forks, ND USA. RP Burd, L (reprint author), Univ N Dakota, Sch Med & Hlth Sci, Dept Pediat, 501 N Columbia Rd, Grand Forks, ND 58202 USA. EM laburd@medicine.nodak.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bakker C, 2002, ACAD PSYCHIATR, V26, P219, DOI 10.1176/appi.ap.26.3.219 Baron-Cohen S, 1999, PSYCHOL MED, V29, P1151, DOI 10.1017/S003329179900896X Baron-Cohen S, 1999, J CHILD PSYCHOL PSYC, V40, P213 BURD L, 1987, J AM ACAD CHILD PSY, V26, P347, DOI 10.1097/00004583-198705000-00012 Church AJ, 2004, ARCH DIS CHILD, V89, P611, DOI 10.1136/adc.2003.031880 CLARKIN JF, 1992, J CONSULT CLIN PSYCH, V60, P904, DOI 10.1037//0022-006X.60.6.904 Cohen D J, 1997, Acta Paediatr Suppl, V422, P106 Costello EJ, 2003, ARCH GEN PSYCHIAT, V60, P837, DOI 10.1001/archpsyc.60.8.837 Dale RC, 2004, ARCH DIS CHILD, V89, P604, DOI 10.1136/adc.2003.031856 Dale RC, 2005, DEV MED CHILD NEUROL, V47, P785, DOI 10.1017/S0012162205001647 Edwards MJ, 2004, NEUROLOGY, V63, P156 Fennig S, 1997, ISRAEL J PSYCHIAT, V34, P239 Freeman RD, 2000, DEV MED CHILD NEUROL, V42, P436, DOI 10.1017/S0012162200000839 Hoekstra PJ, 2004, AM J PSYCHIAT, V161, P1501, DOI 10.1176/appi.ajp.161.8.1501-a Hoekstra PJ, 2004, CELL MOL LIFE SCI, V61, P886, DOI 10.1007/s00018-003-3320-4 Hoekstra PJ, 2002, MOL PSYCHIATR, V7, P437, DOI 10.1038/sj.mp.4000972 Holden RJ, 1995, MED HYPOTHESES, V45, P575, DOI 10.1016/0306-9877(95)90242-2 Hollander E, 1999, AM J PSYCHIAT, V156, P317 Inoff-Germain G, 2003, J CHILD PSYCHOL PSYC, V44, P782, DOI 10.1111/1469-7610.00163 Insel BJ, 2005, SCHIZOPHR RES, V80, P331, DOI 10.1016/j.schres.2005.06.005 KERBESHIAN J, 1988, NEUROSCI BIOBEHAV R, V12, P267, DOI 10.1016/S0149-7634(88)80057-5 Kerbeshian J, 2003, EUR CHILD ADOLES PSY, V12, P103, DOI 10.1007/s00787-003-0325-3 KERBESHIAN J, 1987, CAN J PSYCHIAT, V32, P123 Leonard HL, 2001, INT J NEUROPSYCHOPH, V4, P191 Loiselle CR, 2003, PEDIATR NEUROL, V28, P119, DOI 10.1016/S0887-8994(02)00507-6 Morer A, 2005, BEHAV NEUROL, V16, P1 Muller N, 2000, PSYCHIAT RES, V94, P43, DOI 10.1016/S0165-1781(00)00125-6 Murphy TK, 2001, J NEUROIMMUNOL, V120, P146, DOI 10.1016/S0165-5728(01)00410-6 Singer HS, 2005, NEUROLOGY, V65, P1701, DOI 10.1212/01.wnl.0000183223.69946.f1 Snider LA, 2003, CURR OPIN NEUROL, V16, P359, DOI 10.1097/01.wco.0000073938.19076.31 Stahlberg O, 2004, J NEURAL TRANSM, V111, P891, DOI 10.1007/s00702-004-0115-1 SVERD J, 1993, J AUTISM DEV DISORD, V23, P407, DOI 10.1007/BF01046229 Swedo SE, 2004, PEDIATRICS, V113, P907, DOI 10.1542/peds.113.4.907 Thompson JL, 2004, SCHIZOPHRENIA BULL, V30, P875 Volkmar F, 1999, J AM ACAD CHILD PSY, V38, P1611 Weisz JL, 2004, CLIN DIAGN LAB IMMUN, V11, P330, DOI 10.1128/CDLI.11.2.330-336.2004 Westergaard T, 1999, ARCH GEN PSYCHIAT, V56, P993, DOI 10.1001/archpsyc.56.11.993 Zappella M, 2002, EUR CHILD ADOLES PSY, V11, P18 Zhao G, 2005, J DERMATOL, V32, P91 NR 40 TC 7 Z9 8 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1562-2975 J9 WORLD J BIOL PSYCHIA JI World J. Biol. Psychiatry PY 2007 VL 8 IS 3 BP 201 EP 207 DI 10.1080/15622970601182652 PG 7 WC Psychiatry SC Psychiatry GA 209AL UT WOS:000249360400006 PM 17654411 ER PT J AU Herbrecht, E Poustka, F AF Herbrecht, Evelyn Poustka, Fritz TI Frankfurt group social communication and interaction skills training for children and adolescents with autism spectrum disorders SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE group-based training; autism; social skills; children and adolescents; manual ID BEHAVIORAL TREATMENT; YOUNG-CHILDREN; INTERVENTION; PROGRAM; INDIVIDUALS; CHALLENGES; MODEL AB Objective: Despite the recognition of the need for group-based training programmes for children and adolescents with autistic disorders, there are only very few specific German-speaking training programmes available. Since 2003, a structured group training programme on social skills for children and adolescents with high-functioning autism or Asperger syndrome has been developed and conducted at our department. The training programme focuses on the main deficits of those disorders. Thus, the primary goal is to improve communication and interaction skills. Method: Participants are children and adolescents without significant cognitive and language delays. Principles of intervention include structured formats, combination of theoretical and practical elements, predictable rules, consideration of individual difficulties, and sequential and progressive learning. Techniques range from structured games, the training of affect recognition, group activities, role play, team discussions, and feedback to homework using a newly designed manual on our group-based social skill training programme and curriculum. Generally, three groups of 5-7 participants each and of different age range (children, adolescents) meet weekly / biweekly for 1-1.5 hours (excluding the holidays). Two trainers - who change during the programme - carry out each of the sessions. Trainers meet regularly with the parents to discuss experiences and to provide details of the programme. Results: Acceptance by and satisfaction with the programme are high among participants, as is the mutual recognition of and tolerance of their respective problems. Both feedback from parents and trainers' clinical impressions indicate distinct improvement of verbalization and contact abilities. Participants seem to benefit particularly from role play. Conclusions: Qualtitative measures (impressions of the participants, their parents and their trainers with regard to change in behaviour skills) suggest mounting interaction, communication. and problem-solving skills during the group treatment. An ongoing pilot evaluation also includes measurements of effects in everyday settings. Depending on the results, the training subsequently could be conducted and evaluated in groups. with both pervasive developmental, as well as other psychiatric disorders. C1 Klinikum Johann Wolfgang Goethe Univ, Klin Psychiat & Psychotherapie Kindes & Jugendalt, DE-60528 Frankfurt, Germany. RP Herbrecht, E (reprint author), Klinikum Johann Wolfgang Goethe Univ, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, DE-60528 Frankfurt, Germany. CR Aldred C, 2004, J CHILD PSYCHOL PSYC, V45, P1420, DOI 10.1111/j1469-7610.2004.00338.x Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Barry TD, 2003, J AUTISM DEV DISORD, V33, P685, DOI 10.1023/B:JADD.0000006004.86556.e0 Bolte S, 2006, DIAGNOSTISCHES INTER Bölte Sven, 2002, Int J Circumpolar Health, V61 Suppl 2, P61 BONDY A, 1994, BEHAV MODIF, V25, P725 Drew A, 2002, EUR CHILD ADOLES PSY, V11, P266, DOI 10.1007/s00787-002-0299-6 Eikeseth S, 2002, BEHAV MODIF, V26, P49, DOI 10.1177/0145445502026001004 Goldstein H, 2002, J AUTISM DEV DISORD, V32, P373, DOI 10.1023/A:1020589821992 Gray C., 2000, NEW SOCIAL STORY BOO Happel C., 2003, SOKO AUTISMUS GRUPPE Howlin P., 1998, TEACHING CHILDREN AU Koegel RL, 2001, J CLIN CHILD PSYCHOL, V30, P19, DOI 10.1207/S15374424JCCP3001_4 Krasny L, 2003, CHILD ADOL PSYCH CL, V12, P107, DOI 10.1016/S1056-4993(02)00051-2 Lord C, 2005, J AUTISM DEV DISORD, V35, P695, DOI 10.1007/s10803-005-0017-6 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 McConnell SR, 2002, J AUTISM DEV DISORD, V32, P351, DOI 10.1023/A:1020537805154 MESIBOV GB, 1984, J AUTISM DEV DISORD, V14, P395, DOI 10.1007/BF02409830 MESIBOV GB, 1996, MODEL PROGRAMS CHILD, P215 Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 Panerai S, 2002, J INTELL DISABIL RES, V46, P318, DOI 10.1046/j.1365-2788.2002.00388.x Paul R, 2003, CHILD ADOL PSYCH CL, V12, P87, DOI 10.1016/S1056-4993(02)00047-0 POUSTKA F, 2004, AUTISTISCHE STORUNGE Probst P, 2003, PRAX KINDERPSYCHOL K, V52, P473 Quill K. A., 2000, DO WATCH LISTEN SAY Ruhl D, 2004, DIAGNOSTISCHE BEOBAC STONE WL, 2003, AUTISM, V7, P7 Weiss MJ, 2001, BEHAV MODIF, V25, P785, DOI 10.1177/0145445501255007 WILLIAMS TI, 1989, J AUTISM DEV DISORD, V19, P143, DOI 10.1007/BF02212726 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 31 TC 5 Z9 5 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD JAN PY 2007 VL 35 IS 1 BP 33 EP 40 DI 10.1024/1422-4917.35.1.33 PG 8 WC Psychiatry SC Psychiatry GA 132ZF UT WOS:000243980700004 PM 17230427 ER PT J AU Freitag, CM Retz-Junginger, P Retz, W Seitz, C Palmason, H Meyer, J Rosler, M von Gontard, A AF Freitag, Christine M. Retz-Junginger, Petra Retz, Wolfgang Seitz, Christiane Palmason, Haukur Meyer, Jobst Rosler, Michael von Gontard, Alexander TI German adaptation of the autism-spectrum quotient (AQ): Evaluation and short version AQ-k SO ZEITSCHRIFT FUR KLINISCHE PSYCHOLOGIE UND PSYCHOTHERAPIE LA English DT Article DE screening; autistic disorders; Autism Spectrum Quotient; validity; reliability; sensitivity ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; BROADER PHENOTYPE; FAMILY HISTORY; PARENTS; ADULTS; TWIN; QUESTIONNAIRE; BEHAVIOR; DEFICIT AB Background: Autistic disorders are characterized by deficits in social interaction and communication, and stereotyped and repetitive behaviour. No German-language self-assessment instrument for screening for autistic disorders has been available so far. Methods: Psychometric properties of the Autism Spectrum Quotient (AQ) screening questionnaire were assessed in four samples: two non-clinical, one forensic and one high-functioning autism/Asperger syndrome sample. Results: Due to the partly very low selectivity of individual items, a short version of the questionnaire (AQ-k) was created, containing only sufficiently selective items. A three factor solution (social interaction and spontaneity; imagination and creativity; communication and reciprocity) was obtained by principal components analysis of the AQ-k. Internal consistency of the three factors was between 0.65 and 0.87. Retestreliability as well as external validity were satisfactory. The AQ-k showed a good discriminative validity and good screening properties at a threshold score of 17. Conclusions: The AQ-k is a reliable and valid self-assessment instrument for individuals with normal intelligence from age 16 years on. It is a screening instrument only and should not be used for the diagnosis of an autistic disorder. C1 Univ Klinikum Saarlandes, Klin Kinder & Jugendpsychiat & Psychotherapie, D-66421 Homburg, Germany. Univ Klinikum Saarlandes, Inst Forens Psychiat, Homburg, Germany. Univ Trier, Abt Verhaltensgenet, Trier, Germany. RP Freitag, CM (reprint author), Univ Klinikum Saarlandes, Klin Kinder & Jugendpsychiat & Psychotherapie, Geb 90,Kirrberger Str, D-66421 Homburg, Germany. CR Achenbach T. M., 1997, MANUAL YOUNG ADULT S Achenbach TM, 1991, MANUAL YOUTH SELF RE 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 Bishop DVM, 2004, J CHILD PSYCHOL PSYC, V45, P1431, DOI 10.1111/j.1469-7610.2004.00325.x Bolte S, 2005, Z KINDER JUG-PSYCH, V33, P5, DOI 10.1024/1422-4917.33.1.5 Bolte S, 2000, DIAGNOSTICA, V46, P149, DOI 10.1026//0012-1924.46.3.149 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 Eysenck SBG, 1990, Z DIFFERENTIELLE DIA, V4, P209 FOLSTEIN S, 1977, NATURE, V265, P726, DOI 10.1038/265726a0 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Happe F, 2003, NOVART FDN SYMP, V251, P198 Happe F, 2006, BRAIN COGNITION, V61, P25, DOI 10.1016/j.bandc.2006.03.004 Hollander E, 2003, PSYCHIAT RES, V117, P11, DOI 10.1016/S0165-1781(02)00304-9 Kurita H, 2005, PSYCHIAT CLIN NEUROS, V59, P490, DOI 10.1111/j.1440-1819.2005.01403.x LANDA R, 1992, PSYCHOL MED, V22, P245 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 LEINERT GA, 1998, TESTAUFBAU TESTANALA PICKLES A, 1995, AM J HUM GENET, V57, P717 Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 Piven J, 1999, AM J PSYCHIAT, V156, P557 Piven J, 1997, AM J MED GENET, V74, P398, DOI 10.1002/(SICI)1096-8628(19970725)74:4<398::AID-AJMG11>3.0.CO;2-D Retz-Junginger P, 2002, NERVENARZT, V73, P830, DOI 10.1007/s00115-001-1215-x Rosler M, 2004, NERVENARZT, V75, P888, DOI 10.1007/s00115-003-1622-2 Starr E, 2001, J AUTISM DEV DISORD, V31, P89, DOI 10.1023/A:1005669915105 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Wilcox J, 2003, NEUROPSYCHOBIOLOGY, V47, P171, DOI 10.1159/000071210 Woodbury-Smith MR, 2005, J AUTISM DEV DISORD, V35, P331, DOI 10.1007/s10803-005-3300-7 1993, INT KLASSIFIKATION P NR 31 TC 14 Z9 14 PU HOGREFE & HUBER PUBLISHERS PI GOTTINGEN PA ROHNSWEG 25, D-37085 GOTTINGEN, GERMANY SN 1616-3443 J9 Z KL PSYCH PSYCHOTH JI Z. Klin. Psychol. Psychother. PY 2007 VL 36 IS 4 BP 280 EP 289 DI 10.1026/1616-3443.36.4.280 PG 10 WC Psychology, Clinical SC Psychology GA 225UD UT WOS:000250542600006 ER PT J AU Kozhushko, NY Shaitor, VM Ponomareva, EA Berezhnaya, NF AF Kozhushko, N. Yu. Shaitor, V. M. Ponomareva, E. A. Berezhnaya, N. F. TI Transcranial micropolarization in the complex therapy of early child autism SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE early child autism; transcranial micropolarization; understanding of speech; learning capabilities AB This research presents the results of using transcranial micropolarization technique (TCMP) developed in the Human Brain Institute, Russian Academy of Medical Sciences, in 17 children, aged from 3 to 6 years, with the ICD-10 diagnosis of autism (F84.0). Included in the complex therapy, TCMP allowed to increase significantly the process of formation of higher mental functions and development of communicative skills, mostly due to the substantial improvement of understanding of addressed speech. The positive dynamics of learning capabilities was based on increasing of regulating function of adult's speech with the corresponding growth of adequate behavior of the child at home, studies and public places. CR BEREZHNAYA NF, 2006, DOSHKOLNAYA PEDAGOGI, V4, P56 BOGDANOV OV, 2002, TRANSKRANIALNAYA TRA Domishkevich S.A., 2002, FUNKTSIONALNO UROVNE ILYUKHINA VA, 2004, ZH NEVROPATOL PSIKH, V11, P34 Kovanov V.V., 2001, OPERATIVNAYA KHIRURG LURIYA AR, 1978, YESTESTVENNO NAUCHNY PINCHUK DY, 2001, ZH NEVROPOL PSIKHIAT, V7, P58 PONOMARENKO GN, 1999, FIZICHESKIYE METODY SHELYAKIN AM, 2006, MIKROPOLYARIZATSIYA Sokolov A.N., 2004, DIAGNOSTIKA UROVNYA TIGANOV AS, 2005, ZH NEVROPATOL PSIKH, V8, P4 TSVETKOVA LS, 2000, METODIKA NEYROPSIKHO ZINKEVICHYEVSTI.TD, 2002, PRAKTIKUM PESOCHNOI NR 13 TC 2 Z9 3 PU IZDATELSTVO MEDITSINA PI MOSCOW PA PETROVERIGSKII PER 6-8, K-142 MOSCOW, RUSSIA SN 0044-4588 J9 ZH NEVROL PSIKHIATR JI Z. Nevrol. Psikhiatrii Im S S Korsakova PY 2007 VL 107 IS 10 BP 47 EP 51 PG 7 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 236VG UT WOS:000251330900008 ER PT J AU Shinohe, A Hashimoto, K Nakamura, K Tsujii, M Iwata, Y Tsuchiya, KJ Sekine, Y Suda, S Suzuki, K Sugihara, GI Matsuzaki, H Minabe, Y Suglyama, T Kawai, M Yo, M Takei, N Mori, N AF Shinohe, Atsuko Hashimoto, Kenji Nakamura, Kazuhiko Tsujii, Masatsugu Iwata, Yasuhide Tsuchiya, Kenji J. Sekine, Yoshimoto Suda, Shiro Suzuki, Katsuaki Sugihara, Gen-ichi Matsuzaki, Hideo Minabe, Yoshio Suglyama, Toshiro Kawai, Masayoshi Yo, Masaomi Takei, Nori Mori, Norio TI Increased serum levels of glutamate in adult patients with autism SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE amino acids; autism; D-serme; glutamate; HPLC; human serum ID OBSESSIVE COMPULSIVE SCALE; COMMON DIETARY PROTEINS; CARRIER SLC25A12 GENE; SPECTRUM DISORDERS; D-SERINE; GASTROINTESTINAL SYMPTOMS; CEREBROSPINAL-FLUID; CYTOKINE PRODUCTION; ASSOCIATION; CHILDREN AB Background: Precise mechanisms underlying the pathophysiology of autism are currently unknown. Given the major role of glutamate in brain development, we have hypothesized that glutamatergic neurotransmission plays a role in the pathophysiology of autism. In this study, we studied whether amino acids (glutamate, glutamine, glycine, D-serme, and L-serine) related to glutamatergic neurotransmission are altered in serum of adult patients with autism. Methods: We measured serum levels of amino acids in 18 male adult patients with autism and age-matched 19 male healthy subjects using high-performance liquid chromatography. Results: Serum levels (mean=89.2 mu M, S.D.=21.5) of glutamate in the patients with autism were significantly (t=-4.48, df=35,p < 0.001) higher than those (Mean=61.1 mu M, S.D.= 16.5) of normal controls. In contrast, serum levels of other amino acids (glutamine, glycine, D-serine, L-serine) in the patients with autism did not differ from those of normal controls. There was a positive correlation (r=0.523,p=0.026) between serum glutamate levels and Autism Diagnostic Interview-Revised (ADI-R) social scores in patients. Conclusions: The present study suggests that an abnormality in glutamatergic neurotransmission may play a role in the pathophysiology of autism. (c) 2006 Elsevier Inc. All rights reserved. C1 Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, Chiba 2608670, Japan. Chiba Univ, Grad Sch Med, Dept Psychiat, Chiba 2608670, Japan. Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 4313192, Japan. Chukyo Univ, Fac Sociol, Aichi 4700393, Japan. Aichi Childrens Hlth & Med Ctr, Obu, Aichi 47408710, Japan. RP Hashimoto, K (reprint author), Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, 1-8-1 Inohana, Chiba 2608670, Japan. 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Neuro-Psychopharmacol. Biol. Psychiatry PD DEC 30 PY 2006 VL 30 IS 8 BP 1472 EP 1477 DI 10.1016/j.pnpbp.2006.06.013 PG 6 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 116FT UT WOS:000242788600013 PM 16863675 ER PT J AU Hashimoto, K Iwata, Y Nakamura, K Tsujii, M Tsuchiya, KJ Sekine, Y Suzuki, K Minabe, Y Takei, N Yo, M Mori, N AF Hashimoto, Kenji Iwata, Yasuhide Nakamura, Kazuhiko Tsujii, Masatsugu Tsuchiya, Kenji J. Sekine, Yoshimoto Suzuki, Katsuaki Minabe, Yoshio Takei, Nori Yo, Masaomi Mori, Norio TI Reduced serum levels of brain-derived neurotrophic factor in adult male patients with autism SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE autism; brain-derived neurotrophic factor; neurodevelopmental disorder; serum ID MENTAL-RETARDATION; NEONATAL BLOOD; DISORDERS; CHILDREN; BDNF; NEUROPEPTIDES; PLATELETS; PLASMA AB Background: The precise mechanisms underlying the pathophysiology of autism are currently unknown. Given the key role of brain-derived neurotrophic factor (BDNF) in brain development, we hypothesized that BDNF may play a role in the pathophysiology of autism. In this study, we studied whether serum levels of BDNF are altered in patients with autism. Methods: We measured serum levels of BDNF in 18 adult male patients with autism and 18 age-matched healthy male control subjects. Results: The serum levels of BDNF in patients with autism (25.6 +/- 2.15 ng/ml (mean +/- S.D.)) were significantly (z=-4.42, p < 0.001) lower than those of normal controls (61.6 +/- 10.9 ng/ml (mean S.D.)). Nevertheless, we found no correlations between BDNF levels and clinical variables in autistic patients. Conclusions: This study suggests that reduced BDNF levels may play a role in the pathophysiology of autism. (c) 2006 Elsevier Inc. All rights reserved. C1 Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, Chiba 2608670, Japan. Hamamatsu Univ Sch Med, Dept Psychiat & Neurol, Hamamatsu, Shizuoka 43131, Japan. Chukyo Univ, Fac Sociol, Toyota, Aichi, Japan. Chiba Univ, Dept Psychiat, Grad Sch Med, Chiba, Japan. RP Hashimoto, K (reprint author), Chiba Univ, Ctr Forens Mental Hlth, Div Clin Neurosci, 1-8-1 Inohana, Chiba 2608670, Japan. 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A major focus of interest is the role of efferent and afferent connectivity between the amygdala and the neocortical brain regions, now believed to be critical for the processing of social and emotional perceptions. One possible component is a subcortical neural pathway, which permits rapid and preconscious processing of potentially threatening stimuli, and it leads from the retina to the superior colliculus, to the pulvinar nucleus of the thalamus and then to the amygdala. This pathway is activated by direct eye contact, one of many classes of potential threat, and may be particularly responsive to the 'whites of the eyes'. In humans, autonomic arousal evoked by this stimulus is associated with the activity in specific cortical regions concerned with processing visual information from faces. The integrated functioning of these pathways is modulated by one or more X-linked genes, yet to be identified. 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Trans. R. Soc. B-Biol. Sci. PD DEC 29 PY 2006 VL 361 IS 1476 BP 2129 EP 2141 DI 10.1098/rstb.2006.1935 PG 13 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 114SI UT WOS:000242685500006 PM 17118928 ER PT J AU Hammock, EAD Young, LJ AF Hammock, Elizabeth A. D. Young, Larry J. TI Oxytocin, vasopressin and pair bonding: implications for autism SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES LA English DT Review DE individual differences; regulatory microsatellite; prairie vole; autism; vasopressin; oxytocin ID VOLES MICROTUS-OCHROGASTER; FEMALE PRAIRIE VOLES; SOCIAL RECOGNITION RESPONSES; PARTNER-PREFERENCE FORMATION; NUCLEUS-ACCUMBENS DOPAMINE; RECEPTOR GENE-EXPRESSION; OLFACTORY-BULB; MALE-RATS; SPECIES-DIFFERENCES; MATERNAL-BEHAVIOR AB Understanding the neurobiological substrates regulating normal social behaviours may provide valuable insights in human behaviour, including developmental disorders such as autism that are characterized by pervasive deficits in social behaviour. Here, we review the literature which suggests that the neuropeptides oxytocin and vasopressin play critical roles in modulating social behaviours, with a focus on their role in the regulation of social bonding in monogamous rodents. Oxytocin and vasopressin contribute to a wide variety of social behaviours, including social recognition, communication, parental care, territorial aggression and social bonding. The effects of these two neuropeptides are species-specific and depend on species-specific receptor distributions in the brain. Comparative studies in voles with divergent social structures have revealed some of the neural and genetic mechanisms of social-bonding behaviour. Prairie voles are socially monogamous; males and females form long-term pair bonds, establish a nest site and rear their offspring together. In contrast, montane and meadow voles do not form a bond with a mate and only the females take part in rearing the young. Species differences in the density of receptors for oxytocin and vasopressin in ventral forebrain reward circuitry differentially reinforce social-bonding behaviour in the two species. High levels of oxytocin receptor (OTR) in the nucleus accumbens and high levels of vasopressin 1a receptor (V1aR) in the ventral pallidum contribute to monogamous social structure in the prairie vole. While little is known about the genetic factors contributing to species-differences in OTR distribution, the species-specific distribution pattern of the V1aR is determined in part by a species-specific repetitive element, or 'microsatellite', in the 50 regulatory region of the gene encoding V1aR (avpr1a). This microsatellite is highly expanded in the prairie vole (as well as the monogamous pine vole) compared to a very short version in the promiscuous montane and meadow voles. These species differences in microsatellite sequence are sufficient to change gene expression in cell culture. Within the prairie vole species, intraspecific variation in the microsatellite also modulates gene expression in vitro as well as receptor distribution patterns in vivo and influences the probability of social approach and bonding behaviour. Similar genetic variation in the human AVPR1A may contribute to variations in human social behaviour, including extremes outside the normal range of behaviour and those found in autism spectrum disorders. In sum, comparative studies in pair-bonding rodents have revealed neural and genetic mechanisms contributing to social-bonding behaviour. These studies have generated testable hypotheses regarding the motivational systems and underlying molecular neurobiology involved in social engagement and social bond formation that may have important implications for the core social deficits characterizing autism spectrum disorders. C1 Emory Univ, Yerkes Natl Primate Res Ctr, Ctr Behav Neurosci, Dept Psychiat & Behav Sci, Atlanta, GA 30329 USA. RP Young, LJ (reprint author), Emory Univ, Yerkes Natl Primate Res Ctr, Ctr Behav Neurosci, Dept Psychiat & Behav Sci, Atlanta, GA 30329 USA. 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Trans. R. Soc. B-Biol. Sci. PD DEC 29 PY 2006 VL 361 IS 1476 BP 2187 EP 2198 DI 10.1098/rstb.2006.1939 PG 12 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 114SI UT WOS:000242685500010 PM 17118932 ER PT J AU Boso, M Emanuele, E Minoretti, P Arra, M Politi, P di Nemi, SU Barale, F AF Boso, Marianna Emanuele, Enzo Minoretti, Piercarlo Arra, Mariarosa Politi, Pierluigi di Nemi, Stefania Ucelli Barale, Francesco TI Alterations of circulating endogenous secretory RAGE and S100A9 levels indicating dysfunction of the AGE-RAGE axis in autism SO NEUROSCIENCE LETTERS LA English DT Article DE autistic spectrum disorders; oxidative stress; advanced glycation end products; calgranulins; ELISA ID GLYCATION END-PRODUCTS; VASCULAR COMPLICATIONS; SPECTRUM DISORDERS; ENDOTHELIAL-CELLS; SERUM-LEVELS; CHILDREN; RECEPTOR; PROTEINS; BRAIN AB An excess accumulation of advanced glycation end products (AGEs) has been reported in autism brains. Through their interaction with their putative receptor RAGE, AGEs can promote neuroinflammation, oxidative stress and neuronal degeneration. To shed more light on the possible alterations of the AGEs-RAGE axis in autism, hereto we measured plasma levels of endogenous secretory RAGE (esRAGE) and its proinflammatory ligand S100A9 in 18 young adults with autistic spectrum disorder (ASD) and 18 age- and gender-matched healthy comparison subjects. The Childhood Autism Rating Scale (CARS) was used to assess the severity of autistic symptoms. Significantly reduced levels of esRAGE (P = 0.0023) and elevated concentrations of S100A9 (P = 0.0012) were found in ASD patients as compared to controls. In autistic patients, there was a statistically significant positive correlation between CARS scores and S100A9 levels (r = 0.49, P = 0.035), but no significant correlation was seen between esRAGE and S100A9 values (r = -0.23, P = 0.34). Our results of a significantly reduced peripheral level of esRAGE coupled with elevated S100A9 point to a subtle but definite dysfunction of the AGEs/RAGE axis in autism that could play a role in the pathophysiology of this disorder. (c) 2006 Elsevier Ireland Ltd. All rights reserved. C1 Univ Pavia, Interdept Ctr Res Mol Med, I-27100 Pavia, Italy. Univ Pavia, Dept Appl Hlth & Behav Sci, Sect Psychiat, I-27100 Pavia, Italy. RP Emanuele, E (reprint author), Univ Pavia, Interdept Ctr Res Mol Med, Vialel Taramelli 24, I-27100 Pavia, Italy. 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To automate large-scale reconciliation efforts, we propose a random-arcs-and-nodes model where both nodes (tissue-specific states of biological molecules) and arcs (interactions between them) are represented with random variables. We show how to obtain a non-contradictory model of a molecular network by computing the joint distribution for arc and node variables, and then apply our methodology to a realistic network, generating a set of experimentally testable hypotheses. This network, derived from an automated analysis of over 3,000 full-text research articles, includes genes that have been hypothetically linked to four neurological disorders: Alzheimer's disease, autism, bipolar disorder, and schizophrenia. We estimated that approximately 10% of the published molecular interactions are logically incompatible. Our approach can be directly applied to an array of diverse problems including those encountered in molecular biology, ecology, economics, politics, and sociology. C1 [Rzhetsky, Andrey; Weinreb, Chani] Columbia Univ, Dept Biomed Informat, Ctr Computat Biol & Bioinformat, New York, NY 10027 USA. [Rzhetsky, Andrey; Weinreb, Chani] Columbia Univ, Joint Ctr Syst Biol, New York, NY USA. [Rzhetsky, Andrey] Columbia Univ, Judith P Sulzberger MD Columbia Genome Ctr, New York, NY USA. [Rzhetsky, Andrey] Columbia Univ, Dept Biol, New York, NY USA. [Zheng, Tian] Columbia Univ, Dept Stat, New York, NY USA. RP Rzhetsky, A (reprint author), Columbia Univ, Dept Biomed Informat, Ctr Computat Biol & Bioinformat, New York, NY 10027 USA. EM andrey.rzhetsky@dbmi.columbia.edu RI rzhetsky, andrey/B-6118-2012 FU National Institutes of Health [GM61372, GM070789]; National Science Foundation [0438291, 0121687, 0532231]; Cure Autism Now Foundation; Defense Advanced Research Projects Agency [FA8750-04-2-0123]; [5-T15-LM007079] FX This work was supported by the National Institutes of Health (GM61372 to A. R., GM070789 to T. Z., and training fellowship 5-T15-LM007079 to C. W.), the National Science Foundation ( 0438291 and 0121687 to A. R., and 0532231 to T. Z.), the Cure Autism Now Foundation to A. R., and the Defense Advanced Research Projects Agency (FA8750-04-2-0123 to A. R.). 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Corwin, Thomas E. Kryzak, Lauren A. Smith, Christopher J. Silverman, Jeremy M. Hollander, Eric Buxbaum, Joseph D. TI Family-based association study of TPH1 and TPH2 polymorphisms in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autistic disorder; obsessive-compulsive behaviors; serotonin; tryptophan-hydroxylase; transmission ID TRYPTOPHAN-HYDROXYLASE ISOFORM; PERVASIVE DEVELOPMENTAL DISORDERS; OBSESSIVE-COMPULSIVE BEHAVIORS; WHOLE-BLOOD SEROTONIN; RECEPTOR GENE; 1ST-DEGREE RELATIVES; SPECTRUM DISORDERS; HAPLOTYPE ANALYSIS; ADOLESCENT AUTISM; LINKAGE ANALYSIS AB The TPH1 and TPH2 genes encode the rate-limiting enzymes that control serotonin biosynthesis, and serotonin is clearly altered in autism. In the current study, eight SNPs in the TPH1 gene region and eight SNPs within the TPH2 gene were examined by family-based association tests in a large cohort of 352 families with autism and in clinically defined subsets of these families with either severe obsessive-compulsive behaviors (sOCB) or self-stimulatory behaviors (SSB). We found no evidence for association between autism and single SNPs or haplotypes of the TPH1 and TPH2 genes in the cohort of all families or in the sOCB and SSB subsets. In particular, we failed to replicate the association between autism and variants of the TPH2 gene, rs4341581 (TRANSMIT P=1; PDT P=0.323; FBAT P=0.446) and rs;11179000 (TRANSMIT P=0.174; PDT P=0.293; FBAT P=0.374). Furthermore, no evidence for linkage was observed between autism and SNPs in the TPH1 and TPH2 genes (although linkage at the TPH2 locus was observed in the SSB subset). Thus, it appears unlikely that the TPH1 and TPH2 genes play a significant role in the susceptibility to autism or to autism endophenotypes including sOCB and SSB. (c) 2006 Wiley-Liss, Inc. C1 Mt Sinai Sch Med, Lab Mol Neuropsychiat, Dept Psychiat, New York, NY 10029 USA. Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Geriatr & Adult Dev, New York, NY 10029 USA. RP Buxbaum, JD (reprint author), Mt Sinai Sch Med, Lab Mol Neuropsychiat, Dept Psychiat, 1 Gustave L Levy Pl,Box 1668, New York, NY 10029 USA. 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TI Metabolic endophenotype and related genotypes are associated with oxidative stress in children with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; oxidative stress; genotype; glutathione; methionine ID NEURAL-TUBE DEFECTS; HOMOCYSTEINE METABOLISM; GLUTATHIONE SYNTHESIS; DOWN-SYNDROME; NEURODEGENERATIVE DISORDERS; S-ADENOSYLHOMOCYSTEINE; GENETIC-POLYMORPHISM; PLASMA HOMOCYSTEINE; CEREBROSPINAL-FLUID; LIPID-PEROXIDATION AB Autism is a behaviorally defined neurodevelopmental disorder usually diagnosed in early childhood that is characterized by impairment in reciprocal communication and speech, repetitive behaviors, and social withdrawal. Although both genetic and environmental factors are thought to be involved, none have been reproducibly identified. The metabolic phenotype of an individual reflects the influence of endogenous and exogenous factors on genotype. As such, it provides a window through which the interactive impact of genes and environment may be viewed and relevant susceptibility factors identified. Although abnormal methionine metabolism has been associated with other neurologic disorders, these pathways and related polymorphisms have not been evaluated in autistic children. Plasma levels of metabolites in methionine transmethylation and transsulfuration pathways were measured in 80 autistic and 73 control children. In addition, common polymorphic variants known to modulate these metabolic pathways were evaluated in 360 autistic children and 205 controls. The metabolic results indicated that plasma methionine and the ratio of S-adenosylmethionine (SAM) to S-adenosylhomocysteine (SAH), an indicator of methylation capacity, were significantly decreased in the autistic children relative to age-matched controls. In addition, plasma levels of cysteine, glutathione, and the ratio of reduced to oxidized glutathione, an indication of antioxidant capacity and redox homeostasis, were significantly decreased. Differences in allele frequency and/or significant gene-gene interactions were found for relevant genes encoding the reduced folate carrier (RFC 80G > A), transcobalamin II (TCN2 776G > C), catechol-O-methyltransferase (COMT 472G > A), methylenetetrahydrofolate reductase (MTHFR 677C > T and 1298A > C), and glutathione-S-transferase (GST M1). We propose that an increased vulnerability to oxidative stress (endogenous or environmental) may contribute to the development and clinical manifestations of autism. (c) 2006 Wiley-Liss, Inc. C1 Univ Arkansas Med Sci, Arkansas Childrens Hosp, Dept Pediat, Res Inst, Little Rock, AR 72202 USA. Univ Calif Davis, Genome & Biomed Sci Facil, Davis, CA 95616 USA. Rhinebeck Hlth Ctr, New York, NY USA. Int Child Dev Resource Ctr, Melbourne, FL USA. 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Later in life, signaling pathways are essential in maintaining proper communication between neuronal and non-neuronal cells, and disrupting this balance may result in disorders like Alzheimer's disease. The Wnt/beta-catenin pathway has a well-established role in cancer. Here, we review recent evidence showing the involvement of Wnt/beta-catenin signaling in neurodevelopment as well as in neurodegenerative diseases. We suggest that the onset/development of such pathological conditions may involve the additive effect of genetic variation within Wnt signaling components and of molecules that modulate the activity of this signaling cascade. C1 Univ Washington, Sch Med, Howard Hughes Med Inst, Dept Pharmacol, Seattle, WA 98115 USA. Univ Washington, Sch Med, Inst Stem Cell & Regenerat Med, Seattle, WA 98115 USA. Univ Concepcion, Fac Ciencias Biol, Dept Bioquim & Biol Mol, Concepcion, Chile. RP De Ferrari, GV (reprint author), Univ Washington, Sch Med, Howard Hughes Med Inst, Dept Pharmacol, Seattle, WA 98115 USA. 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Kim, Soo-Jeong Salt, Jeff Leventhal, Bennett L. Lord, Catherine Cook, Edwin H., Jr. TI 5-HTTLPR genotype-specific phenotype in children and adolescents with autism SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID SEROTONIN TRANSPORTER GENE; DIAGNOSTIC OBSERVATION SCHEDULE; DEFICIT HYPERACTIVITY DISORDER; PROMOTER REGION POLYMORPHISM; RIGID-COMPULSIVE BEHAVIORS; PERSONALITY-TRAITS; MULTIPLEX FAMILIES; SYMPTOM DOMAINS; DOUBLE-BLIND; ASSOCIATION AB Objective: The serotonin transporter gene (SLC6A4) is a strong autism candidate gene because of its association with anxiety, aggression and attention, and the effectiveness of selective serotonin reuptake inhibitors (SSRIs) in treating certain behavioral symptoms. In families with individuals with autism, several reports of biased transmission of both alleles (short, long) at the serotonin transporter gene promotor polymorphism (5-HTTLPR) locus of SLC6A4 now exist. The heterogeneity in these reports may be due to clinical heterogeneity. The authors hypothesized that 5-HTTLPR genotypes would be related to variation in specific symptoms in children with autism. Method: The authors explored whether variants of two functional polymorphisms of SLC6A4 (5-HTTLPR, intron 2 variable number tandem repeat [ 2 VNTR]) were related to behavioral characteristics measured by the Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule. Subjects (N = 73, age 3 -19 years old) met diagnostic criteria for autistic disorder based on both measures. Results: Evidence of genotype-phenotype interactions on the Autism Diagnostic Interview-Revised was found with the 5-HTTLPR short group of HTTLPR (S/ L or S/ S genotypes) being rated as more severe on the subdomain "failure to use nonverbal communication to regulate social interaction," and the long group (L/ L genotype) being more severe on the subdomain "stereotyped and repetitive motor mannerisms" and on an aggression measure. In contrast, on the Autism Diagnostic Observation Schedule, the long group was associated with greater severity on directed facial expressions and unusual sensory interests. There were no significant relationships between the intron 2 VNTR genotypes and subdomains or domains of symptoms on the Autism Diagnostic Interview-Revised or the Autism Diagnostic Observation Schedule. Conclusions: These findings provide initial support for genotype-specific phenotypes for 5-HTTLPR in autism based on ratings from the Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule. C1 Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA. Univ Florida, Dept Psychiat, Gainesville, FL 32611 USA. Univ Michigan, Austism & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. RP Cook, EH (reprint author), Univ Illinois, Dept Psychiat, Inst Juvenile Res, MC 747,1747 W Roosevelt Rd,Rm 155, Chicago, IL 60612 USA. 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Previous studies that have measured the corpus callosum in developmental populations have been limited by the use of rather arbitrary methods of subdividing the corpus callosum. The purpose of this study was to measure the corpus callosum in a clinical group of developmentally delayed children using a subdivision that more accurately reflected the anatomical properties of the corpus callosum. Method: The authors applied tractography to subdivide the corpus callosum into regions corresponding to the cortical regions to and from which its fibers travel in a clinical group of very young children with developmental delay, a precursor to general mental retardation, in comparison with typically developing children. Results: The data demonstrate that the midsagittal area of the entire corpus callosum is reduced in children presenting with developmental delay, reflected in the smaller area of each of the fiber-based callosal subdivisions. In addition, while the area of each subdivision was strongly and significantly correlated with the corresponding cortical white matter volume in comparison subjects, this correlation was prominently absent in the developmentally delayed group. Conclusions: A fiber-based subdivision successfully separates lobar regions of the corpus callosum, and the areas of these regions distinguish a developmentally delayed clinical group from the comparison group. This distinction was evident both in the area measurements themselves and in their correlation to the white matter volumes of the corresponding cortical lobes. C1 Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. RP Piven, J (reprint author), Univ N Carolina, Dept Psychiat, CB 3367, Chapel Hill, NC 27599 USA. 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J. Psychiat. PD DEC PY 2006 VL 163 IS 12 BP 2157 EP 2163 DI 10.1176/appi.ajp.163.12.2157 PG 7 WC Psychiatry SC Psychiatry GA 113VL UT WOS:000242626000023 PM 17151168 ER PT J AU Page, LA Daly, E Schmitz, N Simmons, A Toal, F Deeley, Q Ambery, F McAlonan, GM Murphy, KC Murphy, DGM AF Page, Lisa A. Daly, Eileen Schmitz, Nicole Simmons, Andrew Toal, Fiona Deeley, Quinton Ambery, Fiona McAlonan, Grainne M. Murphy, Kieran C. Murphy, Declan G. M. TI In vivo H-1-magnetic resonance spectroscopy study of amygdala-hippocampal and parietal regions in autism SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 4th International Meeting for Autism Research CY MAY 06-07, 2005 CL Boston, MA ID GLUTAMATE-RECEPTOR-6 GENE; ASSOCIATION; LINKAGE; BRAIN AB Objective: The neural basis for autistic spectrum disorders is unclear, but abnormalities in the development of limbic areas and of glutamate have been suggested. Proton magnetic resonance spectroscopy (H-1-MRS) can be used to measure the concentration of brain metabolites. However, the concentration of glutamate/glutamine in brain regions implicated in autistic spectrum disorders has not yet been examined in vivo. Method: The authors used 1H-MRS to investigate the neuronal integrity of the amygdala-hippocampal complex and a parietal control region in adults with autistic spectrum disorders and healthy subjects. Results: People with autistic spectrum disorders had a significantly higher concentration of glutamate/glutamine and creatine/phosphocreatine in the amygdala-hippocampal region but not in the parietal region. Conclusions: Abnormalities in glutamate/glutamine may partially underpin the pathophysiology of autistic spectrum disorders, and the authors confirm earlier reports that limbic areas are metabolically aberrant in these disorders. C1 Inst Psychiat, Div Psychol Med, Sect Brain Maturat, London SE5 8AF, England. Leiden Univ, Med Ctr, Dept Radiol, Leiden, Netherlands. Inst Psychiat, Neuroimaging Res Grp, London, England. Royal Coll Surgeons Ireland, Beaumont Hosp, Dublin 2, Ireland. Univ Hong Kong, Dept Psychiat, Hong Kong, Hong Kong, Peoples R China. RP Murphy, KC (reprint author), Inst Psychiat, Div Psychol Med, Sect Brain Maturat, POB 50,De Crespigny Pk, Denmark Hill, London SE5 8AF, England. EM sphadgm@iop.kcl.ac.uk RI Schmitz, Nicole /F-9471-2011; daly, eileen/B-6716-2011; Murphy, Kieran/D-3577-2012; Simmons, Andrew/B-8848-2008 OI Schmitz, Nicole /0000-0003-4178-4756; Simmons, Andrew/0000-0003-2306-5811 CR Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 Fatemi SH, 2002, BIOL PSYCHIAT, V52, P805, DOI 10.1016/S0006-3223(02)01430-0 Jamain S, 2002, MOL PSYCHIATR, V7, P302, DOI 10.1038/sj/mp/4000979 Jarbrink K, 2001, AUTISM, V5, P7, DOI 10.1177/1362361301005001002 KEMPER TL, 1993, NEUROL CLIN, V11, P175 Murphy DGM, 2002, ARCH GEN PSYCHIAT, V59, P885, DOI 10.1001/archpsyc.59.10.885 ONEILL J, 2003, 11 SCI M TOR ISMRM Polleux F, 2004, MENT RETARD DEV D R, V10, P303, DOI 10.1002/mrdd.20044 Purcell AE, 2001, NEUROLOGY, V57, P1618 Ramoz N, 2004, AM J PSYCHIAT, V161, P662, DOI 10.1176/appi.ajp.161.4.662 Serajee FJ, 2003, J MED GENET, V40, DOI 10.1136/jmg.40.4.e42 Shuang M, 2004, AM J MED GENET B, V131B, P48, DOI 10.1002/ajmg.b.30025 NR 13 TC 71 Z9 76 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 DEC PY 2006 VL 163 IS 12 BP 2189 EP 2192 DI 10.1176/appi.ajp.163.12.2189 PG 4 WC Psychiatry SC Psychiatry GA 113VL UT WOS:000242626000030 PM 17151175 ER PT J AU Blakemore, SJ AF Blakemore, Sarah-Jayne TI Essays in social neuroscience SO AMERICAN JOURNAL OF PSYCHOLOGY LA English DT Book Review ID NEURAL BASIS; PREFRONTAL CORTEX; MENTAL STATES; COOPERATION; COGNITION; PREMOTOR; EMPATHY; AUTISM; TOUCH; PAIN C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. RP Blakemore, SJ (reprint author), UCL, Inst Cognit Neurosci, 17 Queen Sq, London WC1N 3AR, England. EM s.blakemore@ucl.ac.uk CR Anderson SW, 1999, NAT NEUROSCI, V2, P1032 Blakemore SJ, 2005, BRAIN, V128, P1571, DOI 10.1093/brain/awh500 Buccino G, 2001, EUR J NEUROSCI, V13, P400, DOI 10.1046/j.1460-9568.2001.01385.x Cacioppo J. 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J. Psychol. PD WIN PY 2006 VL 119 IS 4 BP 659 EP 664 PG 6 WC Psychology, Multidisciplinary SC Psychology GA 123SF UT WOS:000243315200007 ER PT J AU Spikins, P AF Spikins, Penny TI The secret history of emotion: From Aristotle rhetoric to modern brain science. SO ANTIQUITY LA English DT Book Review ID AUTISM C1 Univ York, Dept Archaeol, York YO10 5DD, N Yorkshire, England. RP Spikins, P (reprint author), Univ York, Dept Archaeol, York YO10 5DD, N Yorkshire, England. CR Baron-Cohen S, 2004, J AUTISM DEV DISORD, V34, P163, DOI 10.1023/B:JADD.0000022607.19833.00 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Bird-David N., 1999, CURR ANTHROPOL, V40, P67 Gosden C., 2004, RETHINKING MAT ENGAG, P33 Griffin J., 2004, HUMAN GIVENS NEW APP Gross Daniel M., 2006, SECRET HIST EMOTION SAHLINS M, 1996, CURR ANTHROPOL, V37, P95 Strathern M., 1988, GENDER GIFT PROBLEMS NR 8 TC 0 Z9 0 PU ANTIQUITY PI YORK PA KINGS MANOR, YORK YO1 7EP, ENGLAND SN 0003-598X J9 ANTIQUITY JI Antiquity PD DEC PY 2006 VL 80 IS 310 BP 1008 EP 1009 PG 2 WC Anthropology; Archaeology SC Anthropology; Archaeology GA 127UO UT WOS:000243612000024 ER PT J AU Sinha, Y Silove, N Wheeler, D Williams, K AF Sinha, Y. Silove, N. Wheeler, D. Williams, K. TI Auditory integration training and other sound therapies for autism spectrum disorders: a systematic review SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Review ID CHILDREN AB Objectives: To determine the effectiveness of auditory integration training (AIT) or other methods of sound therapy in people with autism spectrum disorders (ASD). Study design: A systematic review was carried out of randomised controlled trials (RCTs) of adults or children with ASD. Meta-analysis was attempted. Results: Six RCTs of AIT, including one crossover trial, were identified, with a total of 171 participants aged 3 - 39 years. 17 different outcome measures were used, with only two outcome measures used by three or more studies. Meta-analysis was not possible owing to very high heterogeneity or presentation of data in unusable forms. Three studies did not show any benefit of AIT over control conditions. Three studies reported improvements at 3 months in the AIT group for total mean scores of the Aberrant Behaviour Checklist (ABC), which is of questionable validity. Of these, one study also reported improvements at 3 months in the AIT group for ABC subgroup scores. No significant adverse effects of AIT were reported. Conclusion: At present there is not sufficient evidence to support its use. C1 Childrens Hosp, Ctr Kidney Res, Child Dev Unit, Westmead, NSW 2145, Australia. Childrens Hosp, Dept Gen Paediat, Clin Epidemiol Unit, Westmead, NSW 2145, Australia. Childrens Hosp, Cochrane Child Hlth Field, Westmead, NSW 2145, Australia. RP Sinha, Y (reprint author), Childrens Hosp, Ctr Kidney Res, Child Dev Unit, Locked Bag 4001, Westmead, NSW 2145, Australia. 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TI Amygdala volume and nonverbal social impairment in adolescent and adult males with autism 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 PERVASIVE DEVELOPMENTAL DISORDERS; RECURRENT MAJOR DEPRESSION; SPECTRUM DISORDERS; CHILDREN; RECOGNITION; BRAIN; MRI; HIPPOCAMPUS; DAMAGE; INDIVIDUALS AB Background: Autism is a syndrome of unknown cause, marked by abnormal development of social behavior. Attempts to link pathological features of the amygdala, which plays a key role in emotional processing, to autism have shown little consensus. Objective: To evaluate amygdala volume in individuals with autism spectrum disorders and its relationship to laboratory measures of social behavior to examine whether variations in amygdala structure relate to symptom severity. Design: We conducted 2 cross-sectional studies of amygdala volume, measured blind to diagnosis on high-resolution, anatomical magnetic resonance images. Participants were 54 males aged 8 to 25 years, including 23 with autism and 5 with Asperger syndrome or pervasive developmental disorder not otherwise specified, recruited and evaluated at an academic center for developmental disabilities and 26 age- and sex-matched community volunteers. The Autism Diagnostic Interview-Revised was used to confirm diagnoses and to validate relationships with laboratory measures of social function. Main Outcome Measures: Amygdala volume, judgment of facial expressions, and eye tracking. Results: In study 1, individuals with autism who had small amygdalae were slowest to distinguish emotional from neutral expressions (P=.02) and showed least fixation of eye regions (P=.04). These same individuals were most socially impaired in early childhood, as reported on the Autism Diagnostic Interview-Revised (P <.04). Study 2 showed smaller amygdalae in individuals with autism than in control subjects (P=.03) and group differences in the relation between amygdala volume and age. Study 2 also replicated findings of more gaze avoidance and childhood impairment in participants with autism with the smallest amygdalae. Across the combined sample, severity of social deficits interacted with age to predict different patterns of amygdala development in autism (P=.047). Conclusions: These findings best support a model of amygdala hyperactivity that could explain most volumetric findings in autism. Further psychophysiological and histopathological studies are indicated to confirm these findings. C1 Univ Wisconsin, Waisman Ctr, Waisman Lab Brain Imaging & Behav, Madison, WI 53705 USA. Univ Wisconsin, Dept Phys Med, Madison, WI 53705 USA. 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Gen. Psychiatry PD DEC PY 2006 VL 63 IS 12 BP 1417 EP 1428 DI 10.1001/archpsyc.63.12.1417 PG 12 WC Psychiatry SC Psychiatry GA 111YU UT WOS:000242492600012 PM 17146016 ER PT J AU Wilkinson, KM Rosenquist, C AF Wilkinson, Krista M. Rosenquist, Celia TI Demonstration of a method for assessing semantic organization and category membership in individuals with autism spectrum disorders and receptive vocabulary limitations SO AUGMENTATIVE AND ALTERNATIVE COMMUNICATION LA English DT Article DE AAC display design; mental retardation; matching to sample (MTS) ID STIMULUS-CONTROL; DISABILITIES; VERIFICATION AB A recognized challenge in the field of augmentative and alternative communication (AAC) is the assessment of the individual skills and preferences of potential users of AAC. Particularly in cognitive assessment, many traditional methods are inappropriate because they require the participant to produce a verbal response and/or involve complex verbal instructions. For individuals with limited verbal forms of language, failure at such tasks is relatively uninstructive, either for revealing their functional intellectual status or for developing effective interventions. This paper presents a demonstration of a method developed to evaluate category structure and, thus, semantic organization in individuals with limited verbal skills concomitant to autism spectrum disorder. This method offers a promising tool for assessing clients for AAC. Further potential uses of this method, both clinically and in research, are discussed. C1 Emerson Coll, Boston, MA 02116 USA. Univ Massachusetts, Sch Med, Waltham, MA USA. RP Wilkinson, KM (reprint author), Emerson Coll, 120 Boylston St, Boston, MA 02116 USA. EM Krista_Wilkinson@emerson.edu CR BAUER PJ, 1989, COGNITIVE PSYCHOL, V21, P156, DOI 10.1016/0010-0285(89)90006-6 Beukelman D. 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TI Attentional dysfunction, impulsivity, and resistance to change in a mouse model of fragile X syndrome SO BEHAVIORAL NEUROSCIENCE LA English DT Article; Proceedings Paper CT 35th Annual Meeting of the Society-for-Neuroscience CY NOV 12-16, 2005 CL Washington, DC SP Soc Neurosci DE fragile X syndrome; Fmr1 mouse; attention; autism; error monitoring ID PRENATAL COCAINE EXPOSURE; FMR1 KNOCKOUT MOUSE; IMPAIRED SUSTAINED ATTENTION; MENTAL-RETARDATION; ANIMAL-MODEL; YOUNG MALES; MICE; PHENOTYPE; PERFORMANCE; BEHAVIOR AB On a series of attention tasks, male mice with a mutation targeted to the fragile X mental retardation 1 (Fmr1) gene (Fmr1 knockout [KO] mice) committed a higher rate of premature responses than wild-type littermates, with the largest differences seen when task contingencies changed. This finding indicates impaired inhibitory control, particularly during times of stress or arousal. The KO mice also committed a higher rate of inaccurate responses than controls, particularly during the final third of each daily test session, indicating impaired sustained attention. In the selective attention task, the unpredictable presentation of potent olfactory distractors produced a generalized disruption in the performance of the KO mice, whereas for controls, the disruption produced by the distractors was temporally limited. Finally, the attentional disruption seen following an error was more pronounced for the KO mice than for controls, further implicating impaired regulation of arousal and/or negative affect. The present study provides the first evidence that the Fmr1 KO mouse is impaired in inhibitory control, attention, and arousal regulation, hallmark areas of dysfunction in fragile X syndrome. The resistance to change also seen in these mice provides a behavioral index for studying the autistic features of this disorder. 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Neurosci. PD DEC PY 2006 VL 120 IS 6 BP 1367 EP 1379 DI 10.1037/0735-7044.120.6.1367 PG 13 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 116SM UT WOS:000242822600022 PM 17201482 ER PT J AU Kwasnicka-Crawford, DA Carson, AR Scherer, SW AF Kwasnicka-Crawford, Dorota A. Carson, Andrew R. Scherer, Stephen W. TI IQCJ-SCHIP1, a novel fusion transcript encoding a calmodulin-binding IQ motif protein SO BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS LA English DT Article DE paracentric inversion; schwannomin interacting protein; neurofibromatosis type 2; language disorder; autism; calmodulin ID LANGUAGE-ASSOCIATION CORTEX; BRAIN ABNORMALITIES; GENE-EXPRESSION; HUMAN GENOME; AUTISM; GAP-43; CELLS; IDENTIFICATION; NEUROMODULIN; NEUROGRANIN AB The existence of transcripts that span two adjacent, independent genes is considered rare in the human genome. This study characterizes a novel human fusion gene named IQCJ-SCHIP1. IQCJ-SCHIP1 is the longest isoform of a complex transcriptional unit that bridges two separate genes that encode distinct proteins, IQCJ, a novel IQ motif containing protein and SCHIP1, a schwannomin interacting protein that has been previously shown to interact with the Neurofibromatosis type 2 (NF2) protein. IQCJ-SCHIP1 is located on the chromosome 3q25 and comprises a 1692-bp transcript encompassing 11 exons spanning 828 kb of the genomic DNA. We show that IQCJ-SCHIP1 mRNA is highly expressed in the brain. Protein encoded by the IQCJ-SCHIP1 gene was localized to cytoplasm and actin-rich regions and in differentiated PC12 cells was also seen in neurite extensions. (c) 2006 Elsevier Inc. All rights reserved. C1 Hosp Sick Children, Dept Genet, Toronto, ON M5G 1X8, Canada. Hosp Sick Children, Dept Genom Biol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Mol & Med Genet, Toronto, ON, Canada. 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PD DEC 1 PY 2006 VL 350 IS 4 BP 890 EP 899 DI 10.1016/j.bbrc.2006.09.136 PG 10 WC Biochemistry & Molecular Biology; Biophysics SC Biochemistry & Molecular Biology; Biophysics GA 100TD UT WOS:000241690800013 PM 17045569 ER PT J AU Andrieux, A Salin, P Schweitzer, A Begou, M Pachoud, B Brun, P Gory-Faure, S Kujala, P Suaud-Chagny, MF Hofle, G Job, D AF Andrieux, Annie Salin, Paul Schweitzer, Annie Begou, Melina Pachoud, Bastien Brun, Philippe Gory-Faure, Sylvie Kujala, Pekka Suaud-Chagny, Marie-Francoise Hoefle, Gerhard Job, Didier TI Microtubule stabilizer ameliorates synaptic function and behavior in a mouse model for schizophrenia SO BIOLOGICAL PSYCHIATRY LA English DT Article DE epothilone; microtubule; schizophrenia; STOP protein; synaptic plasticity ID ACTIN CYTOSKELETON; ANTITUMOR AGENT; STOP PROTEINS; AUTISM; GENES; MUTATION; MICE; PATHOPHYSIOLOGY; NEUREGULIN-1; NEUROLIGINS AB Background: Recent data suggest that cytoskeletal defects may play a role in schizophrenia. We previously imitated features of schizophrenia in an animal model by disrupting gene coding for a microtubule-associated protein called STOP. STOP-null mice display synaptic defects in glutamatergic neurons, byper-dopaminergy, and severe behavioral disorders. Synaptic and behavioral deficits are amended by neuroleptic treatment in STOP-null mice, providing an attractive model to test new antipsychotic agents. We examined the effects of a taxol-related microtubule stabilizer, epothilone D. Methods. Mice were treated either with vehicle alone or with epothilone D. Treatment effects on synaptic function were assessed using electron-microscopy quantification of synaptic vesicle pools and electrophysiology in the CA 1 region of the hippocampus, Dopamine transmission was investigated using electrochemical assays. Behavior was principally assessed using tests of maternal skills. Results: In STOP-null mice, treatment with epothilone D increased synaptic vesicle pools, ameliorated both short- and long-term forms of synaptic plasticity in glutamatergic neurons, and had a dramatic beneficial effect on mouse behavior. Conclusions: A microtubule stabilizer can have a beneficial effect on synaptic function and behavior, suggesting new possibilities,for treatment of schizophrenia. C1 CEA Grenoble, INSERM, Lab Cytosquelette, U366,Dept Reponse & Dynam Cellulaire, F-38054 Grenoble, France. Fac Med Laennec, CNRS, UMR5167, Lyon, France. UCBL, Lab Neuropharmacol & Neurochim, INSERM, Inst Fed Neurosci Lyon, Lyon, France. Netherlands Canc Inst, Amsterdam, Netherlands. German Res Ctr Biotechnol, Braunschweig, Germany. RP Andrieux, A (reprint author), CEA Grenoble, INSERM, Lab Cytosquelette, U366,Dept Reponse & Dynam Cellulaire, 17 Rue Martyrs, F-38054 Grenoble, France. 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Psychiatry PD DEC 1 PY 2006 VL 60 IS 11 BP 1224 EP 1230 DI 10.1016/j.biopsych.2006.03.048 PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 108ZW UT WOS:000242278700008 PM 16806091 ER PT J AU Molnar, MJ Bencsik, P AF Molnar, Maria J. Bencsik, Peter TI Establishing a neurological-psychiatric biobank: Banking, informatics, ethics SO CELLULAR IMMUNOLOGY LA English DT Article; Proceedings Paper CT International Conference of Immunogenomics and Immunomics CY OCT 08-12, 2006 CL Budapest, HUNGARY DE neurology; psychiatry; biobanking; database ID GENETICS AB The recent development of genetic databases and biobanks in a number of countries reflects scientist's beliefs in the future health benefits to be derived from genetic research. The NEPSYBANK is a national program of the Hungarian Clinical Neurogenetic Society with comprehensive participation of the Neurology and Psychiatry Departments of Medical Universities and the National Institute of Psychiatry and Neurology. The NEPSYBANK forms a part of the national biobank project (www.biobank.hu). The goal is to establish nationwide collaboration and common biobanking standards on quality, access, and protection of integrity in the field of neurology and psychiatry. Biological materials and databases are already collected in stroke, epilepsy, multiple sclerosis, motoneuron diseases, dementia, movement disorders, schizophrenia, and alcohol addiction. In peripheral neuropathies, neuropathic pain syndromes, muscle diseases, migraine, myasthenia gravis, depression, panic disease, anxiety, autism, and software development is in progress. The resources have been expanded by continued prospective collection of samples and data and important bottlenecks in sample purification, sample retrieval, in protection of the integrity of the research participants, as well as in guaranteeing the security and confidentiality of the participant's information have been harmonized. The development of uniform consent management, comprehensive sample overview and quality standards for health care-related biobanking may provide a unique opportunity for Hungary in molecular clinically oriented research. The program is a diseased-based research biobank with comprehensive collection of phenotypic and environmental information as well as biobanking of DNA, RNA or buffy coat, plasma, and erythrocytes stored at -80 degrees C. The biobank has a neuro pathological part as well: storing conventional pathology and biopsy specimens. The analytical and informational demands being created by biobanking requires a "connectivity of community" that has not traditionally been present in the life sciences. As you put more resources into something, your silos tend to become taller, and we need to avoid this. The life science and healthcare community should be ignored working in individual "silos." (c) 2007 Elsevier Inc. All rights reserved. C1 Natl Inst Psychiat & Neurol, H-1021 Budapest, Hungary. Semmelweis Univ, Dept Pediat 1, Budapest, Hungary. RP Molnar, MJ (reprint author), Natl Inst Psychiat & Neurol, Huvosvolgyi Str 116, H-1021 Budapest, Hungary. EM molnarm@opni.hu CR Calkins ME, 2007, SCHIZOPHRENIA BULL, V33, P33, DOI 10.1093/schbul/sbl044 Corrigan Oonagh P, 2006, Stud Hist Philos Biol Biomed Sci, V37, P550, DOI 10.1016/j.shpsc.2006.06.004 Elston RC, 2006, STAT MED, V25, P3049, DOI 10.1002/sim.2650 Gibbons Susan M C, 2005, Eur J Health Law, V12, P103, DOI 10.1163/1571809054640659 Myhr K-M, 2006, Acta Neurol Scand Suppl, V183, P37 Tanaka F, 2006, ANN NY ACAD SCI, V1086, P1, DOI 10.1196/annals.1377.011 Thornton M, 2005, DRUG DISCOV TODAY, V10, P1369, DOI 10.1016/S1359-6446(05)03560-9 Williams RW, 2006, MAMM GENOME, V17, P496, DOI 10.1007/s00335-006-0006-x NR 8 TC 13 Z9 16 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0008-8749 J9 CELL IMMUNOL JI Cell. Immunol. PD DEC PY 2006 VL 244 IS 2 BP 101 EP 104 DI 10.1016/j.cellimm.2007.02.013 PG 4 WC Cell Biology; Immunology SC Cell Biology; Immunology GA 172AO UT WOS:000246776700007 PM 17448454 ER PT J AU Liu, XC Hubbard, JA Fabes, RA Adam, JB AF Liu, Xianchen Hubbard, Julie A. Fabes, Richard A. Adam, James B. TI Sleep disturbances and correlates of children with autism spectrum disorders SO CHILD PSYCHIATRY & HUMAN DEVELOPMENT LA English DT Article DE autistic spectrum disorder; sleep patterns; sleep problems; risk factors ID SCHOOL-AGED CHILDREN; PREVALENCE; PATTERNS; BEHAVIOR; HABITS AB This study examined sleep patterns, sleep problems, and their correlates in children with autism spectrum disorders (ASD). Subjects consisted of 167 ASD children, including 108 with autistic disorder, 27 with Asperger's syndrome, and 32 with other diagnoses of ASD. Mean age was 8.8 years (SD = 4.2), 86% were boys. Parents completed a self-administered child sleep questionnaire. Results showed that average night sleep duration was 8.9 h (SD = 1.8), 16% of children shared a bed with parent. About 86% of children had at least one sleep problem almost every day, including 54% with bedtime resistance, 56% with insomnia, 53% with parasomnias, 25% with sleep disordered breathing, 45% with morning rise problems, and 31% with daytime sleepiness. Multivariate logistic regression analyses indicated that younger age, hypersensitivity, co-sleeping, epilepsy, attention-deficit/hyperactivity disorder (ADHD), asthma, bedtime ritual, medication use, and family history of sleep problems were related to sleep problems. Comorbid epilepsy, insomnia, and parasomnias were associated with increased risk for daytime sleepiness. Results suggest that both dyssomnias and parasomnias are very prevalent in children with ASD. Although multiple child and family factors are associated with sleep problems, other comorbid disorders of autism may play a major role. 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Tsai, Katherine TI Parenting interventions for children with autism spectrum and disruptive behavior disorders: Opportunities for cross-fertilization SO CLINICAL CHILD AND FAMILY PSYCHOLOGY REVIEW LA English DT Review DE autism spectrum disorders; disruptive behavior disorders; parent education; parent training; treatment ID ONSET CONDUCT PROBLEMS; PERVASIVE DEVELOPMENTAL DISORDERS; HEAD-START CHILDREN; INTERACTION THERAPY; FOLLOW-UP; YOUNG-CHILDREN; ANTISOCIAL-BEHAVIOR; TREATING CHILDREN; TRAINING-PROGRAM; LANGUAGE DELAYS AB Empirical support exists for parent training/education (PT/PE) interventions for children with disruptive behavior disorders (DBD) and autism spectrum disorders (ASD). While the models share common roots, current approaches have largely developed independently and the research findings have been disseminated in two different literature traditions: mental health and developmental disabilities. 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Child Fam. Psychol. Rev. PD DEC PY 2006 VL 9 IS 3-4 BP 181 EP 200 DI 10.1007/s10567-006-0010-4 PG 20 WC Psychology, Clinical SC Psychology GA 114YI UT WOS:000242701200003 PM 17053963 ER PT J AU Serretti, A Calati, R Mandelli, L De Ronchi, D AF Serretti, Alessandro Calati, Raffaella Mandelli, Laura De Ronchi, Diana TI Serotonin transporter gene variants and behavior: A comprehensive review SO CURRENT DRUG TARGETS LA English DT Review DE serotonin transporter; phenotype; complex disorder; genetics; psychiatry ID ANTIDEPRESSANT-INDUCED MANIA; REGULATORY REGION POLYMORPHISM; OBSESSIVE-COMPULSIVE DISORDER; TRYPTOPHAN-HYDROXYLASE GENE; ANXIETY-RELATED TRAITS; POSITRON-EMISSION-TOMOGRAPHY; FAMILY-BASED ASSOCIATION; STRESSFUL LIFE EVENTS; FUNCTIONAL POLYMORPHISM; PROMOTER POLYMORPHISM AB The serotonin system modulates affective, cognitive and behavioral processes. A key molecular structure of this system, the serotonin transporter (SERT) gene, has been associated with many human behaviors, both normal and pathological. This article aim is a comprehensive overview of the human behavioral features influenced by SERT gene variants and to suggest some comprehensive hypotheses. In particular, the SERTPR insertion/deletion polymorphism has been related to hippocampal volume and amygdala response and it has been found to influence anxiety-related personality traits and anxiety disorders; in mood disorders it showed some influences on age at onset, periodicity, illness recurrence, rapid cycling, antidepressants response and depressive reaction to stressful life events. Psychosomatic disorders, suicide, alcoholism, smoking, eating disorders, attention deficit hyperactivity disorders and autism have been also found to be related to SERTPR variants. SERT gene variants seem therefore to modulate a wide range of aspects in both normal and affected individuals, many of which are possibly due to indirect correlations between such human features. C1 Univ Bologna, Inst Psychiat, I-40123 Bologna, Italy. RP Serretti, A (reprint author), Univ Bologna, Inst Psychiat, Viale Carlo Pepoli 5, I-40123 Bologna, Italy. 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EM ouriel@limsi.fr CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Russell J., 1996, AGENCY ITS ROLE MENT NR 2 TC 0 Z9 0 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1094-9313 J9 CYBERPSYCHOL BEHAV JI CyberPsychol. Behav. PD DEC PY 2006 VL 9 IS 6 BP 677 EP 678 PG 2 WC Communication; Psychology, Applied SC Communication; Psychology GA 120TL UT WOS:000243108800044 ER PT J AU Trepagnier, CY Sebrechts, MM Finkelmeyer, A Stewart, W Woodford, J AF Trepagnier, Cheryl Y. Sebrechts, Marc M. Finkelmeyer, Andreas Stewart, Willie, Jr. Woodford, Jordana TI Acceptance of a virtual social environment by pre-schoolers with autism spectrum disorder SO CYBERPSYCHOLOGY & BEHAVIOR LA English DT Meeting Abstract C1 Catholic Univ Amer, Washington, DC 20064 USA. EM trepagnier@cua.edu NR 0 TC 3 Z9 3 PU MARY ANN LIEBERT INC PI NEW ROCHELLE PA 140 HUGUENOT STREET, 3RD FL, NEW ROCHELLE, NY 10801 USA SN 1094-9313 J9 CYBERPSYCHOL BEHAV JI CyberPsychol. Behav. PD DEC PY 2006 VL 9 IS 6 BP 723 EP 723 PG 1 WC Communication; Psychology, Applied SC Communication; Psychology GA 120TL UT WOS:000243108800119 ER PT J AU Pellicano, E Maybery, M Durkin, K Maley, A AF Pellicano, E Maybery, M Durkin, K Maley, A TI Multiple cognitive capabilities/deficits in children with an autism spectrum disorder: "Weak" central coherence and its relationship to theory of mind and executive control SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; DEVELOPMENTAL DISORDERS; VERBAL-ABILITY; INDIVIDUALS; PERFORMANCE; ATTENTION; ADULTS; PRESCHOOLERS; IMPAIRMENTS; ADOLESCENTS AB This study examined the validity of "weak" central coherence (CC) in the context of multiple cognitive capabilities/deficits in autism. Children with an autism spectrum disorder (ASD) and matched typically developing children were administered tasks tapping visuospatial coherence, false-belief understanding and aspects of executive control. Significant group differences were found in all three cognitive domains. Evidence of local processing on coherence tasks was widespread in the ASD group, but difficulties in attributing false beliefs and in component,,. of executive functioning were present in fewer of the children with ASD. This cognitive profile was generally similar for younger and older children with ASD. Furthermore, weak CC was unrelated to false-belief understanding, but aspects of coherence (related to integration) were associated with aspects of executive control. Few associations were found between cognitive variables and indices of autistic symptomatology. Implications for CC theory are discussed. C1 Univ Oxford, Pk Hosp Children, Sect Child & Adolescent Psychiat, Oxford OX3 7LQ, England. Univ Western Australia, Nedlands, WA 6009, Australia. Univ Strathclyde, Glasgow G1 1XQ, Lanark, Scotland. RP Pellicano, E (reprint author), Univ Oxford, Pk Hosp Children, Sect Child & Adolescent Psychiat, Old Rd, Oxford OX3 7LQ, England. 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PD WIN PY 2006 VL 18 IS 1 BP 77 EP 98 DI 10.1017/S0954579406060056 PG 22 WC Psychology, Developmental SC Psychology GA 019ZA UT WOS:000235876100005 PM 16478553 ER PT J AU Campbell, R Lawrence, K Mandy, W Mitra, C Jeyakuma, L Skuse, D AF Campbell, R Lawrence, K Mandy, W Mitra, C Jeyakuma, L Skuse, D TI Meanings in motion and faces: Developmental associations between the processing of intention from geometrical animations and gaze detection accuracy SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID ASPERGER-SYNDROME; EYE-GAZE; AUTISTIC INDIVIDUALS; FUNCTIONING AUTISM; MENTAL STATES; PERCEPTION; CHILDREN; MIND; RECOGNITION; BRAIN AB Aspects of face processing, on the one hand, and theory of mind (ToM) tasks, on the other hand, show specific impairment in autism. We aimed to discover whether a correlation between tasks tapping these abilities was evident in typically developing children at two developmental stages. One hundred fifty-four normal children (6-8 years and 16-18 years) and 13 high-IQ autistic children (11-17 years) were tested on a range of face-processing and IQ tasks, and a ToM test based oil the attribution of intentional movement to abstract shapes in a cartoon. By midchildhood, the ability accurately and spontaneously to infer the locus of attention of a face with direct or averted gaze was specifically associated with the ability to describe geometrical animations using mental state terms. Other face-processing and animation descriptions failed to show the association. Autistic adolescents were impaired at both gaze processing and ToM descriptions. using these tests. Mentalizing and gaze perception accuracy are associated in typically developing children and adolescents. The findings are congruent with the possibility that common neural Circuitry underlies, at least in part, processing implicated in these tasks. They are also congruent with the possibility that autism may lie at one end of a developmental continuum with respect to these skills, and to the factor(s) underpinning them. C1 UCL, Dept Human Commun Sci, London WC1 N1PF, England. Inst Child Hlth, London, England. RP Campbell, R (reprint author), UCL, Dept Human Commun Sci, London WC1 N1PF, England. 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Psychopathol. PD WIN PY 2006 VL 18 IS 1 BP 99 EP 118 DI 10.1017/S0954579406060068 PG 20 WC Psychology, Developmental SC Psychology GA 019ZA UT WOS:000235876100006 PM 16478554 ER PT J AU de Bruin, EI Verheij, F Wiegman, T Ferdinand, RF AF de Bruin, Esther I. Verheij, Fop Wiegman, T. Ferdinand, Robert F. TI Differences in finger length ratio between males with autism, pervasive developmental disorder-not otherwise specified, ADHD, and anxiety disorders SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID 4TH DIGIT LENGTH; SEXUAL ORIENTATION; 2ND; TESTOSTERONE; PREDICTOR; SYMPTOMS; LINKAGE; HOXA1; CHILD; MEN AB Children with autism have a relatively shorter index finger (2D) compared with their ring finger (4D). It is often presumed that the 2D:4D ratio is associated with fetal testosterone levels and that high fetal testosterone levels could play a role in the aetiology of autism. It is unknown whether this effect is specific to autism. In this study, 2D:4D ratios of 144 males aged 6 to 14 years (mean age 9y 1mo [SD 1y 11mo]) with psychiatric disorders were compared with those of 96 males aged 6 to 13 years from the general population (mean age 9y 1mo [SD 1y 10mo]). Psychiatric disorders were divided into autism/Asperger syndrome (n=24), pervasive developmental disorder-not otherwise specified (PDD-NOS; n=26), attention-deficit-hyperactivity disorder (ADHD)/oppositional defiant disorder (ODD; n=68), and anxiety disorders (n=26). Males with autism/Asperger syndrome (p < 0.05) and ADHD/ODD (p < 0.05) had significantly lower (though not significantly; p=0.52) ratios than males with an anxiety disorder, and males with autism/Asperger syndrome had lower ratios than those in the comparison group. These results indicated that higher fetal testosterone levels may play a role, not only in the origin of autism, but also in the aetiology of PDD-NOS and of ADHD/ODD. Males with anxiety disorders might have been exposed to lower prenatal testosterone levels. C1 Sophia Childrens Univ Hosp, Erasmus Med Ctr Rotterdam, Dept Child & Adolescent Psychiat, NL-3015 Rotterdam, Netherlands. RP Ferdinand, RF (reprint author), Sophia Childrens Univ Hosp, Erasmus Med Ctr Rotterdam, Dept Child & Adolescent Psychiat, Dr Molewaterpl 60, NL-3015 Rotterdam, Netherlands. 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EM rebecca_knickmeyer@med.unc.edu RI Hoekstra, Rosa/G-2410-2011; Knickmeyer, Rebecca/G-8128-2014 OI Knickmeyer, Rebecca/0000-0001-7708-1388 CR Abbott DH, 1997, ANDROGEN EXCESS DISORDERS IN WOMEN, P369 Baron-Cohen S, 2005, SCIENCE, V310, P819, DOI 10.1126/science.1115455 Burgess B, 1996, AM J MED GENET, V64, P376, DOI 10.1002/ajmg.1320640203 EVANS AL, 1988, CHILD CARE HLTH DEV, V14, P59, DOI 10.1111/j.1365-2214.1988.tb00563.x Gillberg C., 1984, DEV MED CHILD NEUROL, V26, P122 Levene H., 1960, CONTRIBUTIONS PROBAB, V1, P278 Weichold K., 2003, GENDER DIFFERENCES P, P241, DOI DOI 10.1017/CB09780511489716.013 World Health Organization, 1994, INT CLASS DIS Worley G, 2002, PEDIATRICS, V110, P897, DOI 10.1542/peds.110.5.897 NR 9 TC 25 Z9 26 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD DEC PY 2006 VL 48 IS 12 BP 1007 EP 1008 DI 10.1017/S0012162206222229 PG 2 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 114LS UT WOS:000242668300018 PM 17109794 ER PT J AU Dosman, CF Drmic, IE Brian, JA Senthilselvan, A Harford, M Smith, R Roberts, SW AF Dosman, Cara F. Drmic, Irene E. Brian, Jessica A. Senthilselvan, Ambikaipakan Harford, Mary Smith, Ryan Roberts, S. Wendy TI Ferritin as an indicator of suspected iron deficiency in children with autism spectrum disorder: prevalence of low serum ferritin concentration SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Letter C1 Univ Alberta, Glenrose Rehabil Hosp, Edmonton, AB, Canada. Univ York, Dept Psychol, York YO10 5DD, N Yorkshire, England. Univ Toronto, Hosp Sick Children, Child Dev Ctr, Toronto, ON, Canada. Univ Alberta, Dept Publ Hlth Sci, Edmonton, AB, Canada. RP Dosman, CF (reprint author), Univ Alberta, Glenrose Rehabil Hosp, Edmonton, AB, Canada. 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Med. Child Neurol. PD DEC PY 2006 VL 48 IS 12 BP 1008 EP 1009 DI 10.1017/S0012162206232225 PG 2 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 114LS UT WOS:000242668300019 PM 17109795 ER PT J AU Knickmeyer, RC Baron-Cohen, S AF Knickmeyer, Rebecca Christine Baron-Cohen, Simon TI Fetal testosterone and sex differences SO EARLY HUMAN DEVELOPMENT LA English DT Article; Proceedings Paper CT Neonatal Update Conference on Science of Newborn Care CY DEC 06-08, 2006 CL London, ENGLAND DE testosterone; sex differences ID PRENATAL TESTOSTERONE; VERBAL-ABILITY; CHILDREN; BEHAVIOR; AUTISM; DIFFERENTIATION; POPULATION; HORMONE; INFANTS; MIND AB Experiments in animals leave no doubt that androgens, including testosterone, produced by the testes in fetal and/or neonatal life act on the brain to induce sex differences in neural structure and function. In this article, we argue that prenatal and neonatal testosterone exposure are strong candidates for having a causal role in sexual dimorphism in human behaviour, including social development. (c) 2006 Elsevier Ireland Ltd. All rights reserved. C1 Univ N Carolina, Dept Psychiat, Neurosci Hosp 7023, Chapel Hill, NC 27599 USA. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. RP Knickmeyer, RC (reprint author), Univ N Carolina, Dept Psychiat, Neurosci Hosp 7023, CB 7160, Chapel Hill, NC 27599 USA. EM rebecca_knickmeyer@med.unc.edu RI Knickmeyer, Rebecca/G-8128-2014 OI Knickmeyer, Rebecca/0000-0001-7708-1388 CR ABRAMOVI.DR, 1974, J OBSTET GYN BR COMM, V81, P448 Arnold AP, 2004, ENDOCRINOLOGY, V145, P1057, DOI 10.1210/en.2003-1491 AUYEUNG B, IN PRESS EUR J ENDOC Baird G, 2006, LANCET, V368, P210, DOI 10.1016/S0140-6736(06)69041-7 Bar-On A, 1999, BRIT J SOC WORK, V29, P5 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x BARONCOHEN S, 1995, STIMULATION THEORY D BENENSON JF, 1993, CHILD DEV, V64, P544, DOI 10.1111/j.1467-8624.1993.tb02927.x Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 CHAPMAN E, IN PRESS J SOC NEURO CONNELLAN J, 2001, INFANT BEHAV DEV, V23, P113 De Vries GJ, 2002, HORMONES BRAIN BEHAV, P137 Fechner P. 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Dev. PD DEC PY 2006 VL 82 IS 12 BP 755 EP 760 DI 10.1016/j.earlhumdev.2006.09.014 PG 6 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA 114WP UT WOS:000242696600002 ER PT J AU Starr, EA Foy, JB Cramer, KA Singh, H AF Starr, Elizabeth A. Foy, Janis B. Cramer, Kenneth A. Singh, Henareet TI How are schools doing? Parental perceptions of children with autism spectrum disorders, Down syndrome and learning disabilities: A comparative analysis SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; PERSONNEL PREPARATION; MENTAL DISABILITIES; EDUCATION; STUDENTS AB Parents of 209 children (162 mates and 46 females) with autism spectrum disorders, Down syndrome or learning disabilities ranging in age from 4 to 21 years were surveyed about their perceptions of the education of their children. Items on the survey were categorized into 7 areas: school personnel's knowledge about the disability, best practices, behavioural concerns, parent/school collaboration, education team, individual education plan, and miscellaneous other items. Group differences were observed on a number of items and in almost every case parents in the learning disabilities group rated the items significantly lower than one or more of the other groups. In addition, numerous items were paired such that parents were asked to rate if a certain educational "best practice" was being utilized with their child and if they felt their child required it. Examination of the paired items indicated many significant differences between what parents felt was being offered their child, and what their child needed to achieve their maximum potential across diagnostic groups. The implications of these and other results are discussed. C1 Univ Windsor, Fac Educ, Windsor, ON N9B 3P4, Canada. 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L., 1997, FOCUS AUTISM OTHER D, V12, P67 Westling DL, 1996, EDUC TRAIN MENT RET, V31, P86 Westling DL, 1999, EDUC TRAIN MENT RET, V34, P43 Wing L, 2005, HDB AUTISM PERVASIVE, V1, P583 NR 26 TC 9 Z9 9 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 DEC PY 2006 VL 41 IS 4 BP 315 EP 332 PG 18 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 109HV UT WOS:000242299700001 ER PT J AU Cannella-Malone, H Sigafoos, J O'Reilly, M de la Cruz, B Edrisinha, C Lancioni, GE AF Cannella-Malone, Helen Sigafoos, Jeff O'Reilly, Mark de la Cruz, Berenice Edrisinha, Chaturi Lancioni, Giulio E. TI Comparing video prompting to video modeling for teaching daily living skills to six adults with developmental disabilities SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID MULTIPLE-TREATMENT INTERFERENCE; ALTERNATING-TREATMENTS DESIGN; MENTAL-RETARDATION; AUTISM; CHILDREN; TECHNOLOGY; DISORDER; MODERATE AB We compared two procedures (video prompting versus video modeling) for teaching six adults with developmental disabilities to set a table and put away groceries. Video prompting involved 10 separate video clips, each showing one step of the task analysis. Video modeling involved a single video showing all 10 steps from beginning to end. After watching the respective video clips, participants were given the opportunity to complete the task. Video prompting and video modeling procedures were counter-balanced across tasks and participants and compared in an alternating treatments design. Video prompting was effective in promoting rapid acquisition across both tasks in all but one case. Video modeling, in contrast, was generally shown to be ineffective. These data suggest that the number, duration, and/or Perspective from which the video clips are filmed may influence their effectiveness as a teaching tool for individuals with developmental disabilities. C1 Ohio State Univ, Sch Phys Act & Educ Serv, Columbus, OH 43210 USA. Univ Tasmania, Hobart, Tas 7001, Australia. Univ Texas, Austin, TX 78712 USA. Univ Bari, I-70121 Bari, Italy. RP Cannella-Malone, H (reprint author), Ohio State Univ, Sch Phys Act & Educ Serv, 356G Arps Hall,1945 N High St, Columbus, OH 43210 USA. EM malone.175@osu.edu RI Malone, Helen/E-3150-2012 CR Alberto PA, 2005, RES DEV DISABIL, V26, P327, DOI 10.1016/j.ridd.2004.11.002 BANDURA A, 1986, SOCIAL FDN THOUGHT A BARLOW DH, 1984, SINGLE CASE EXPT DES Belfiore P. 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Train. Dev. Disabil. PD DEC PY 2006 VL 41 IS 4 BP 344 EP 356 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 109HV UT WOS:000242299700003 ER PT J AU Van Laarhoven, T Van Laarhoven-Myers, T AF Van Laarhoven, Toni Van Laarhoven-Myers, Traci TI Comparison of three video-based instructional procedures for teaching daily living skills to persons with developmental disabilities SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID SEVERE MENTAL-RETARDATION; INTELLECTUAL DISABILITIES; SECONDARY STUDENTS; PURCHASING SKILLS; RETARDED ADULTS; COMPUTER; CHILDREN; AUTISM; SELF; ACQUISITION AB This study compared the effectiveness of three different video-based instructional sequences, all used in conjunction with the system of least prompts, for teaching three different daily living skills to three young adults with developmental disabilities. The video-based instructional sequences (i.e., video rehearsal, video rehearsal plus photos, and video-rehearsal plus in-vivo video prompting) were evaluated using an adapted alternating treatments design. Results indicated that all of the procedures were effective in increasing independent responding from baseline levels for all participants with the video-rehearsal plus in vivo prompting (Video/In-vivo) and video rehearsal plus photo (Video/Photo) conditions being more efficient in terms of sessions to reach criterion. Two of the three participants engaged in more independent correct responding when they were taught skills with the Video-In-vivo condition, while the other participant engaged in more independent responding on the target skill when the Video/Photo condition was the instructional procedure. In addition, the skills generalized to untrained settings. C1 No Illinois Univ, Dept Teaching & Learning, De Kalb, IL 60115 USA. 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TI Effects of early sensorimotor disorder on contextual learning in autism SO EUROPEAN REVIEW OF APPLIED PSYCHOLOGY-REVUE EUROPEENNE DE PSYCHOLOGIE APPLIQUEE LA English DT Article DE autism; early development; context learning; attention; inhibition ID SELECTIVE ATTENTION; INHIBITION; CHILDREN; SCHIZOPHRENIA; DEFICITS; INFANCY; BRAIN; TASKS AB Cognitive explanations of autism often involve higher order cognitive functions developing late in childhood, such as theory of mind, executive functions or central coherence. In home videos of infants later diagnosed with autism, children display early signs of developmental disorders, for example impaired sensorimotor functions, attention to social and non-social stimuli and a lack of circadian regulation. We propose that these early signs need to be understood using a framework of context learning. It is also important to understand the role for context understanding in guiding the maturation of behavior. The role for inhibition in context learning as understood within learning theory provides us with helpful tools for this analysis. Our research aim is not to identify and explain early markers for autism, but to understand the cognitive developmental pathway set into rolling by an early impairment. This will help us understand the seemingly unrelated symptoms that define the complex syndrome of autism. (c) 2006 Elsevier Masson SAS. All rights reserved. C1 Lund Univ, S-22222 Lund, Sweden. RP Bjorne, P (reprint author), Lund Univ, S-22222 Lund, Sweden. 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Rev. Appl. Psychol.-Rev. Eur. Psychol. Appl. PD DEC PY 2006 VL 56 IS 4 BP 247 EP 252 DI 10.1016/j.erap.2005.09.005 PG 6 WC Psychology, Applied SC Psychology GA 114WM UT WOS:000242696300006 ER PT J AU [Anonymous] AF [Anonymous] TI Increased autism risk in children SO FORTSCHRITTE DER NEUROLOGIE PSYCHIATRIE LA German DT News Item NR 0 TC 0 Z9 0 PU GEORG THIEME VERLAG KG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0720-4299 EI 1439-3522 J9 FORTSCHR NEUROL PSYC JI Forschritte Neurol. Psychiatr. PD DEC PY 2006 VL 74 IS 12 BP 683 EP 683 PG 1 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 123LX UT WOS:000243298500005 ER PT J AU Lewandowski, TA AF Lewandowski, Thomas A. TI Questions regarding environmental mercury release, special education rates, and autism disorder: An ecological study of Texas by Palmer et al. SO HEALTH & PLACE LA English DT Editorial Material DE mercury; Texas; autism ID UNITED-STATES AB Palmer et al. present an analysis in which they look for an association between Toxic Release Inventory (TRI) reporting data for mercury and rates of autism and special education enrollment in Texas. In their analysis, the link between TRI release data and actual mercury exposure is not clear at all, and thus the conclusions drawn from the analysis are questionable. (c) 2005 Elsevier Ltd. All rights reserved. C1 Gradient Corp, Seattle, WA 98101 USA. RP Lewandowski, TA (reprint author), Gradient Corp, 600 Stewart St,Suite 803, Seattle, WA 98101 USA. EM tlewandowski@gradientcorp.com CR Carrington CD, 2002, RISK ANAL, V22, P689, DOI 10.1111/0272-4332.00061 Dabeka R, 2004, FOOD ADDIT CONTAM, V21, P434, DOI 10.1080/02652030410001670184 DEB S, 1994, BRIT J PSYCHIAT, V165, P395, DOI 10.1192/bjp.165.3.395 PALMER RF, 2005, IN PRESS HLTH PLACE Seigneur C, 2004, ENVIRON SCI TECHNOL, V38, P555, DOI 10.1021/es034109t NR 5 TC 2 Z9 2 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 1353-8292 J9 HEALTH PLACE JI Health Place PD DEC PY 2006 VL 12 IS 4 BP 749 EP 750 DI 10.1016/j.healthplace.2005.10.005 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 067EI UT WOS:000239284100034 PM 16337825 ER PT J AU Palmer, RF AF Palmer, Raymond F. TI Response to Thomas A. Lewandowski: Questions regarding environmental mercury release, special education rates, and autism disorder: an ecological study of Texas by Palmer et al. SO HEALTH & PLACE LA English DT Letter EM palmerr@uthscsa.edu CR Bradstreet JJ, 2003, J AM PHYS SURG, V8, P76 Geier DA, 2004, INT J TOXICOL, V23, P369, DOI 10.1080/10915810490902038 Menounou N, 2003, ARCH ENVIRON CON TOX, V45, P11, DOI 10.1007/s00224-002-2120-4 PALMER RF, 2005, HEALTH PLACE, V12, P83 NR 4 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 1353-8292 J9 HEALTH PLACE JI Health Place PD DEC PY 2006 VL 12 IS 4 BP 751 EP 752 DI 10.1016/j.healthplace.2005.10.002 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 067EI UT WOS:000239284100035 ER PT J AU [Anonymous] AF [Anonymous] TI Engineers and autism SO IEEE SPECTRUM LA English DT Editorial Material NR 0 TC 0 Z9 0 PU IEEE-INST ELECTRICAL ELECTRONICS ENGINEERS INC PI PISCATAWAY PA 445 HOES LANE, PISCATAWAY, NJ 08855-4141 USA SN 0018-9235 EI 1939-9340 J9 IEEE SPECTRUM JI IEEE Spectr. PD DEC PY 2006 VL 43 IS 12 BP 10 EP 10 PG 1 WC Engineering, Electrical & Electronic SC Engineering GA 116CB UT WOS:000242779000010 ER PT J AU Geschwind, D AF Geschwind, D. TI Deciphering complexity in autism genetics: Endophenotypes and pathway analysis SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Meeting Abstract CT 16th Biennial Meeting of the International-Society-for-Developmental-Neuroscience CY AUG 24-28, 2006 CL Banff, CANADA SP Int Soc Dev Neurosci NR 0 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD DEC PY 2006 VL 24 IS 8 BP 474 EP 474 DI 10.1016/j.ijdevneu.2006.09.012 PG 1 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 128NE UT WOS:000243663700015 ER PT J AU Sebat, J Lakshmi, B Troge, J Martin, C Spence, S Ledbetter, D Gilliam, TC Ye, K Geschwind, D Sutcliffe, J Wigler, M AF Sebat, J. Lakshmi, B. Troge, J. Martin, C. Spence, S. Ledbetter, D. Gilliam, T. C. Ye, K. Geschwind, D. Sutcliffe, J. Wigler, M. TI High-resolution analysis of genome copy number variation in autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Meeting Abstract CT 16th Biennial Meeting of the International-Society-for-Developmental-Neuroscience CY AUG 24-28, 2006 CL Banff, CANADA SP Int Soc Dev Neurosci C1 Cold Spring Harbor Lab, Cold Spring Harbor, NY USA. Emory Univ, Sch Med, Atlanta, GA 30322 USA. Stony Brook Univ, Stony Brook, NY USA. Calif State Univ Los Angeles, Los Angeles, CA 90032 USA. Columbia Univ, Ctr Med, New York, NY 10027 USA. Univ Chicago, Chicago, IL 60637 USA. Vanderbilt Univ, Nashville, TN 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 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD DEC PY 2006 VL 24 IS 8 BP 474 EP 474 DI 10.1016/j.ijdevneu.2006.09.013 PG 1 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 128NE UT WOS:000243663700016 ER PT J AU Buxbaum, JD Barreto, M Cai, G Goldsmith, J Hollander, E Ramoz, N Reichert, J Sakurai, T Silverman, J Smith, C AF Buxbaum, J. D. Barreto, M. Cai, G. Goldsmith, J. Hollander, E. Ramoz, N. Reichert, J. Sakurai, T. Silverman, J. Smith, C. TI Linkage and association analysis across an autism susceptibility locus on chromosome 2q in autism: Functional analysis of AGC1/SLC25A12 SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Meeting Abstract CT 16th Biennial Meeting of the International-Society-for-Developmental-Neuroscience CY AUG 24-28, 2006 CL Banff, CANADA SP Int Soc Dev Neurosci DE myelin; gene; mouse RI Barreto, Marta/F-5591-2012 OI Barreto, Marta/0000-0001-6464-548X NR 0 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD DEC PY 2006 VL 24 IS 8 BP 507 EP 508 DI 10.1016/j.ijdevneu.2006.09.092 PG 2 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 128NE UT WOS:000243663700089 ER PT J AU Frackowiak, J Cohen, IL Jenkins, E Flory, M Mazur-Kolecka, B AF Frackowiak, J. Cohen, I. L. Jenkins, E. Flory, M. Mazur-Kolecka, B. TI Formation of neuronal processes in a cell culture model of neuronal differentiation in autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Meeting Abstract CT 16th Biennial Meeting of the International-Society-for-Developmental-Neuroscience CY AUG 24-28, 2006 CL Banff, CANADA SP Int Soc Dev Neurosci DE autism; neuronal progenitor cells; neuronal processes; cell culture C1 New York State Inst Basic Res Dev Disabil, New York, NY USA. NR 0 TC 1 Z9 1 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD DEC PY 2006 VL 24 IS 8 BP 533 EP 533 DI 10.1016/j.ijdevneu.2006.09.149 PG 1 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 128NE UT WOS:000243663700146 ER PT J AU Mazur-Kolecka, B Cohen, IL Jenkins, EC Kaczmarski, W Flory, M Frackowiak, J AF Mazur-Kolecka, B. Cohen, I. L. Jenkins, E. C. Kaczmarski, W. Flory, M. Frackowiak, J. TI A new cell culture model to study alterations of early neuronal development in autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Meeting Abstract CT 16th Biennial Meeting of the International-Society-for-Developmental-Neuroscience CY AUG 24-28, 2006 CL Banff, CANADA SP Int Soc Dev Neurosci DE autism; neuronal progenitor cells; neurogenesis; cell culture C1 New York State Inst Basic Res Dev Disabil, New York, NY 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 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD DEC PY 2006 VL 24 IS 8 BP 533 EP 533 DI 10.1016/j.ijdevneu.2006.09.150 PG 1 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 128NE UT WOS:000243663700147 ER PT J AU Sokol, D Maloney, B Kardatzke, D Chen, D Lahiri, D AF Sokol, D. Maloney, B. Kardatzke, D. Chen, D. Lahiri, D. TI Role of two Alzheimer's disease protein markers: Amyloid precursor protein and acetyleholinesterase with aggression in autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Meeting Abstract CT 16th Biennial Meeting of the International-Society-for-Developmental-Neuroscience CY AUG 24-28, 2006 CL Banff, CANADA SP Int Soc Dev Neurosci DE autism; Alzheimers disease; markers C1 Indiana Univ, Sch Med, Indiana, PA USA. RI Maloney, Bryan/C-4924-2011 OI Maloney, Bryan/0000-0003-2364-9649 NR 0 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD DEC PY 2006 VL 24 IS 8 BP 551 EP 551 DI 10.1016/j.ijdevneu.2006.09.190 PG 1 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 128NE UT WOS:000243663700187 ER PT J AU Rajakumar, B Chang, J Rajakumar, R AF Rajakumar, B. Chang, J. Rajakumar, R. TI Disrupted development of thalamocortical fibres leads to imbalance in excitation: inhibition ratio in adult cerebral cortex SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Meeting Abstract CT 16th Biennial Meeting of the International-Society-for-Developmental-Neuroscience CY AUG 24-28, 2006 CL Banff, CANADA SP Int Soc Dev Neurosci DE autism; subplate; GABAergic interneurons; functional domain C1 Univ Western Ontario, London, ON N6A 3K7, Canada. NR 0 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0736-5748 J9 INT J DEV NEUROSCI JI Int. J. Dev. Neurosci. PD DEC PY 2006 VL 24 IS 8 BP 592 EP 592 DI 10.1016/j.ijdevneu.2006.09.285 PG 1 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 128NE UT WOS:000243663700282 ER PT J AU Guo, YQ AF Guo Yanqing TI Training parents and professionals to help children with autism in China: The contribution of behaviour analysis SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Article AB A training programme is presented with two parts. (1) Professional training is received by graduate students at the Institute for Mental Health of Beijing University, based on the principles of behaviour assessment and modification, radical behaviourism, and applied research methods. (2) Parent training focused oil parents with autistic children. using the behaviour analysis and modification methods. China has between 400,000 and 800,000 children with autism. In comparison to its fast economic growth the development of social welfare and social insurance systems are far behind. Once the child is diagnosed with autism, the parents or the primary caregivers of the child, not the government or the community, take the responsibility for the child's rehabilitation. The diagnosis of autism Was first introduced in China in 1982, and for years the work was based on clinical appearances and diagnosis. The main mission of child psychiatrists was early diagnosis, but there was little change obtained with autistic children. From the year 2000 more people were interested in rehabilitation rather than in diagnosis and medical treatments. Behaviour analysis methods are now extensively used in interventions in children with autism in this Country. There is a great need in China for this kind of work, but there are few professionals with the appropriate scientific knowledge and skills to,work with autistic children, These professionals will help to further develop the area of behaviour analysis in China. C1 Peking Univ, Inst Mental Hlth, Beijing 100083, Peoples R China. RP Guo, YQ (reprint author), Peking Univ, Inst Mental Hlth, Beijing 100083, Peoples R China. EM gyq1201@sohu.com NR 0 TC 1 Z9 1 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD DEC PY 2006 VL 41 IS 6 BP 523 EP 526 DI 10.1080/00207590500492575 PG 4 WC Psychology, Multidisciplinary SC Psychology GA 121GX UT WOS:000243147200010 ER PT J AU Gena, A AF Gena, Angeliki TI The effects of prompting and social reinforcement on establishing social interactions with peers during the inclusion of four children with autism in preschool SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Article ID GENERAL-EDUCATION CLASSROOMS; SEVERE DISABILITIES; YOUNG-CHILDREN; STUDENTS; SETTINGS; SCHOOL; INTERVENTIONS; MODERATE; SKILLS; INSTRUCTION AB Inclusion in "regular" schools has become a considerable option for children with autism only in recent years, but we are still far from having a global appreciation of the needs that arise upon the inclusion of children with Such a severe disability. The main purpose of the present Study vas to identify empirically supported procedures that may improve the social interactions of children with autism upon their inclusion in the "regular" preschool. The identification of the needs of preschoolers with autism in Greek schools, as well as the specific skills that Would be taught, were based oil normative data collected and analysed in a series of prior Studies. A long-lasting controversy has been going on between professionals who either advocate For "schools for all children," or stress the importance of making individualized decisions based on each child's needs during the inclusion process. The present study demonstrated that social reinforcement in combination with prompting procedures, provided by a shadow teacher, were effective in increasing the social initiations as well as appropriate responding to peers' initiations of four children with autism during interactions With their classmates in preschool. More importantly, the treatment benefits were obtained in a natural setting, and the initiations and replies were not cliche statements but involved generalized language use appropriate to the social context, and generalized to new therapists. C1 Natl & Kapodistrian Univ Athens, Athens, Greece. RP Gena, A (reprint author), Natl & Kapodistrian Univ Athens, Athens, Greece. 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J. Psychol. PD DEC PY 2006 VL 41 IS 6 BP 541 EP 554 DI 10.1080/00207590500492658 PG 14 WC Psychology, Multidisciplinary SC Psychology GA 121GX UT WOS:000243147200012 ER PT J AU Ricciardi, JN Luiselli, JK Camare, M AF Ricciardi, Joseph N. Luiselli, James K. Camare, Marianne TI Shaping approach responses as intervention for specific phobia in a child with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE contact desensitization; specific phobia; autism; changing-criterion design AB We evaluated contact desensitization (reinforcing approach responses) as intervention for specific phobia with a child diagnosed with autism. During hospital-based intervention, the boy was able to encounter previously avoided stimuli. Parental report suggested that results were maintained postdischarge. C1 Hampstead Hosp, Hampstead, NH 03841 USA. RP Ricciardi, JN (reprint author), Hampstead Hosp, 218 East Rd, Hampstead, NH 03841 USA. EM jricciardi@hampsteadhospital.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Erfanian N., 1990, BEHAV RESIDENTIAL TR, V5, P55, DOI 10.1002/bin.2360050106 Jones KM, 1999, J APPL BEHAV ANAL, V32, P95, DOI 10.1901/jaba.1999.32-95 Rapp JT, 2005, BEHAV THER, V36, P101, DOI 10.1016/S0005-7894(05)80058-9 NR 4 TC 18 Z9 18 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 WIN PY 2006 VL 39 IS 4 BP 445 EP 448 DI 10.1901/jaba.2006.158-05 PG 4 WC Psychology, Clinical SC Psychology GA 114SD UT WOS:000242685000006 PM 17236342 ER PT J AU Shabani, DB Fisher, WW AF Shabani, Daniel B. Fisher, Wayne W. TI Stimulus fading and differential reinforcement for the treatment of needle phobia in a youth with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; diabetes; fading; medical non-compliance; needle phobia; systematic desensitization AB Stimulus fading in the form of gradually increased exposure to a fear-evoking stimulus, often combined with differential reinforcement, has been used to treat phobias in children who are otherwise normal and in children with autism. In this investigation, we applied stimulus fading plus differential reinforcement with an adolescent with autism and diabetes whose needle phobia had prevented medical monitoring of his blood glucose levels for over 2 years. Results showed that the treatment was successful in obtaining daily blood samples for measuring glucose levels. RP Fisher, WW (reprint author), Munroe Meyer Inst, 985450 Nebraska Med Ctr, Omaha, NE 68198 USA. EM wfisher@unmc.edu CR Braff M., 1979, J DENT CHILD, V46, P404 Davidson MB, 2004, DIABETES RES CLIN PR, V64, P229, DOI 10.1016/j.diabres.2004.03.006 DeLeon IG, 1996, J APPL BEHAV ANAL, V29, P519, DOI 10.1901/jaba.1996.29-519 Jones KM, 1999, J APPL BEHAV ANAL, V32, P95, DOI 10.1901/jaba.1999.32-95 LOVE SR, 1990, J APPL BEHAV ANAL, V23, P379, DOI 10.1901/jaba.1990.23-379 MCDOWALL RH, 1995, J CLIN ANESTH, V7, P273, DOI 10.1016/0952-8180(95)00017-C Zambanini A, 1997, DIABETIC MED, V14, P321, DOI 10.1002/(SICI)1096-9136(199704)14:4<321::AID-DIA356>3.0.CO;2-H NR 7 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 WIN PY 2006 VL 39 IS 4 BP 449 EP 452 DI 10.1901/jaba.2006.30-05 PG 4 WC Psychology, Clinical SC Psychology GA 114SD UT WOS:000242685000007 PM 17236343 ER PT J AU Beadle-Brown, J Murphy, G Wing, L AF Beadle-Brown, Julie Murphy, Glynis Wing, Lorna TI The Camberwell Cohort 25 years on: Characteristics and changes in skills over time SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE autism; outcome changes in skills; severe intellectual disability; social impairment ID SEVERE INTELLECTUAL DISABILITIES; RECEPTIVE LANGUAGE DISORDER; MENTALLY-RETARDED ADULTS; ADAPTIVE-BEHAVIOR; FOLLOW-UP; DOWNS-SYNDROME; SOCIAL IMPAIRMENT; RESIDENTIAL CARE; CHILDREN; AUTISM AB Background This study presents data on the characteristics of the Camberwell Cohort, 25 years after they were first assessed in the 1970s [Wing & Gould (1979) journal of Autism and Childhood Schizophrenia vol. 9, pp. 11-29]. It also presents data on changes over time which adds to that presented in Beadle-Brown et al. [Journal of Intellectual Disability Research (2000) vol. 32, pp. 195-206]. Methods Measures of level of skills, ability and behaviour, including self-care, educational, social skills, cognitive ability and challenging behaviour, were conducted with as many of the cohort as possible. In addition, background information was collected on diagnosis, placement history, daytime activity and family contact. Results The cohort (n = 91) now aged between 27 and 42 years were living mostly in the community (68%) or with their parents (27%). Sixty-four per cent of the sample who could be tested (n = 36) had an IQ below 50, 73% were socially impaired and 72% had some form of autistic spectrum disorder. There were few changes over time between time 2 (1980s) and time 3 - as reported in Beadle-Brown et al., most changes occurred during childhood and early adolescence. However, for those who had been in institutional care for more than 3 years, there were a number of self-care skills which significantly increased between time 2 and time 3 (after a move into the community). C1 Univ Kent, Tizard Ctr, Canterbury CT2 7LZ, Kent, England. Univ Lancaster, Inst Hlth Res, Lancaster, England. RP Beadle-Brown, J (reprint author), Univ Kent, Tizard Ctr, Canterbury CT2 7LZ, Kent, England. EM j.d.beadle-brown@kent-ac.uk CR Bayley N., 1969, BAYLEY SCALES INFANT Beadle-Brown J, 2000, J INTELL DISABIL RES, V44, P12, DOI 10.1046/j.1365-2788.2000.00245.x Beadle-Brown J, 2002, J AUTISM DEV DISORD, V32, P195, DOI 10.1023/A:1015401814041 Beadle-Brown J, 2005, AM J MENT RETARD, V110, P1, DOI 10.1352/0895-8017(2005)110<1:LOFPWS>2.0.CO;2 Braddock D, 2001, MENT RETARD DEV D R, V7, P115, DOI 10.1002/mrdd.1016 CAMBRIDGE P, 2001, 12 YEARS ON OUTCOMES Carr J, 1995, DOWNS SYNDROME CHILD Carr J, 2003, J APPL RES INTELLECT, V16, P29, DOI 10.1046/j.1468-3148.2003.00129.x Carr J, 2000, J APPL RES INTELLECT, V13, P1, DOI 10.1046/j.1468-3148.2000.00003.x CONROY J, 1996, DEINSTITUTIONALIZATI Conroy J. W., 1985, PENNHURST LONGITUDIN CORNWELL AC, 1969, AM J MENT DEF, V74, P341 Edgerton R. B., 1967, CLOAK COMPETENCE STI EDGERTON RB, 1976, J MENTAL DEFICIENCY, V10, P485 EDGERTON RB, 1988, AM J MENT RETARD, V92, P331 EDGERTON RB, 1984, AM J MENT DEF, V88, P345 FELCE D, 1984, BEHAV RES THER, V22, P299, DOI 10.1016/0005-7967(84)90010-X Felce D, 2001, MENT RETARD DEV D R, V7, P75, DOI 10.1002/mrdd.1011 GILLBERG C, 1987, J AUTISM DEV DISORD, V17, P273, DOI 10.1007/BF01495061 Gould E., 1994, CARE COMMUNITY 5 YEA HEMMING H, 1981, AM J MENT DEF, V86, P157 Howlin P, 2000, J CHILD PSYCHOL PSYC, V41, P561, DOI 10.1017/S0021963099005806 JACOBSON JW, 1990, J AUTISM DEV DISORD, V20, P205, DOI 10.1007/BF02284719 KLEINBERG J, 1983, AM J MENT DEF, V88, P21 Leiter R. G., 1980, LEITER INT PERFORMAN Lerman P, 2005, MENT RETARD, V43, P25, DOI 10.1352/0047-6765(2005)43<25:LCIABO>2.0.CO;2 Lotter V., 1978, AUTISM REAPPRAISAL C, P475 LOVELAND KA, 1988, AM J MENT RETARD, V93, P84 LOWE K, 1993, J INTELL DISABIL RES, V37, P3 Mansell J, 2002, J INTELL DISABIL RES, V46, P625, DOI 10.1046/j.1365-2788.2002.00440.x Mawhood L, 2000, J CHILD PSYCHOL PSYC, V41, P547, DOI 10.1017/S002196309900579X McCarthy J. J., 1961, ILLINOIS TEST PSYCHO Murphy GH, 2005, J AUTISM DEV DISORD, V35, P405, DOI 10.1007/s10803-005-5030-2 Nihira K, 1993, AAMR ADAPTIVE BEHAV RASMUSSEN DE, 1994, AM J MENT RETARD, V99, P151 Reynell J., 1969, REYNELL DEV LANGUAGE REYNELL JK, 1977, REYNELL LANGUAGE DEV RUTTER M, 1994, CHILD ADOL PSYCH CL, P569 RUTTER M, 1970, SEMIN PSYCHIAT, V2, P435 RUTTER M, 1967, BRIT J PSYCHIAT, V113, P1183, DOI 10.1192/bjp.113.504.1183 SCHATZ J, 1995, J AUTISM DEV DISORD, V25, P51, DOI 10.1007/BF02178167 SHAH A, 1986, SCI SERVICE MENTAL R, P132 SILVERSTEIN AB, 1988, AM J MENT RETARD, V92, P455 SMITH B, 1992, J CHILD PSYCHOL PSYC, V33, P1039, DOI 10.1111/j.1469-7610.1992.tb00924.x Stutsman R., 1931, MENTAL MEASUREMENT P Wechsler D, 1949, WECHSLER INTELLIGENC Wing JK, 1972, EVALUATING COMMUNITY WING L, 1971, PSYCHOL MED, V1, P405 WING L, 1968, SOC PSYCHIATR, V3, P116, DOI 10.1007/BF00577835 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1978, J AUTISM CHILD SCHIZ, V8, P79, DOI 10.1007/BF01550280 NR 51 TC 9 Z9 9 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 DEC PY 2006 VL 19 IS 4 BP 317 EP 329 DI 10.1111/j.1468-3148.2005.00289.x PG 13 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 111WQ UT WOS:000242487000004 ER PT J AU Lewis, N AF Lewis, Nicola TI Autism and Asperger syndrome SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Book Review C1 Dept Psychol, Cwmbran NP44 8YN, Torfaen, Wales. RP Lewis, N (reprint author), Dept Psychol, Alders House,Llanfrechfa Grange, Cwmbran NP44 8YN, Torfaen, Wales. EM Nicola.Lewis2@gwent.wales.nhs.uk CR HOWLIN P, 2004, AUTISM ASPERGERS SYN NR 1 TC 0 Z9 0 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 DEC PY 2006 VL 19 IS 4 BP 391 EP 393 DI 10.1111/j.1468-3148.2006.00273.x PG 3 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 111WQ UT WOS:000242487000011 ER PT J AU Butter, E Mulick, J AF Butter, Eric Mulick, James TI Preliminary reliability and validity of a measure to evaluate core symptoms of autism: The Ohio Autism Clinical Impressions Scale (OACIS) SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Conference on New Clinical Drug Evaluation Unit Meeting CY JUN 12-15, 2006 CL Boca Raton, FL SP Natl Inst Mental Hlth C1 Ohio State Univ, Columbus, OH 43210 USA. NR 0 TC 0 Z9 0 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 DEC PY 2006 VL 16 IS 6 BP 651 EP 652 PG 2 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 127RZ UT WOS:000243605300007 ER PT J AU Pandina, GJ Bossie, CA Zhu, Y Flanders, S AF Pandina, Gahan J. Bossie, Cynthia A. Zhu, Young Flanders, Scott TI The aberrant behavior checklist: Use in clinical trials of pediatric autism SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Conference on New Clinical Drug Evaluation Unit Meeting CY JUN 12-15, 2006 CL Boca Raton, FL SP Natl Inst Mental Hlth C1 Janssen Pharmaceut, Titusville, NJ USA. Ortho McNeil Janssen Sci Affairs LLC, Titusville, NJ USA. Ortho McNeil Janssen Sci Affairs LLC, Grayslake, IL USA. NR 0 TC 1 Z9 1 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 DEC PY 2006 VL 16 IS 6 BP 661 EP 662 PG 2 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 127RZ UT WOS:000243605300024 ER PT J AU Lee, DO Ousley, OY AF Lee, Douglas O. Ousley, Opal Y. TI Attention-deficit hyperactivity disorder symptoms in a clinic sample of children and adolescents with pervasive developmental disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DEFICIT/HYPERACTIVITY DISORDER; ASPERGER-SYNDROME; FOLLOW-UP; REFERRED SAMPLE; NORMATIVE DATA; PHARMACOTHERAPY; COMORBIDITY; RATINGS; AUTISM; CHILDHOOD AB Objectives: The aims of this systematic chart review were to determine the frequency of attention-deficit/hyperactivity disorder (ADHD) in a clinic sample of children and adolescents with autism spectrum disorders (ASD), to compare ADHD symptoms in children with Autistic Disorder, Asperger's Disorder, and pervasive developmental disorders-not otherwise specified (PDD-NOS), to compare ADHD symptoms in individuals with and without ADHD-related chief complaints, and to determine the correlation between ADHD Rating Scale (ADHD RS) scores and age. Method: This systematic chart review examined data from children and adolescents who were consecutively referred to a university-based autism psychopharmacology program. All individuals were diagnosed by semistructured interview for ASD and ADHD, and ADHD symptoms were assessed using ADHD RS scores. Results: Of 83 children, 78% fulfilled Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV) criteria for ADHD and exceeded the 93(rd) percentile norm for the ADHD RS. Hyperactivity-impulsivity scores were significantly greater in individuals with autism than those with other ASDs. DSM-IV ADHD diagnosis was represented equally in individuals with and without ADHD as their chief complaints. ADHD RS hyperactivityimpulsivity and total scores were negatively correlated with age. Conclusion: ADHD symptoms are pervasive in clinically referred children and adolescents with ASD. C1 Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, Atlanta, GA 30322 USA. RP Lee, DO (reprint author), Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Div Child & Adolescent Psychiat, 1551 Shoup Court, Atlanta, GA 30322 USA. 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E., 1995, GILLIAM AUTISM RATIN Goldstein S, 2004, J AUTISM DEV DISORD, V34, P329, DOI 10.1023/B:JADD.0000029554.46570.68 Gomez R, 2003, PSYCHOL ASSESSMENT, V15, P3, DOI 10.1037/1040-3590.15.1.3 Goodman R, 1999, J CHILD PSYCHOL PSYC, V40, P791, DOI 10.1017/S0021963099004096 HART EL, 1995, J ABNORM CHILD PSYCH, V23, P729, DOI 10.1007/BF01447474 Hollander E, 2003, LANCET, V362, P732, DOI 10.1016/S0140-6736(03)14236-5 Kaufman J, 1997, J AM ACAD CHILD PSY, V36, P980, DOI 10.1097/00004583-199707000-00021 Klin A, 2005, J AUTISM DEV DISORD, V35, P221, DOI 10.1007/s10803-005-2001-6 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x Kube DA, 2002, CLIN PEDIATR, V41, P461, DOI 10.1177/000992280204100702 LAHEY BB, 1994, AM J PSYCHIAT, V151, P1673 Mitsis EM, 2000, J AM ACAD CHILD PSY, V39, P308, DOI 10.1097/00004583-200003000-00012 Nam CB, 2004, POPUL RES POLICY REV, V23, P327, DOI 10.1023/B:POPU.0000040045.51228.34 Nicolson R, 2000, J AUTISM DEV DISORD, V30, P461, DOI 10.1023/A:1005511809545 PATERNITE CE, 1995, J ABNORM CHILD PSYCH, V23, P453, DOI 10.1007/BF01447208 PEARSON DA, 1994, J AUTISM DEV DISORD, V24, P395, DOI 10.1007/BF02172125 Posey DJ, 2000, HARVARD REV PSYCHIAT, V8, P45, DOI 10.1093/hrp/8.2.45 Rapport MD, 1999, J CHILD PSYCHOL PSYC, V40, P1169, DOI 10.1017/S0021963099004618 Steinhausen HC, 2003, J AM ACAD CHILD PSY, V42, P1085, DOI 10.1097/01.CHI.0000070241.24125.A3 Wozniak J, 1997, J AM ACAD CHILD PSY, V36, P1552, DOI 10.1016/S0890-8567(09)66564-3 Yoshida Y, 2004, EUR CHILD ADOLES PSY, V13, P307, DOI 10.1007/s00787-004-0391-1 NR 37 TC 82 Z9 86 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 DEC PY 2006 VL 16 IS 6 BP 737 EP 746 DI 10.1089/cap.2006.16.737 PG 10 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 127RZ UT WOS:000243605300036 PM 17201617 ER PT J AU Ivanov, I Klein, M Green, WH Coffey, B AF Ivanov, Iliyan Klein, Martha Green, Wayne Hugo Coffey, Barbara TI The challenges of psychopharmacological management of children with severe developmental disabilities SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID VALPROIC ACID; RISPERIDONE; DISORDERS; ADOLESCENTS; PHARMACOKINETICS; ANTIPSYCHOTICS; CARBAMAZEPINE; BEHAVIOR; AUTISM; EDEMA C1 NYU, Ctr Child Study, New York, NY 10016 USA. Mt Sinai Sch Med, New York, NY USA. Childrens Aid Soc, New York, NY USA. RP Coffey, B (reprint author), NYU, Ctr Child Study, 577 1st Ave, New York, NY 10016 USA. EM barbara.coffey@med.nyu.edu CR Airaksinen EM, 2000, EPILEPSIA, V41, P1214, DOI 10.1111/j.1528-1157.2000.tb00328.x Aman MG, 2002, AM J PSYCHIAT, V159, P1337, DOI 10.1176/appi.ajp.159.8.1337 Baldassano CF, 1996, J CLIN PSYCHIAT, V57, P422 Bertoldo M, 2002, J AM ACAD CHILD PSY, V41, P632, DOI 10.1097/00004583-200206000-00002 DeVane CL, 2001, CLIN PHARMACOKINET, V40, P509, DOI 10.2165/00003088-200140070-00003 Findling RL, 2004, J CLIN PSYCHIAT, V65, P30 Good CR, 2003, J AM ACAD CHILD PSY, V42, P2, DOI 10.1097/01.CHI.0000024908.60748.05 Hirsch E, 2003, CNS DRUGS, V17, P633, DOI 10.2165/00023210-200317090-00003 Hollander E, 2003, LANCET, V362, P732, DOI 10.1016/S0140-6736(03)14236-5 Kielinen M, 2004, AUTISM, V8, P49, DOI 10.1177/1362361304040638 King BH, 2000, J AUTISM DEV DISORD, V30, P439, DOI 10.1023/A:1005555624566 Lauterbach EC, 1998, NEUROPSY NEUROPSY BE, V11, P157 Masi G, 2004, CNS DRUGS, V18, P1031, DOI 10.2165/00023210-200418140-00006 Muñoz-Yunta J A, 2003, Rev Neurol, V36 Suppl 1, pS61 Patel NC, 2005, J CHILD ADOL PSYCHOP, V15, P270, DOI 10.1089/cap.2005.15.270 Pine D S, 1999, Paediatr Drugs, V1, P183, DOI 10.2165/00128072-199901030-00003 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Sanders RD, 1998, J CLIN PSYCHIAT, V59, P689, DOI 10.4088/JCP.v59n1208e Schreier HA, 1998, J CHILD ADOL PSYCHOP, V8, P49, DOI 10.1089/cap.1998.8.49 Schur SB, 2003, J AM ACAD CHILD PSY, V42, P132, DOI 10.1097/01.CHI.0000037017.34553.2E Simeon J, 2002, PROG NEURO-PSYCHOPH, V26, P267, DOI 10.1016/S0278-5846(01)00264-0 Spina E, 2000, THER DRUG MONIT, V22, P481, DOI 10.1097/00007691-200008000-00019 Turgay A, 2002, PEDIATRICS, V110, DOI 10.1542/peds.110.3.e34 van Wattum PJ, 2001, J AM ACAD CHILD PSY, V40, P866, DOI 10.1097/00004583-200108000-00003 WILDER BJ, 1992, J CLIN PSYCHOPHARM, V12, pS64 NR 25 TC 0 Z9 0 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 DEC PY 2006 VL 16 IS 6 BP 793 EP 799 DI 10.1089/cap.2006.16.793 PG 7 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 127RZ UT WOS:000243605300041 PM 17201623 ER PT J AU Juranek, J Filipek, PA Berenji, GR Modahl, C Osann, K Spence, MA AF Juranek, Jenifer Filipek, Pauline A. Berenji, Gholam R. Modahl, Charlotte Osann, Kathryn Spence, M. Anne TI Association between amygdala volume and anxiety level: Magnetic resonance imaging (MRI) study in autistic children SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID PEDIATRIC-PATIENTS; HUMAN BRAIN; DISORDERS; ADULTS AB Our objective was to evaluate brain-behavior relationships between amygdala volume and anxious/depressed scores on the Child Behavior Checklist in a well-characterized population of autistic children. Volumes for the amygdala, hippocampus, and whole brain were obtained from three-dimensional magnetic resonance images (MRIs) captured from 42 children who met the criteria for autistic disorder. Anxious/depressed symptoms were assessed in these children by the Anxious/Depressed subscale of the Child Behavior Checklist. To investigate the association between anxious/ depressed scores on the Child Behavior Checklist and amygdala volume, data were analyzed using linear regression methods with Pearson correlation coefficients. A multivariate model was used to adjust for potential covariates associated with amygdala volume, including age at MRI and total brain size. We found that anxious/depressed symptoms were significantly correlated with increased total amygdala volume (r = .386, P =.012) and right amygdala volume (r = .469, P = .002). The correlation between anxious/depressed symptoms and left amygdala volume did not reach statistical significance (r = .249, P = .112). Child Behavior Checklist anxious/depressed scores were found to be a significant predictor of amygdala total (P = .014) and right amygdala (P = .002) volumes. In conclusion, we have identified a significant brain-behavior relationship between amygdala volume and anxious/depressed scores on the Child Behavior Checklist in our autistic cohort. This specific relationship has not been reported in autism. However, the existing literature on human psychiatry and behavior supports our reported evidence for a neurobiologic relationship between symptoms of anxiety and depression with araygdala structure and function. Our results highlight the importance of characterizing comorbid psychiatric symptomatology in autism. The abundance of inconsistent findings in the published literature on autism might reflect differences between study populations regarding age at MRI, level of impairment within autistic subjects, and underlying anxiety level in the selected study groups. 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Child Neurol. PD DEC PY 2006 VL 21 IS 12 BP 1051 EP 1058 DI 10.2310/7010.2006.00237 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 122DX UT WOS:000243207000009 PM 17156697 ER PT J AU Fombonne, E AF Fombonne, Eric TI Response to the management of autism and its related disorders - Reply SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Letter ID PERVASIVE DEVELOPMENTAL DISORDERS; PREVALENCE C1 Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3H 1P3, Canada. RP Fombonne, E (reprint author), Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3H 1P3, Canada. CR Fombonne E, 2005, J CLIN PSYCHIAT, V66, P3 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Fombonne E, 2006, PEDIATRICS, V118, pE139, DOI 10.1542/peds.2005-2993 Institute of Medicine, 2004, IMM SAF REV VACC AUT LAIDLER JR, 2005, PEDIATRICS, V116, P120 Parker SK, 2004, PEDIATRICS, V114, P793, DOI 10.1542/peds.2004-0434 *STAT CAL, 2005, Q CLIENT CHAR REP IN U.S. Census Bureau, 2006, STAT COUNT QUICKFACT Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 9 TC 0 Z9 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD DEC PY 2006 VL 67 IS 12 BP 2030 EP 2031 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120LI UT WOS:000243085800026 ER PT J AU Slaff, I AF Slaff, Ilana TI Response to the management of autism and its related disorders SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Letter ID PERVASIVE DEVELOPMENTAL DISORDERS C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. RP Slaff, I (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. CR Aman MG, 2005, J CLIN PSYCHIAT, V66, P38 Findling RL, 2005, J CLIN PSYCHIAT, V66, P26 Fombonne E, 2005, J CLIN PSYCHIAT, V66, P3 Greenspan S. I., 1998, CHILD SPECIAL NEEDS MAUGH TH, 2005, LOS ANGELES TIM 0713 *NEW YORK STAT DEP, CLIN PRACT GUID GUID, P13 NR 6 TC 0 Z9 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD DEC PY 2006 VL 67 IS 12 BP 2030 EP 2030 PG 1 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120LI UT WOS:000243085800025 PM 17194285 ER PT J AU Aman, MG AF Aman, Michael G. TI Response to the management of autism and its related disorders - Reply SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Letter C1 Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. RP Aman, MG (reprint author), Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. CR Greenspan S. I., 1998, CHILD SPECIAL NEEDS Greenspan S. I., 1997, J DEV LEARNING DISOR, V1, P87 Metz B, 2005, CONTROVERSIAL THERAPIES FOR DEVELOPMENTAL DISABILITES: FAD, FASHION, AND SCIENCE IN PROFESSIONAL PRACTICE, P237 NR 3 TC 0 Z9 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD DEC PY 2006 VL 67 IS 12 BP 2031 EP 2032 PG 2 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120LI UT WOS:000243085800028 ER PT J AU Findling, RL AF Findling, Robert L. TI Response to the management of autism and its related disorders - Reply SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Letter C1 Univ Hosp Case Med Ctr, Cleveland, OH USA. RP Findling, RL (reprint author), Univ Hosp Case Med Ctr, Cleveland, OH USA. NR 0 TC 0 Z9 0 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD DEC PY 2006 VL 67 IS 12 BP 2031 EP 2031 PG 1 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120LI UT WOS:000243085800027 ER PT J AU Hinton, VJ Nereo, NE Fee, RJ Cyrulnik, SE AF Hinton, Veronica J. Nereo, Nancy E. Fee, Robert J. Cyrulnik, Shana E. TI Social behavior problems in boys with duchenne muscular dystrophy SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE duchenne muscular dystrophy; behavior; behavioral phenotype; social problems ID CHRONIC PHYSICAL DISORDERS; VERBAL WORKING-MEMORY; CHRONIC ILLNESS; MENTAL-RETARDATION; PSYCHOLOGICAL ADJUSTMENT; CHILDREN; AUTISM; CORTICOSTEROIDS; DISABILITIES; ADOLESCENTS AB Duchenne muscular dystrophy (DMD) is a chronic, progressive pediatric disease that affects both muscle and brain. The objectives of the study were to examine parent reported behavior in children with DMD, investigate the influence of chronic illness, intellectual ability and etiology on behavior, and determine whether a specific behavioral profile is associated with DMD. Parental ratings of boys with DMD (n = 181) on the Child Behavior Checklist behavior scales were examined and compared to reported findings of children with other chronic illnesses, unaffected siblings of boys with DMD (n = 86), and children with cerebral palsy (CP) (n = 42). Increased ratings of general behavior problems were reported, and neither physical progression nor intellectual level contributed to behavioral ratings. Among the children with DMD, the Social Problem behavior scale had the greatest number of "clinically significant" ratings (34%). Between-group comparisons showed significantly more boys with DMD were rated as having social behavior problems than either the sibling or CP comparison groups. In addition to the increase in reported behavioral problems likely related to the effects of chronic illness, boys with DMD may be at heightened risk for specific social behavior problems. The specificity of the findings of the behavior profile in DMD may be partially due to the lack of dystrophin isoforms in the central nervous system, and not solely a reactive response to the illness. C1 Columbia Univ, Coll Phys & Surg, Gertrude H Sergievsky Ctr, New York, NY 10032 USA. Columbia Univ, Coll Phys & Surg, Dept Neurol, New York, NY 10032 USA. Hosp Special Surg, Dept Rehabil, New York, NY USA. RP Hinton, VJ (reprint author), Columbia Univ, Coll Phys & Surg, Gertrude H Sergievsky Ctr, 630 W 168th St P&S Box 16, New York, NY 10032 USA. 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TI Reliable classification of case-control studies of autistic disorder and obstetric complications SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article; Proceedings Paper CT 97th Annual Scientific Assembly of the Southern-Medical-Association CY NOV, 2003 CL Atlanta, GA SP SO Med Assoc DE case-control study; infant low birth weight; labor complications; pervasive child developmental disorders; pregnancy complications ID MINOR PHYSICAL ANOMALIES; JERUSALEM INFANT-DEVELOPMENT; DIAGNOSTIC OBSERVATION SCHEDULE; RECEPTIVE LANGUAGE DISORDER; UTAH EPIDEMIOLOGIC SURVEY; SEVERE MENTAL-RETARDATION; RATING SURVEY PQRS; FOLLOW-UP; CHILDHOOD SCHIZOPHRENIA; PERINATAL COMPLICATIONS AB Several reports have suggested an association between obstetric complications and autistic disorder. Since conclusions may be drawn from case-control studies, a methodology to identify case-control studies of autistic disorder and obstetric complications for qualitative and quantitative reviews is needed. We sought to establish the feasibility of blinding of reports as a means to remove biases in meta-analyses of case-control studies of autism and obstetric complications. Therefore, we located published reports of case-control studies of autistic disorder and obstetric complications by a literature search and additional articles. The methods or other appropriate portions of the articles were blindly reviewed for the presence or absence of obstetric complications in cases with autistic disorder matched with at least one control without autistic disorder. Good inter-rater reliability was obtained for case-control studies of autistic disorder (74.6% agreement and kappa=.451) and for obstetric complications (84.0% agreement and kappa=.658). 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Recent genetic evidence implicates involvement of a gene encoding tryptophan 2,3-dioxygenase, a rate-limiting enzyme in tryptophan's major metabolic pathway, the kynurenine pathway, in autism. To test activity of the kynurenine pathway in autism, plasma kynurenine levels were measured in 30 drug-free autistic children (mean age (SD)=6 years 0 months (2 years 9 months)) and 29 age-, race- and gender-matched healthy comparison subjects (mean age (SD)=6 years 5 months (2 years 6 months)) using high-performance liquid chromatography. No difference was found in plasma kynurenine levels between the study groups. In the autistic children, plasma kynurenine levels did not correlate with autistic behaviors or IQ. These results do not support a role for abnormal global function of the kynurenine pathway; however, the status of this pathway in the brain remains unknown. C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. 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Genet. PD DEC PY 2006 VL 85 IS 3 BP 187 EP 191 DI 10.1007/BF02935329 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 159PV UT WOS:000245879500005 PM 17406092 ER PT J AU Herring, S Gray, K Taffe, J Tonge, B Sweeney, D Einfeld, S AF Herring, S. Gray, K. Taffe, J. Tonge, B. Sweeney, D. Einfeld, S. TI Behaviour and emotional problems in toddlers with pervasive developmental disorders and developmental delay: associations with parental mental health and family functioning SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE behaviour and emotional problems; children; developmental delay; family; pervasive developmental disorders ID PRESCHOOL-CHILDREN; AUTISTIC-CHILDREN; INTELLECTUAL DISABILITY; SPECTRUM DISORDERS; ASSESSMENT DEVICE; MATERNAL STRESS; YOUNG-CHILDREN; MOTHERS; INTERVENTION; FATHERS AB Background Behavioural and emotional problems occur at a high rate in children and adolescents with intellectual disability, often from a young age. Some studies have indicated that children and adolescents with autism present with even higher rates. Less is known about the presentation, development and family impact of these difficulties in young children with autism. This study aimed to explore these issues in toddlers with pervasive developmental disorders (PDDs), those with delay without a PDD, and their families. Methods Participants were 123 children aged 20-51 months, referred to a developmental assessment clinic. Parents completed a checklist on child behavioural and emotional problems, and individual questionnaires on family functioning, their own mental health, and stress in relation to parenting their child. The child's language and cognitive skills, adaptive functioning and behaviour were assessed by standardized measures. Measures were repeated 1 year postdiagnosis. Behavioural and emotional problems in young children with a PDD were compared with those in children with developmental delay without a PDD, and their impact on parental outcomes explored over time. Results Initial and follow-up measures of child behaviour and emotional problems, parent mental health problems, parent stress and family functioning were significantly correlated, providing some evidence of stability over time. Child emotional and behavioural problems contributed significantly more to mother stress, parent mental health problems, and perceived family dysfunction than child diagnosis (PDD/non-PDD), delay or gender. Compared with mothers, all fathers reported significantly less stress in relation to parenting their child. Conclusion Results highlighted the importance of addressing emotional and behavioural problems in very young children with autism and/or developmental delay. 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P., 1988, USERS GUIDE GEN HLTH Gray DE, 1997, SOC SCI MED, V44, P1097, DOI 10.1016/S0277-9536(96)00237-7 Hastings RP, 2002, J INTELLECT DEV DIS, V27, P149, DOI 10.1080/1366825021000008657 Hastings RP, 2003, J INTELL DISABIL RES, V47, P231, DOI 10.1046/j.1365-2788.2003.00485.x Hastings RP, 2005, J AUTISM DEV DISORD, V35, P635, DOI 10.1007/s10803-005-0007-8 HOLROYD J, 1976, AM J MENT DEF, V80, P431 Hudson AM, 2003, J INTELL DISABIL RES, V47, P238, DOI 10.1046/j.1365-2788.2003.00486.x Johnson E, 2002, CHILD CARE HLTH DEV, V28, P123 KOEGEL RL, 1992, J AUTISM DEV DISORD, V22, P205, DOI 10.1007/BF01058151 KONSTANTAREAS MM, 1989, J CHILD PSYCHOL PSYC, V30, P459, DOI 10.1111/j.1469-7610.1989.tb00259.x KONSTANTAREAS MM, 1992, J AUTISM DEV DISORD, V22, P217, DOI 10.1007/BF01058152 Lecavalier L, 2006, J INTELL DISABIL RES, V50, P172, DOI 10.1111/j.1365-2788.2005.00732.x 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 MILGRAM NA, 1988, J AUTISM DEV DISORD, V18, P415, DOI 10.1007/BF02212196 MRUZEK DW, 2006, 5 ANN INT M AUT RES Olsson MB, 2001, J INTELL DISABIL RES, V45, P535, DOI 10.1046/j.1365-2788.2001.00372.x Rivers JW, 2003, J AUTISM DEV DISORD, V33, P383, DOI 10.1023/A:1025006727395 Sanders JL, 1997, CHILD FAM BEHAV THER, V19, P15, DOI 10.1300/J019v19n04_02 Schopler E, 1990, PSYCHOEDUCATIONAL PR Sparrow S, 1984, VINELAND ADAPTIVE BE *SPSS INC, 2003, SPSS VERS 12 WIND Stata, 2005, STAT STAT SOFTW REL Tomanik S, 2004, J INTELLECT DEV DIS, V29, P16, DOI 10.1080/13668250410001662892 Tonge BJ, 2003, INT REV RES MENT RET, V26, P61, DOI 10.1016/S0074-7750(03)01002-4 Wechsler D, 2004, WECHSLER PRESCHOOL P, V3rd WOLF LC, 1989, J AUTISM DEV DISORD, V19, P157, DOI 10.1007/BF02212727 Yirmiya N, 2005, J CHILD PSYCHOL PSYC, V46, P69, DOI 10.1111/j.1469-7610.2004.00334.x NR 48 TC 152 Z9 153 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 DEC PY 2006 VL 50 BP 874 EP 882 DI 10.1111/j.1365-2788.2006.00904.x PN 12 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 102SA UT WOS:000241832400003 PM 17100948 ER PT J AU Lewis, P Abbeduto, L Murphy, M Richmond, E Giles, N Bruno, L Schroeder, S Anderson, J Orsmond, G AF Lewis, P. Abbeduto, L. Murphy, M. Richmond, E. Giles, N. Bruno, L. Schroeder, S. Anderson, J. Orsmond, G. TI Psychological well-being of mothers of youth with fragile X syndrome: syndrome specificity and within-syndrome variability SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; Down syndrome; fragile X syndrome; intellectual disability; mental health; parents ID MENTAL-RETARDATION; SPECTRUM DISORDER; YOUNG-CHILDREN; DOWN-SYNDROME; AUTISM; SYMPTOMS; STRESS; MALES; BEHAVIOR; FAMILY AB Background Research on parental well-being has focused largely on Down syndrome and autism; however, fragile X syndrome is likely to pose different challenges for parents compared with these other diagnostic conditions. Moreover, there is considerable variability among youth with fragile X syndrome; for example, 25% to 33% of affected youth meet criteria for a co-morbid diagnosis of autism. It is likely that parents of youth with fragile X syndrome will experience different degrees and patterns of stress, depending on whether their offspring do or do not have a co-morbid diagnosis of autism. In the present study, we compared mothers of three groups of young males on measures of psychological well-being and stress: those with fragile X syndrome and a co-morbid diagnosis of autism; those with fragile X syndrome alone; and those with Down syndrome. Method The sample consisted of mothers of adolescent and young adult males with fragile X syndrome and co-morbid autism (n = 9), fragile X syndrome alone (n = 19), and Down syndrome (n = 19). We screened all youth for autism using the Autism Behavior Checklist, which was completed by mothers, fathers and teachers, and the youth who scored above the suggested cut-off were evaluated by a licensed psychologist to determine autism status. The three groups of youth did not differ in chronological age (16.4, 15.8 and 16.0 years, respectively) or non-verbal mental age (3.8, 3.9 and 3.8 years, respectively). Several self-report measures were completed by mothers. These measures assessed current mental health status (e.g. the Center for Epidemiological Studies Depression Scale), perceptions of their son's and family's functioning (e.g. the Positive Affect Index, which measures closeness felt by the mother to her son and also reciprocated closeness felt by the son towards the mother, as perceived by the mother), and approach to coping with their son's disability [e.g. the Multidimensional Coping Inventory (COPE), which measures emotion-focused and problem-solving focused coping]. Results The results suggest that fragile X syndrome creates more challenges to maternal psychological well-being than Down syndrome, and that the combination of fragile X syndrome and autism can be particularly challenging. Differences among groups, however, were manifested mainly as concerns about the affected son and about relationships within the family rather than as lower levels of mental health. Thus, mothers of sons with fragile X syndrome, regardless of the son's autism status, reported more pessimism about the son's future and more conflict within the family than mothers of sons with Down syndrome. Additionally, mothers of sons with fragile X syndrome and co-morbid autism reported lower levels of reciprocated closeness than the other two groups of mothers. Conclusion We consider possible causes of these maternal differences, the implications for clinical practice, needs for future research, and the importance of understanding child and contextual factors as well as the dynamics leading to these differences. C1 Univ Wisconsin, Waisman Ctr Mental Retardat & Human Dev, Madison, WI 53706 USA. Kennedy Krieger Inst, Baltimore, MD USA. Johns Hopkins Univ, Baltimore, MD USA. Boston Univ, Boston, MA 02215 USA. RP Lewis, P (reprint author), 1500 Highland Ave, Madison, WI USA. EM lewis@waisman.wisc.edu 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, 2004, AM J MENT RETARD, V109, P237, DOI 10.1352/0895-8017(2004)109<237:PWACIM>2.0.CO;2 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey DB, 2001, J AUTISM DEV DISORD, V31, P165 Bailey DB, 2004, DEVELOPMENTAL LANGUAGE DISORDERS: FROM PHENOTYPES TO ETIOLOGIES, P121 Bengston V. L., 1973, THEOR DEV WORKSH NAT CAMPBELL A, 1976, QUALITY AM LIFE PERS CARVER CS, 1989, J PERS SOC PSYCHOL, V56, P267, DOI 10.1037//0022-3514.56.2.267 Cohen IL, 1995, DEV BRAIN DYSFUNCT, V8, P252 Demark JL, 2003, AM J MENT RETARD, V108, P314, DOI 10.1352/0895-8017(2003)108<314:BRBAAF>2.0.CO;2 DUNST CJ, 1986, AM J MENT RETARD, V90, P403 Dykens E. M., 2000, GENETICS MENTAL RETA Franke P, 1996, AM J MED GENET, V64, P334, DOI 10.1002/(SICI)1096-8628(19960809)64:2<334::AID-AJMG20>3.3.CO;2-C FRIEDRICH WN, 1983, AM J MENT DEF, V88, P41 Goodlin-Jones BL, 2004, J DEV BEHAV PEDIATR, V25, P392, DOI 10.1097/00004703-200412000-00002 Hagerman R. J, 1999, NEURODEVELOPMENTAL D HAGERMAN RJ, 1986, AM J MED GENET, V23, P359, DOI 10.1002/ajmg.1320230128 Hessl D, 2005, AM J MED GENET B, V139B, P115, DOI 10.1002/ajmg.b.30241 Hessl D, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.5.e88 Hodapp RM, 1997, AM J MENT RETARD, V102, P67, DOI 10.1352/0895-8017(1997)102<0067:DAIBEO>2.0.CO;2 HOLM S, 1979, SCAND J STAT, V6, P65 Johnston C, 2001, AM J MED GENET, V103, P314, DOI 10.1002/ajmg.1561 Kasari C, 1997, J AUTISM DEV DISORD, V27, P39, DOI 10.1023/A:1025869105208 Kau ASM, 2004, AM J MED GENET A, V126A, P9, DOI 10.1002/ajmg.a.20218 Kaufmann WE, 2004, AM J MED GENET A, V129A, P225, DOI 10.1002/ajmg.a.30229 Krug D. A., 1980, AUTISM SCREENING INS LEVIN JR, 1994, PSYCHOL BULL, V115, P153, DOI 10.1037//0033-2909.115.1.153 Lewis P, 2006, J INTELL DISABIL RES, V50, P532, DOI 10.1111/j.1365-2788.2006.00803.x Luecking RG, 1997, ADOLESCENTS WITH DOWN SYNDROME, P235 Ly TM, 2002, J DEV BEHAV PEDIATR, V23, P322 MARCOVITCH S, 1986, DEV BEHAV PEDIAT, V7, P247 Moos R. H., 1981, FAMILY ENV SCALE MAN Abbeduto L, 2004, DEVELOPMENTAL LANGUAGE DISORDERS: FROM PHENOTYPES TO ETIOLOGIES, P77 Philofsky A, 2004, AM J MENT RETARD, V109, P208, DOI 10.1352/0895-8017(2004)109<208:LACFAA>2.0.CO;2 Radloff L.S., 1997, APPL PSYCH MEAS, V3, P385 REISS AL, 1990, J AM ACAD CHILD PSY, V29, P885, DOI 10.1097/00004583-199011000-00007 Ricci LA, 2003, J INTELL DISABIL RES, V47, P273, DOI 10.1046/j.1365-2788.2003.00489.x ROGERS SJ, 2001, DEV BEHAV PEDIAT, V22, P409 Sarimski K, 1997, EUR CHILD ADOLES PSY, V6, P26 SOBESKY WE, 1994, J AM ACAD CHILD PSY, V33, P247, DOI 10.1097/00004583-199402000-00014 Sobesky WE, 1996, AM J MED GENET, V64, P340, DOI 10.1002/(SICI)1096-8628(19960809)64:2<340::AID-AJMG21>3.0.CO;2-E Thorndike RL, 1986, STANFORD BINET INTEL WALKER LS, 1992, J PEDIATR PSYCHOL, V17, P327, DOI 10.1093/jpepsy/17.3.327 NR 43 TC 30 Z9 30 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 DEC PY 2006 VL 50 BP 894 EP 904 DI 10.1111/j.1365-2788.2006.00907.x PN 12 PG 11 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 102SA UT WOS:000241832400005 PM 17100950 ER PT J AU Gray, DE AF Gray, D. E. TI Coping over time: the parents of children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; coping; family ID MOTHERS; ADAPTATION; STRATEGIES; SUPPORT; FATHERS; STRESS AB Background Although coping with autism has been examined in a number of papers, virtually no research exists on how families cope over time. This paper reports the results of a longitudinal study of parents coping with autism over a period of approximately a decade. Methods The research method for the study was based on ethnographic methods that emphasized in-depth interviews and participant observation. The sample for this study consisted of 28 parents (19 mothers and nine fathers) of children with autism. The instrument for the interviews consisted of questions concerning: the child's medical history and referral experience, the child's present symptomatology, the effects of the child's problems on the parent's well-being, the effects of autism on the family's social life, parental coping strategies, illness conceptualization and the parents' expectations for the future. Results and conclusions Coping strategies changed from the time of the initial study, as fewer parents coped through reliance on service providers, family support, social withdrawal and individualism and relatively more parents coped through their religious faith and other emotion-focused strategies. The results tentatively support previous research on coping that indicates that aging is linked to the use of more emotion-focused coping strategies. C1 Univ New England, Sch Social Sci, Armidale, NSW, Australia. RP Gray, DE (reprint author), Univ New England, Sch Social Sci, Armidale, NSW, Australia. EM dgray@pobox.une.edu.au CR Aldwin C. M., 1991, J GERONTOL B-PSYCHOL, V46, P174, DOI 10.1093/geronj/46.4.P174 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 BURY M, 1991, SOCIOL HEALTH ILL, V13, P451, DOI 10.1111/j.1467-9566.1991.tb00522.x DeMeyer M. K., 1979, PARENTS CHILDREN AUT Erlandson D, 1993, DOING NATURALISTIC I Gray David E., 1992, Australia and New Zealand Journal of Developmental Disabilities, V18, P83 GRAY DE, 1994, SOCIOL HEALTH ILL, V16, P275, DOI 10.1111/1467-9566.ep11348729 Gray DE, 2003, SOC SCI MED, V56, P631, DOI 10.1016/S0277-9536(02)00059-X Hastings RP, 2005, AUTISM, V9, P377, DOI 10.1177/1362361305056078 Lazarus R. S., 1996, HDB EMOTION ADULT DE, P289, DOI 10.1016/B978-012464995-8/50017-0 LAZARUS RS, 1993, PSYCHOSOM MED, V55, P234 MARCUS L, 1977, AM J ORTHOPSYCHIAT, V47, P383 Marcus L. M., 1997, HDB AUTISM PERVASIVE, P631 MILGRAM NA, 1988, J AUTISM DEV DISORD, V18, P415, DOI 10.1007/BF02212196 THOITS PA, 1995, J HLTH SOCIAL BEHAV, P53, DOI DOI 10.2307/2626957 NR 17 TC 54 Z9 55 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 DEC PY 2006 VL 50 BP 970 EP 976 DI 10.1111/j.1365-2788.2006.00933.x PN 12 PG 7 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 102SA UT WOS:000241832400012 PM 17100957 ER PT J AU Kern, P Aldridge, D AF Kern, Petra Aldridge, David TI Using embedded music therapy interventions to support outdoor play of young children with autism in an inclusive community-based child care program SO JOURNAL OF MUSIC THERAPY LA English DT Article ID ENVIRONMENT; BEHAVIORS; STUDENTS AB For young children with autism enrolled in community-based inclusive child care programs, outdoor play can be a major challenge. The aim of this music therapy intervention was to improve peer interactions and meaningful play on the playground for four boys with autism by adding an outdoor music center and using original songs composed for each participant. A collaborative approach was used to support the implementation of the intervention by the children's teachers, engaging classroom peers as formal and informal helpers. The effects of the interventions were examined using a multiple baseline design with four conditions replicated across the four children. The results indicate that the musical adaptation of the playground itself did not improve social interactions of children with autism significantly, but it facilitated their play and involvement with peers by attraction to the sound and opportunity to use the instruments. The song interventions produced desirable peer interaction outcomes, and the collaborative consultative approach enabled teachers to implement interventions successfully in ongoing playground routines. In addition, peer-mediated strategies increased peer interactions and meaningful play on the playground. C1 Univ N Carolina, Frank Porter Graham Child Dev Inst, Chapel Hill, NC 27515 USA. Univ Witten Herdecke, Chair Qualitiat Res Med, Witten, Germany. RP Kern, P (reprint author), Univ Windsor, Sch Mus, 401 Sunset Ave, Windsor, ON N9B 3P4, Canada. EM pkern@uwindsor.ca CR Alberto P. 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PD WIN PY 2006 VL 43 IS 4 PG 25 WC Music; Rehabilitation SC Music; Rehabilitation GA 137EC UT WOS:000244274800001 ER PT J AU Kay, S Harchik, AE Luiselli, JK AF Kay, S Harchik, AE Luiselli, JK TI Elimination of drooling by an adolescent student with autism attending public high school SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID CHILDREN; MANAGEMENT AB We evaluated a multicomponent intervention that successfully eliminated drooling by a 17-year-old student with autism who attended a public high school. The student was taught to perform compensatory responses (wiping his mouth and swallowing saliva), received positive reinforcement for having a "dry mouth," and was given opportunities to monitor his appearance. Implemented in a multiple-baseline design across three school locations, intervention was applied with high integrity and judged positively by staff. C1 May Ctr Child Dev, W Springfield, MA 01089 USA. May Inst, W Springfield, MA 01089 USA. RP Kay, S (reprint author), May Ctr Child Dev, 511 Main St, W Springfield, MA 01089 USA. EM skay@mayinstitute.org CR DiSalvo C., 2002, FOCUS AUTISM OTHER D, V17, P198, DOI DOI 10.1177/10883576020170040201 DRABMAN RS, 1979, BEHAV THER, V10, P46, DOI 10.1016/S0005-7894(79)80008-8 DUNN KW, 1987, DEV MED CHILD NEUROL, V29, P305 Haring T. G., 1991, CRITICAL ISSUES LIVE, P195 HUNT P, 1994, J ASSOC PERS SEVERE, V19, P200 Kennedy C. H., 1997, J BEHAV ED, V7, P167, DOI [10.1023/ A:1022888924438, DOI 10.1023/A:1022888924438] KENNEDY CH, 2004, INCLUSION STUDENTS S LUISELLI JK, 2002, BEHAV PSYCHOL SCH IN MCCLANNAHAN LE, 1990, J APPL BEHAV ANAL, V23, P469, DOI 10.1901/jaba.1990.23-469 Reddihough DS, 1999, J DEV PHYS DISABIL, V11, P17, DOI 10.1023/A:1021804500520 NR 10 TC 18 Z9 18 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 WIN PY 2006 VL 8 IS 1 BP 24 EP 28 DI 10.1177/10983007060080010401 PG 5 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 000HP UT WOS:000234452200004 ER PT J AU Delano, M Snell, ME AF Delano, M Snell, ME TI The effects of social stories on the social engagement of children with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID SKILLS; STUDENTS; BEHAVIOR; INTERVENTION; PEERS AB A multiple-probe design across participants was used to evaluate the effects of social stories on the duration of appropriate social engagement and the frequency of 4 social skills in 3 elementary-age students with autism. The social skills were seeking attention, initiating comments, initiating requests, and making contingent responses. Following the intervention, which consisted of reading individualized social stories, answering comprehension questions, and participating in a 10-min play session, the duration of social engagement increased for all 3 students with both a training peer and a novel peer. The number of target social skills displayed during the 10-min play sessions increased after the intervention was introduced. Two students demonstrated generalization to a classroom setting. These findings suggest that the use of social stories without additional social skill interventions may be effective in increasing the duration of social engagement and the frequency of specific social skills. C1 Florida State Univ, Coll Educ, Tallahassee, FL 32306 USA. RP Delano, M (reprint author), Florida State Univ, Coll Educ, 205 Stone Bldg, Tallahassee, FL 32306 USA. 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Interv. PD WIN PY 2006 VL 8 IS 1 BP 29 EP 42 DI 10.1177/10983007060080010501 PG 14 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 000HP UT WOS:000234452200005 ER PT J AU Sansosti, FJ Powell-Smith, KA AF Sansosti, FJ Powell-Smith, KA TI Using social stories to improve the social behavior of children with Asperger syndrome SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID AUTISM AB To date, the empirical support for the use of social story interventions for children with Asperger syndrome (AS) is small. The purpose of this study was to examine the effects of individualized social story interventions on the social behavior of three children with AS. Using a multiple-baseline-across-participants design, social stories were implemented, and direct observations of the participants' identified target behaviors were conducted three times per week during unstructured school activities (e.g., recess). Data revealed an increase in the social behavior of two of the three participants when the treatment was implemented. Unfortunately, maintenance of target behaviors was not observed. These data provide some initial support for the use of social stories to teach social skills to children diagnosed with AS. However, failure to demonstrate skill maintenance and poor results for one participant highlight possible limitations of the social story intervention and suggest a strong need for further research. Recommendations for future research endeavors and the potential benefits of social story interventions are discussed. C1 Dist Sch Board Pasco Cty, Dept Student Serv, Land O Lakes, FL 34638 USA. Univ S Florida, Sch Psychol Program, Tampa, FL USA. RP Sansosti, FJ (reprint author), Dist Sch Board Pasco Cty, Dept Student Serv, 7227 Land O Lakes Blvd, Land O Lakes, FL 34638 USA. EM sansost@pasco.k12.fl.us CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ATWOOD T, 1998, ASPERGERS SYNDROME G Barry L. M., 2004, FOCUS AUTISM OTHER D, V19, P45, DOI DOI 10.1177/10883576040190010601 BRADY MP, 1987, J AUTISM DEV DISORD, V17, P375, DOI 10.1007/BF01487067 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Church C., 2000, FOCUS AUTISM OTHER D, V15, P12, DOI DOI 10.1177/108835760001500102 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x FERRON J, 2002, AM ED RES ASS C NEW Gray C., 1995, TEACHING CHILDREN AU, P219 Gray C. A., 1993, FOCUS AUTISTIC BEHAV, V8, P1, DOI DOI 10.1177/108835769300800101 Gray C.A., 1998, ASPERGER SYNDROME HI, P167 Hayes S. C., 1999, SCI PRACTITIONER RES HYMAN SL, 2001, J AM MED ASS, V285 Kazdin A. 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R., 2000, ASPERGER SYNDROME, P25 Volkmar FR, 2000, AM J PSYCHIAT, V157, P262, DOI 10.1176/appi.ajp.157.2.262 Williams K., 1995, FOCUS AUTISTIC BEHAV, V10, P9 Wing Lorna, 2000, ASPERGER SYNDROME, P418 NR 32 TC 39 Z9 39 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 WIN PY 2006 VL 8 IS 1 BP 43 EP 57 DI 10.1177/10983007060080010601 PG 15 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 000HP UT WOS:000234452200006 ER PT J AU [Anonymous] AF [Anonymous] TI New resources for individuals with autism SO JOURNAL OF PSYCHOSOCIAL NURSING AND MENTAL HEALTH SERVICES LA English DT News Item CR 2006, TRAVEL AUTISM VACATI 2006, D FLUTIE FDN AUSTISM NR 2 TC 0 Z9 0 PU SLACK INC PI THOROFARE PA 6900 GROVE RD, THOROFARE, NJ 08086 USA SN 0279-3695 J9 J PSYCHOSOC NURS JI J. Psychosoc. Nurs. Ment. Health Serv. PD DEC PY 2006 VL 44 IS 12 BP 11 EP 11 PG 1 WC Nursing SC Nursing GA V59LO UT WOS:000204018400012 ER PT J AU Nettle, D AF Nettle, Daniel TI Schizotypy and mental health amongst poets, visual artists, and mathematicians SO JOURNAL OF RESEARCH IN PERSONALITY LA English DT Article DE schizotypy; psychopathology; creativity; poetry; artists; mathematics ID PSYCHOSIS-PRONE SUBJECTS; FUNCTIONING AUTISM; CREATIVITY; SCHIZOPHRENIA; TRAITS; PSYCHOPATHOLOGY; PSYCHOTICISM; ASSOCIATION; DISORDERS; QUOTIENT AB Many researchers have found evidence of an association between creativity and the predisposition to mental illness. However, a number of questions remain unanswered. First, it is not clear whether healthy creatives have a milder loading on schizotypal traits than people who suffer serious psychopathology, or whether they have an equal loading, but other mediating characteristics. Second, most of the existing research has concentrated on artistic creativity, and the position of other creative domains is not yet clear. The present study compares schizotypy profiles using the O-LIFE inventory in a large sample of poets, artists, mathematicians, the general population, and psychiatric patients. Poets and artists have levels of unusual experiences that are higher than controls, and as high as schizophrenia patients. However, they are relatively low on the dimension of introvertive anhedonia. Mathematicians are lower than controls on unusual experiences. The results suggest that artistic creatives and psychiatric patients share a tendency to unusual ideas and experiences, but creative groups are distinguished by the absence of anhedonia and avolition. 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Breitenbach-Koller, L. Poustka, A. TI Mutations in the ribosomal protein gene RPL10 suggest a novel modulating disease mechanism for autism SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; autistic disorder; ribosomal protein; Xq28; translation ID PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN TRANSPORTER 5-HTT; X MENTAL-RETARDATION; SACCHAROMYCES-CEREVISIAE; SUBUNIT PROTEIN; GENOMEWIDE SCREEN; SPECTRUM; HIPPOCAMPUS; INDIVIDUALS; CHROMOSOME AB Autism has a strong genetic background with a higher frequency of affected males suggesting involvement of X-linked genes and possibly also other factors causing the unbalanced sex ratio in the etiology of the disorder. We have identified two missense mutations in the ribosomal protein gene RPL10 located in Xq28 in two independent families with autism. We have obtained evidence that the amino-acid substitutions L206M and H213Q at the C-terminal end of RPL10 confer hypomorphism with respect to the regulation of the translation process while keeping the basic translation functions intact. This suggests the contribution of a novel, possibly modulating aberrant cellular function operative in autism. Previously, we detected high expression of RPL10 by RNA in situ hybridization in mouse hippocampus, a constituent of the brain limbic system known to be afflicted in autism. Based on these findings, we present a model for autistic disorder where a change in translational function is suggested to impact on those cognitive functions that are mediated through the limbic system. C1 DKFZ, Div Mol Genome Anal, D-69120 Heidelberg, Germany. Paris Lodron Univ Salzburg, Dept Cell Biol, Salzburg, Austria. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. RP Poustka, A (reprint author), DKFZ, Div Mol Genome Anal, Neuenheimer Feld 580, D-69120 Heidelberg, Germany. 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Rev. Neurosci. PD DEC PY 2006 VL 7 IS 12 BP 942 EP 951 DI 10.1038/nrn2024 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 107KH UT WOS:000242169300013 PM 17115076 ER PT J AU Geier, DA Geier, MR AF Geier, David A. Geier, Mark R. TI A clinical trial of combined anti-androgen and anti-heavy metal therapy in autistic disorders SO NEUROENDOCRINOLOGY LETTERS LA English DT Article DE autistic; DMSA; heavy metal; testosterone ID CENTRAL PRECOCIOUS PUBERTY; MERCURY; INDIVIDUALS; TAP-144-SR; ACETATE AB BACKGROUND: A medical hypothesis has suggested that some autism spectrum disorders (ASDs) may result from interactions between the methionine cycle-trans-sulfuration and androgen pathways following exposure to mercury. METHODS: The IRB of the Institute for Chronic Illnesses approved the present study. A novel treatment was utilized combining LUPRON (R) (leuprolide acetate, TAP Pharmaceuticals, Inc.) and CHEMET (R) (meso-2, 3-dimercaptosuccinic acid - DMSA, McNeil Consumer Products Company) on 11 consecutive children with ASDs. RESULTS: A significant (p < 0.01) overall improvement from the 70-79th percentile of severity (median baseline score=87) at baseline to the 40-49th percentile of severity (median end of study period score=63) at the end of the study was observed for patients treated for a median of approximately 4 months. Significant improvements in sociability, cognitive awareness, behavior, and clinical symptoms/behaviors of hyperandrogenemia were also observed. Significant decreases in blood androgens and increases in urinary heavy metal concentrations were observed. Minimal drug adverse effects were found. 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Although studies have investigated the neural correlates of intelligence quotient (IQ) and ASD in intellectually unimpaired subjects, these issues have not been addressed in intellectually impaired subjects. We studied 63 intellectually disabled adolescents receiving additional learning support and 72 controls using whole brain tissue volumes extracted from native space and voxel-based morphometry (VBM) in normalised space. We applied a qualitative and quantitative review of VBM preprocessing and modified the optimised method to establish optimum co-registration of the brains in normalised space. We report tissue density differences at cluster level with adjustment for underlying smoothness. Individuals with intellectual disability had smaller total white matter and total brain tissue volumes than controls, as well as reduced grey matter density in the right cerebellar hemisphere and left temporoparietal cortex, and reduced white matter density in the posterior corpus callosum. Intellectually disabled subjects were additionally subgrouped according to their degree of reported autistic features. Reduced grey matter density was detected in the thalamus of subjects with autistic features scoring within the pervasive developmental disorder range as compared to subjects below the threshold for ASD, and increased white matter density was detected in the left superior temporal gyrus of subjects scoring above the threshold for autism as compared to subjects below the threshold for ASD. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Edinburgh, Royal Edinburgh Hosp, Div Psychiat, Edinburgh EH10 5HF, Midlothian, Scotland. RP Spencer, MD (reprint author), Univ Edinburgh, Royal Edinburgh Hosp, Div Psychiat, Edinburgh EH10 5HF, Midlothian, Scotland. 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NR 0 TC 1 Z9 1 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2006 VL 31 SU 1 BP S9 EP S10 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 108BS UT WOS:000242215900029 ER PT J AU Jacob, S Brune, CW Carter, CS Leventhal, B Lord, C Cook, EH AF Jacob, Suma Brune, Camille W. Carter, C. S. Leventhal, Bennett Lord, Catherine Cook, Edwin H. TI Association of the oxytocin receptor gene (OXTR) in Caucasian children and adolescents with autism SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the American-College-of-Neuropsychopharmacolgy CY DEC 03-07, 2006 CL Hollywood, FL SP Amer Coll Neuropsychopharmacol C1 Univ Illinois, Chicago, IL USA. NR 0 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2006 VL 31 SU 1 BP S210 EP S210 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 108BS UT WOS:000242215900558 ER PT J AU Narasimhan, M Bruce, TO Ballard, JF Patkar, A Masand, P Rech, R AF Narasimhan, Meera Bruce, Travis O. Ballard, John F. Patkar, Ashwin Masand, Prakash Rech, Richard TI An open-label trial of aripiprazole in the treatment of autism and its correlation to whole blood serotonin levels and serotonin transporter (5HTTPLR) function SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the American-College-of-Neuropsychopharmacolgy CY DEC 03-07, 2006 CL Hollywood, FL SP Amer Coll Neuropsychopharmacol C1 Univ S Carolina, Columbia, SC 29208 USA. NR 0 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2006 VL 31 SU 1 BP S259 EP S260 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 108BS UT WOS:000242215900681 ER PT J AU Prasad, HC Blakely, RD Sutcliffe, JS AF Prasad, Harish C. Blakely, Randy D. Sutcliffe, James S. TI Autism-associated serotonin transporter variants confer gain of function phenotypes arising through distinct mechanisms SO NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 45th Annual Meeting of the American-College-of-Neuropsychopharmacolgy CY DEC 03-07, 2006 CL Hollywood, FL SP Amer Coll Neuropsychopharmacol C1 Vanderbilt Univ, Nashville, TN USA. NR 0 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0893-133X J9 NEUROPSYCHOPHARMACOL JI Neuropsychopharmacology PD DEC PY 2006 VL 31 SU 1 BP S82 EP S83 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 108BS UT WOS:000242215900237 ER PT J AU Blaxill, MF AF Blaxill, Mark F. TI Why are so many children sick? A review of the time trend evidence and related controversies in autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1149 EP 1149 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300031 ER PT J AU Kahler, SG AF Kahler, S. G. TI Dietary and intestinal issues in autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR C1 Univ Arkansas Med Sci, Little Rock, AR 72205 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1150 EP 1150 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300032 ER PT J AU Herbert, M AF Herbert, Martha TI Autism: A brain disorder or a disorder that affects the brain? SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR DE autism; brain; complex systems; connectivity; gene-environment interaction C1 Harvard Univ, Massachusetts Gen Hosp, Harvard Sch Med, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1151 EP 1152 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300037 ER PT J AU Pessah, I AF Pessah, Isaac TI Toward understanding autism's complexities. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR C1 Univ Calif Davis, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1152 EP 1152 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300038 ER PT J AU Bradstreet, J AF Bradstreet, Jeff TI Autism: The clinical picture. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR C1 Florida Hosp Celebrat, Intl Child Dev Resource Ctr, Melbourne, FL USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1154 EP 1154 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300045 ER PT J AU Herbert, M Pessah, I AF Herbert, Martha Pessah, Isaac TI Advancing the science of autism spectrum disorders: Introduction and overview. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR C1 Harvard Univ, Massachusetts Gen Hosp, Harvard Med Sch, Boston, MA USA. Univ Calif Davis, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1154 EP 1154 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300044 ER PT J AU Pessah, I AF Pessah, Isaac TI Critical mechanisms, moving targets: Understanding immune system modulation in autism risk. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR C1 Univ Calif Davis, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1155 EP 1155 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300049 ER PT J AU Rossignol, D Mumper, E James, J Melnyk, S Rossignol, L AF Rossignol, Dan Mumper, Elizabeth James, Jill Melnyk, Stepan Rossignol, Lanier TI Hyperbaric oxygen therapy in autistic children improves symptomology, decreases markers of inflammation, and has neutral effects on oxidative stress. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR DE autism; hyperbaric oxygen therapy; inflammation C1 Univ Virginia, Dept Family Med, Charlottesville, VA USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1155 EP 1156 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300050 ER PT J AU Rossignol, D AF Rossignol, Dan TI Evidence of impaired mercury efflux in autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR C1 Univ Virginia, Dept Family Med, Charlottesville, VA USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1173 EP 1173 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300100 ER PT J AU ter Schure, A Yager, J AF ter Schure, A. Yager, J. TI Examining databases used to evaluate trends in neuro development disorders. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR DE autism; thimerosal; database-analysis C1 Elect Power Res Inst, Air Qual Hlth & Risk Assesment, Palo Alto, CA USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1182 EP 1182 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300125 ER PT J AU Graves, JT Walker, SJ AF Graves, J. T. Walker, S. J. TI Microarray analysis of TNFRSF and other cytokine mRNAS differentially regulated in autistic, EBV-immortalized B-lymphocytes. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR DE autism; cell culture; gene expression C1 Wake Forest Univ, Sch Med, Dept Physiol & Pharmacol, Winston Salem, NC 27109 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1184 EP 1184 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300132 ER PT J AU Kahler, SG Cooper, E Gaylor, D AF Kahler, S. G. Cooper, E. Gaylor, D. TI Peptiduria in autism and related disorders: An exploratory study. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR C1 Univ Arkansas Med Sci, Little Rock, AR 72205 USA. Murdoch Childrens Res Inst, Parkville, Vic, Australia. Gaylor & Assoc Eureka, Springs, AR USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1184 EP 1185 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300133 ER PT J AU Owens, SE Summar, ML Haines, JL Aschner, M AF Owens, S. E. Summar, M. L. Haines, J. L. Aschner, M. TI Genetic susceptibility in autism. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR DE genetics; mercury; autism C1 Vanderbilt Univ, Sch Med, Dept Pediat, Nashville, TN 37212 USA. Vanderbilt Univ, Sch Med, Ctr Human Genet Res, Nashville, TN 37212 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1184 EP 1184 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300131 ER PT J AU Walker, SJ Nelson, A Blaxill, M Aschner, M AF Walker, S. J. Nelson, A. Blaxill, M. Aschner, M. TI Transport of ethylmercury and methylmercury in an in vitro blood-brain barrier model. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR DE autism; blood brain barrier; ethylmercury C1 Wake Forest Univ, Sch Med, Dept Physiol & Pharmacol, Winston Salem, NC 27109 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1185 EP 1185 PG 1 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300134 ER PT J AU Melnyk, S Jernigan, S Savenka, A James, SJ AF Melnyk, Stepan Jernigan, Stefanie Savenka, Alena James, S. Jill TI Increased intracellular free radical production and decreased glutathione redox ratio in lymphoblastoid cell lines from autistic children. SO NEUROTOXICOLOGY LA English DT Meeting Abstract CT 23rd International Neurotoxicology Conference CY SEP 17-21, 2006 CL Little Rock, AR DE autism; oxidative stress; Thimerosal C1 Univ Arkansas Med Sci, Arkansas Childrens Hosp Res Inst, Little Rock, AR 72205 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0161-813X J9 NEUROTOXICOLOGY JI Neurotoxicology PD DEC PY 2006 VL 27 IS 6 BP 1190 EP 1191 PG 2 WC Neurosciences; Pharmacology & Pharmacy; Toxicology SC Neurosciences & Neurology; Pharmacology & Pharmacy; Toxicology GA 122FO UT WOS:000243211300150 ER PT J AU Traboulsi, EI Koenekoop, R Stone, EM AF Traboulsi, Elias I. Koenekoop, Robert Stone, Edwin M. TI Lumpers or splitters? The role of molecular diagnosis in leber congenital amaurosis SO OPHTHALMIC GENETICS LA English DT Editorial Material DE leber congenital amaurosis; classification; Joubert syndrome; CEP290 gene; blindness congenital; review; perspective; editorial; retinal dystrophy; genetic testing ID MUTATIONS; GENE AB Clarification and classification of the congenital form of blindness known as Leber congenital amaurosis (LCA) continues to provide its challenges and dilemmas. Until recently, seven genes have been identified that cause LCA. Clarifying the relation between LCA and associated neurological abnormalities such as autism, seizures, and hypotony, and unraveling the relationship between the ocular LCA phenotype and that associated with distinct systemic entities such as Joubert syndrome, Senior-Loken syndrome and Saldino-Mainzer syndrome has taken on new importance with the discovery that a substantial proportion of patients with LCA have mutations in the CEP290 gene that causes Joubert syndrome. This commentary explores the implications of this recent discovery and revisits the classification of LCA. C1 Cole Eye Inst, Ctr Genet Eye Dis, Cleveland, OH 44195 USA. McGill Univ, Montreal Childrens Hosp, Res Inst, McGill Ocular Genet Lab, Montreal, PQ H3H 1P3, Canada. Univ Iowa, Carver Coll Med, Iowa City, IA 52242 USA. Howard Hughes Med Inst, Iowa City, IA 52242 USA. 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Tobi, Hilde TI Pervasive developmental disorder, behavior problems, and psychotropic drug use in children and adolescents with mental retardation SO PEDIATRICS LA English DT Article DE mental retardation; children; adolescents; psychopharmacology; pervasive developmental disorder; behavior problems; psychotropic agents ID AUTISM SPECTRUM DISORDERS; INTELLECTUAL DISABILITY; PSYCHIATRIC-DISORDERS; RISPERIDONE; SCALES; PSYCHOPHARMACOLOGY; POPULATION; PREVALENCE; INSTRUMENT; MEDICATION AB OBJECTIVE. This study investigated the interrelationship between psychopharmaco-therapy in general and the use of specific psychotropic drugs and pervasive developmental disorder and other behavior problems in children and adolescents with mental retardation. METHODS. A total of 862 participants 4 to 18 years of age, including all levels of mental retardation, were recruited through facilities for children with mental retardation in Friesland, the Netherlands. Information on medication was collected through parent interviews. Behavior problems were investigated with a standardized parent questionnaire (Developmental Behavior Checklist). A pervasive developmental disorder classification was based on the Pervasive Developmental Disorder in Mental Retardation Scale, completed by psychologists or teachers. Logistic regression analysis was used to investigate the relationship between the use of psychotropic drugs and pervasive developmental disorder and other behavioral problems, in the presence of possible confounders. RESULTS. One of 10 participants used psychotropic medication. The main factors associated with psychotropic drug use were pervasive developmental disorder and disruptive behavior. The level of functioning was also associated. Self-absorbed behavior was statistically significantly associated with clonidine use and disruptive behavior with stimulant use. Pervasive developmental disorder and communication problems were the main factors associated with the use of antipsychotic drugs. Age also played a role, whereas gender, living situation, and level of mental retardation did not. CONCLUSIONS. Antipsychotic drugs were associated with pervasive developmental disorder, whereas clonidine and stimulants were associated with self-absorbed and disruptive behavior, respectively. Although clonidine and risperidone are not registered for the problems reported and the other nonstimulants were only sometimes used on-label, their use was associated with specific psychiatric or behavioral problems. C1 Univ Groningen, Ctr Child & Adolescent Psychiat, Med Ctr, Accare Univ, NL-9700 AR Groningen, Netherlands. Univ Groningen, Inst Drug Explorat, Dept Social Pharm Pharmacoepidemiol & Pharmacothe, Groningen, Netherlands. Social Sci Wageningen Univ Res, Res Methodol Grp, Wageningen, Netherlands. RP de Bildt, A (reprint author), Univ Groningen, Ctr Child & Adolescent Psychiat, Med Ctr, Accare Univ, POB 660, NL-9700 AR Groningen, Netherlands. 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TI Lack of correlation between digit ratio (2D : 4D) and Baron-Cohen's "Reading the Mind in the Eyes" test, empathy, systemising, and autism-spectrum quotients in a general population sample SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE digit ratio (2D : 4D); prenatal testosterone; empathising; systemising; autism phenotype; sex differences ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME; FETAL TESTOSTERONE; FINGER-LENGTH; 2ND; ADULTS; CHILDREN; PERSONALITY; DISORDERS AB The second-to-fourth digit ratio (2D:4D) is sexually differentiated and is a likely biomarker for the organisational (permanent) effects of prenatal testosterone on the human brain. Recent research has highlighted a possible role of prenatal testosterone levels in both the etiology of autism-spectrum disorders and in sex and individual differences in cognitive styles of the normal mind (Baron-Cohen's Extreme Male Brain Theory of Autism and Empathising/Systemising Theory). Importantly, autistic children present lower (hypermasculinised) 2D:4D than healthy controls. Based on these accounts, we investigated the relation of 2D:4D with Baron-Cohen's measures of empathising ("Reading the Mind in the Eyes" test, RMET; Empathy Quotient, EQ), systemising (Systemising Quotient, SQ), and autistic-like traits (Autism-Spectrum Quotient, AQ) in the general population (N = 423 Austrian adults). Whereas sex differences into the expected direction and of expected size were obtained for all variables and internal scale consistencies tallied to retrievable reference values, 213:413 was unrelated to RMET, EQ, SQ, and AQ scores. Candidate explanations for this lack of correlation might be possible developmental timing differences in the expression of 2D:4D and empathising/systemising, qualitative (as opposed to quantitative) functional differences between the normal and the autistic mind, or the suboptimal psychometric properties of the measures. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ Vienna, Sch Psychol, Dept Basic Psychol Res, Vienna, Austria. RP Voracek, M (reprint author), Univ Vienna, Sch Psychol, Dept Basic Psychol Res, Waehringer Guertel 18, Vienna, Austria. 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Clin. North Amer. PD DEC PY 2006 VL 29 IS 4 BP 1059 EP + DI 10.1016/j.psc.2006.08.004 PG 19 WC Psychiatry SC Psychiatry GA 118ZT UT WOS:000242982700013 PM 17118282 ER PT J AU Sakurai, T Ramoz, N Reichert, JG Corwin, TE Kryzak, L Smith, CJ Silverman, JM Hollander, E Buxbaum, JD AF Sakurai, Takeshi Ramoz, Nicolas Reichert, Jennifer G. Corwin, Thomas E. Kryzak, Lauren Smith, Christopher J. Silverman, Jeremy M. Hollander, Eric Buxbaum, Joseph D. TI Association analysis of the NrCAM gene in autism and in subsets of families with severe obsessive-compulsive or self-stimulatory behaviors SO PSYCHIATRIC GENETICS LA English DT Article DE autism disorder; AUTS1; behaviors; brain; cell adhesion molecule; drug addiction; receptor; 7q31 ID PERVASIVE DEVELOPMENTAL DISORDERS; CHROMOSOME 7Q; SUSCEPTIBILITY GENES; SPECTRUM DISORDERS; SYMPTOM DOMAINS; CANDIDATE GENES; GENOMIC SCREEN; NR-CAM; LINKAGE; ETIOLOGY AB Objectives An autism susceptibility locus (AUTS1, MIM#608636) has been identified in chromosome 7q31. NrCAM is a candidate gene for AUTS1 because it is expressed in the brain and encodes a receptor involved in nervous system development. Polymorphisms in NrCAM have been reported to be associated with autism susceptibility and with substance abuse, implicating NrCAM in reward circuitry. Self-stimulatory, perseverative behavior in autism might be due to defects in reward circuitry. In addition, models of drug addiction have also borrowed from models of obsessive-compulsive behavior designed to reduce anxiety. Thus, our goals were to replicate previous associations of NrCAM with autism, making use of a large cohort, and to clarify whether NrCAM was associated with a specific endophenotype of autism in the repetitive behaviors and stereotyped interests domains. Methods We genotyped six NrCAM single nucleotide polymorphisms in 352 families and we tested for association between these, polymorphisms and autism in the entire cohort and in two subsets, one with severe obsessive-compulsive behaviors and one with pronounced self-stimulatory behaviors. Results We found no association between single nucleotide polymorphisms of NrCAM and autism in our large cohort, or in the severe obsessive-compulsive behavior and self-stimulatory behavior subsets. However, we observed a significant overtransmission (21 transmitted vs 6 nontransmitted, X = 12.054, P = 0.0005) of the haplotype G-G-A-G-C-A of rs722519-rs1269622-rs405945-rs6958498-rs401433-rs439587 in the severe obsessive-compulsive behavior subset, likely driven by the G-C haplotype of rs6958498-rs401433, which itself showed significant overtransmission (31 transmitted vs 13 nontransmitted, X = 8.844, P = 0.003). Conclusions Overtransmission of particular haplotypes of NrCAM, that may relate to the expression level of NrCAM in the brain, appeared to be associated with autism in the severe obsessive-compulsive behavior subset. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Pharmacol & Biol Chem, New York, NY 10029 USA. Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA. Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. RP Buxbaum, JD (reprint author), Mt Sinai Sch Med, Dept Psychiat, 1 Gustave L Levy Pl,Box 1668, New York, NY 10029 USA. 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Genet. PD DEC PY 2006 VL 16 IS 6 BP 251 EP 257 DI 10.1097/01.ypg.0000242196.81891.c9 PG 7 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 114QN UT WOS:000242680800011 PM 17106428 ER PT J AU Wang, YF Su, YJ AF Wang, Yifang Su, Yanjie TI Theory of mind in old adults: The performance on Happe's stories and faux pas stories SO PSYCHOLOGIA LA English DT Article DE theory of mind; old adults; strange stories; faux pas stories ID FALSE BELIEF; CHILDREN; GENDER; AGE; REPRESENTATION; AUTISM AB Theory of mind abilities in old adults did not receive attention until Happe, Winner, and Brownell (1998) found that the theory of mind performance improved with advancing age. However, Maylor, Moulson, Muncer, and Taylor (2002) and Sullivan and Ruffman (2004) reported that the old adults performed worse than the young adults on theory of mind stories. We used "strange stories" (Happe et al., 1998; Maylor et al., 2002) and faux pas stories (Stone Baron-Cohen, Calder, Keane, & Young, 2003) separately to examine the theory of mind abilities of an old and a young group with IQ and educational level matched. We found that the performance of the old group was worse than that of the young group on the faux pas stories, especially in the faux pas understanding, but no significant difference existed between the two age groups in the strange stories understanding. Moreover, the performance on the faux pas and strange stories for both old and young adults was separately independent of fluid intelligence, full-scale IQ, verbal IQ, and performance IQ. C1 Peking Univ, Dept Psychol, Beijing 100871, Peoples R China. Capital Normal Univ, Beijing, Peoples R China. RP Su, YJ (reprint author), Peking Univ, Dept Psychol, Beijing 100871, Peoples R China. 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James Frith, Uta Happe, Francesca TI Autism spectrum disorder and psychopathy: shared cognitive underpinnings or double hit? SO PSYCHOLOGICAL MEDICINE LA English DT Article ID ASPERGERS SYNDROME; EXECUTIVE DYSFUNCTION; CHILDREN; RESPONSES; VIOLENCE; OTHERS; QUESTIONNAIRE; IMPAIRMENT; TENDENCIES; CHILDHOOD AB Background. We measured psychopathic traits in boys with autism spectrum disorder (ASD) selected for difficult and aggressive behaviour. We asked (1) whether psychopathic tendencies can be measured in ASD independent of the severity of autistic behaviour; (ii) whether individuals with ASD with callous-unemotional (CU) traits differ in their cognitive profile from those without such traits; and (iii) how the cognitive data from this study compare with previous data of Youngsters with psychopathic tendencies. Method. Twenty-eight ASD boys were rated on psychopathic tendencies, autistic traits and a range of cognitive measures assessing mentalizing ability, executive functions, emotion recognition and ability to make moral-conventional distinction. Results. Our results indicate that psychopathic tendencies are not related to severity of ASD. In addition., such tendencies do not seem to be related to core autistic cognitive deficits, specifically in 'mind-reading' or executive function. Boys with co-occurring ASD and CU tendencies share some behaviours and aspects of cognitive profile with boys who have psychopathic tendencies alone. Conclusions. Callous/psychopathic acts in a small number of individuals with ASD probably reflect a 'double hit' involving an additional impairment of empathic response to distress Cues, which is not part and parcel of ASD itself. C1 UCL, Dept Psychol, London WC1E 6BT, England. Kings Coll London, Inst Psychiat, London WC2R 2LS, England. 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Rec. PD WIN PY 2006 VL 56 IS 1 BP 3 EP 21 PG 19 WC Psychology, Multidisciplinary SC Psychology GA 008CG UT WOS:000235017200001 ER PT J AU Wellman, HM Fang, FX Liu, D Zhu, LQ Liu, GX AF Wellman, Henry M. Fang, Fuxi Liu, David Zhu, Liqi Liu, Guoxiong TI Scaling of theory-of-mind understandings in Chinese children SO PSYCHOLOGICAL SCIENCE LA English DT Article ID CANTONESE-SPEAKING CHILDREN; MENTAL STATE LANGUAGE; FALSE BELIEF; DEAFNESS; CULTURE; EMOTION; AUTISM AB Prior research demonstrates that understanding of theory of mind develops at different paces in children raised in different cultures. Are these differences simply differences in timing, or do they represent different patterns of cultural learning? That is, to what extent are sequences of theory-of-mind understanding universal, and to what extent are they culture-specific? 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PD DEC PY 2006 VL 17 IS 12 BP 1075 EP 1081 DI 10.1111/j.1467-9280.2006.01830.x PG 7 WC Psychology, Multidisciplinary SC Psychology GA 117IL UT WOS:000242866500012 PM 17201790 ER PT J AU Lakes, K Lopez, SR Garro, LC AF Lakes, Kimberley Lopez, Steven R. Garro, Linda C. TI Cultural competence and psychotherapy: Applying anthropologically informed conceptions of culture SO PSYCHOTHERAPY LA English DT Article DE culture; psychotherapy; cultural competence; narratives; autism ID CHILDREN; ILLNESS; AUTISM; HEALTH; DISPARITIES; SERVICES; LESSONS; MODEL; CARE AB The authors apply two contemporary notions of culture to advance the conceptual basis of cultural competence in psychotherapy: Kleinman's (1995) definition of culture as what is at stake in local, social worlds, and Mattingly and Lawlor's (2001) concept of shared narratives between practitioners and patients. The authors examine these cultural constructs within a clinical case of an immigrant family caring for a young boy with an autism-spectrum disorder. Their analysis suggests that the socially based model of culture and the concept of shared narratives have the potential to broaden and enrich the definition of cultural competence beyond its current emphasis on the presumed cultural differences of specific racial and ethnic minority groups. C1 Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. Calif State Univ San Bernardino, San Bernardino, CA 92407 USA. RP Lopez, SR (reprint author), Univ Calif Los Angeles, Dept Psychol, 1285 Franz Hall,Box 951563, Los Angeles, CA 90095 USA. 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Panyavin, Ivan S. Calkins, Monica E. Kohler, Christian Siegel, Steven J. Schachter, Michael Gur, Raquel E. Gur, Ruben C. TI Self-face recognition and theory of mind in patients with schizophrenia and first-degree relatives SO SCHIZOPHRENIA RESEARCH LA English DT Article DE schizophrenia; endophenotype; face processing; theory of mind; self-face; schizotypal traits ID SCHIZOTYPAL PERSONALITY-TRAITS; AUDITORY HALLUCINATIONS; NORMAL ADULTS; BODY-IMAGE; PERCEPTION; EXPRESSION; EMOTIONS; BEHAVIOR; AUTISM; BRAIN AB Objective: The hypothesized relationship between theory of mind (ToM) and self-face recognition as well as its potential genetic associations has not been previously explored in patients with schizophrenia and in first-degree relatives with schizotypal personality traits. Method. Ten patients diagnosed with schizophrenia, 10 of their first-degree relatives and 10 healthy controls were included. To assess self-face recognition (SFR), participants were presented images of faces of themselves and others and asked to make rapid 'unfamiliar', 'familiar' and 'self' judgments. As a measure of ToM, subjects were administered the Revised Mind in the Eyes Test (MET [Baron-Cohen, S., Wheelwright, S., Hill, J., Raste, Y, and Plumb, I., 2001. The "Reading the Mind in the Eyes" Test revised version: a study with normal adults, and adults with Asperger syndrome or high-functioning autism. J Child Psychol Psychiatry 42 (2), 241-251.]). Schizotypal characteristics in relatives and controls were assessed using a modified version of the Schizotypal Personality Questionnaire (SPQ [Raine, A., 1991. The SPQ: a scale for the assessment of schizotypal personality based on DSM-III-R criteria. Schizophrenia Bulletin 17(4), 555-564.]). Results: Patients took longer and were less accurate on the SFR task than their relatives who in turn performed worse than healthy controls. Specific ToM deficits in schizophrenia were replicated. There was a relationship between accuracy rates on the MET and SFR tasks. High levels of schizotypal traits such as social anxiety, constricted affect and no close friends were important for both tasks. Conclusions: Face recognition deficits and ToM deficits in schizophrenia are apparent. The critical influence of high levels of select schizotypal traits is also highlighted. A deficit in relatives of schizophrenia patients raises the possibility that ToM and face recognition deficits may be candidate endophenotypes for schizophrenia. Support for the hypothesized link between ToM and face recognition is provided. (c) 2006 Elsevier B.V. All rights reserved. C1 Drexel Univ, Dept Psychol, Philadelphia, PA 19104 USA. Univ Penn, Dept Neurosci, Philadelphia, PA 19104 USA. RP Irani, F (reprint author), Drexel Univ, Dept Psychol, 3141 Chestnut St, Philadelphia, PA 19104 USA. 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TI Characterizing sleep in children with autism spectrum disorders: A multidimensional approach SO SLEEP LA English DT Article DE insomnia; polysomrography; children's sleep habits questionnaire; child behavior checklist; autism diagnostic observation schedule ID PERVASIVE DEVELOPMENTAL DISORDERS; SCHOOL-AGED CHILDREN; PARENTS CONCERNS; PATTERNS; BEHAVIOR; PREVALENCE; APNEA AB Study Objectives: To relate parentally reported sleep concerns in autism spectrum disorders (ASD) to polysomnographic (PSG) findings and measures of daytime behavior and autism symptomatology. Design: Cross-sectional study involving validated questionnaires, sleep histories and diaries, 2 nights of PSG, and the Autism Diagnostic Observation Schedule (ADOS). Setting: Vanderbilt University General Clinical Research Center Sleep Core Participants: 21 children with ASD and 10 typically developing (TD) children, aged 4-10 years. Children were free of psychotropic medications, with no history of mental retardation or epileptic seizures. Interventions: N/A Measurements and Results: Children with ASD were defined as "good sleepers" (10 children) and "poor sleepers" (11 children) on the basis of parental report; the age-comparable TD children were all reported by their parents to be good sleepers. Poor sleepers with ASD showed prolonged sleep latency and decreased sleep efficiency on night 1 of PSG and differed on insomnia-related subscales of the Children's Sleep Habits Questionnaire (CSHQ; increased sleep onset delay and decreased sleep duration). The good sleepers with ASD did not differ from the TD children in sleep architecture or on CSHQ domains. As compared with ASD good sleepers, the ASD poor sleepers also had higher scores related to affective problems on the Child Behavior Checklist and more problems with reciprocal social interaction on the ADOS. Conclusions: Parentally reported sleep concerns of insomnia in children with ASD are substantiated by validated sleep questionnaires and by PSG. Furthermore, good sleepers with ASD showed fewer affective problems and better social interactions than ASD poor sleepers. C1 Vanderbilt Univ, Sch Med, Med Ctr, Dept Neurol,Sleep Disorders Div, Nashville, TN 37232 USA. Vanderbilt Univ, Sch Med, Kennedy Ctr, Nashville, TN 37232 USA. Vanderbilt Univ, Sch Med, Dept Biostat, Nashville, TN 37232 USA. Vanderbilt Univ, Sch Med, Childrens Hosp, Dept Pediat, Nashville, TN 37232 USA. Univ Michigan, Sch Med, Dept Neurol, Ann Arbor, MI USA. RP Malow, BA (reprint author), Vanderbilt Univ, Sch Med, Med Ctr, Dept Neurol,Sleep Disorders Div, S Garage Med Bldg,Room 2219,2311 Pierce Ave, Nashville, TN 37232 USA. 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TI Model syndromes for investigating social cognitive and affective neuroscience: a comparison of autism and Williams syndrome SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE LA English DT Article DE autism; Williams syndrome; face processing; emotion processing; amygdala AB Autism and Williams syndrome are genetically based neurodevelopmental disorders that present strikingly different social phenotypes. Autism involves fundamental impairments in social reciprocity and communication, whereas people with Williams syndrome are highly sociable and engaging. This article reviews the behavioral and neuroimaging literature that has explored the neurocognitive mechanisms that underlie these contrasting social phenotypes, focusing on studies of face processing. The article concludes with a discussion of how the social phenotypes of both syndromes may be characterized by impaired connectivity between the amygdala and other critical regions in the 'social brain'. C1 [Tager-Flusberg, Helen] Boston Univ, Dept Anat & Neurobiol, Sch Med, Boston, MA 02118 USA. RP Tager-Flusberg, H (reprint author), Boston Univ, Dept Anat & Neurobiol, Sch Med, 715 Albany St L-814, Boston, MA 02118 USA. EM htagerf@bu.edu RI Joseph, Roy/D-8530-2015 FU [U19 DC 03610]; [U54 MH 66398]; [RO1 HD 33470]; [RO3 HD 51943]; [K01 MH 73944] FX Preparation of this article was supported by the following grants: U19 DC 03610 (HTF, RMJ), U54 MH 66398 (HTF), RO1 HD 33470 (HTF, DPS), RO3 HD 51943 (DPS) and K01 MH 73944 (RMJ). 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Cogn. Affect. Neurosci. PD DEC PY 2006 VL 1 IS 3 BP 175 EP 182 DI 10.1093/scan/nsl035 PG 8 WC Neurosciences; Psychology; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA V20GZ UT WOS:000208129800003 PM 18985104 ER PT J AU Marco, EJ Skuse, DH AF Marco, Elysa J. Skuse, David H. TI Autism-lessons from the X chromosome SO SOCIAL COGNITIVE AND AFFECTIVE NEUROSCIENCE LA English DT Article DE autism; X chromosome; social cognition; genetics AB Recognized cases of autism spectrum disorders are on the rise. It is unclear whether this increase is attributable to secular trends in biological susceptibility, or to a change in diagnostic practices and recognition. One hint concerning etiological influences is the universally reported male excess (in the range of 4: 1 to 10: 1). Evidence suggests that genetic influences from the X chromosome play a crucial role in engendering this male vulnerability. In this review, we discuss three categories of genetic disease that highlight the importance of X-linked genes in the manifestation of an autistic phenotype: aneuploides (Turner syndrome and Klinefelter syndrome), trinucleotide expansions (Fragile X syndrome) and nucleotide mutations (Rett Syndrome, Neuroligins 3 & 4, and SLC6A8). The lessons from these diseases include an understanding of autistic features as a broad phenotype rather than as a single clinical entity, the role of multiple genes either alone or in concert with the manifestation of autistic features, and the role of epigenetic factors such as imprinting and X-inactivation in the expression of disease severity. Better understanding of the clinical phenotypes of social cognition and the molecular neurogenetics of X-linked gene disorders will certainly provide additional tools for understanding autism in the years to come. 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The group fixated the location of the mouth in facial expressions more than did matched controls, even when the mouth was not shown, even in faces that were inverted and most noticeably at latencies of 200-400 ms. Comparisons with a computational model of visual saliency argue that the abnormal bias for fixating the mouth in autism is not driven by an exaggerated sensitivity to the bottom-up saliency of the features, but rather by an abnormal top-down strategy for allocating visual attention. C1 [Neumann, Dirk; Adolphs, Ralph] CALTECH, Computat & Neural Syst Program, Pasadena, CA 91125 USA. [Spezio, Michael L.; Adolphs, Ralph] CALTECH, Div Humanities & Social Sci, Pasadena, CA 91125 USA. [Piven, Joseph] Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. RP Adolphs, R (reprint author), CALTECH, Computat & Neural Syst Program, HSS 228-77, Pasadena, CA 91125 USA. EM radolphs@hss.caltech.edu FU NIMH; Cure Autism Now Foundation; Autism Speaks FX This research was supported by grants from the NIMH, the Cure Autism Now Foundation, and Autism Speaks. The authors would like to thank the participants and their families for making this study possible, Dr Frederic Gosselin for helpful advice on the using the 'Bubbles' method, and Robert Hurley for support in conducting the experiment. 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TI Wisconsin Twin Panel: Current directions and findings SO TWIN RESEARCH AND HUMAN GENETICS LA English DT Article ID BEHAVIORAL-INHIBITION; CHILDHOOD TEMPERAMENT; POSITIVE EMOTIONALITY; CHILDREN; ANXIETY; ASSOCIATION; ENVIRONMENT; DISORDERS; TODDLER; INFANT AB The Wisconsin Twin Panel is based on the population of all twins born in the state of Wisconsin, United States. Our research focus is the etiology and developmental course of early emotions, temperament, childhood anxiety and impulsivity, the autism spectrum, auditory and tactile sensory sensitivity, and related psychobiological and behavioral phenotypes. We employ a range of research methods including structured interviews with caregivers, observer ratings, child self-report, home-based behavioral batteries, biological measures of basal and reactive cortisol, palm prints, birth records, genotyping, cognitive testing, and questionnaires. 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TI Enhanced anxiety and stress-induced corticosterone release are associated with increased Crh expression in a mouse model of Rett syndrome SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE autism; corticotropin-releasing hormone; methyl-CpG-binding protein 2 ID CPG-BINDING-PROTEIN; METHYL-CPG; TRANSCRIPTIONAL REPRESSION; HISTONE DEACETYLASE; BEHAVIORAL-ASPECTS; DNA METHYLATION; MECP2; MICE; DYSFUNCTION; PLASTICITY AB Rett syndrome (RTT), a postnatal neurodevelopmental disorder, is caused by mutations in the methyl-CpG-binding protein 2 (MECP2) gene. Children with RTT display cognitive and motor abnormalities as well as autistic features. We studied mice bearing a truncated Mecp2 allele (Mecp2(308/Y) mice) and found evidence of increased anxiety-like behavior and an abnormal stress response as evidenced by elevated serum corticosterone levels. We found increased corticotropin-releasing hormone (Crh) gene expression in the paraventricular nucleus of the hypothalamus, the central amygdala, and the bed nucleus of the stria terminalis. Finally, we discovered that MeCP2 binds the Crh promoter, which is enriched for methylated CpG dinucleotides. In contrast, the MeCP2308 protein was not detected at the Crh promoter. This study identifies Crh as a target of MeCP2 and implicates Crh overexpression in the development of specific features of the Mecp2(308/Y) mouse, thereby providing opportunities for clinical investigation and therapeutic intervention in RTT. C1 Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA. Baylor Coll Med, Med Scientist Training Program, Houston, TX 77030 USA. Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Verna & Marrs McLean Dept Biochem & Mol Biol, Houston, TX 77030 USA. Baylor Coll Med, Natl Ctr Macromol Imaging, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. Baylor Coll Med, Howard Hughes Med Inst, Houston, TX 77030 USA. RP Zoghbi, HY (reprint author), Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA. 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Natl. Acad. Sci. U. S. A. PD NOV 28 PY 2006 VL 103 IS 48 BP 18267 EP 18272 DI 10.1073/pnas.0608702103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 111PJ UT WOS:000242465200043 PM 17108082 ER PT J AU Feng, JN Schroer, R Yan, J Song, WJ Yang, CM Bockholt, A Cook, EH Skinner, C Schwartz, CE Sommer, SS AF Feng, Jinong Schroer, Richard Yan, Jin Song, Wenjia Yang, Chunmei Bockholt, Anke Cook, Edwin H., Jr. Skinner, Cindy Schwartz, Charles E. Sommer, Steve S. TI High frequency of neurexin 1 beta signal peptide structural variants in patients with autism SO NEUROSCIENCE LETTERS LA English DT Article DE autism; beta-neurexin genes; NLGN4 gene; mutation detection ID BETA-NEUREXINS; DOVAM-S; GENES; MUTATIONS; PROTEINS; NLGN4 AB Neuroligins are postsynaptic membrane cell-adhesion molecules which bind to beta-neurexins, a family of proteins that act as neuronal cell surface receptors. To explore the possibility that structural variants in the P-neurexin genes predispose to autism, the coding regions and associated splice junctions of three beta-neurexin genes were scanned with detection of virtually all mutations-SSCP (DOVAM-S) in 72 Caucasian patients with autism. In addition, segments of the neurexin 1 beta gene were sequenced in 131 additional Caucasian and 61 Afro-American patients with autism from South Carolina and the, Midwest. Two putative missense structural variants were identified in the neurexin 1 beta gene in four Caucasian patients with autism and not in 535 healthy Caucasian controls (4/203 vs. 0/535, P=0.0056). Initial family data suggest that incomplete penetrance may occur. In addition, no structural variant was found in the neurexin 20 gene and the neurexin 3 beta gene. In the context of all available data, we conclude that mutations of the neurexin 1 beta gene may contribute to autism susceptibility. (c) 2006 Elsevier Ireland Ltd. All rights reserved. C1 City Hope Natl Med Ctr, Dept Mol Genet, Duarte, CA 91010 USA. Greenwood Genet Ctr, JC Self Res Inst, Greenwood, SC 29646 USA. Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA. RP Sommer, SS (reprint author), City Hope Natl Med Ctr, Dept Mol Genet, 1500 E Duarte Rd, Duarte, CA 91010 USA. 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Lett. PD NOV 27 PY 2006 VL 409 IS 1 BP 10 EP 13 DI 10.1016/j.neulet.2006.08.017 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 106LK UT WOS:000242101800003 PM 17034946 ER PT J AU Nicolson, R DeVito, TJ Vidal, CN Sui, YH Hayashi, KM Drost, DJ Williamson, PC Rajakumar, N Toga, AW Thompson, PM AF Nicolson, Rob DeVito, Timothy J. Vidal, Christine N. Sui, Yihong Hayashi, Kiralee M. Drost, Dick J. Williamson, Peter C. Rajakumar, Nagalingam Toga, Arthur W. Thompson, Paul M. TI Detection and mapping of hippocampal abnormalities in autism SO PSYCHIATRY RESEARCH-NEUROIMAGING LA English DT Article; Proceedings Paper CT 50th Annual Meeting of the American-Academy-of-Child-and-Adolescent-Psychiatry CY OCT 14-19, 2003 CL Miami, FL SP Amer Acad Child & Adolescent Psychiat DE autism; hippocampus; MRI ID MEDIAL TEMPORAL-LOBE; STRUCTURAL ABNORMALITIES; ONSET SCHIZOPHRENIA; SPECTRUM DISORDERS; HUMAN BRAIN; AMYGDALA; CHILDREN; MRI; RECOGNITION; VOLUMES AB Brain imaging studies of the hippocampus in autism have yielded inconsistent results. In this study, a computational mapping strategy was used to examine the three-dimensional profile of hippocampal abnormalities in autism. Twenty-one mates with autism (age: 9.5 +/- 3.3 years) and 24 male controls (age: 10.3 +/- 2.4 years) underwent a volumetric magnetic resonance imaging scan at 3 Tesla. The hippocampus was delineated, using an anatomical protocol, and hippocampal volumes were compared between the two groups. Hippocampal traces were also converted into three-dimensional parametric surface meshes, and statistical brain maps were created to visualize morphological differences in the shape and thickness of the hippocampus between groups. Parametric surface meshes and shape analysis revealed subtle differences between patients and controls, particularly in the right posterior hippocampus. These deficits were significant even though the groups did not differ significantly with traditional measures of hippocampal volume. These results suggest that autism may be associated with subtle regional reductions in the size of the hippocampus. The increased statistical and spatial. power of computational mapping methods provided the ability to detect these differences, which were not found with traditional volumetric methods. (c) 2006 Elsevier Ireland Ltd. All rights reserved. C1 Univ Western Ontario, Dept Psychiat, London, ON N6A 3K7, Canada. 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D., 2005, HDB AUTISM PERVASIVE, P365 Williams DL, 2005, J AUTISM DEV DISORD, V35, P747, DOI 10.1007/s10803-005-0021-x Woods RP, 2003, NEUROIMAGE, V19, P1829, DOI 10.1016/S1053-8119(03)00243-X YEARGINALLSOP M, 2003, JAMA-J AM MED ASSOC, V289, P48 NR 57 TC 45 Z9 48 PU ELSEVIER IRELAND LTD PI CLARE PA ELSEVIER HOUSE, BROOKVALE PLAZA, EAST PARK SHANNON, CO, CLARE, 00000, IRELAND SN 0925-4927 J9 PSYCHIAT RES-NEUROIM JI Psychiatry Res. Neuroimaging PD NOV 22 PY 2006 VL 148 IS 1 BP 11 EP 21 DI 10.1016/j.pscychresns.2006.02.005 PG 11 WC Clinical Neurology; Neuroimaging; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 114LY UT WOS:000242668900002 PM 17056234 ER PT J AU de Dios, JG Balaguer-Santamaria, JA AF de Dios, J. Gonzalez Balaguer-Santamaria, J. A. TI What can we expect of collaborative review groups of Cochrane Collaboration in neuropaediatrics? SO REVISTA DE NEUROLOGIA LA Spanish DT Review DE clinical trials; Cochrane Collaboration; evidence-based decision-making; evidence-based medicine; paediatric neurology; systematic reviews ID AUTISTIC SPECTRUM DISORDERS; EPILEPSY-SOCIETY GUIDE; PAPER-BASED JOURNALS; SYSTEMATIC REVIEWS; ANDALUSIA-EPILEPSY; THERAPY 2005; REFRACTORY EPILEPSY; DIAGNOSTIC-TESTS; PARTIAL SEIZURES; DECISION-MAKING AB Introduction. Cochrane Collaboration (CC) contains detailed, critical and up-to-date systematic reviews (SR) of the best scientific evidence available. Aim. To analyse the bibliometric characteristics of the SR related to paediatric neurology published in the 50 Collaborative Review Groups (CRG) of the CC. Materials and methods. Bibliometric analysis of the Database of Systematic Reviews in Cochrane Library, Issue 2, 2005 (n = 2.231 SR). The variables recorded were: number of SR and protocols in any CRG, authors and clusters of secondary research, dates (late review and update), type of study, critical review of the SR and conclusions. Results. Nine published SR about neuropaediatrics: the Epilepsy Group (24 SR), the Neuromuscular Disease Group (16), the Neonatal Group (16), the Developmental, Psychosocial and Learning Problems Group (10), the Pain, Palliative Care and Supportive Care Group (4), the Movement Disorders Group (3), the Injuries Group (3), the Infections Disease Group (3) and the Acute Respiratory Infections Group (2). The three main thematic areas were treatment of epilepsy (pharmacologic and non-pharmacologic), neonatal neurology (mainly intraventricular haemorrhage and perinatal asphyxia) and miscellanea (autism spectrum disorder headache, cerebral palsy, myasthenia gravis, Guillain-Barre syndrome, Bell's palsy and bacterial meningitis). All the SR were about treatment interventions. Conclusions. Paediatric neurology SR are infrequent (3.6% of the 2.231 SR published in CC), and helps an evidence-based decision-making in a few areas: pharmacologic treatment of epilepsy, management of intraventricular haemorrhage of preterm infants and bacterial meningitis. Many therapies in paediatric neurology persist with no supporting evidence, and we detected no SR about important neurological issues in childhood as attention-deficit hyperactivity disorder, mental retardation and hypotonia. C1 Univ Miguel Hernandez, Hosp Univ San Juan, Dept Pediat, Alicante, Spain. Univ Rovira & Virgili, Hosp Univ St Joan, Dept Pediat, Tarragona, Spain. RP de Dios, JG (reprint author), Prof Manuel Sala,6,3 A, E-03003 Alicante, Spain. 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Neurologia PD NOV 16 PY 2006 VL 43 IS 10 BP 589 EP 597 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA 116QC UT WOS:000242816400003 ER PT J AU Ouali, A Cherif, AR Krebs, MO AF Ouali, Abdelaziz Cherif, Amar Ramdane Krebs, Marie-Odile TI Data mining based Bayesian networks for best classification SO COMPUTATIONAL STATISTICS & DATA ANALYSIS LA English DT Article DE data mining; bio-informatics; gene; schizophrenia; Bayesian networks ID RECEPTOR GENE; PROBABILISTIC NETWORKS; SCHIZOPHRENIA; ASSOCIATION; ONSET; ANOMALIES; DISEASE; AUTISM; AGE AB Schizophrenia is a frequent and devastating disorder beginning in early adulthood. Until now, the heterogeneity of this disease has been a major pitfall for identifying the aetiological, genetic or environmental factors. Age at onset or several other quantitative variables could allow categorizing more homogeneous subgroups of patients, although there is little information on the boundaries for such categories. The Bayesian networks classifier (BNs) approach is one of the most popular formalisms for reasoning under uncertainty. Using a data set including genotypes of selected candidate genes for schizophrenia, BNs were used to determine the best cut-off point for three continuous variables (i.e. age at onset of schizophrenia (AFC & AFE) and neurological soft signs (NSS)). (c) 2005 Elsevier B.V. All rights reserved. C1 Univ Paris 05, Fac Med Paris Descartes, INSERM, E0117, F-75014 Paris, France. Univ Versailles, PRISM Lab, F-78035 Versailles, France. RP Ouali, A (reprint author), Univ Paris 05, Fac Med Paris Descartes, INSERM, E0117, 2 Ter Rue Alesia, F-75014 Paris, France. 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Stat. Data Anal. PD NOV 15 PY 2006 VL 51 IS 2 BP 1278 EP 1292 DI 10.1016/j.csda.2005.09.012 PG 15 WC Computer Science, Interdisciplinary Applications; Statistics & Probability SC Computer Science; Mathematics GA 111VU UT WOS:000242484200062 ER PT J AU State, MW AF State, Matthew W. TI A surprising METamorphosis: Autism genetics finds a common functional variant SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Editorial Material ID SPECTRUM DISORDERS; GASTROINTESTINAL SYMPTOMS; INTERNEURON DEVELOPMENT; CHILDREN; ASSOCIATION; TRANSCRIPTION; HISTORY; MEASLES; MUMPS; MET C1 Yale Univ, Sch Med, Program Neurogenet, Dept Child Psychiat, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dept Genet, New Haven, CT 06520 USA. RP State, MW (reprint author), Yale Univ, Sch Med, Program Neurogenet, Dept Child Psychiat, 230 S Frontage Rd, New Haven, CT 06520 USA. 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Levitt, Pat TI A genetic variant that disrupts MET transcription is associated with autism SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article DE autism spectrum disorder; association; candidate gene; hepatocyte growth factor; hepatocyte growth factor receptor ID HEPATOCYTE GROWTH-FACTOR; INFLAMMATORY-BOWEL-DISEASE; GASTROINTESTINAL SYMPTOMS; INTERNEURON DEVELOPMENT; SUSCEPTIBILITY LOCUS; SPECTRUM DISORDERS; MUCOSAL REPAIR; PHENOTYPE; HAPLOTYPES; MONOCYTES AB There is strong evidence for a genetic predisposition to autism and an intense interest in discovering heritable risk factors that disrupt gene function. Based on neurobiological findings and location within a chromosome 7q31 autism candidate gene region, we analyzed the gene encoding the pleiotropic MET receptor tyrosine kinase in a family based study of autism including 1,231 cases. MET signaling participates in neocortical and cerebellar growth and maturation, immune function, and gastrointestinal repair, consistent with reported medical complications in some children with autism. Here, we show genetic association (P = 0.0005) of a common C allele in the promoter region of the MET gene in 204 autism families. The allelic association at this MET variant was confirmed in a replication sample of 539 autism families (P = 0.001) and in the combined sample (P = 0.000005). Multiplex families, in which more than one child has autism, exhibited the strongest allelic association (P = 0.000007). In case-control analyses, the autism diagnosis relative risk was 2.27 (95% confidence interval: 1.41-3.65; P = 0.0006) for the CC genotype and 1.67 (95% confidence interval: 1.11-2.49; P = 0.012)for the CG genotype compared with the GG genotype. Functional assays showed that the C allele results in a 2-fold decrease in MET promoter activity and altered binding of specific transcription factor complexes. These data implicate reduced MET gene expression in autism susceptibility, providing evidence of a previously undescribed pathophysiological basis for this behaviorally and medically complex disorder. C1 Vanderbilt Univ, Dept Pharmacol, Nashville, TN 37203 USA. Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37203 USA. Vanderbilt Univ, Vanderbilt Kennedy Ctr Res Human Dev, Nashville, TN 37203 USA. Univ Naples, Dept Child Neuropsychiat, I-80131 Naples, Italy. Assoc Anni Verdi ONLUS, I-00148 Rome, Italy. IRCCS, Sci Inst Res Hospitalizat & Hlth Care, Unit Neurol & Clin Neurophysiopathol, I-94018 Troina, Italy. SW Autism Res & Resource Ctr, Phoenix, AZ 85006 USA. Ctr Autism Res & Ecuc, Phoenix, AZ 85012 USA. Univ Rome, Lab Mol Psychiat Neurogenet, I-00155 Rome, Italy. IRCCS Fdn Santa Lucia, I-00179 Rome, Italy. RP Levitt, P (reprint author), Vanderbilt Univ, Dept Pharmacol, Nashville, TN 37203 USA. 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Natl. Acad. Sci. U. S. A. PD NOV 7 PY 2006 VL 103 IS 45 BP 16834 EP 16839 DI 10.1073/pnas.0605296103 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 104PB UT WOS:000241969500039 PM 17053076 ER PT J AU Cherkassky, VL Kana, RK Keller, TA Just, MA AF Cherkassky, Vladimir L. Kana, Rajesh K. Keller, Timothy A. Just, Marcel Adam TI Functional connectivity in a baseline resting-state network in autism SO NEUROREPORT LA English DT Article DE autism; corpus callosum; functional connectivity; functional magnetic resonance imaging (fMRI); resting-state network ID SENTENCE COMPREHENSION; DEFAULT MODE; BRAIN; CONSCIOUSNESS AB Brain activity in people with high-functioning autism has been shown to be atypical in a number of ways, including reduced synchronization across areas of activation measured by functional magnetic resonance imaging. This activation atypicality has been observed mostly during the performance of cognitive tasks. This study compares the resting-state network of 57 participants with autism and 57 control participants matched for age and intelligence quotient. The results indicate that both groups have a resting-state network that is very similar both in volume and in organization, but in autism this network is much more loosely connected. This functional underconnectivity was observed in the anterior-posterior connections. The results expand the theory of cortical underconnectivity in autism to the resting state of the brain. C1 Carnegie Mellon Univ, Dept Psychol, Ctr Cognit Brain Imaging, Pittsburgh, PA 15213 USA. RP Cherkassky, VL (reprint author), Carnegie Mellon Univ, Dept Psychol, Ctr Cognit Brain Imaging, Pittsburgh, PA 15213 USA. 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Rivlin, Joseph Roberts, Wendy Senman, Lili Summers, Anne Szatmari, Peter Wong, Virginia Vincent, John B. Zeesman, Susan Osborne, Lucy R. Cardy, Janis Oram Kere, Juha Scherer, Stephen W. Hannula-Jouppi, Katariina TI Absence of a paternally inherited FOXP2 gene in developmental verbal dyspraxia SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID MATERNAL UNIPARENTAL DISOMY; SILVER-RUSSELL-SYNDROME; LANGUAGE IMPAIRMENT; CHROMOSOME REARRANGEMENTS; SUSCEPTIBILITY GENE; GROWTH-RETARDATION; SEVERE SPEECH; DISORDER; AUTISM; 7Q31 AB Mutations in FOXP2 cause developmental verbal dyspraxia (DVD), but only a few cases have been described. We characterize 13 patients with DVD-5 with hemizygous paternal deletions spanning the FOXP2 gene, 1 with a translocation interrupting FOXP2, and the remaining 7 with maternal uniparental disomy of chromosome 7 (UPD7), who were also given a diagnosis of Silver-Russell Syndrome (SRS). Of these individuals with DVD, all 12 for whom parental DNA was available showed absence of a paternal copy of FOXP2. Five other individuals with deletions of paternally inherited FOXP2 but with incomplete clinical information or phenotypes too complex to properly assess are also described. Four of the patients with DVD also meet criteria for autism spectrum disorder. Individuals with paternal UPD7 or with partial maternal UPD7 or deletion starting downstream of FOXP2 do not have DVD. Using quantitative real-time polymerase chain reaction, we show the maternally inherited FOXP2 to be comparatively underexpressed. Our results indicate that absence of paternal FOXP2 is the cause of DVD in patients with SRS with maternal UPD7. The data also point to a role for differential parent-of-origin expression of FOXP2 in human speech development. C1 Hosp Sick Children, Ctr Appl Genom, Dept Genet, N York Gen Hosp, Toronto, ON M5G 1L7, Canada. 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Volkmar, Fred TI Head circumference and height in autism: A study by the Collaborative Program of Excellence in Autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE autism; autism-spectrum disorder; head circumference; macrocephaly; height ID PERVASIVE DEVELOPMENTAL DISORDERS; BRAIN VOLUME; CHILDREN; INDIVIDUALS; SPECTRUM; GROWTH; PREVALENCE; BIRTH; SIZE; LIFE AB Data from 10 sites of the NICHD/NIDCD Collaborative Programs of Excellence in Autism were combined to Study the distribution of head circumference and relationship to demographic and clinical variables. Three hundred thirty-eight probands with autism-spectruin disorder (ASD) including 208 probands with autism were studied along with 147 parents: 149 siblings, and typically developing controls. ASDs were diagnosed, and head circumference and clinical variables measured in a standardized manner across all sites. All Subjects with autism met ADI-R, ADOS-G, DSM-IV, and ICD-10 criteria. The results show the distribution of standardized head circumference in autism is normal in shape, and the mean, variance; and rate of macrocephaly but not microcephaly are increased. Head circumference tends to be large relative to height in autism. No site, gender, age, SES, verbal, or non-verbal IQ effects were present in the autism sample. In addition to autism itself, standardized height and average parental head circumference were the most important factors predicting head circumference in individuals with autism. Mean standardized head circumference and rates of macrocephaly were similar in probands with autism and their parents. Increased head circumference was associated with a higher (more severe) ADI-R social algorithm score. Macrocephaly is associated with delayed onset of language. Although mean head circumference and rates of macrocephaly are increased in autism, a high degree of variability is present, underscoring the complex clinical heterogeneity of the disorder. The wide distribution of head circumference in autism has major implications for genetic, neuroimaging, and other neurobiological research. (c) 2006 Wiley-Liss, Inc. C1 Dept Psychiat, Salt Lake City, UT USA. Univ Utah, Inst Brain, Salt Lake City, UT USA. Brigham Young Univ, Provo, UT 84602 USA. Univ Calif Irvine, Irvine, CA USA. Univ Washington, Seattle, WA 98195 USA. Harvard Univ, Boston, MA 02115 USA. Albert Einstein Univ, New York, NY USA. Boston Univ, Boston, MA 02215 USA. Johns Hopkins Univ, Baltimore, MD USA. Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Univ Rochester, Rochester, NY USA. Univ Pittsburgh, Pittsburgh, PA USA. Univ Calif Los Angeles, Los Angeles, CA USA. Yale Univ, New Haven, CT USA. RP Lainhart, JE (reprint author), Utah Autism Res Program, 421 Wakara Way,Suite 143, Salt Lake City, UT 84108 USA. 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J. Med. Genet. A PD NOV 1 PY 2006 VL 140A IS 21 BP 2257 EP 2274 DI 10.1002/ajmg.a.31465 PG 18 WC Genetics & Heredity SC Genetics & Heredity GA 103SF UT WOS:000241906300001 PM 17022081 ER PT J AU Brady, N Skinner, D Roberts, J Hennon, E AF Brady, Nancy Skinner, Debra Roberts, Joanne Hennon, Elizabeth TI Communication in young children with fragile X syndrome: A qualitative study of mothers' perspectives SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Article DE fragile X; communication disorders; parents; preschool children; qualitative research analysis ID BEHAVIORAL-PHENOTYPE; ADAPTIVE-BEHAVIOR; LANGUAGE; MALES; INTERVENTION; AUTISM; DISABILITIES; ADOLESCENTS; EXPERIENCES; SYMPTOMS AB Purpose: To provide descriptive and qualitative information about communication in young children with fragile X syndrome (FXS) and about how families react to and accommodate communication differences in their children. Method: In-depth interviews were conducted with 55 mothers of young children with FXS. Interviewers asked mothers to describe their children's communication, strategies they used to help promote their children's communication, communication-related frustrations, their expectations for their children, and the roles that they perceive for themselves. Results: Over half the children were nonverbal and learning to communicate with augmentative and alternative communication. Mothers reported using strategies that were developmentally appropriate and recommended by early childhood experts, such as reading and talking to their children. Many mothers identified challenges faced in helping their child to communicate, and some cited difficulty obtaining speech-language services as a challenge. Mothers identified their roles as caregiver, teacher, therapist, and advocate. Conclusions: The perspectives offered by mothers are valuable because they indicate how children with FXS communicate in natural contexts. Information about mothers' expectations and roles may help clinicians to be sensitive to variables that will affect working with young children and their families. C1 Univ Kansas, Lawrence, KS 66045 USA. Univ N Carolina, Chapel Hill, NC USA. RP Brady, N (reprint author), Univ Kansas, 1052 Dole,1000 Sunnyside Dr, Lawrence, KS 66045 USA. 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TI Predicting lexical density growth rate in young children with autism spectrum disorders SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Article DE autism; spoken language; predictors ID JOINT ATTENTION; FOLLOW-UP; COMMUNICATION INTERVENTIONS; DEVELOPMENTAL-DISABILITIES; LANGUAGE-DEVELOPMENT; PRESCHOOLERS; PROGNOSIS; DEFICITS; LEVEL; PLAY AB Purpose: The purpose of this longitudinal correlational study was to test whether an environmental variable and 4 child variables predicted growth rate of number of different nonimitative words used (i.e., lexical density). Method: Thirty-five young (age range 21-54 months) children with autism spectrum disorders (ASD) who were initially nonverbal or low verbal participated in the study. Lexical density was measured at 3 times: at entry into the study as well as 6 months and 12 months after entry into the study. Growth curve analysis was used to test the associations. The predictive value of the putative predictors in the model was tested after controlling for initial expressive language impairment. Results: Initial frequency of intentional communication and diversity of object play were predictors of lexical density growth above and beyond initial expressive language impairment (both pseudo R(2)S =.14). Conclusions: Intentional communication and diversity of object play may represent important prelinguistic goals for young children with ASD. These skills not only have been shown to be malleable through treatment, but they also provide a context for linguistic input from others that may facilitate language development. C1 Vanderbilt Univ, Nashville, TN 37203 USA. RP Yoder, PJ (reprint author), Vanderbilt Univ, 230 Appleton Pl, Nashville, TN 37203 USA. 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J. Speech-Lang. Pathol. PD NOV PY 2006 VL 15 IS 4 BP 378 EP 388 DI 10.1044/1058-0360(2006/035) PG 11 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 114DI UT WOS:000242646500009 PM 17102148 ER PT J AU Dickson, CA Deutsch, CK Wang, SS Dube, WV AF Dickson, Chata A. Deutsch, Curtis K. Wang, Sharon S. Dube, William V. TI Matching-to-sample assessment of stimulus overselectivity in students with intellectual disabilities SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID SEVERE MENTAL-RETARDATION; OVER-SELECTIVITY; CHILDREN; ATTENTION; ADOLESCENTS; AUTISM; DISCRIMINATION; ADULTS AB A delayed matching-to-sample task with multiple sample stimuli was used to evaluate stimulus overselectivity in 70 individuals attending residential special-education schools. A Mental Age Equivalent score (MAE) was obtained for each student using the Peabody Picture Vocabulary Test. Twenty-one participants failed to complete matching-to-sample pretests (mean MAE = 3.70 years). Results on the multiple-sample test for the remaining 49 participants indicated no overselectivity for 14 students (mean MAE = 7.44 years) and were consistent with overselectivity for 35 students (mean MAE = 5.28 years). Performances of students with overselectivity were more variable than those with no overselectivity. The MAE scores were related to both matching-to-sample performance and stimulus overselectivity. C1 Univ Massachusetts, Sch Med, Shriver Ctr, Amherst, MA 01003 USA. RP Dube, WV (reprint author), UMMS Shriver Ctr, Dept Psychol Sci, 200 Trapelo Rd, Waltham, MA 02452 USA. EM william.dube@umassmed.edu CR Anderson S. R., 1996, BEHAV INTERVENTION Y, P181 BAILEY SL, 1981, J APPL BEHAV ANAL, V14, P239, DOI 10.1901/jaba.1981.14-239 DICKSON CA, IN PRESS RES DEV DIS Dube WV, 1999, J APPL BEHAV ANAL, V32, P25, DOI 10.1901/jaba.1999.32-25 Dunn L. 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J. Ment. Retard. PD NOV PY 2006 VL 111 IS 6 BP 447 EP 453 DI 10.1352/0895-8017(2006)111[447:MAOSOI]2.0.CO;2 PG 7 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 108ZF UT WOS:000242277000006 PM 17029502 ER PT J AU Beversdorf, DQ AF Beversdorf, David Q. TI Noradrenergic modulation of cognition and autism spectrum disorders SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 131st Annual Meeting of the American-Neurological-Association CY OCT 08-11, 2006 CL Chicago, IL SP Amer Neurol Assoc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD NOV PY 2006 VL 60 IS 5 BP 625 EP 625 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 112RQ UT WOS:000242545100030 ER PT J AU Isenberg, N AF Isenberg, N. TI Disruption of the mirror neuron system in autism: An fMRI stud of social and instrumental gesture SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 131st Annual Meeting of the American-Neurological-Association CY OCT 08-11, 2006 CL Chicago, IL SP Amer Neurol Assoc C1 JFK Med Ctr, Dept Neurosci, Edison, NJ 08818 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD NOV PY 2006 VL 60 IS 5 BP 627 EP 628 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 112RQ UT WOS:000242545100036 ER PT J AU Barbaresi, WJ Katusic, SK Voigt, RG AF Barbaresi, William J. Katusic, Slavica K. Voigt, Robert G. TI Autism - A review of the state of the science for pediatric primary health care clinicians SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; INTENSIVE BEHAVIORAL TREATMENT; SPECTRUM DISORDERS; YOUNG-CHILDREN; COGNITIVE PROFILES; GASTROINTESTINAL DISORDERS; DIAGNOSTIC INTERVIEW; MENTAL-RETARDATION; MODIFIED CHECKLIST; MEDICAL DISORDERS AB Autism is a complex neurodevelopmental disorder characterized by impaired reciprocal social interaction, impaired communication, and restricted, repetitive, or stereotyped behaviors. Autism seems to affect more children than was previously believed, although this phenomenon may be due to broadening of the diagnostic criteria and increased awareness of the condition. Recent research has clearly indicated the importance of early identification, since early intensive treatment is associated with better long-term outcome. There are many controversies and competing theories about the etiology and treatment of autism, often leaving families confused about the best course of treatment and intervention. Pediatric primary health care clinicians have an important role in both the early identification and ongoing management of children with autism. It is, therefore, essential that primary care clinicians have up-to-date information about the science of autism. C1 Mayo Clin & Mayo Fdn, Coll Med, Dept Pediat & Adolescent Med, Div Dev & Behav Pediat, Rochester, MN 55905 USA. Mayo Clin & Mayo Fdn, Coll Med, Dept Hlth Res, Div Epidemiol, Rochester, MN 55905 USA. Mayo Clin & Mayo Fdn, Coll Med, Dana Child Dev & Learning Disorders Program, Rochester, MN 55905 USA. RP Barbaresi, WJ (reprint author), Mayo Clin & Mayo Fdn, Coll Med, Dept Pediat & Adolescent Med, Div Dev & Behav Pediat, 200 1st St SW, Rochester, MN 55905 USA. 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Pediatr. Adolesc. Med. PD NOV PY 2006 VL 160 IS 11 BP 1167 EP 1175 DI 10.1001/archpedi.160.11.1167 PG 9 WC Pediatrics SC Pediatrics GA 102HN UT WOS:000241801700011 PM 17088521 ER PT J AU Mazefsky, CA Oswald, DP AF Mazefsky, Carla A. Oswald, Donald P. TI The discriminative ability and diagnostic utility of the ADOS-G, ADI-R, and GARS for children in a clinical setting SO AUTISM LA English DT Article DE assessment; autism; clinical sample; differential diagnosis ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGERS-DISORDER; AUTISTIC DISORDER; DSM-IV; INTERVIEW; ADOLESCENTS; STABILITY; SPECTRUM AB Recent years have seen a surge of interest in assessment instruments for diagnosing autism in children. Instruments have generally been developed and evaluated from a research perspective. The Autism Diagnostic Observation Schedule-Generic (ADOS-G), Autism Diagnostic Interview-Revised (ADI-R), and Gilliam Autism Rating Scale (GARS) have received considerable attention and are widely used. The objective of this study was to explore the diagnostic utility and discriminative ability of these tools using a clinical population of children referred to a specialty diagnostic clinic over a 3 year time span. The results indicated that the ADOS-G and ADI-R led to approximately 75 percent agreement with team diagnoses, with most inconsistencies being false positive diagnoses based on the measures. The GARS was generally ineffective at discriminating between children with various team diagnoses and consistently underestimated the likelihood of autism. The findings have important implications for the use of these measures in both research and clinical practice. C1 Virginia Commonwealth Univ, Dept Psychiat, Richmond, VA 23298 USA. Univ Pittsburgh, Pittsburgh, PA USA. RP Oswald, DP (reprint author), Virginia Commonwealth Univ, Dept Psychiat, Box 980489, Richmond, VA 23298 USA. EM doswald@vcu.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 de Bildt A, 2004, J AUTISM DEV DISORD, V34, P129 Gilchrist A, 2001, J CHILD PSYCHOL PSYC, V42, P227, DOI 10.1017/S0021963001006631 Gilliam J. E., 1995, GILLIAM AUTISM RATIN Hill A, 2001, PSYCHOPATHOLOGY, V34, P187, DOI 10.1159/000049305 Klin A, 2005, J AUTISM DEV DISORD, V35, P221, DOI 10.1007/s10803-005-2001-6 Klinger LG, 2000, J CLIN CHILD PSYCHOL, V29, P479, DOI 10.1207/S15374424JCCP2904_3 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., 1997, HDB AUTISM PERVASIVE, P460 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 Macintosh KE, 2004, J CHILD PSYCHOL PSYC, V45, P421, DOI 10.1111/j.1469-7610.2004.00234.x Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 Midence K., 1999, AUTISM, V3, P273, DOI [10.1177/1362361399003003005, DOI 10.1177/1362361399003003005] Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 RUTTER M, 2003, AUTISM DIAGNOSTIC IN SCHOPLER E, 1998, ASPERGER SYNDROME HI South M, 2002, J AUTISM DEV DISORD, V32, P593, DOI 10.1023/A:1021211232023 Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 Volkmar FR, 2000, AM J PSYCHIAT, V157, P262, DOI 10.1176/appi.ajp.157.2.262 NR 22 TC 35 Z9 36 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 NOV PY 2006 VL 10 IS 6 BP 533 EP 549 DI 10.1177/136236130606850S PG 17 WC Psychology, Developmental SC Psychology GA 109WY UT WOS:000242341500002 PM 17088271 ER PT J AU Elfert, M Mirenda, P AF Elfert, Miriam Mirenda, Pat TI The experiences of behavior interventionists who work with children with autism in families' homes SO AUTISM LA English DT Article DE autism; behavior intervention; Canada; coping; family; stress ID STRESSORS; HEALTH AB This study examined the experiences of 65 behavior interventionists (BIs) who provide 1:1 home-based instruction to children with autism in two Canadian provinces. Dependent variables included occupational stress; the relationships among stress, strain, and coping; the relationship between stress and the characteristics of both challenging families and children with autism; and the most and least rewarding aspects of BIs' jobs. The two most stressful work roles for BIs were role overload (the extent to which job demands exceed personal/workplace resources) and role boundary (the extent to which the individual experiences conflicting role demands at work). Significant relationships were found between coping and both stress and strain; however, coping did not moderate the relationship between stress and strain. Significant correlations were found between BI stress and both sensory-related behaviors and social unrelatedness in children with autism. The implications for the BIs, the families, and the agencies are discussed. C1 Univ British Columbia, Fac Educ, Vancouver, BC V6T 1Z4, Canada. RP Mirenda, P (reprint author), Univ British Columbia, Fac Educ, 2125 Main Mall, Vancouver, BC V6T 1Z4, Canada. EM pat.mirenda@ubc.ca CR BARON RM, 1986, J PERS SOC PSYCHOL, V51, P1173, DOI 10.1037/0022-3514.51.6.1173 ELFERT M, 2006, UNPUB MAKING DIFFERE ELFERT M, 2002, UNPUB ESSENCE BEING FLETCHER BC, 1991, J ADV NURS, V16, P1078, DOI 10.1111/j.1365-2648.1991.tb03369.x Huck SW, 2000, READING STAT RES Krug DA, 1993, AUTISM SCREENING INS Leaf R., 1999, WORK PROGR BEHAV MAN Maurice C., 1993, LET ME HEAR YOUR VOI McBride SL, 1997, TOP EARLY CHILD SPEC, V17, P209 Moos RH, 1994, FAMILY ENV SCALE MAN Osipow S. H., 1984, APPLIED SOCIAL PSYCH, V5, P67 Osipow S. H., 1998, OCCUPATIONAL STRESS OSIPOW SH, 1988, J VOCAT BEHAV, V32, P1, DOI 10.1016/0001-8791(88)90002-4 Scott J., 1996, BEHAV INTERVENTION Y, P231 Smith K A, 2000, HIV Clin Trials, V1, P16, DOI 10.1310/4VD1-WGAU-VX2L-V3JE STEWART MJ, 1994, CAN J PUBLIC HEALTH, V85, P180 Wasik B. H., 2001, HOME VISITING PROCED West M, 1988, Health Visit, V61, P366 West M A, 1988, Health Visit, V61, P305 NR 19 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 NOV PY 2006 VL 10 IS 6 BP 577 EP 591 DI 10.1177/1362361306068502 PG 15 WC Psychology, Developmental SC Psychology GA 109WY UT WOS:000242341500005 PM 17088274 ER PT J AU Konstantareas, MM Papageorgiou, V AF Konstantareas, M. Mary Papageorgiou, Vaya TI Effects of temperament, symptom severity and level of functioning on maternal stress in Greek children and youth with ASD SO AUTISM LA English DT Article DE autism spectrum disorder; emotion regulation; maternal stress; temperament ID YOUNG-CHILDREN; BEHAVIOR; AUTISM; PSYCHOPATHOLOGY; DISABILITIES; PARENTS; BIRTH AB This study examined the effect of child temperament, symptom severity, verbal ability and level of functioning on maternal stress in 43 Greek mothers of children and young people with autism spectrum disorder. Symptom severity was assessed by the CARS, level of functioning by the PEP, temperament by the Dimensions of Temperament Scale (DOTS-R) and maternal stress by the Clarke Modification of Holroyd's Questionnaire on Resources and Stress (QRS). Lower-functioning children and those with high activity level, low flexibility and low mood scores were perceived to be more stressful. Counter to expectation, children with ASD who were rated high on rhythmicity and task orientation were perceived as more stressful. Best predictors of maternal stress were high activity level, low mood and high symptom severity. Mothers of non-verbal children were more stressed than those of verbal. The relevance of child temperament for understanding maternal stress is discussed with particular relevance to the Greek culture and available supports. C1 Univ Guelph, Dept Psychol, Guelph, ON N1G 2W1, Canada. Med Psychopaedol Ctr, Thessaloniki, Greece. RP Konstantareas, MM (reprint author), Univ Guelph, Dept Psychol, Guelph, ON N1G 2W1, Canada. EM mkonstan@uoguelph.ca CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x BEBKO JM, 1987, J AUTISM DEV DISORD, V17, P565, DOI 10.1007/BF01486971 Dodge KA, 2003, DEV PSYCHOL, V39, P349, DOI 10.1037/0012-1649.39.2.349 Eisenberg N, 2001, CHILD DEV, V72, P1112, DOI 10.1111/1467-8624.00337 Eisenberg N, 2002, ADV CHILD DEV BEHAV, V30, P189, DOI 10.1016/S0065-2407(02)80042-8 Frick PJ, 2004, J CLIN CHILD ADOLESC, V33, P2, DOI 10.1207/S15374424JCCP3301_1 Giancola PR, 1998, J ABNORM PSYCHOL, V107, P629, DOI 10.1037/0021-843X.107.4.629 Golding LA, 2003, ACSMS HEALTH FIT J, V7, P3 Goldsmith H.H., 1991, EXPLORATIONS TEMPERA, P249, DOI DOI 10.1007/978-1-4899-0643-4_16 Grych JH, 1999, DEV PSYCHOL, V35, P893, DOI 10.1037//0012-1649.35.4.893 Holroyd J., 1974, J COMMUNITY PSYCHOL, V2, P92, DOI 10.1002/1520-6629(197401)2:1<92::AID-JCOP2290020133>3.0.CO;2-A Honjo S, 1998, EARLY HUM DEV, V51, P123, DOI 10.1016/S0378-3782(97)00102-3 HUNTINGTON GS, 1993, INF MENTAL HLTH J, V14, P49, DOI 10.1002/1097-0355(199321)14:1<49::AID-IMHJ2280140105>3.0.CO;2-B Kasari C, 1997, J AUTISM DEV DISORD, V27, P39, DOI 10.1023/A:1025869105208 KOCHANSKA G, 1993, CHILD DEV, V64, P324 KONSTANTAREAS MM, 1989, J CHILD PSYCHOL PSYC, V30, P459, DOI 10.1111/j.1469-7610.1989.tb00259.x KONSTANTAREAS MM, IN PRESS J AUTISM DE KONSTANTAREAS MM, 1992, J AUTISM DEV DISORD, V22, P217, DOI 10.1007/BF01058152 KRAUSS MW, 1993, AM J MENT RETARD, V97, P393 MARCHANT HJ, 1987, P NIPR S POLAR BIOL, V0001 MAZIADE M, 1990, ARCH GEN PSYCHIAT, V47, P477 PAPAGEORGIOU V, 2002, GOOD AUTISM PRACTICE, V3, P75 Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x RATEKIN C, 1996, DEV DISABILITIES B, V24, P18 Rothbart MK, 2001, CHILD DEV, V72, P1394, DOI 10.1111/1467-8624.00355 ROTHBART MK, 1995, HDB CHILD PSYCHOL, V3 SCHOPLER E, 1976, PSYCHOEDUCATIONAL PR Schopler E., 1988, CHILDHOOD AUTISM RAT Thomas A., 1963, BEHAV INDIVIDUALITY TRUTE B, 1988, J MARITAL FAM THER, V14, P185, DOI 10.1111/j.1752-0606.1988.tb00734.x VAUGHN BE, 1994, AM J MENT RETARD, V98, P607 Windle M., 1992, PSYCHOL ASSESSMENT, V4, P228, DOI 10.1037/1040-3590.4.2.228 Windle M., 1986, J ADOLESCENT RES, V1, P213, DOI 10.1177/074355488612007 WINDLE M, 1989, J PERS ASSESS, V53, P685, DOI 10.1207/s15327752jpa5304_5 NR 35 TC 19 Z9 19 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 NOV PY 2006 VL 10 IS 6 BP 593 EP 607 DI 10.1177/1362361306068511 PG 15 WC Psychology, Developmental SC Psychology GA 109WY UT WOS:000242341500006 PM 17088275 ER PT J AU Knott, F Dunlop, AW MacKay, T AF Knott, Fiona Dunlop, Aline-Wendy MacKay, Tommy TI Living with ASD SO AUTISM LA English DT Article DE autistic spectrum disorders; parent report; self-report; social competence; social skills ID HIGH-FUNCTIONING CHILDREN; AUTISM AB Social interaction and understanding in autistic spectrum disorder (ASD) are key areas of concern to practitioners and researchers alike. However, there is a relative lack of information about the skills and competencies of children and young people with ASD who access ordinary community facilities including mainstream education. In particular, contributions by parents and their children have been under-utilized. Using two structured questionnaires, 19 children with ASD reported difficulties with social skills including social engagement and temper management and also reported difficulties with social competence, affecting both friendships and peer relationships. Parents rated the children's social skill and competence as significantly worse than did the children themselves, but there was considerable agreement about the areas that were problematic. Using an informal measure to highlight their children's difficulties, parents raised issues relating to conversation skills, social emotional reciprocity and peer relationships. The implications for assessment and intervention are discussed. C1 Univ Reading, Sch Psychol, Reading RG6 6AL, Berks, England. Univ Strathclyde, Glasgow G1 1XQ, Lanark, Scotland. RP Knott, F (reprint author), Univ Reading, Sch Psychol, Earley Gate, Reading RG6 6AL, Berks, England. EM f.j.knott@reading.ac.uk CR Bauminger N, 2003, J AUTISM DEV DISORD, V33, P489, DOI 10.1023/A:1025827427901 Bauminger N, 2002, J AUTISM DEV DISORD, V32, P283, DOI 10.1023/A:1016378718278 BAUMINGER N, 2001, RES BASIS AUTISM INT Carter A. S., 2005, HDB AUTISM PERVASIVE, V1 DUNLOP AW, 2002, DEV SOCIAL INTERACTI FEIN D, 1986, J AM ACAD CHILD PSY, V25, P198, DOI 10.1016/S0002-7138(09)60227-2 Gifford-Smith ME, 2003, J SCHOOL PSYCHOL, V41, P235, DOI 10.1016/S0022-4405(03)00048-7 Koning C, 2001, AUTISM, V5, P23, DOI 10.1177/1362361301005001003 LITTLE L, 2002, J AM ACAD CHILD ADOL, V40, P995 Mesman J, 2000, J AM ACAD CHILD PSY, V39, P1371, DOI 10.1097/00004583-200011000-00011 POMEROY C, 1998, ASPERGERS SYNDROME H Rogers SJ, 2000, J AUTISM DEV DISORD, V30, P399, DOI 10.1023/A:1005543321840 Sofronoff K, 2004, AUTISM, V8, P301, DOI 10.1177/136261304045215 Spence S., 2002, CHILD ADOLESCENT MEN, V8, P84 Spence S. H., 1995, SOCIAL SKILLS TRAINI VOLKMAR F, 1997, HDB AUTISM PERVASIVE Wrobel NH, 1998, PSYCHOL SCHOOLS, V35, P17 NR 17 TC 27 Z9 27 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 NOV PY 2006 VL 10 IS 6 BP 609 EP 617 DI 10.1177/1362361306068510 PG 9 WC Psychology, Developmental SC Psychology GA 109WY UT WOS:000242341500007 PM 17088276 ER PT J AU Howard, B Cohn, E Orsmond, GI AF Howard, Brooke Cohn, Ellen Orsmond, Gael I. TI Understanding and negotiating friendships SO AUTISM LA English DT Article DE adolescent; Asperger syndrome; autism; friendship ID HIGH-FUNCTIONING CHILDREN; AUTISM; LONELINESS AB This case study explored perceptions of friendship of an adolescent with Asperger syndrome. Data were collected through semi-structured interviews, photographs taken by the adolescent, and quality of life and friendship measures. Data were analyzed using grounded theory principles and organized into three themes: (1) characteristics of a friend, (2) family involvement, and (3) enjoyment of friendships and desire to have them. The adolescent appeared to enjoy having friends, was interested in pursuing friendships, and had a basic understanding of many characteristics of friendships. He described negotiating his own and his friend's focused interests. Family members played important roles in the establishment and maintenance of the adolescent's friendships. C1 Boston Univ, Boston, MA 02215 USA. RP Howard, B (reprint author), 429 Norfolk St 11, Somerville, MA 02143 USA. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bauminger N, 2003, J AUTISM DEV DISORD, V33, P489, DOI 10.1023/A:1025827427901 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Bauminger N, 2003, AUTISM, V7, P81, DOI 10.1177/1362361303007001007 BIGELOW BJ, 1975, DEV PSYCHOL, V11, P105 BOIVIN M, 1994, J SOCIAL PERSONAL RE, V11, P471 BUHRMESTER D, 1990, CHILD DEV, V61, P1101, DOI 10.1111/j.1467-8624.1990.tb02844.x CESARONI L, 1991, J AUTISM DEV DISORD, V21, P303, DOI 10.1007/BF02207327 Geisthardt CL, 2002, EDUC TRAIN MENT RET, V37, P235 Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hurlbutt K., 2002, FOCUS AUTISM OTHER D, V17, P103, DOI [10.1177/10883576020170020501, DOI 10.1177/10883576020170020501] JACKSON L, 2000, FREAKS GEEKS ASPERGE Jones R. S. P., 2001, J LEARNING DISABILIT, V5, P35, DOI DOI 10.1177/146900470100500104 LAWSON W, 2001, LIFE BEHIND GLASS PE Lawson W, 2003, LEARNING AND BEHAVIOR PROBLEMS IN ASPERGER SYNDROME, P177 Mounts N., 2000, FAMILY PEERS LINKING, P169 NEWCOMB AF, 1995, PSYCHOL BULL, V117, P306, DOI 10.1037//0033-2909.117.2.306 Patrick DL, 2002, J ADOLESCENCE, V25, P287, DOI 10.1006/yjado.471 Stoddart K, 1999, AUTISM, V3, P255, DOI DOI 10.1177/1362361399003003004 Strauss A., 1998, BASICS QUALITATIVE R Wang C, 1997, HEALTH EDUC BEHAV, V24, P369, DOI 10.1177/109019819702400309 NR 21 TC 13 Z9 13 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 NOV PY 2006 VL 10 IS 6 BP 619 EP 627 DI 10.1177/1362361306068508 PG 9 WC Psychology, Developmental SC Psychology GA 109WY UT WOS:000242341500008 PM 17088277 ER PT J AU Benderix, Y Nordstrom, B Sivberg, B AF Benderix, Ylva Nordstrom, Berit Sivberg, Bengt TI Parents' experience of having a child with autism and learning disabilities living in a group home - A case study SO AUTISM LA English DT Article DE autism; exhaustion; group home; parents; respite; Sweden ID STRESS AB Some children with autism and learning disabilities also have aberrant behaviours that are difficult to regulate and stressful for both the child and family members. This case study concerns experiences of 10 parents from five families before and 2 years after entrusting their 10- to 11-year-old child with autism to a group home. Hermeneutic phenomenological analysis of narrative interviews with the parents before the child's moving showed them experiencing grief and sorrow, total exhaustion because of inability to regulate their child's behaviours, social isolation, and negative effects on the child's siblings, but experiencing themselves as more sympathetic than previously towards other people with problems. Two years later they experienced relief for the family due to the group home arrangement and the child's improvement, but with an ethical dilemma which made them feel guilty, despite increased hope for the future. Some also felt unhappy with the staff situation at the group home. C1 Lund Univ, Fac Med, Div Hlth Sci, SE-22100 Lund, Sweden. RP Benderix, Y (reprint author), Lund Univ, Fac Med, Div Hlth Sci, POB 157, SE-22100 Lund, Sweden. EM ylva.benderix@med.lu.se CR BAGENHOLM A, 1991, J MENTAL DEFICIENCY, V35, P210 Banks Martha E, 2003, Cultur Divers Ethnic Minor Psychol, V9, P367, DOI 10.1037/1099-9809.9.4.367 BENDERIX Y, 2004, IN PRESS J PEDIA MAY Dumas J. 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N., 2005, VOICES SPECTRUM PARE 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 NOV PY 2006 VL 10 IS 6 BP 643 EP 644 DI 10.1177/1362361306068513 PG 2 WC Psychology, Developmental SC Psychology GA 109WY UT WOS:000242341500010 ER PT J AU Stein, CM Millard, C Kluge, A Miscimarra, LE Cartier, KC Freebairn, LA Hansen, AJ Shriberg, LD Taylor, HG Lewis, BA Iyengar, SK AF Stein, Catherine M. Millard, Christopher Kluge, Amy Miscimarra, Lara E. Cartier, Kevin C. Freebairn, Lisa A. Hansen, Amy J. Shriberg, Lawrence D. Taylor, H. Gerry Lewis, Barbara A. Iyengar, Sudha K. TI Speech sound disorder influenced by a locus in 15q14 region SO BEHAVIOR GENETICS LA English DT Article DE phonology; speech; language; parent-of-origin; allele-sharing ID PRADER-WILLI-SYNDROME; QUANTITATIVE-TRAIT LOCUS; AUTISM SUSCEPTIBILITY GENES; FAMILY-BASED ASSOCIATION; LANGUAGE IMPAIRMENT; DEVELOPMENTAL DYSLEXIA; READING-DISABILITY; CHROMOSOME 7Q; ANGELMAN-SYNDROME; CANDIDATE GENE AB Despite a growing body of evidence indicating that speech sound disorder (SSD) has an underlying genetic etiology, researchers have not yet identified specific genes predisposing to this condition. The speech and language deficits associated with SSD are shared with several other disorders, including dyslexia, autism, Prader-Willi Syndrome (PWS), and Angelman's Syndrome ( AS), raising the possibility of gene sharing. Furthermore, we previously demonstrated that dyslexia and SSD share genetic susceptibility loci. The present study assesses the hypothesis that SSD also shares susceptibility loci with autism and PWS. To test this hypothesis, we examined linkage between SSD phenotypes and microsatellite markers on the chromosome 15q14-21 region, which has been associated with autism, PWS/AS, and dyslexia. Using SSD as the phenotype, we replicated linkage to the 15q14 region (P = 0.004). Further modeling revealed that this locus influenced oral-motor function, articulation and phonological memory, and that linkage at D15S118 was potentially influenced by a parent-of-origin effect (LOD score increase from 0.97 to 2.17, P = 0.0633). These results suggest shared genetic determinants in this chromosomal region for SSD, autism, and PWS/AS. C1 Case Western Reserve Univ, Dept Epidemiol & Biostat, Cleveland, OH 44106 USA. Case Western Reserve Univ, Rainbow Babies & Childrens Hosp, Dept Pediat, Cleveland, OH 44106 USA. Univ Wisconsin, Waisman Ctr, Madison, WI 53706 USA. RP Iyengar, SK (reprint author), Case Western Reserve Univ, Dept Epidemiol & Biostat, Wolstein Res Bldg,Room 1315,2103 Cornell Rd, Cleveland, OH 44106 USA. 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Genet. PD NOV PY 2006 VL 36 IS 6 BP 858 EP 868 DI 10.1007/s10519-006-9090-7 PG 11 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 210IC UT WOS:000249448900006 PM 16786424 ER PT J AU Jones, EA Carr, EG Feeley, KM AF Jones, Emily A. Carr, Edward G. Feeley, Kathleen M. TI Multiple effects of joint attention intervention for children with autism SO BEHAVIOR MODIFICATION LA English DT Article DE autism; joint attention; discrete trial instruction; pivotal response training ID COMMUNICATION-SKILLS; BEHAVIOR; INFANTS; PEERS; DELAY AB Joint attention refers to an early developing set of behaviors that plays a critical role in both social and language development and is specifically impaired in children with autism. In a series of three studies, preschool teachers demonstrated the effectiveness of discrete trial instruction and pivotal response training strategies to teach joint attention to 5 children with autism (Study 1). Parents of 2 of the 5 children also taught joint attention at home and in the community (Study 2). Several additional dependent measures demonstrated collateral improvements in expressive language and social-communicative characteristics that were socially validated by parent raters (Study 3). Results are discussed with respect to the importance of addressing different forms of joint attention, the necessity to extend intervention to naturalistic contexts and joint attention partners, the pivotal nature of joint attention, and whether intervention adequately addresses both the form and social function of joint attention. C1 Long Isl Univ, Dept Psychol, Brookville, NY 11548 USA. SUNY Stony Brook, Dept Psychol, Dev Disabil Inst, Stony Brook, NY 11794 USA. 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Modificat. PD NOV PY 2006 VL 30 IS 6 BP 782 EP 834 DI 10.1177/0145445506289392 PG 53 WC Psychology, Clinical SC Psychology GA 093JE UT WOS:000241163800003 PM 17050765 ER PT J AU Carr, EG Blakeley-Smith, A AF Carr, Edward G. Blakeley-Smith, Audrey TI Classroom intervention for illness-related problem behavior in children with developmental disabilities SO BEHAVIOR MODIFICATION LA English DT Article DE autism; problem behavior; illness; classroom intervention ID ADULTS AB There is growing evidence of an association between physical illness and problem behavior in children with developmental disabilities. Such behavior can compromise school performance. Therefore, the purpose of the present study was to evaluate, using a group design, the effectiveness of medical intervention alone (N = 11) versus behavioral plus medical intervention (N = 10) for illness-related problem behavior in a school setting. Following intervention, the behavioral plus medical intervention group showed lower levels of problem behavior and completed more academic tasks than did the medical intervention alone group. The results are discussed with respect to the concept of illness and pain as a setting event for problem behavior. The need for research to develop algorithms that allow one to select the best combination of medical and behavioral interventions for specific illnesses and contexts is noted. C1 SUNY Stony Brook, Dept Psychol, Dev Disabil Inst, Stony Brook, NY 11794 USA. Univ Colorado Denver & Hlth Sci Ctr, Dept Psychiat, Denver, CO USA. RP Carr, EG (reprint author), SUNY Stony Brook, Dept Psychol, Dev Disabil Inst, Stony Brook, NY 11794 USA. CR AMAN MG, 1985, AM J MENT DEF, V89, P492 Bijou S. W., 1961, CHILD DEV Bosch J, 1997, MENT RETARD, V35, P124, DOI 10.1352/0047-6765(1997)035<0124:ROMCIT>2.0.CO;2 Bruininks R. 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Parvenski, Tom TI The River Street Autism Program - A case study of a regional service center behavioral intervention program SO BEHAVIOR MODIFICATION LA English DT Article DE autism; early intensive behavioral intervention; quality programming; quality of life ID CHILDREN; LANGUAGE; INDIVIDUALS AB An urgent demand from Connecticut parents for behavioral intervention resulted in the development of the River Street Autism Program (RSAP). This research-to-practice program implements intervention service based on empirical research findings conducted with children diagnosed with autism and pervasive developmental disorders. RSAP is provided through a regional service center and provides services for children entering the program at 2 to 5 years old. Because of the diverse nature of the districts served by RSAP, the delivered services varied according to the needs of the districts, available funding, and family preferences. Program evaluation data were therefore examined with regard to outcomes for children who received programs with differing numbers of treatment components. Treatment components that varied across children were treatment intensity, duration, extent of family participation, staff training, and supervision. Outcome data revealed that families reported greater gains in child functioning and quality of life when children received programs with more treatment components. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey DB, 1998, EXCEPT CHILDREN, V64, P313 CHARLOP MH, 1985, J APPL BEHAV ANAL, V18, P155, DOI 10.1901/jaba.1985.18-155 *CONN STAT DEP ED, 2002, CLASS SPEC ED TABL 2 *CONN STAT DEP ED, 1998, REP CONN TAST FORC I Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 DYER K, 1990, J APPL BEHAV ANAL, V23, P515, DOI 10.1901/jaba.1990.23-515 DYER K, 1989, J ASSOC PERS SEVERE, V14, P184 DYER K, 1987, RES DEV DISABIL, V8, P606 DYER K, 1987, J SPEECH HEAR DISORD, V52, P335 DYER K, 1996, INNOVATIONS, P345 Egel A. 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Modificat. PD NOV PY 2006 VL 30 IS 6 BP 925 EP 943 DI 10.1177/0145445506291395 PG 19 WC Psychology, Clinical SC Psychology GA 093JE UT WOS:000241163800009 PM 17050771 ER PT J AU Casey, SD Merical, CL AF Casey, Sean D. Merical, Cheryl L. TI The use of functional communication training without additional treatment procedures in an inclusive school setting SO BEHAVIORAL DISORDERS LA English DT Article ID INTERMITTENT REINFORCEMENT; NEGATIVE REINFORCEMENT; DISRUPTIVE BEHAVIOR; EXTINCTION; MAINTENANCE; CHILDREN; INTERVENTION; ACQUISITION; PUNISHMENT; AUTISM AB Functional communication training (FCT) is an intervention frequently used for students with developmental disabilities to reduce problematic behaviors and to increase prosocial behaviors. This intervention appears to be very effective when the communication responses trained are matched to the function of the student's problematic behaviors. In most cases, however, FCT is implemented as part of an intervention package. As a result, there is little research showing FCT to be effective without additional treatment components. In this investigation, the results of a brief functional analysis conducted with a student with autism in an inclusive school setting revealed that the student's self-injury served as a negative reinforcement function. We used a multiple baseline design across classrooms to evaluate the effects of FCT in the absence of augmentative procedures. The results of this study indicate that ameliorating the student's self-injury occurred with implementing the FCT procedure in isolation, providing growing support for using FCT without augmentative procedures. C1 Penn State Univ, Malvern, PA 19355 USA. RP Casey, SD (reprint author), Penn State Univ, 30 E Swedesford Rd, Malvern, PA 19355 USA. 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Disord. PD NOV PY 2006 VL 32 IS 1 BP 46 EP 54 PG 9 WC Psychology, Clinical; Psychology, Educational SC Psychology GA 175CP UT WOS:000246990500004 ER PT J AU Butter, EM Mulick, JA Metz, B AF Butter, Eric M. Mulick, James A. Metz, Bernard TI Eight case reports of learning recovery in children with pervasive developmental disorders after early intervention SO BEHAVIORAL INTERVENTIONS LA English DT Article ID INTENSIVE BEHAVIORAL TREATMENT; AUTISM; MODEL AB Early intensive behavioral intervention (EIBI) is often recommended for children with Pervasive Developmental Disorders (PDD). It is an empirically supported treatment designed to address the core symptoms of autism including language delays, social and play skills, and restricted and repetitive behaviors as well as other related deficits in cognition and adaptive behavior. Though there are a growing number of research studies supporting EIBI, many questions remain about the nature and stability of best outcomes. The current study provides case descriptions of eight children previously diagnosed with an autism spectrum disorder and mental retardation who, after EIBI treatment, no longer met behavioral criteria for mental retardation or a PDD. The average gain in IQ standard scores was 34.6 (+/- 13.2) points; and, the average gain in adaptive behavior standard scores was 43 (+/- 25.3) points. Nonverbal IQ standard scores (mean = 93 +/- 12.6) and academic achievement standard scores (mean = 105.3 +/- 18.7) ended within the average range. Language skills remained impaired for seven children. The cases support findings of other researchers that learning recovery in autism and PDD is possible and may be related to intensive behavioral treatment. Individual differences in response to EIBI treatment are discussed. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Ohio State Univ, Columbus, OH 43210 USA. 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TI Using analog assessment procedures for determining the effects of a gluten-free and casein-free diet on rate of problem behaviors for an adolescent with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article ID FUNCTIONAL-ANALYSIS; SELF-INJURY AB The behavioral effects of a gluten/casein-free diet were evaluated for an adolescent with autism who displayed several forms of aberrant behavior. An analog assessment was used to measure behavioral response rates within four conditions with type of diet controlled using a BABA design. Results suggested that a gluten/casein-free diet did not serve as an abolishing operation for assessed problem behaviors. Both the limitations and generality of this finding are discussed. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Murdoch Ctr, Psychol Serv, Butner, NC 27509 USA. RP Irvin, DS (reprint author), Murdoch Ctr, Psychol Serv, POB 3000,1600 E C St, Butner, NC 27509 USA. EM hserve@aol.com CR IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 KNIVSBERG AM, 2002, J HUMAN NUTR DIETETI, V15, P261 OReilly MF, 1997, J APPL BEHAV ANAL, V30, P165, DOI 10.1901/jaba.1997.30-165 SHATTOCK P, 2000, EXPERT OPINION THERA, V6, P175 SHAW W, 2002, BIOL TREATMENTS AUTI, P79 NR 5 TC 5 Z9 5 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD NOV PY 2006 VL 21 IS 4 BP 281 EP 286 DI 10.1002/bin.205 PG 6 WC Psychology, Clinical SC Psychology GA 114OU UT WOS:000242676300005 ER PT J AU Bidaud, I Mezghrani, A Swayne, LA Monteil, A Lory, P AF Bidaud, Isabelle Mezghrani, Alexandre Swayne, Leigh Anne Monteil, Arnaud Lory, Philippe TI Voltage-gated calcium channels in genetic diseases SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH LA English DT Article; Proceedings Paper CT 9th European Symposium on Calcium-Binding Proteins in Normal and Transformed Cells CY JUL 19-22, 2006 CL Strasbourg, FRANCE HO Ecole Superieure Biotechnol DE calcium channelopathies; hypokalemic periodic paralysis; long QT syndrome; ataxia; migraine; epilepsy; autism ID HYPOKALEMIC PERIODIC PARALYSIS; EPISODIC ATAXIA TYPE-2; IDIOPATHIC GENERALIZED EPILEPSY; FAMILIAL HEMIPLEGIC MIGRAINE; STATIONARY NIGHT BLINDNESS; CHILDHOOD ABSENCE EPILEPSY; SKELETAL-MUSCLE; PROGRESSIVE ATAXIA; CA2+ CHANNELS; MOUSE MODELS AB Voltage-gated calcium channels (VGCCs) mediate calcium entry into excitable cells in response to membrane depolarization. During the past decade, our understanding of the gating and functions of VGCCs has been illuminated by the analysis of mutations linked to a heterogeneous group of genetic diseases called "calcium channelopathies". Calcium channelopathies include muscular, neurological, cardiac and vision syndromes. Recent data suggest that calcium channelopathies result not only from electrophysiological defects but also from altered alpha(1)/Ca-v subunit protein processing, including folding, posttranslational modifications, quality control and trafficking abnormalities. Overall, functional analyses of VGCC mutations provide a more comprehensive view of the corresponding human disorders and offer important new insights into VGCC function. Ultimately, the understanding of these pathogenic channel mutations should lead to improved treatments of such hereditary diseases in humans. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Montpellier 1, INSERM, CNRS, UMR 5203,U661,IGF,Dept Physiol, F-34094 Montpellier 05, France. Univ Montpellier 2, INSERM, CNRS, UMR 5203,U661,IGF,Dept Physiol, F-34094 Montpellier, France. RP Lory, P (reprint author), Univ Montpellier 1, INSERM, CNRS, UMR 5203,U661,IGF,Dept Physiol, 141 Rue Cardonille, F-34094 Montpellier 05, France. 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SO BIOLOGICAL PSYCHIATRY LA English DT Article DE attention; autism spectrum disorders; bipolar disorder; cauclate volume; executive function; neuroimaging ID ASPERGERS-SYNDROME; BIPOLAR DISORDER; BASAL GANGLIA; EXECUTIVE DYSFUNCTION; GROWTH-PATTERNS; YOUNG-CHILDREN; ANATOMICAL MRI; HUMAN BRAIN; AUTISM; ATTENTION AB Background: Impaired neuropsychological test performance, especially on tests of executive function and attention, is often seen in children diagnosed with autism spectrum disorders (ASD). Structures involved in fronto-striatal circuitry, such as the caudate nucleus, may support these cognitive abilities. However, few studies have examined caudate volumes specifically in children with ASD, or correlated caudate volumes to cognitive ability. Methods: Neuropsychological test scores and caudate volumes of children with ASD were compared to those of children with bipolar disorder (BD) and of typically developing (TD) children. The relationship between test performance and caudate volumes was analyzed. Results. The ASD group displayed larger Tight and left caudate volumes, and modest executive deficits, compared to ID controls. While caudate volume inversely predicted performance on the Wisconsin Card Sorting Test in all participants, it differentially predicted performance on measures of attention across the ASD, BD and TD groups. Conclusions. Larger caudate volumes were related to impaired problem solving. On a test of attention, larger left caudate volumes predicted increased impulsivity and more omission errors in the ASD group as compared to the TD group, however smaller volume predicted poorer discriminant responding as compared to the BD group. C1 Rutgers State Univ, Ctr Alcohol Studies, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Dept Psychiat, Newark, NJ 07103 USA. Janssen Pharmaceut Inc, Trenton, NJ USA. Univ Calif Davis, Dept Psychiat, Davis, CA 95616 USA. 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Psychiatry PD NOV 1 PY 2006 VL 60 IS 9 BP 942 EP 950 DI 10.1016/j.biopsych.2006.03.071 PG 9 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 100TL UT WOS:000241691600007 PM 16950212 ER PT J AU Castelli, F AF Castelli, Fulvia TI The Valley task: Understanding intention from goal-directed motion in typical development and autism SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID ATTRIBUTION; CHILDREN; MIND AB A novel paradigm investigates the ability to understand an agent's intended goal in children with autism (N = 25), typically developing children (N = 46), and adults (N = 16 + 12) by watching a non-human agent's kinematic properties alone. Computer animations depict a circle at the bottom of a U-shaped valley rolling up and down its slopes and getting closer to a target resting at the top of either side of the valley. The circle's persistent motion and improving attempts evoke the attribution of the intention to reach the target, regardless of whether the circle fails or attains its goal. Children with autism are as able as controls to infer an agent's intended-goal, disregarding its failure to reach the target. In addition, the study showed that the perception of persistent motion is a sufficient but not a necessary cue for very young children and children with autisn to attribute intention to an agent, whereas adults consider the persistent motion cue as a sufficient and necessary cue to attribute intention to an agent. C1 CALTECH, Div Humanities & Social Sci, Pasadena, CA 91125 USA. RP Castelli, F (reprint author), CALTECH, Div Humanities & Social Sci, Pasadena, CA 91125 USA. EM fulvia@hss.caltech.edu CR ABELL F, 2000, J COGNITIVE DEV, V15, P1 Aldridge MA, 2000, DEVELOPMENTAL SCI, V3, P294, DOI 10.1111/1467-7687.00123 Baron-Cohen S, 1993, UNDERSTANDING OTHER BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Bowler D, 2000, AUTISM, V4, P147, DOI 10.1177/1362361300004002004 Carpenter M, 2001, J AUTISM DEV DISORD, V31, P589, DOI 10.1023/A:1013251112392 Castelli F, 2002, BRAIN, V125, P1839, DOI 10.1093/brain/awf189 Csibra G, 1999, COGNITION, V72, P237, DOI 10.1016/S0010-0277(99)00039-6 GERGELY G, 1995, COGNITION, V56, P165, DOI 10.1016/0010-0277(95)00661-H HEIDER F, 1944, AM J PSYCHOL, V57, P1377 Klin A, 2000, J CHILD PSYCHOL PSYC, V41, P831, DOI 10.1017/S0021963099006101 Leslie A.M., 1994, MAPPING MIND DOMAIN Meltzoff AN, 1995, DEV PSYCHOL, V31, P1, DOI DOI 10.1037/0012-1649.31.5.838 Michotte A., 1963, PERCEPTION CAUSALITY Montgomery DE, 1999, BRIT J DEV PSYCHOL, V17, P245, DOI 10.1348/026151099165258 Perner J, 1989, Child Dev, V60, P688 Phillips W, 1998, BRIT J DEV PSYCHOL, V16, P337 PREMACK D, 1994, MAPPING MIND DOMAIN Russell J, 2001, J CHILD PSYCHOL PSYC, V42, P317, DOI 10.1017/S0021963001006874 Wellman HM, 2001, CHILD DEV, V72, P655, DOI 10.1111/1467-8624.00304 NR 21 TC 6 Z9 6 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0261-510X J9 BRIT J DEV PSYCHOL JI Br. J. Dev. Psychol. PD NOV PY 2006 VL 24 BP 655 EP 668 DI 10.1348/026151005X54209 PN 4 PG 14 WC Psychology, Developmental SC Psychology GA 106HB UT WOS:000242090500001 ER PT J AU Whitehouse, AJO Maybery, MT Durkin, K AF Whitehouse, Andrew J. O. Maybery, Murray T. Durkin, Kevin TI The development of the picture-superiority effect SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID VISUAL COMPLEXITY; NAME AGREEMENT; CHILDREN; NORMS; PERFORMANCE; FAMILIARITY; AUTISM; SPEECH; MEMORY; WORDS AB When pictures and words are presented serially in an explicit memory task, recall of the pictures is superior. While this effect is well established in the adult population, little is known of the development of this picture-superiority effect in typical development. This task was administered to 80 participants from middle childhood to adolescence. The magnitude of the picture superiority effect increased with age. 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TI Digit ratio and faculty membership: Implications for the relationship between prenatal testosterone and academia SO BRITISH JOURNAL OF PSYCHOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME; FINGER-LENGTH; CEREBRAL LATERALIZATION; FETAL TESTOSTERONE; SPATIAL COGNITION; HAND PREFERENCE; 2ND; CHILDREN AB Digit ratio (length of index finger divided by length of ring finger) is an index of exposure to prenatal testosterone. Prenatal testosterone slows the growth rate of the left side of the brain while enhancing growth of the right side. Right hemisphere processing is associated with better visual-spatial and mathematical abilities, as is digit ratio. Thus, traditional sex differences in visual-spatial and mathematical abilities can be attributed to differences in exposure to prenatal testosterone, indexed by a sex dimorphic pattern in digit ratio (female = 1.00, male = 0.98 for UK samples). Additionally, the digit ratio is a marker for within-sex variance in visual-spatial ability. This study examines the digit ratio of an academic sample. No sex differences are found and there is a significant difference between the Science Faculty and Social Science Faculty. Social Scientists of both sexes have a ratio consistent with the male norm (0.98) whilst Scientists have a digit ratio consistent with the female norm (1.00). These results are discussed in terms of the lower normal range of male testosterone being associated with highest visual spatial abilities. Relationships with fertility and Dyslexia are also identified. C1 Univ Bath, Dept Psychol, Bath BA2 7AY, Avon, England. RP Brosnan, MJ (reprint author), Univ Bath, Dept Psychol, Bath BA2 7AY, Avon, England. 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J. Psychol. PD NOV PY 2006 VL 97 BP 455 EP 466 DI 10.1348/000712605X85808 PN 4 PG 12 WC Psychology, Multidisciplinary SC Psychology GA 103ZJ UT WOS:000241925400002 PM 17018183 ER PT J AU Fletcher-Watson, S Leekam, SR Turner, MA Moxon, L AF Fletcher-Watson, S. Leekam, S. R. Turner, M. A. Moxon, L. TI Do people with autistic spectrum disorder show normal selection for attention? Evidence from change blindness SO BRITISH JOURNAL OF PSYCHOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; WEAK CENTRAL COHERENCE; DETECT CHANGES; CHILDREN; INDIVIDUALS; SCENES; DISENGAGEMENT; ADOLESCENTS; INFORMATION; PRECEDENCE AB People in the general population are typically very poor at detecting changes in pictures of complex scenes. The degree of this 'change blindness', however, varies with the content of the scene: when an object is semantically important or contextually inappropriate, people may be more effective at detecting changes. Two experiments investigated change blindness in people with autism, who are known from previous research to be efficient in detecting features yet poor at processing stimuli for meaning and context. The first experiment measured the effect of semantic information while the second investigated the role of context in directing attention., In each task, participants detected the dissimilarity between pairs of images. Both groups showed a main effect of image type in both experimental tasks, showing that their attention was directed to semantically meaningful and contextually inappropriate items. However, the autistic group also showed a greater difficulty detecting changes to semantically marginal items in the first experiment. Conclusions point to a normal selection of items for attention in people with autism spectrum disorders, although this may be combined with difficulty switching or disengaging attention. C1 Univ Durham, Dept Psychol, Sci Labs, Durham DH1 3LE, England. 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J. Neurol. Sci. PD NOV PY 2006 VL 33 IS 4 BP 339 EP 340 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 106NX UT WOS:000242108700001 PM 17168157 ER PT J AU Doja, A Roberts, W AF Doja, Asif Roberts, Wendy TI Immunizations and autism: A review of the literature SO CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES LA English DT Review ID THIMEROSAL-CONTAINING VACCINES; INFLAMMATORY-BOWEL-DISEASE; DEVELOPMENTAL DISORDERS; RUBELLA VACCINATION; SPECTRUM DISORDER; EPIDEMIOLOGIC EVIDENCE; CAUSAL ASSOCIATION; MEASLES; CHILDREN; MUMPS AB Because of a temporal correlation between the first notable signs and symptoms of autism and the routine childhood vaccination schedule, many parents have become increasingly concerned regarding the possible etiologic role vaccines may play in the development of autism. In particular, some have suggested all association between the Measles-Mumps-Rubella vaccine and autism. Our literature review found very few Studies supporting this theory, with the overwhelming majority showing no causal association between the Measles-Mumps-Rubella vaccine and autism. The vaccine preservative thimerosal has alternatively been hypothesized to have a possible causal role in autism. Again, no convincing evidence was found to support this claim, nor for the use of chelation therapy in autism. With decreasing uptake of immunizations in children and the inevitable occurrence of measles outbreaks, it is important that clinicians be aware of the literature concerning vaccinations and autism so that they may have informed discussions with parents and caregivers. C1 Childrens Hosp Eastern Ontario, Div Neurol, Ottawa, ON K1H 8L1, Canada. Hosp Sick Children, Div Dev Paediat, Toronto, ON M5G 1X8, Canada. RP Doja, A (reprint author), Childrens Hosp Eastern Ontario, Div Neurol, 401 Smyth Rd, Ottawa, ON K1H 8L1, Canada. 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J. Neurol. Sci. PD NOV PY 2006 VL 33 IS 4 BP 341 EP 346 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 106NX UT WOS:000242108700002 PM 17168158 ER PT J AU Gastgeb, HZ Strauss, MS Minshew, NJ AF Gastgeb, Holly Zajac Strauss, Mark S. Minshew, Nancy J. TI Do individuals with autism process categories differently? The effect of typicality and development SO CHILD DEVELOPMENT LA English DT Article; Proceedings Paper CT Biennial Meeting of the Society-for-Research-in-Child-Development CY APR 07-10, 2005 CL Atlanta, GA SP Soc Res Child Dev ID INFANT FORM CATEGORIES; FUSIFORM FACE AREA; LEVEL CATEGORIZATION; CHILDREN; RECOGNITION; ADULTS; INFORMATION; PERCEPTION; DEFICITS; SKILLS AB This study examined the effect of exemplar typicality on reaction time and accuracy of categorization. High-functioning children (age 9-12), adolescents (age 13-16), and adults with autism (age 17-48) and matched controls were tested in a category verification procedure. 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PD NOV-DEC PY 2006 VL 77 IS 6 BP 1717 EP 1729 DI 10.1111/j.1467-8624.2006.00969.x PG 13 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 104JM UT WOS:000241954700015 PM 17107456 ER PT J AU Farrant, BM Fletcher, J Maybery, MT AF Farrant, Brad M. Fletcher, Janet Maybery, Murray T. TI Specific language impairment, theory of mind, and visual perspective taking: Evidence for simulation theory and the developmental role of language SO CHILD DEVELOPMENT LA English DT Article ID FALSE BELIEF; CHILDRENS KNOWLEDGE; AUTISM; CONSCIOUSNESS; CHIMPANZEES; COGNITION AB Recent research has found that the acquisition of theory of mind (ToM) is delayed in children with specific language impairment (SLI). The present study used a battery of ToM and visual perspective taking (VPT) tasks to investigate whether the delayed acquisition of ToM in children with SLI is associated with delayed VPT development. 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PD NOV-DEC PY 2006 VL 77 IS 6 BP 1842 EP 1853 DI 10.1111/j.1467-8624.2006.00977.x PG 12 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 104JM UT WOS:000241954700023 PM 17107464 ER PT J AU Guillem, P Cans, C Guinchat, V Ratel, M Jouk, PS AF Guillem, Pascale Cans, Christine Guinchat, Vincent Ratel, Marc Jouk, Pierre-Simon TI Trends, perinatal characteristics, and medical conditions in pervasive developmental disorders SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID INFANTILE-AUTISM; RISK-FACTORS; FRENCH CLASSIFICATION; EPIDEMIOLOGIC SURVEY; POPULATION; PREVALENCE; REGISTER; CHILDREN AB Our aim was to study trends in the prevalence of pervasive developmental disorders (PDD) and to quantify their association with morphogenetic anomalies and with perinatal characteristics such as gestational age, birthweight, and hospitalization in a neonatal care unit. Data from a French morbidity register of childhood disabilities with the use of consistent definitions over time within the same geographical area were analyzed. The data of a total of 454 children (312 males, 142 females) with PDD, born between 1980 and 1993 and residing in Isere county, were recorded at the age of 7 years. The overall prevalence of PDD was 22.2 out of every 10 000. There was a significant increase, from 14.7 to 30.8 out of every 10 000, during the period of study. Among these children with PDD, morphogenetic anomalies were observed in 12.1% (95% confidence interval [CI] 9.3-15.5), and the hospitalization rate during the neonatal period was 22% (95% CI 17.0-27.5), which is significantly higher than the observed rates in the general population. The increase in the prevalence of PDD, the association with perinatal risk factors, and the high rate of neonatal hospitalization require further studies to investigate the reasons for and mechanisms of these developmental disorders. C1 RHEOP Isere, Ctr Dept Sante, F-38000 Grenoble, France. Grenoble Univ Hosp, Dept Med Informat & Data Proc, Grenoble, France. Grenoble Univ Hosp, Dept Psychiat, Grenoble, France. Grenoble Univ Hosp, Unit Childhood Psychiat, Dept Psychiat, Grenoble, France. Grenoble Univ Hosp, Dept Genet, Grenoble, France. RP Guillem, P (reprint author), RHEOP Isere, Ctr Dept Sante, 23 Ave Albert 1er Belgique, F-38000 Grenoble, France. 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Med. Child Neurol. PD NOV PY 2006 VL 48 IS 11 BP 896 EP 900 DI 10.1017/S0012162206001964 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 102RN UT WOS:000241831100009 PM 17044957 ER PT J AU Tordjman, S AF Tordjman, S. TI From a categorical diagnostic approach to a dimensional approach for mental disorders : interest of sex differences SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE anorexia; autistic disorder; communication; emotional expression; sex differences; social interaction ID PLAY-BEHAVIOR; AUTISM; SOCIALIZATION; EXPRESSION; TODDLERS; GIRLS; BOYS AB A strong prevalence of females or males is often found in mental disorders. Based on examples of anorexia (90% females) and autistic disorder (80 to 90% males), arguments that allow a better understanding of these different sex ratios are presented. The role of certain sociocultural factors in the onset of anorexia is developed. The predominance of males in autistic disorder has led to genetic and hormone-based biological hypotheses. However, it is also possible that the cultural representation of sex roles and its effects (expectation, different attitudes and behaviors depending on the child's gender) influence the development of social interaction and communication domains which are impaired in autistic disorder. Indeed, according to most studies, parents solicit and stimulate more social interaction and communication (eye contact specially during the first months of life, vocalizations then verbal language, emotional expression) in girls than in boys during the first three years of life, which corresponds to the period when autistic disorder appears. It is possible that because girls are more solicited than boys in social interaction and communication domains, during a sensitive (or critical) period of development, we may observe that girls show less autistic impairment in reciprocal social interaction and verbal or non-verbal communication, which are two of the three main domains of autistic disorder. It is also possible that impairments in social interaction and communication maybe identified earlier for girls than for boys, which could lead to earlier therapeutic care for girls. Indeed, if parents have greater expectations for girls in social interaction and/or communication domains, they may worry more for their girl than for their boy with regard to developmental delay in these domains, and then may ask for professional advice earlier. This is what we have observed in our clinical practice and research, in which we conducted a follow-up in young girls showing autistic disorder aged two and half years old and who evolved positively; in contrast we have observed that parents bring their son for professional advice later, after kindergarten begins. Finally, a more complex, non-linear model is proposed in which biological genetic factors (such as sex-linked chromosomes) and/or hormonal factors (such as sex hormones) may play a role in differentiation of girls' and boys' behavior from birth. These different behaviors would induce differentiated expectations and attitudes in parents depending on the child's gender, which in turn would reinforce sex-related characteristic behaviors in the child. Thus, there may be a continuum in different behavioral domains (for example, boys would interact and communicate less than girls, and girls would express more their emotions), with mental disorders occurring at the extremes of this continuum (for example, autistic disorder for certain boys and anxiety disorder for certain girls). This hypothesis fits within an integrated psycho-biological approach that takes into account sex differences in mental disorders; it stems from a model in which a dimensional conception of mental disorders replaces a categorical nosographical one. New perspectives could be envisioned concerning the identification, follow-up and treatment of mental disorders (or sub-types of mental disorders), which are currently considered to belong to different nosographical categories, but which could overlap through shared common dimensions. C1 Hosp Univ Psychiat Enfant Adolescent Rennes, Ctr Hosp Guillaume Regnier, F-35000 Rennes, France. Univ Rennes 1, F-35014 Rennes, France. CNRS, UMR 7593, F-75700 Paris, France. RP Tordjman, S (reprint author), Hosp Univ Psychiat Enfant Adolescent Rennes, Ctr Hosp Guillaume Regnier, 154 Rue Chatillon, F-35000 Rennes, France. 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PD NOV-DEC PY 2006 VL 32 IS 6 BP 988 EP 994 PN 1 PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 146WH UT WOS:000244964900009 PM 17372544 ER PT J AU Auyeung, B Baron-Cohen, S Chapman, E Knickmeyer, R Taylor, K Hackett, G AF Auyeung, Bonnie Baron-Cohen, Simon Chapman, Emma Knickmeyer, Rebecca Taylor, Kevin Hackett, Gerald TI Foetal testosterone and the child systemizing quotient SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Article; Proceedings Paper CT 4th Ferring Pharmaceuticals International Paediatric Endocrinology Symposium CY 2006 CL Paris, FRANCE SP Ferring Pharmaceut ID CONGENITAL ADRENAL-HYPERPLASIA; CENTRAL NERVOUS-SYSTEM; SEX-DIFFERENCES; SPATIAL ABILITIES; MENTAL ROTATION; DIETHYLSTILBESTROL DES; ASPERGER-SYNDROME; AUTISM; ANDROGENS; PLAY AB This study examines foetal testosterone (fT) levels (measured in amniotic fluid) as a candidate biological factor, influencing sex differences in systemizing. Systemizing is a cognitive process, defined as the drive to analyze or construct systems. A recent model of psychological sex differences suggests that this is a major dimension in which the sexes differ, with males being more drawn to systemize than females. Participants included 204 children (93 female), age 6-9 years, taking part in a long-term study on the effects of M The systemizing quotient - children's version was administered to these mothers to answer on behalf of their child. Males (mean = 27.79 +/- 7.64) scored significantly higher than females (mean = 22.59 +/- 7.53), confirming that boys systemize to a greater extent than girls. Stepwise regression analysis revealed that fT was the only significant predictor of systemizing preference when the sexes were examined together. Sex was not included in the final regression model, suggesting that Er levels play a greater role than the child's sex in terms of differences in systemizing preference. 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J. Endocrinol. PD NOV PY 2006 VL 155 SU 1 BP S123 EP S130 DI 10.1530/eje.1.02260 PG 8 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 113NR UT WOS:000242605100019 ER PT J AU Skuse, DH AF Skuse, David H. TI Sexual dimorphism in cognition and behaviour: the role of X-linked genes SO EUROPEAN JOURNAL OF ENDOCRINOLOGY LA English DT Article; Proceedings Paper CT 4th Ferring Pharmaceuticals International Paediatric Endocrinology Symposium CY 2006 CL Paris, FRANCE SP Ferring Pharmaceut ID TURNER-SYNDROME; MOUSE-BRAIN; CHROMOSOME COMPLEMENT; EVOLUTION; AUTISM; EXPRESSION; MICE; FEMALES; INACTIVATION; MUTATIONS AB Chimpanzees and humans last shared a common ancestor between 5 and 7 million years ago; 99% of the two species' DNA is identical. Yet, since the paths of primate evolution diverged, there have been remarkable developments in the behavioural and cognitive attainments of our species, which ultimately reflect subtle differences in gene structure and function. These modifications have occurred despite evolutionary constraints upon the diversity of genetic influences, on the development and function of neural tissue. Significant species differences can be observed both at the levels of function (gene expression) and structure (amino acid sequence). Protein evolution is driving an accelerating increase in brain complexity and size. Playing centre stage, in terms of the proportion of genes involved in brain development and cognitive function, is the X chromosome. Recently, it has become clear that a long-standing theory, implicating X-linked genes in a sexually antagonistic evolutionary role, is probably correct. Genes on the sex chromosomes can directly influence sexual dimorphism in cognition and behaviour, independent of the action of sex steroids. Mechanisms by which sex-chromosomal effects, due to X-linked genes, influence neural development or function are reviewed. These include the biased expression of genes subject to X-inactivation. haploin-sufficiency (in males) for non-inactivated genes with no Y homology, sex-specific brain functions and genomic imprinting of X-linked loci. Evidence supporting each of these mechanisms is available from both human and animal models. Recently, the first candidate genes have been discovered. C1 Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. RP Skuse, DH (reprint author), Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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The children performed two tasks in which they had to discriminate whether images of faces presented sequentially in pairs were identical. The images showed four different categories of gaze: direct gaze, eyes averted (left or right) and closed eyes but there was no instruction to focus on the direction of gaze. Images of motorbikes were used as control stimuli. Faces evoked strong activity over posterior brain regions at about 100 ms in both groups of children. A response at 140 ms to faces observed over extrastriate cortices, thought to be homologous to the N170 in adults, was weak and bilateral in both groups and somewhat weaker (approaching significance) in the children with autism than in the control children. The response to motorbikes differed between the groups at 100 and 140 ms. Averted eyes evoked a strong right lateralized component at 240 ms in the normally developing children that was weak in the clinical group. 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TI The safety of dental amalgam in children SO EXPERT OPINION ON DRUG SAFETY LA English DT Review DE amalgam; children; mercury ID RANDOMIZED CLINICAL-TRIAL; THIMEROSAL-CONTAINING VACCINES; AUTISTIC SPECTRUM DISORDER; RESISTANT ORAL BACTERIA; LOW-LEVEL EXPOSURE; MERCURY EXPOSURE; INORGANIC MERCURY; ANTIBIOTIC-RESISTANCE; COPROPORPHYRINOGEN OXIDASE; RETROSPECTIVE COHORT AB The safety of mercury-containing dental amalgam has been hotly debated for well over a century. Dental exposures from mercury have been suggested as the cause of numerous diseases including multiple sclerosis, autism and many others. Known health effects of mercury exposure include CNS and renal damage. However, these effects have only been shown at occupational or higher levels of exposure, and have not been conclusively shown to be present at levels of mercury exposure consistent with that from dental amalgam fillings. The use of mercury amalgam fillings remains a state-of-the-art treatment for dental caries throughout the world. Although there have been a small number of peer-reviewed reports examining the health effects of dental mercury in children, only very recently have the only randomised, controlled clinical trials (two) of the safety of mercury amalgam been published. The purpose of this review is to discuss the scientific evidence on the safety of the use of mercury-containing dental amalgam as a treatment for dental caries. C1 Univ Washington, Sch Dent, Dept Oral Med, Seattle, WA 98195 USA. RP Martin, MD (reprint author), Univ Washington, Sch Dent, Dept Oral Med, Box 356370, Seattle, WA 98195 USA. 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This study investigated whether first-degree relatives of individuals with autism spectrum disorders (ASDs) demonstrate a specific profile of performance on a range of components of executive function (EF), to determine whether EF deficits represent possible endophenotypes for autism. Parents and siblings of ASD and control probands were tested on EF tasks measuring planning, set-shifting, inhibition and generativity. ASD parents showed poorer performance than control parents on a test of ideational fluency or generativity, and ASD fathers demonstrated a weakness in set-shifting to a previously irrelevant dimension. ASD siblings revealed a mild reduction in ideational fluency and a weakness in non-verbal generativity when compared with control siblings. Neither ASD parents nor siblings displayed significant difficulties with planning or inhibition. These results indicated that the broad autism phenotype may not be characterized primarily by impairments in planning and cognitive flexibility, as had been previously proposed. Weaknesses in generativity emerged as stronger potential endophenotypes in this study, suggesting that this aspect of EF should play a central role in cognitive theories of autism. However, discrepancies in the EF profile demonstrated by parents and siblings suggest that factors related to age or parental responsibility may affect the precise pattern of deficits observed. C1 Univ Western Australia, Sch Psychol, Crawley, WA 6009, Australia. Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. Univ Western Australia, Ctr Clin Res Neuropsychiat, Nedlands, WA 6009, Australia. Univ Western Australia, Sch Psychiat & Clin Neurosci, Crawley, WA 6009, Australia. Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. RP Wong, D (reprint author), Univ Western Australia, Sch Psychol, 35 Stirling Highway, Crawley, WA 6009, Australia. 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In this review, we discuss the roles of the neuropeptides oxytocin and vasopressin in the regulation of social bonding as well as related social behaviors which culminate in the formation of social relationships in animal models. The formation of social bonds is a hierarchical process involving social motivation and approach, the processing of social stimuli and formation of social memories, and the social attachment itself. Oxytocin and vasopressin have been implicated in each of these processes. Specifically, these peptides facilitate social affiliation and parental nurturing behavior, are essential for social recognition in rodents, and are involved in the formation of selective mother-infant bonds in sheep and pair bonds in monogamous voles. 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These findings may have important implications for understanding and treating clinical disorders marked by social deficits and/or disrupted attachment. This review focuses on advances made to date in the effort to forge links between basic and clinical research in the area of neuropeptides and social behavior. The literature on oxytocin and its involvement in stress response, affiliation, and prosocial behavior is reviewed, and the implications of these findings for such disorders as autism as well as other social and stress-related disorders including social phobia, post-traumatic stress disorder, and some personality disorders are considered. Finally, unresolved issues and directions for future research are discussed. (c) 2006 Elsevier Inc. All rights reserved. C1 Mt Sinai Sch Med, New York, NY 10029 USA. RP Bartz, JA (reprint author), Mt Sinai Sch Med, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA. 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Secretin receptor-deficient mice are overtly normal and fertile; however, synaptic plasticity in the hippocampus is impaired and there are slightly fewer dendritic spines in the CA1 hippocampal pyramidal cells. Furthermore, secretin receptor-deficient mice show abnormal social and cognitive behaviors. These findings suggest that the secretin receptor system has an important role in the central nervous system relating to social behavior. C1 Ohio State Univ, Ctr Mol & Human Genet, Columbus Childrens Res Inst, Columbus, OH 43205 USA. Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Div Neurosci, Houston, TX 77030 USA. Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA. Jichi Med Sch, Dept Pediat, Tochigi 3290498, Japan. Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. Natl Ctr Neurol & Psychiat, Tokyo 1878502, Japan. Wellcome Trust Sanger Inst, Cambridge, England. RP Nishijima, I (reprint author), Ohio State Univ, Ctr Mol & Human Genet, Columbus Childrens Res Inst, Columbus, OH 43205 USA. 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Mol. Genet. PD NOV 1 PY 2006 VL 15 IS 21 BP 3241 EP 3250 DI 10.1093/hmg/ddl402 PG 10 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 097EP UT WOS:000241430000014 PM 17008357 ER PT J AU Wasserman, S Iyengar, R Chaplin, WF Watner, D Waldoks, SE Anagnostou, E Soorya, L Hollander, E AF Wasserman, Stacey Iyengar, Rupa Chaplin, William F. Watner, Dryden Waldoks, Shulamit E. Anagnostou, Evdokia Soorya, Latha Hollander, Eric TI Levetiracetam versus placebo in childhood and adolescent autism: a double-blind placebo-controlled study SO INTERNATIONAL CLINICAL PSYCHOPHARMACOLOGY LA English DT Article DE anticonvulsants; autism; levetiracetam ID TRIAL; DIVALPROEX; DISORDERS; CHILDREN AB The purpose of this study was to determine the safety and efficacy of the anticonvulsant levetiracetam in the treatment of children with autism. A previous open-label study in autistic children treated with levetiracetam demonstrated effectiveness in hyperactivity, impulsivity/ aggression, and mood lability. Twenty patients with autism ranging from 5 to 17 years of age were entered into a 10-week, placebo-controlled, double-blind trial of levetiracetam versus placebo. The mean maximum dosage for levetiracetam was 862.50 +/- 279.19 mg/day. We evaluated global improvement of autism with the Clinical Global Impression-improvement (CGI-I) Scale and aggression and affective instability with the Aberrant Behavior Checklist (ABC) parent and teacher ratings. We measured repetitive behaviors using the Children's Yale-Brown Obsessive-Compulsive Scale (CY-BOCS) score and impulsivity and hyperactivity with the Conners' Rating Scale-Revised: Long Version for parent and teacher. 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PD NOV PY 2006 VL 21 IS 6 BP 363 EP 367 DI 10.1097/01.yic.0000224787.13782.0f PG 5 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 144DH UT WOS:000244775200006 PM 17012983 ER PT J AU Baron, CA Liu, SY Hicks, C Gregg, JP AF Baron, Colin A. Liu, Stephenie Y. Hicks, Chindo Gregg, Jeffrey P. TI Utilization of lymphoblastoid cell lines as a system for the molecular modeling of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; lymphoblastoid cell lines; gene expression; microarray; blood genomics; PathwayAssist ID PERVASIVE DEVELOPMENTAL DISORDERS; GENE-EXPRESSION; DIAGNOSTIC INTERVIEW; SUSCEPTIBILITY LOCI; GENOMEWIDE SCREEN; PHARMACOTHERAPY; ABNORMALITIES; SEROTONIN; RESOURCE; ETIOLOGY AB In order to provide an alternative approach for understanding the biology and genetics of autism, we performed statistical analysis of gene expression profiles of lymphoblastoid cell lines derived from children with autism and their families. The goal was to assess the feasibility of using this model in identifying autism-associated genes. Replicate microarray experiments demonstrated that expression data from the cell lines were consistent and highly reproducible. Further analyses identified differentially expressed genes between cell lines derived from children with autism and those derived from their normally developing siblings. These genes were then used to identify biochemical pathways potentially involved in autism. This study suggests that lymphoblastoid cell lines may be a viable tool for identifying genes associated with autism. C1 Univ Calif Davis, Dept Pathol & Lab Med, Sacramento, CA 95817 USA. Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. RP Gregg, JP (reprint author), Univ Calif Davis, Dept Pathol & Lab Med, Sacramento, CA 95817 USA. 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Autism Dev. Disord. PD NOV PY 2006 VL 36 IS 8 BP 973 EP 982 DI 10.1007/s10803-006-0134-x PG 10 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800003 PM 16845580 ER PT J AU Rutherford, MD Pennington, BF Rogers, SJ AF Rutherford, M. D. Pennington, Bruce F. Rogers, Sally J. TI The perception of animacy in young children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; perception; animacy; theory of mind; intentionality ID ASPERGER-SYNDROME; BIOLOGICAL MOTION; SOCIAL CAUSALITY; BRAIN; COMMUNICATION; ATTRIBUTION; LANGUAGE; RECOGNITION; SENSITIVITY; MOVEMENT AB Visual perception may be a developmental prerequisite to some types of social understanding. The ability to perceive social information given visual motion appears to develop early. However, children with autism have profound deficits in social cognitive function and may fail to see social motion in the same way that typically developing children do. We tested the hypothesis that children with autism fail to discriminate animate motion, using a novel paradigm involving simple geometric figures. The subjects were 23 children with autism (c.a. 70.7 mos.), 18 children with other developmental disabilities (c.a. 68.2 mos.), and 18 typically developing children (c.a. 46.4 mos.). Children saw two circles moving on a screen and were rewarded for identifying the one that moved as if animate. A control condition required children to identify the heavier of two objects. Children with autism initially showed a deficit in categorizing objects as animate (though no deficit on the control task), but showed no deficit in this ability after they had reached criterion in the training phase. These results are discussed in terms of the social orienting theory of autism, and the possibility that animacy perception might be preserved in autism, even if it is not used automatically. C1 McMaster Univ, Hamilton, ON L8S 4K1, Canada. 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Autism Dev. Disord. PD NOV PY 2006 VL 36 IS 8 BP 983 EP 992 DI 10.1007/s10803-006-0136-8 PG 10 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800004 PM 16897392 ER PT J AU Toth, K Munson, J Meltzoff, AN Dawson, G AF Toth, Karen Munson, Jeffrey Meltzoff, Andrew N. Dawson, Geraldine TI Early predictors of communication development in young children with autism spectrum disorder: Joint attention, imitation, and toy play SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; language; communication; joint attention; imitation; play ID DIAGNOSTIC OBSERVATION SCHEDULE; RECEPTIVE LANGUAGE DISORDER; NONVERBAL-COMMUNICATION; INFANTILE-AUTISM; SYMBOLIC PLAY; 2ND YEAR; INFANCY; BEHAVIOR; DELAY; 6-MONTH-OLDS AB This study investigated the unique contributions of joint attention, imitation, and toy play to language ability and rate of development of communication skills in young children with autism spectrum disorder (ASD). Sixty preschool-aged children with ASD were assessed using measures of joint attention, imitation, toy play, language, and communication ability. Two skills, initiating protodeclarative joint attention and immediate imitation, were most strongly associated with language ability at age 3-4 years, whereas toy play and deferred imitation were the best predictors of rate of communication development from age 4 to 6.5 years. The implications of these results for understanding the nature and course of language development in autism and for the development of targeted early interventions are discussed. C1 Univ Washington, Dept Psychol, Autism Ctr, CHDD, Seattle, WA 98195 USA. RP Toth, K (reprint author), Univ Washington, Dept Psychol, Autism Ctr, CHDD, 357920, Seattle, WA 98195 USA. 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Autism Dev. Disord. PD NOV PY 2006 VL 36 IS 8 BP 1007 EP 1024 DI 10.1007/s10803-006-0142-x PG 18 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800006 PM 16845576 ER PT J AU Schlooz, WAJM Hulstijn, W van den Broek, PJA van der Pijll, ACAM Gabreels, F van der Gaag, RJ Rotteveel, JJ AF Schlooz, Wim A. J. M. Hulstijn, Wouter van den Broek, Pieter J. A. van der Pijll, Angela C. A. M. Gabreels, Fons van der Gaag, Rutger J. Rotteveel, Jan J. TI Fragmented visuospatial processing in children with pervasive developmental disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pervasive developmental disorder; central coherence; rey complex figure task; children's embedded figure test; local and global processing ID OSTERRIETH COMPLEX FIGURE; HIGH-FUNCTIONING AUTISM; TOURETTE-SYNDROME; SPECTRUM DISORDERS; ASPERGER-SYNDROME; VISUAL-SEARCH; MEMORY; INDIVIDUALS; PERFORMANCE; ABILITIES AB Children diagnosed with Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS) and Asperger Syndrome (AS) may be characterised by a similar perceptual focus on details as children with autistic disorder (AD). This was tested by analysing their performance in a visuoperceptual task [the Children's Embedded Figure Test (CEFT)] and a graphic reproduction task [the Rey Complex Figure Task (Rey CFT)]. Control groups were children with Tourette Syndrome (TS) and typically developing children. The TS sample performed similarly to the normal control group in both tasks. The CEFT results did not show the expected preference for local processing in children with PDD-NOS. However, the Rey CFT data revealed that the children with this lesser variant of PDD processed visuospatial information in a fragmented way and were deficient in global processing. C1 UMCN St Radboud ACKJON Lingewal, Dept Child Psychiat, Nijmegen, Netherlands. Radboud Univ Nijmegen, NICI, Nijmegen, Netherlands. UMCN St Radboud, Dept Med Psychol, Nijmegen, Netherlands. UMCN St Radboud, Dept Child Neurol IKNC, Nijmegen, Netherlands. RP Schlooz, WAJM (reprint author), UMCN St Radboud ACKJON Lingewal, Dept Child Psychiat, Nijmegen, Netherlands. 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Three (M:F = 1:2) had normal development to age 22, 35, and 42 months, with onset of autism upon recovery from severe malaria, attended by prolonged high fever, convulsions, and in one case prolonged loss of consciousness. In four other cases (M:F = 3:1), the temporal relationship between onset of autism and severe infection was close, but possibly spurious since malaria is common in Tanzania and there were indications of abnormal development in the child or a family member. In seven cases, (M:F = 6:1) autism onset was unrelated to malaria. The excess of non-verbal cases (N = 10) is related local diagnostic practice. C1 Johns Hopkins Univ, Sch Med, Baltimore, MD 21210 USA. Msimbazi Mseto Primary Sch, Autism Unit, Dar Es Salaam, Tanzania. Univ Dar Es Salaam, Coll Hlth Sci, Muhimbili Univ, Dept Psychiat, Dar Es Salaam, Tanzania. Tufts Univ, New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. Tufts Univ, Sch Med, Boston, MA 02111 USA. 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Autism Dev. Disord. PD NOV PY 2006 VL 36 IS 8 BP 1039 EP 1051 DI 10.1007/s10803-006-0143-9 PG 13 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800008 PM 16897390 ER PT J AU Schneider, CK Melmed, RD Enriquez, FJ Barstow, LE Ranger-Moore, J Ostrem, JA AF Schneider, Cindy K. Melmed, Raun D. Enriquez, F. Javier Barstow, Leon E. Ranger-Moore, James Ostrem, James A. TI Oral human immunoglobulin for children with autism and gastrointestinal dysfunction: A prospective, open-label study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; autistic disorder; immunoglobulin; gastrointestinal dysfunction; mucosal immunity ID IMMUNE GLOBULIN THERAPY; BIRTH-WEIGHT INFANTS; REGRESSIVE AUTISM; DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; CROHNS-DISEASE; AUTOANTIBODIES; ENTEROCOLITIS; AUTOIMMUNITY; DIARRHEA AB Immunoglobulin secretion onto mucosal surfaces is a major component of the mucosal immune system. We hypothesized that chronic gastrointestinal (GI) disturbances associated with autistic disorder (AD) may be due to an underlying deficiency in mucosal immunity, and that orally administered immunoglobulin would be effective in alleviating chronic GI dysfunction in these individuals. In this pilot study, twelve male subjects diagnosed with AD were evaluated using a GI severity index (GSI) while receiving daily dosing with encapsulated human immunoglobulin. Following eight weeks of treatment, 50% of the subjects met prespecified criteria for response in GI signs and symptoms and showed significant behavioral improvement as assessed by the Autism Behavior Checklist and parent and physician rated Clinical Global Impression of Improvement. C1 Protein Therapeut Inc, Tucson, AZ USA. SW Autism Res & Resource Ctr, Phoenix, AZ USA. Univ Arizona, Hlth Sci Ctr, Ctr Canc, Biometry Unit, Tucson, AZ USA. RP Ostrem, JA (reprint author), Protein Therapeut Inc, Tucson, AZ USA. 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Autism Dev. Disord. PD NOV PY 2006 VL 36 IS 8 BP 1053 EP 1064 DI 10.1007/s10803-006-0141-y PG 12 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800009 PM 16845577 ER PT J AU Macintosh, K Dissanayake, C AF Macintosh, Kathleen Dissanayake, Cheryl TI Social skills and problem behaviours in school aged 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; social skills; problem behaviours; SSRS AB The social skills and problem behaviours of children with high-functioning autism and Asperger's Disorder were compared using parent and teacher reports on the Social Skills Rating System. The participants were 20 children with high-functioning autism, 19 children with Asperger's Disorder, and 17 typically developing children, matched on chronological and overall mental age. The children with autism and Asperger's Disorder were not differentiated on any social skill or problem behaviour based either on teacher or parent report. However, both clinical groups demonstrated significant social skill deficits and problem behaviours relative to the typically developing children, and the original standardization sample. The findings were compatible with the view that autism and Asperger's Disorder belong on a single spectrum of disorder. 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 Achenbach T. M., 1983, MANUAL CHILD BEHAV C American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 Bryson S. 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R., 2000, ASPERGER SYNDROME, P25 Volkmar FR, 1998, AUTISM, V2, P45, DOI DOI 10.1177/1362361398021005 Wing L., 1996, AUTISTIC SPECTRUM GU WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wing Lorna, 2000, ASPERGER SYNDROME, P418 World Health Organization, 1993, INT CLASS DIS ZWAIGENBAUM L, 1999, HDB PSYCHOSOCIAL CHA, P275 NR 44 TC 51 Z9 53 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 NOV PY 2006 VL 36 IS 8 BP 1065 EP 1076 DI 10.1007/s10803-006-0139-5 PG 12 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800010 PM 16865549 ER PT J AU Cohen, IL Tsiouris, JA AF Cohen, Ira L. Tsiouris, John A. TI Maternal recurrent mood disorders and high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high-functioning autism; recurrent depression; internalizing behaviors ID PERVASIVE DEVELOPMENTAL DISORDERS; PDD BEHAVIOR INVENTORY; PSYCHIATRIC-DISORDERS; FAMILY-HISTORY; MAJOR DEPRESSION; EARLY-ONSET; CHILDREN; SPECTRUM; PATTERNS; PARENTS AB A quantitative examination was made of the association of parental mood and anxiety disorders with severity of disability within a large sample of young children with Pervasive Developmental Disorder (PDD). Maternal recurrent mood disorders were associated with elevated cognitive and adaptive functioning in their affected children, parent reports of increased behavior problems and teacher reports of an internalizing behavioral style. Maternal histories of anxiety disorders and paternal depression or anxiety disorders were not associated with levels of adaptive/cognitive functioning or levels of maladaptive behaviors in the children. Various genetic models are discussed. It is hypothesized that genes associated with recurrent depression in women may exert a "protective" effect on cognition and adaptive functioning in children with PDD. C1 New York State Inst Basic Res Dev Disabil, Staten Isl, NY 10314 USA. RP Cohen, IL (reprint author), New York State Inst Basic Res Dev Disabil, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA. EM Ira.Cohen@omr.state.ny.us CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT Benazzi F, 2003, COMPR PSYCHIAT, V44, P102, DOI 10.1053/comp.2003.50015 Biederman J, 2001, AM J PSYCHIAT, V158, P49, DOI 10.1176/appi.ajp.158.1.49 Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 Cassano GB, 2004, AM J PSYCHIAT, V161, P1264, DOI 10.1176/appi.ajp.161.7.1264 Cohen IL, 2003, J AUTISM DEV DISORD, V33, P47, DOI 10.1023/A:1022278420716 Cohen IL, 2003, J AUTISM DEV DISORD, V33, P31, DOI 10.1023/A:1022226403878 Cohen IL, 2003, CLIN GENET, V64, P190, DOI 10.1034/j.1399-0004.2003.00115.x COHEN IL, 1988, AM J MENT RETARD, V92, P436 DeLong GR, 1999, NEUROLOGY, V52, P911 DELONG GR, 1988, J AUTISM DEV DISORD, V18, P593 DeLong R, 2004, J NEUROPSYCH CLIN N, V16, P199, DOI 10.1176/appi.neuropsych.16.2.199 DELONG R, 1994, DEV MED CHILD NEUROL, V36, P441 Fombonne E, 1997, J CHILD PSYCHOL PSYC, V38, P667, DOI 10.1111/j.1469-7610.1997.tb01694.x Ghaziuddin M, 1998, J AUTISM DEV DISORD, V28, P111, DOI 10.1023/A:1026036514719 Griffiths R., 1984, ABILITIES YOUNG CHIL KESSLER RC, 1994, ARCH GEN PSYCHIAT, V51, P8 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 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 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Piven J, 1999, AM J PSYCHIAT, V156, P557 PIVEN J, 1991, J AM ACAD CHILD PSY, V30, P471, DOI 10.1097/00004583-199105000-00019 Robins L. 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PD NOV PY 2006 VL 36 IS 8 BP 1077 EP 1088 DI 10.1007/s10803-006-0145-7 PG 12 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800011 PM 16897389 ER PT J AU Muller, E Schuler, A AF Muller, Eve Schuler, Adriana TI Verbal marking of affect by children with asperger syndrome and high functioning autism during spontaneous interactions with family members SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger Syndrome; high functioning autism; affect; emotion; language; spontaneous interaction ID EMOTION; INDIVIDUALS; LANGUAGE; MOTHERS; PEOPLE; STATES AB Verbal marking of affect by older children with Asperger Syndrome (AS) and high functioning autism (HFA) during spontaneous interactions is described. Discourse analysis of AS and HFA and typically developing children included frequency of affective utterances, affective initiations, affective labels and affective explanations, attribution of affective responses to self and others, and positive and negative markers of affect. Findings indicate that children with AS and HFA engaged in a higher proportion of affect marking and provided a higher proportion of affective explanations than typically developing children, yet were less likely to initiate affect marking sequences or talk about the affective responses of others. No significant differences were found between groups in terms of the marking of positive and negative affect. C1 Natl Assoc State Directors Special Educ, Project Forum, Alexandria, VA 22314 USA. San Francisco State Univ, Dept Special Educ, San Francisco, CA 94132 USA. RP Muller, E (reprint author), Natl Assoc State Directors Special Educ, Project Forum, 1800 Diagonal Rd,Suite 320, Alexandria, VA 22314 USA. EM eve.muller@nasdse.org CR ATKINSON M, 1999, DISCOURSE READER ATTWOOD A, 1988, J AUTISM DEV DISORD, V18, P241, DOI 10.1007/BF02211950 ATTWOOD A, 1998, ASPERGERS SYNDROME G BEEGHLY M, 1986, BRIT J DEV PSYCHOL, V4, P247 Capps L., 1998, AUTISM, V2, P325, DOI DOI 10.1177/1362361398024002 CAPPS L, 2000, J ABNORMAL CHILD PSY, V2, P193 CAPPS L, 1992, J AUTISM DEV DISORD, V29, P57 Cervantes CA, 1998, DEV PSYCHOL, V34, P88, DOI 10.1037/0012-1649.34.1.88 DAWSON G, 1990, J ABNORM CHILD PSYCH, V18, P335, DOI 10.1007/BF00916569 FAY W, 1980, LANGUAGE INTERVENTIO Gillott A, 2001, AUTISM, V5, P277, DOI 10.1177/1362361301005003005 Goodwin Charles, 1992, RETHINKING CONTEXT L HOBSON RP, 1989, J AUTISM DEV DISORD, V19, P601, DOI 10.1007/BF02212860 Kanner L, 1943, NERV CHILD, V2, P217 KIM J, 2000, INT J RES PRACTICE, V11, P117 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x Langdell T., 1981, THESIS U LONDON LANGDELL T, 1978, J CHILD PSYCHOL PSYC, V19, P255, DOI 10.1111/j.1469-7610.1978.tb00468.x LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LOVELAND K, 2001, DEV AUTISM PERSPECTI Martin J.R., 2000, EVALUATION TEXT AUTH MULLER E, 2004, THESIS U CALIFORNIA Ochs Elinor, 2001, LIVING NARRATIVE CRE PRIOR M, 1990, J CHILD PSYCHOL PSYC, V31, P587, DOI 10.1111/j.1469-7610.1990.tb00799.x QUILL K, 1995, TEACHING AUTISTIC CH RASCO L, 1999, 1999 BIENN M SOC RES RICKS DM, 1975, J AUTISM CHILD SCHIZ, V5, P191, DOI 10.1007/BF01538152 RICKS DM, 1979, BEFORE SPEECH, P245 SIGMAN M, 1986, J CHILD PSYCHOL PSYC, V27, P647, DOI 10.1111/j.1469-7610.1986.tb00189.x SNOW ME, 1987, J AM ACAD CHILD PSY, V26, P836, DOI 10.1097/00004583-198726060-00006 TAGERFLUSBERG H, 1995, BRIT J DEV PSYCHOL, V13, P45 TAGERFLUSBERG H, 1995, APPL PSYCHOLINGUIST, V16, P241, DOI 10.1017/S0142716400007281 Wechsler D., 1974, MANUAL WECHSLER INTE WETHERBY A, 1997, HDB AUTISM DEV DISOR YIRMIYA N, 1989, J CHILD PSYCHOL PSYC, V30, P725, DOI 10.1111/j.1469-7610.1989.tb00785.x YIRMIYA N, 1992, CHILD DEV, V63, P150, DOI 10.1111/j.1467-8624.1992.tb03603.x NR 36 TC 8 Z9 8 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 NOV PY 2006 VL 36 IS 8 BP 1089 EP 1100 DI 10.1007/s10803-006-0146-6 PG 12 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800012 PM 16897388 ER PT J AU Lecavalier, L AF Lecavalier, Luc TI Behavioral and emotional problems in young people with pervasive developmental disorders: Relative prevalence, effects of subject characteristics, and empirical classification SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Pervasive Developmental Disorder; behavior problems; prevalence; cluster analysis; Nisonger Child Behavior Rating Form ID RATED CHILD-BEHAVIOR; NATIONAL US SAMPLE; RATING FORM; MENTAL-RETARDATION; AUTISM; COMMUNITY; CHECKLIST; NORMS; DISABILITIES; INDIVIDUALS AB Parents or teachers rated 487 non-clinically referred young people with Pervasive Developmental Disorders on the Nisonger Child Behavior Rating Form. The objectives of the study were to examine the relative prevalence of specific behavior problems, assess the impact of subject characteristics, and derive an empirical classification of behavioral and emotional problems for this population. Results indicated that the youngsters experienced high rates of behavior and emotional problems. Cluster analysis suggested that six- and eight-cluster solutions best fit the ratings provided by parents and teachers, respectively. Both parent and teacher cluster solutions contained groups of children characterized as problem free, well adapted, hyperactive, anxious, and with undifferentiated behavior disturbances. The empirically derived clusters were supported by data external to the analyses. C1 Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. RP Lecavalier, L (reprint author), Ohio State Univ, Nisonger Ctr, 305 McCampbell Hall,1581 Dodd Dr, Columbus, OH 43210 USA. 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Autism Dev. Disord. PD NOV PY 2006 VL 36 IS 8 BP 1101 EP 1114 DI 10.1007/s10803-006-0147-5 PG 14 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800013 PM 16897387 ER PT J AU Reed, P AF Reed, Phil TI The effect of retention interval on stimulus over-selectivity using a matching-to-sample paradigm SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; overselectivity; delayed matching-to-sample; memory; humans ID MULTIPLE VISUAL CUES; AUTISTIC-CHILDREN; OVERSELECTIVITY; MEMORY; DEFICITS AB The conditions under which stimulus over-selectivity occurred were studied using a matching-to-sample procedure with non-autistic adults. A matching-to-sample discrimination learning task with a number of sample-comparison retention intervals was used. The results demonstrated that an increase in retention interval increased the degree of stimulus overselectivity displayed. In addition, it was shown that the matching-to-sample procedure is suitable for eliciting overselectivity in a non-autistic adult sample. C1 Univ Coll Swansea, Dept Psychol, Swansea SA2 8PP, W Glam, Wales. RP Reed, P (reprint author), Univ Coll Swansea, Dept Psychol, Singleton Pk, Swansea SA2 8PP, W Glam, Wales. EM p.reed@swansea.ac.uk CR BICKEL WK, 1984, J AUTISM DEV DISORD, V14, P137, DOI 10.1007/BF02409657 Dube W. V., 1999, EXPT ANAL HUMAN BEHA, V13, P267 Dube WV, 1997, J EXP ANAL BEHAV, V68, P303, DOI 10.1901/jeab.1997.68-303 Dube WV, 1999, J APPL BEHAV ANAL, V32, P25, DOI 10.1901/jaba.1999.32-25 Gibson E, 2005, J AUTISM DEV DISORD, V35, P851, DOI 10.1007/s10803-005-0030-9 Jolliffe T, 1999, COGNITION, V71, P149, DOI 10.1016/S0010-0277(99)00022-0 KOEGEL RL, 1977, J EXP CHILD PSYCHOL, V24, P299, DOI 10.1016/0022-0965(77)90008-X KOEGEL RL, 1973, J EXP CHILD PSYCHOL, V15, P442, DOI 10.1016/0022-0965(73)90094-5 KOVATTAN.PM, 1974, J AUTISM CHILD SCHIZ, V4, P251, DOI 10.1007/BF02115231 LOVAAS OI, 1971, BEHAV RES THER, V9, P305, DOI 10.1016/0005-7967(71)90042-8 LOVAAS OI, 1971, J ABNORM PSYCHOL, V77, P211, DOI 10.1037/h0031015 Mottron L, 1999, J CHILD PSYCHOL PSYC, V40, P743, DOI 10.1017/S0021963098003795 Reed P, 2005, J AUTISM DEV DISORD, V35, P601, DOI 10.1007/s10803-005-0004-y SONOYAMA S, 1986, JAPANESE J BEHAV THE, V12, P62 WAYLAND S, 1985, BRAIN COGNITION, V4, P338, DOI 10.1016/0278-2626(85)90026-0 White KG, 2002, PSYCHON B REV, V9, P426, DOI 10.3758/BF03196301 NR 16 TC 10 Z9 10 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 NOV PY 2006 VL 36 IS 8 BP 1115 EP 1121 DI 10.1007/s10803-006-0148-4 PG 7 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800014 PM 16874563 ER PT J AU Tsakanikos, E Costello, H Holt, G Bouras, N Sturmey, P Newton, T AF Tsakanikos, Elias Costello, Helen Holt, Geraldine Bouras, Nick Sturmey, Peter Newton, Tim TI Psychopathology in adults with autism and intellectual disability SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; intellectual disability; psychiatric co-morbidity ID PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHIATRIC-DISORDERS; PREVALENCE; SYMPTOMS AB There have been few studies of psychopathology in adult with autism. This study examined psychiatric co-morbidity in 147 adults with intellectual disability (ID) and autism and 605 adults with ID but without autism. After controlling for the effects of gender, age, psychotropic medication and level of ID, people with autism and ID were no more likely to receive a psychiatric diagnosis than people with ID only. People with autism were less likely to receive a diagnosis of personality disorder. These findings cast doubts on the hypothesis that adults with ID and autism are more vulnerable to certain psychiatric disorders than non-autistic adults with ID. C1 Kings Coll London, Inst Psychiat, NHiLD York Clin, Guys Hosp, London SE1 3RR, England. Kings Coll London, Inst Psychiat, Estia Ctr, London SE5 8AF, England. CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA. CUNY, Grad Ctr, Flushing, NY 11367 USA. Kings Coll London, GKT Med & Dent Sch, London WC2R 2LS, England. RP Bouras, N (reprint author), Kings Coll London, Inst Psychiat, NHiLD York Clin, Guys Hosp, 47 Weston St, London SE1 3RR, England. EM nick.bouras@kcl.ac.uk RI Tsakanikos, Elias/B-4881-2011 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Aylward EH, 2002, NEUROLOGY, V59, P175 Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 Bouras N, 2003, J INTELL DISABIL RES, V47, P439, DOI 10.1046/j.1365-2788.2003.00514.x Bradley EA, 2004, J AUTISM DEV DISORD, V34, P151, DOI 10.1023/B:JADD.0000022606.97580.19 CLARKE DJ, 1989, BRIT J PSYCHIAT, V155, P692 Deb S., 2001, PRACTICE GUIDELINES Deb S, 2001, J INTELL DISABIL RES, V45, P495 EISENBERG L, 1958, PSYCHOPATHOLOGY SOUR, P3 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 1997, J AM ACAD CHILD PSY, V36, P1561, DOI 10.1016/S0890-8567(09)66566-7 Ghaziuddin M, 2002, J AUTISM DEV DISORD, V32, P299, DOI 10.1023/A:1016330802348 GILLBERG C, 1999, PSYCHIAT BEHAV DISOR, P73 GILLBERG C, 1991, J AUTISM DEV DISORD, V21, P61, DOI 10.1007/BF02206998 Gillberg C, 2000, ACTA PSYCHIAT SCAND, V102, P321, DOI 10.1034/j.1600-0447.2000.102005321.x Giovanardi Rossi P, 2000, Brain Dev, V22, P102, DOI 10.1016/S0387-7604(99)00124-2 HOWLIN P, 1997, AUTISM PREPARATION A Howlin P, 2000, AUTISM, V4, P63, DOI DOI 10.1177/1362361300004001005 LAINHART JE, 1999, MOL PSYCHIATR, V4, P303 Matson J. L., 1995, DIAGNOSTIC ASSESSMEN Morgan C. N., 2003, PSYCHIAT B, V27, P378, DOI 10.1192/pb.27.10.378 Moss S, 1998, J INTELL DISABIL RES, V42, P173, DOI 10.1046/j.1365-2788.1998.00116.x Mouridsen SE, 1999, PSYCHOPATHOLOGY, V32, P177, DOI 10.1159/000029087 PETTY LK, 1984, ARCH GEN PSYCHIAT, V41, P129 Piven J, 1999, AM J PSYCHIAT, V156, P557 Posey DJ, 2000, HARVARD REV PSYCHIAT, V8, P45, DOI 10.1093/hrp/8.2.45 Seltzer MM, 2003, J AUTISM DEV DISORD, V33, P565, DOI 10.1023/B:JADD.0000005995.02453.0b Sturmey P, 2001, J AM ACAD CHILD PSY, V40, P621, DOI 10.1097/00004583-200106000-00005 VOLKMAR FR, 1991, AM J PSYCHIAT, V148, P1705 VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 32 TC 44 Z9 44 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 NOV PY 2006 VL 36 IS 8 BP 1123 EP 1129 DI 10.1007/s10803-006-0149-3 PG 7 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800015 PM 16855878 ER PT J AU Eberhart, CG Copeland, J Abel, TW AF Eberhart, Charles G. Copeland, Joshua Abel, Ty W. TI Brief report: S6 ribosomal protein phosphorylation in autistic frontal cortex and cerebellum: A tissue array analysis SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism tissue array; S6; tuberous sclerosis; Cowden disease ID TUBEROUS SCLEROSIS COMPLEX; SPECTRUM DISORDERS; CORTICAL DYSPLASIA; COWDEN-SYNDROME; MICROARRAYS; PREVALENCE; MTOR AB Few autistic brain samples are available for study, limiting investigations into molecular and histopathological abnormalities associated with this common disease. To facilitate distribution of samples, we have constructed a tissue array containing cerebral and cerebellar cores from 5 autistic children, 1 girl with Rett syndrome, and 5 age-matched controls. To demonstrate the utility of this resource, we examined phosphorylation of the S6 ribosomal protein, a signaling event regulated by the genes mutated in tuberous sclerosis and Cowden disease. We hypothesized that the molecular pathways altered in these inherited conditions associated with autism might be dysregulated in sporadic autistic cases as well. However, no consistent alterations in S6 phosphorylation were detected in autistic tissues compared to controls in the brain regions analyzed. C1 Johns Hopkins Univ, Baltimore, MD USA. RP Eberhart, CG (reprint author), Johns Hopkins Univ, Baltimore, MD USA. 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Autism Dev. Disord. PD NOV PY 2006 VL 36 IS 8 BP 1131 EP 1135 DI 10.1007/s10803-006-0135-9 PG 5 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800016 PM 16845579 ER PT J AU Correia, C Coutinho, AM Diogo, L Grazina, M Marques, C Miguel, T Ataide, A Almeida, J Borges, L Oliveira, C Oliveira, G Vicente, AM AF Correia, Catarina Coutinho, Ana M. Diogo, Luisa Grazina, Manuela Marques, Carla Miguel, Teresa Ataide, Assuncao Almeida, Joana Borges, Luis Oliveira, Catarina Oliveira, Guiomar Vicente, Astrid M. TI Brief report: High frequency of biochemical markers for mitochondrial dysfunction in autism: No association with the mitochondrial aspartate/glutamate carrier SLC25A12 gene SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; mitochondrial dysfunction; lactate/pyruvate ratio; SLC25A12 gene; genetic association ID SPECTRUM DISORDERS; CHILDREN AB In the present study we confirm the previously reported high frequency of biochemical markers of mitochondrial dysfunction, namely hyperlactacidemia and increased lactate/pyruvate ratio, in a significant fraction of 210 autistic patients. We further examine the involvement of the mitochondrial aspartate/glutamate carrier gene (SLC25A12) in mitochondrial dysfunction associated with autism. We found no evidence of association of the SLC25A12 gene with lactate and lactate/pyruvate distributions or with autism in 241 nuclear families with one affected individual. We conclude that while mitochondrial dysfunction may be one of the most common medical conditions associated with autism, variation at the SLC25A12 gene does not explain the high frequency of mitochondrial dysfunction markers and is not associated with autism in this sample of autistic patients. C1 Inst Nacl Saude Dr Ricardo Jorge, P-1649016 Lisbon, Portugal. Direccao Reg Educ Regiao Ctr, Coimbra, Portugal. Ctr Neurociencias & Biol Celular, Coimbra, Portugal. Hosp Pediat Coimbra, Ctr Desenvolvimento Crianca, Coimbra, Portugal. Gulbenkian Inst Sci, P-2781 Oeiras, Portugal. RP Vicente, AM (reprint author), Inst Nacl Saude Dr Ricardo Jorge, Av Padre Cruz, P-1649016 Lisbon, Portugal. 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Autism Dev. Disord. PD NOV PY 2006 VL 36 IS 8 BP 1137 EP 1140 DI 10.1007/s10803-006-0138-6 PG 4 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800017 PM 17151801 ER PT J AU Wing, L Gould, J AF Wing, Lorna Gould, Judith TI Letter to the editor: Comment on "The adult Asperger assessment (AAA): A diagnostic method", Simon Baron-Cohen, Sally Wheelwright, Janine Robinson and Marc Woodbury-Smith, Journal of Autism and Developmental Disorders vol 35(6) SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID INTERVIEW C1 Ctr Social & Commun Disorders, Bromley BR2 9HT, Kent, England. RP Wing, L (reprint author), Ctr Social & Commun Disorders, Elliot House,Masons Hill, Bromley BR2 9HT, Kent, England. EM Elliot.House@nas.org.uk CR Baron-Cohen S, 2005, J AUTISM DEV DISORD, V35, P807, DOI 10.1007/s10803-005-0026-5 Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 Minshew NJ, 2005, J AUTISM DEV DISORD, V35, P877, DOI 10.1007/s10803-005-0035-4 Shea V, 2005, J AUTISM DEV DISORD, V35, P871, DOI 10.1007/s10803-005-0032-7 Wing L, 2002, J CHILD PSYCHOL PSYC, V43, P307, DOI 10.1111/1469-7610.00023 WING L, 1978, J AUTISM CHILD SCHIZ, V8, P79, DOI 10.1007/BF01550280 NR 6 TC 1 Z9 1 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 NOV PY 2006 VL 36 IS 8 BP 1141 EP 1142 DI 10.1007/s10803-006-0289-5 PG 2 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800018 PM 17080268 ER PT J AU Hill, EL Berthoz, S AF Hill, Elisabeth L. Berthoz, Sylvie TI Response to "Letter to the editor: The overlap between Alexithymia and Asperger's syndrome", Fitzgerald and Bellgrove, Journal of Autism and Developmental Disorders, 36(4) SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID SPECTRUM DISORDER; CINGULATE CORTEX; VALIDITY; AWARENESS; EMOTIONS; SCALE; BRAIN; FMRI; MIND C1 Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. Univ Paris 05, Inst Mutualiste Montsouris, Dept Psychiat Adolescents & Young Adults, Paris, France. RP Hill, EL (reprint author), Univ London Goldsmiths Coll, Dept Psychol, New Cross, London SE14 6NW, England. 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J., 1997, DISORDERS AFFECT REG, P190, DOI 10.1017/CBO9780511526831.012 Vorst HCM, 2001, PERS INDIV DIFFER, V30, P413, DOI 10.1016/S0191-8869(00)00033-7 NR 21 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 NOV PY 2006 VL 36 IS 8 BP 1143 EP 1145 DI 10.1007/s10803-006-0287-7 PG 3 WC Psychology, Developmental SC Psychology GA 117OY UT WOS:000242883800019 PM 17080269 ER PT J AU Antrop, I Stock, P Verte, S Wiersema, JR Baeyens, D Roeyers, H AF Antrop, Inge Stock, Pieter Verte, Sylvie Wiersema, Jan Roelt Baeyens, Dieter Roeyers, Herbert TI ADHD and delay aversion: the influence of non-temporal stimulation on choice for delayed rewards SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE delay aversion ID DEFICIT-HYPERACTIVITY DISORDER; RESPONSE-INHIBITION; DIAGNOSTIC INTERVIEW; CONTROL CHILDREN; EVENT-RATE; ATTENTION; AUTISM; AD/HD; TASK; RELIABILITY AB Background: Delay aversion, the motivation to escape or avoid delay, results in preference for small immediate over large delayed rewards. Delay aversion has been proposed as one distinctive psychological process that may underlie the behavioural symptoms and cognitive deficits of attention deficit/hyperactivity disorder (ADHD). Furthermore, the delay aversion hypothesis predicts that ADHD children's preference for immediate small over large delayed rewards will be reduced when stimulation, which makes time appear to pass more quickly, is added to the delay interval. The current paper tests these predictions. Methods: A group of children with a diagnosis of ADHD (with or without oppositional defiant disorder (ODD)), a group with a diagnosis of high-functioning autism (HFA), and a normal control group were compared on an experimental paradigm giving repeated choices between small immediate and large delayed rewards (Maudsley Index of Delay Aversion-MIDA) under two conditions (stimulation and no stimulation). Results: As predicted, ADHD children displayed a stronger preference than the HFA and control children for the small immediate rewards under the no-stimulation condition. The ADHD children preferences were normalised under the stimulation condition with no differences between the groups. This pattern of results was the same whether the ADHD children had comorbid ODD or not. Discussion: The findings from the MIDA are consistent with the delay aversion hypothesis of ADHD in showing that preference for small immediate rewards over large delayed rewards is a specific feature of ADHD and that this preference can be reduced by the addition of stimulation. Further research is required to better understand the emotional and motivational mechanisms underpinning delay aversion. C1 State Univ Ghent Hosp, Dept Child & Adolescent Psychiat, B-9000 Ghent, Belgium. Univ Ghent, B-9000 Ghent, Belgium. RP Antrop, I (reprint author), State Univ Ghent Hosp, Dept Child & Adolescent Psychiat, De Pintelaan 185, B-9000 Ghent, Belgium. 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TI Global and Local Processing in Adult Humans (Homo sapiens), 5-Year-Old Children (Homo sapiens), and Adult Cotton-Top Tamarins (Saguinus oedipus) SO JOURNAL OF COMPARATIVE PSYCHOLOGY LA English DT Article DE global precedence; local bias; perception; discrimination; cotton-top tamarins AB This study compared adults (Homo sapiens), young children (Homo sapiens), and adult tamarins (Saguinus oedipus) while they discriminated global and local properties of stimuli. Subjects were trained to discriminate a circle made of circle elements from a square made of square elements and were tested with circles made of squares and squares made of circles. Adult humans showed a global bias in testing that was unaffected by the density of the elements in the stimuli. Children showed a global bias with dense displays but discriminated by both local and global properties with sparse displays. Adult tamarins' biases matched those of the children. 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Comp. Psychol. PD NOV PY 2006 VL 120 IS 4 BP 323 EP 330 DI 10.1037/0735-7036.120.4.323 PG 8 WC Behavioral Sciences; Psychology; Psychology, Multidisciplinary; Zoology SC Behavioral Sciences; Psychology; Zoology GA V33ZM UT WOS:000209056700001 PM 17115853 ER PT J AU Gallagher, L AF Gallagher, L. TI Autism: Complex genetics - Complex phenotype SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE autistic spectrum disorder; genetics C1 Univ Dublin Trinity Coll, Dublin 2, Ireland. NR 0 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 NOV PY 2006 VL 50 BP 782 EP 782 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500008 ER PT J AU Howlin, P AF Howlin, P. TI Improving the quality of autism intervention research SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE autism; ASD; intervention research C1 Inst Psychiat, London, England. NR 0 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 NOV PY 2006 VL 50 BP 782 EP 782 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500009 ER PT J AU Murphy, D AF Murphy, D. TI Biological differences in autism - So what? SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE autistic spectrum disorder; neurobiology; neurotransmitters C1 Inst Psychiat, London, England. NR 0 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 NOV PY 2006 VL 50 BP 782 EP 782 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500007 ER PT J AU Ousely, OY Rockers, K Walker, E Coleman, K Cubells, JF AF Ousely, O. Y. Rockers, K. Walker, E. Coleman, K. Cubells, J. F. TI Autism-spectrum and schizophrenia-prodrome symptoms in young adults with 22q11 Deletion Syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE 2q11DS; psychosis; autistic spectrum disorder C1 Emory Univ, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA. Emory Univ, Dept Human Genet, Atlanta, GA 30322 USA. Emory Univ, Dept Psychol, Atlanta, GA 30322 USA. NR 0 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 NOV PY 2006 VL 50 BP 785 EP 785 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500015 ER PT J AU Freitag, CM Haberlen, M von Gontard, A Reith, W Krick, C AF Freitag, C. M. Haeberlen, M. von Gontard, A. Reith, W. Krick, C. TI Motion perception in autism: A functional MRI study SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE autism; fMRI; motion perception C1 Saarland Univ Hosp, Dept Child & Adolescent Psychiat, Homburg, Germany. Saarland Univ Hosp, Dept Neuroradiol, Homburg, Germany. NR 0 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 NOV PY 2006 VL 50 BP 786 EP 786 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500019 ER PT J AU Toal, F Daly, EM Page, L Deeley, Q Cutter, B Deeley, Q Hallaghan, B Chitnis, XA Curran, S Robertson, D Murphy, C Murphy, KMC Murphy, DGM AF Toal, F. Daly, E. M. Page, L. Deeley, Q. Cutter, B. Deeley, Q. Hallaghan, B. Chitnis, X. A. Curran, S. Robertson, D. Murphy, C. Murphy, K. M. C. Murphy, D. G. M. TI The relationship between clinical phenotype and brain anatomy in autistic spectrum disorder: An sMRI study SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE autism; Asperger; phenotype; sMRI C1 Beaumont Hosp, Dept Psychiat, Royal Coll Surg Ireland, Dublin 9, Ireland. Inst Psychiat, Sect Brain Maturat, Dept Psychol Med, London, England. RI daly, eileen/B-6716-2011; Murphy, Kieran/D-3577-2012 NR 0 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 NOV PY 2006 VL 50 BP 786 EP 786 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500018 ER PT J AU Tartaglia, NR Hansen, RL Reynolds, A Hessl, D Bacalman, S Goodlin-Jones, B Deprey, L Hagerman, RJ AF Tartaglia, N. R. Hansen, R. L. Reynolds, A. Hessl, D. Bacalman, S. Goodlin-Jones, B. Deprey, L. Hagerman, R. J. TI Attention deficit hyperactivity disorder and autism spectrum disorders in males with XXY, XYY and XXYY syndromes SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE sex chromosome aneuploidy; XXY; XYY; XXYY; ADHD; autism C1 Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Childrens Hosp, Denver, CO 80218 USA. NR 0 TC 4 Z9 4 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 NOV PY 2006 VL 50 BP 787 EP 787 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500020 ER PT J AU Jacobs, D Willekens, D de Die-Smulders, C Fryns, JP Steyaert, J AF Jacobs, D. Willekens, D. de Die-Smulders, C. Fryns, J. -P. Steyaert, J. TI Autism spectrum disorders, delusions and overvalued ideas in juvenile myotonic dystrophy SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE myotonic dystrophy; psychosocial functioning C1 Univ Limburg, Acad Hosp Maastricht, Dept Clin Genet, Maastricht, Netherlands. Katholieke Univ Leuven, Dept Child & Adolescent Psychiat, Louvain, Belgium. Katholieke Univ Leuven, Ctr Human Genet, Louvain, Belgium. RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 NR 0 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 NOV PY 2006 VL 50 BP 789 EP 789 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500027 ER PT J AU Hagerman, PJ Goetz, CG Leehey, MA Zhang, L Li, L Nguyen, D Hall, D Tartaglia, N Cogswell, J Farrell, GF Tassone, F Maselli, R Hagerman, RJ Berry-Kravis, E AF Hagerman, P. J. Goetz, C. G. Leehey, M. A. Zhang, L. Li, L. Nguyen, D. Hall, D. Tartaglia, N. Cogswell, J. Farrell, G. F. Tassone, F. Maselli, R. Hagerman, R. J. Berry-Kravis, E. TI Peripheral neuropathy in fragile X-associated tremor/ataxia syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE autism; neurodegeneration; RNA toxicity; fragile X syndrome C1 Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Davis, CA 95616 USA. Rush Univ, Ctr Med, Dept Neurol Sci, Chicago, IL 60612 USA. Univ Colorado, Hlth Sci Ctr, Dept Neurol, Denver, CO USA. Univ Calif Davis, Med Ctr, Dept Neurol, Sacramento, CA 95817 USA. N Carolina State Univ, Dept Stat, Raleigh, NC 27695 USA. Univ Calif Davis, Sch Med, Div Biostat, Davis, CA 95616 USA. Univ Calif Davis, Med Ctr, MIND Inst, Sacramento, CA 95817 USA. Univ Calif Davis, Med Ctr, EMG Lab, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Pediat, Sacramento, CA 95817 USA. Rush Univ, Med Ctr, Dept Neurol Sci, Chicago, IL 60612 USA. Rush Univ, Med Ctr, Dept Pediat, Chicago, IL 60612 USA. Rush Univ, Med Ctr, Dept Biochem, Chicago, IL 60612 USA. NR 0 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 NOV PY 2006 VL 50 BP 793 EP 793 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500037 ER PT J AU Steyaert, J Castermans, D Devos, R Creemers, J Fryns, JP Devriendt, K AF Steyaert, J. Castermans, D. Devos, R. Creemers, J. Fryns, J. -P. Devriendt, K. TI Studies of three candidate genes suggests that errors in the regulated secretion pathway may underlie autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract DE genetics; candidate genes; autism C1 UZ Leuven, Louvain, Belgium. RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 NR 0 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 NOV PY 2006 VL 50 BP 796 EP 796 PN 11 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 087WM UT WOS:000240773500044 ER PT J AU Jacquemont, ML Sanlaville, D Redon, R Raoul, O Cormier-Daire, V Lyonnet, S Amiel, J Le Merrer, M Heron, D de Blois, MC Prieur, M Vekemans, M Carter, NP Munnich, A Colleaux, L Philippe, A AF Jacquemont, M-L Sanlaville, D. Redon, R. Raoul, O. Cormier-Daire, V. Lyonnet, S. Amiel, J. Le Merrer, M. Heron, D. de Blois, M-C Prieur, M. Vekemans, M. Carter, N. P. Munnich, A. Colleaux, L. Philippe, A. TI Array-based comparative genomic hybridisation identifies high frequency of cryptic chromosomal rearrangements in patients with syndromic autism spectrum disorders SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; COPY NUMBER VARIATION; 45,X/46,XY MOSAICISM; INFANTILE-AUTISM; MICROARRAY; DELETIONS; CGH; TWIN; ABNORMALITIES; DUPLICATIONS AB Background: Autism spectrum disorders ( ASD) refer to a broader group of neurobiological conditions, pervasive developmental disorders. They are characterised by a symptomatic triad associated with qualitative changes in social interactions, defect in communication abilities, and repetitive and stereotyped interests and activities. ASD is prevalent in 1 to 3 per 1000 people. Despite several arguments for a strong genetic contribution, the molecular basis of a most cases remains unexplained. About 5% of patients with autism have a chromosome abnormality visible with cytogenetic methods. The most frequent are 15q11 - q13 duplication, 2q37 and 22q13.3 deletions. Many other chromosomal imbalances have been described. However, most of them remain undetectable using routine karyotype analysis, thus impeding diagnosis and genetic counselling. Methods and results: 29 patients presenting with syndromic ASD were investigated using a DNA microarray constructed from large insert clones spaced at approximately 1 Mb intervals across the genome. Eight clinically relevant rearrangements were identified in 8 (27.5%) patients: six deletions and two duplications. Altered segments ranged in size from 1.4 to 16 Mb ( 2 - 19 clones). No recurrent abnormality was identified. Conclusion: These results clearly show that array comparative genomic hybridisation should be considered to be an essential aspect of the genetic analysis of patients with syndromic ASD. Moreover, besides their importance for diagnosis and genetic counselling, they may allow the delineation of new contiguous gene syndromes associated with ASD. Finally, the detailed molecular analysis of the rearranged regions may pave the way for the identification of new ASD genes. C1 Hop Necker Enfants Malad, INSERM, U781, F-75015 Paris, France. Hop Necker Enfants Malad, Dept Genet, F-75015 Paris, France. Wellcome Trust Sanger Inst, Cambridge, England. Hop La Pitie Salpetriere, Dept Genet, Paris, France. RP Philippe, A (reprint author), Hop Necker Enfants Malad, INSERM, U781, 149 Rue Sevres, F-75015 Paris, France. 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Med. Genet. PD NOV PY 2006 VL 43 IS 11 BP 843 EP 849 DI 10.1136/jmg.2006.043166 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 101YW UT WOS:000241778500002 PM 16840569 ER PT J AU Janusonis, S Anderson, GM Shifrovich, I Rakic, P AF Janusonis, Skirmantas Anderson, George M. Shifrovich, Ilya Rakic, Pasko TI Ontogeny of brain and blood serotonin levels in 5-HT1A receptor knockout mice: potential relevance to the neurobiology of autism SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE autism; blood platelets; brain development; hyperserotonemia; 5-hydroxytryptamine (serotonin); 5-HT1A ID NORMAL ANXIETY-LIKE; 5-HYDROXYTRYPTAMINE RELEASE; PLATELET SEROTONIN; SMALL-INTESTINE; TRYPTOPHAN; MODEL; MOUSE; RAT; MECHANISMS; EXPRESSION AB The most consistent neurochemical finding in autism has been elevated group mean levels of blood platelet 5-hydroxytryptamine (5-HT, serotonin). The origin and significance of this platelet hyperserotonemia remain poorly understood. The 5-HT1A receptor plays important roles in the developing brain and is also expressed in the gut, the main source of platelet 5-HT. Post-natal tissue levels of 5-HT, 5-hydroxyindoleacetic acid (5-HIAA) and tryptophan were examined in the brain, duodenum and blood of 5-HT1A receptor-knockout and wild-type mice. At 3 days after birth, the knockout mice had lower mean brain 5-HT levels and normal mean platelet 5-HT levels. Also, at 3 days after birth, the mean tryptophan levels in the brain, duodenum and blood of the knockout mice were around 30% lower than those of the wild-type mice. By 2 weeks after birth, the mean brain 5-HT levels of the knockout mice normalized, but their mean platelet 5-HT levels became 24% higher than normal. The possible causes of these dynamic shifts were explored by examining correlations between central and peripheral levels of 5-HT, 5-HIAA and tryptophan. The results are discussed in relation to the possible role of 5-HT in the ontogeny of autism. 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PD NOV PY 2006 VL 17 IS 11 BP 717 EP 727 DI 10.1016/j.jnutbio.2006.02.001 PG 11 WC Biochemistry & Molecular Biology; Nutrition & Dietetics SC Biochemistry & Molecular Biology; Nutrition & Dietetics GA 100CN UT WOS:000241644900001 PM 16650750 ER PT J AU Shastri, M Alla, L Sabaratnam, M AF Shastri, Manan Alla, Lakshmiramana Sabaratnam, Manga TI Aripiprazole use in individuals with intellectual disability and psychotic or behaviourat disorders: a case series SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Article DE aripiprazole; schizophrenia; intellectual disability; psychotic disorders; behavioural disorders; challenging behaviour ID MENTAL HANDICAP; PSYCHIATRIC-DISORDERS; SCHIZOPHRENIA; RETARDATION; EPILEPSY; ILLNESS; ADULTS; DRUGS; TERM AB People with intellectual disabilities may be at greater risk of developing movement disorders as a consequence of their underlying neurological damage, especially when they are treated with typical antipsychotic agents. Aripiprazole is a novel antipsychotic quinolone derivative that has been approved for the treatment of schizophrenia in adults. However, there are few reports on the use of aripiprazole in people with intellectual disabilities. Herein, we report on the use of aripiprazole in five individuals with intellectual disabilities and psychotic illness (four cases) or challenging behaviour (one case). Four of the five patients had an additional diagnosis of schizophrenia and one had autism spectrum disorder and challenging behaviour. Issues related to the usefulness of aripiprazole in the management of schizophrenia and challenging behaviour in people with intellectual disabilities are also discussed. Aripiprazole was well tolerated and effective in each of the cases and appears to be a safe and efficacious alternative in the management of patients with both intellectual disabilities and schizophrenia. 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Psychopharmacol. PD NOV PY 2006 VL 20 IS 6 BP 863 EP 867 DI 10.1177/0269881106067765 PG 5 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 108EZ UT WOS:000242224400016 PM 16891339 ER PT J AU Friedlander, AH Vagiela, JA Paterno, VI Mahler, ME AF Friedlander, Arthur H. Vagiela, John A. Paterno, Victoria I. Mahler, Michael E. TI The neuropathology, medical management and dental implications of autism SO JOURNAL OF THE AMERICAN DENTAL ASSOCIATION LA English DT Review DE autism; neurodevelopmental disorders; Asperger's syndrome; pervasive developmental disorder; adverse effects; dental treatment ID ADVERSE DRUG-INTERACTIONS; DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; SLEEP PROBLEMS; CHILDREN; FAMILIES; DIAGNOSIS; PREVALENCE; SYMPTOMS; PATTERNS AB Background. A paucity of information exists in the dental literature about autism and its dental implications. Types of Studies Reviewed. The authors conducted a MEDLINE search for the period 2000 through 2006, using the term "autism," with the aim of defining the condition's clinical manifestations, dental and medical treatment and dental implications. Results. Autism is a severe developmental. brain disorder that appears in infancy, persists throughout life, and is characterized by impaired social interaction, abnormalities in communication (both verbal and nonverbal and restricted interests. Often accompanying the disorder are behavioral disturbances-such as self-mutilation, aggression, psychiatric symptoms and seizures-that necessitate the administration of multiple medications to help the affected person participate effectively in the educational and rehabilitative process. Clinical Implications. Dentists caring for people with autism must be familiar with the manifestations of the, disease and its associated features so that they can garner the maximum level of patient cooperation. 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Both children taught themselves to read before 5 years of age but showed minimal comprehension; both displayed obsessional reading and difficulties in social skills and attention. Brain CT scans were normal. Hyperlexia has been associated with hyperactivation of the left superior temporal cortex; we conclude that the orthographic route is a probable mechanism for the development of hyperlexia. (c) 2006 Elsevier B.V. All rights reserved. C1 Colegio Mayor Nuestra Senora Rosario, Sch Med, Neurosci Unit, Grp Neurosci, Bogota, Colombia. RP Talero-Gutierrez, C (reprint author), Calle 63D 24-31, Bogota, Colombia. 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This article discusses the evidence for the case that some children with autism may become autistic from neuronal cell death or brain damage sometime after birth as result of insult; and addresses the hypotheses that toxicity and oxidative stress may be a cause of neuronal insult in autism. The article first describes the Purkinje cell loss found in autism, Purkinje cell physiology and vulnerability, and the evidence for postnatal cell loss. Second, the article describes the increased brain volume in autism and how it may be related to the Purkinje cell loss. Third, the evidence for toxicity and oxidative stress is covered and the possible involvement of glutathione is discussed. Finally, the article discusses what may be happening over the course of development and the multiple factors that may interplay and make these children more vulnerable to toxicity, oxidative stress, and neuronal insult. C1 Univ Texas, SW Med Ctr, Dept Psychiat, Dallas, TX 75390 USA. 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Differences in clinical characteristics between CMV-related and unrelated SNHL cases were scrutinized. Methods. Using dried umbilical cord, we have recently developed a polymerase chain reaction (PCR)-based assay for the retrospective detection of congenital CMV infection. Medical records of 7 CMV-related patients identified from 31 SNHL patients by the assay were evaluated for the following: type and degree of hearing impairment, computed tomographic scan results, mental retardation, cerebral palsy, autism, and other multiple disorders. Results. Clinical characteristics of the seven CMV-related SNHL cases were as follows: 1) six of the seven exhibited severe bilateral SNHL, whereas one had severe unilateral SNHL in the right ear. Although the hearing levels of CMV-related patients were more greatly impaired than those of CMV-negative patients, there was no hearing impairment pattern specific to the CMV-related patients; 2) five patients had mental retardation, which was more frequent than in CMV-negative patients; 3) birth weights of the CMV-positive cases were relatively lower. Discussion: Although CMV-positive cases are clinically indistinguishable from CMV-negative cases, our PCR system allowed the retrospective diagnosis of CMV-related SNHL. Conclusion. CMV-related SNHL tends to accompany mental retardation and low birth weight more frequently than does CMV-negative SNHL. C1 Fukushima Med Univ, Dept Otolaryngol, Fukushima, Japan. Fukushima Med Univ, Dept Microbiol, Fukushima, Japan. Fukushima Rehabil Ctr, Dept Otolaryngol, Fukushima, Japan. Natl Inst Infect Dis, Dept Virol, Tokyo, Japan. RP Ogawa, H (reprint author), Fukushima Med Univ, Dept Otolaryngol, Fukushima, Japan. 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PD NOV PY 2006 VL 21 IS 5 BP 587 EP 596 DI 10.1111/j.1468-0017.2006.00293.x PG 10 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 099VT UT WOS:000241626000004 ER PT J AU Schellenberg, GD Dawson, G Sung, YJ Estes, A Munson, J Rosenthal, E Rothstein, J Flodman, P Smith, M Coon, H Leong, L Yu, CE Stodgell, C Rodier, PM Spence, MA Minshew, N McMahon, WM Wijsman, EM AF Schellenberg, G. D. Dawson, G. Sung, Y. J. Estes, A. Munson, J. Rosenthal, E. Rothstein, J. Flodman, P. Smith, M. Coon, H. Leong, L. Yu, C-E Stodgell, C. Rodier, P. M. Spence, M. A. Minshew, N. McMahon, W. M. Wijsman, E. M. TI Evidence for multiple loci from a genome scan of autism kindreds SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; autism spectrum disorder; linkage; genome scan; chromosome 7 ID SUSCEPTIBILITY GENE; TRANSLOCATION BREAKPOINT; DIAGNOSTIC INTERVIEW; SPECTRUM DISORDERS; INFANTILE-AUTISM; LINKAGE ANALYSIS; CHROMOSOME 7Q; SCREEN; SUPPORT; IDENTIFICATION AB We performed a genome-wide linkage scan using highly polymorphic microsatellite markers. To minimize genetic heterogeneity, we focused on sibpairs meeting the strict diagnosis of autism. In our primary analyses, we observed a strong linkage signal (P= 0.0006, 133.16 cM) on chromosome 7q at a location coincident with other linkage studies. When a more relaxed diagnostic criteria was used, linkage evidence at this location was weaker (P = 0.01). The sample was stratified into families with only male affected subjects ( MO) and families with at least one female affected subject (FC). The strongest signal unique to the MO group was on chromosome 11 (P = 0.0009, 83.82 cM), and for the FC group on chromosome 4 (P = 0.002, 111.41 cM). We also divided the sample into regression positive and regression negative families. The regression-positive group showed modest linkage signals on chromosomes 10 ( P= 0.003, 0 cM) and 14 ( P = 0.005, 104.2 cM). More significant peaks were seen in the regression negative group on chromosomes 3 ( P= 0.0002, 140.06 cM) and 4 ( P = 0.0005, 111.41 cM). Finally, we used language acquisition data as a quantitative trait in our linkage analysis and observed a chromosome 9 signal ( 149.01 cM) of P = 0.00006 and an empirical P-value of 0.0008 at the same location. Our work provides strong conformation for an autism locus on 7q and suggestive evidence for several other chromosomal locations. Diagnostic specificity and detailed analysis of the autism phenotype is critical for identifying autism loci. C1 Puget Sound Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, Seattle, WA 98108 USA. Univ Washington, Dept 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. Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. Univ Washington, Dept Psychiat & Behav Sci, Seattle, WA 98195 USA. Univ Washington, Dept Med, Div Med Genet, Seattle, WA 98195 USA. Univ Washington, Dept Biostat, Seattle, WA 98195 USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. Univ Utah, Dept Psychiat, Div Child & Adolescent Psychiat, Salt Lake City, UT 84112 USA. Univ Rochester, Med Ctr, Dept OB GYN, Rochester, NY 14627 USA. Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA 15260 USA. RP Schellenberg, GD (reprint author), Vet Affairs Med Ctr, 182B,1660 S Columbian Rd, Seattle, WA 98108 USA. 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Psychiatr. PD NOV PY 2006 VL 11 IS 11 BP 1049 EP 1060 DI 10.1038/sj.mp.4001874 PG 12 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 099FG UT WOS:000241578100009 PM 16880825 ER PT J AU Hughes, V AF Hughes, Virginia TI A shot of fear SO NATURE MEDICINE LA English DT News Item AB Spooked by reports that vaccines might cause diseases such as autism, many parents choose not to vaccinate their kids. But when their decision endangers others, asks Virginia Hughes, should the government step in? CR 2003, NAT MED, V362, P1498 1998, NAT MED, V351, P637 2004, NAT MED, V101, P13391 2003, NAT MED, V21, P4003 2004, NAT MED, V114, P187 2006, NAT MED, V355, P447 NR 6 TC 2 Z9 2 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK STREET, 9TH FLOOR, NEW YORK, NY 10013-1917 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 2006 VL 12 IS 11 BP 1228 EP 1229 DI 10.1038/nm1106-1228 PG 2 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 102WU UT WOS:000241844900007 PM 17088878 ER PT J AU Lee, LC Zachary, AA Leffell, MS Newschaffer, CJ Matteson, KJ Tyler, JD Zimmerman, AW AF Lee, Li-Ching Zachary, Andrea A. Leffell, Mary S. Newschaffer, Craig J. Matteson, Karla J. Tyler, John D. Zimmerman, Andrew W. TI HLA-DR4 in families with autism SO PEDIATRIC NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; RHEUMATOID-ARTHRITIS; SPECTRUM DISORDER; ASSOCIATION; MHC; LOCUS; DRB1; DR4 AB Autoimmune disorders are observed with increased frequency among parents of individuals with autism, particularly mothers. Because there is evidence supporting an association between autoimmune disorders and specific alleles of the human leukocyte antigen (HLA) system, we examined HLA types and subtypes in families with autism. Two groups were studied: 16 families selected from a geographically defined area in eastern Tennessee have males with a diagnosis of autism; and 33 families selected across all regions in the United States have multiple males having autism diagnosis. The HLA-DR4 frequencies of mothers, fathers, and children in these two groups were compared with a reference series of 475 normal, unrelated Caucasians. Results of HLA typing indicated that mothers and their sons in the geographically defined group had a significantly higher frequency of DR4 than normal control subjects (odds ratio = 5.54, 95% confidence interval = 1.74-18.67 and odds ratio = 4.20, 95% confidence interval = 1.37-13.27, respectively). No significant difference in the distribution of HLA alleles was evident between the United States-all region group and control subjects. Findings of this study are consistent with a hypothesis that prenatal maternal-fetal immune interaction can affect fetal brain development in a population residing in a geographically defined region. Such immune interactions may involve HLA and related genes in both genetic and epigenetic mechanisms during pregnancy. (c) 2006 by Elsevier Inc. All rights reserved. C1 Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Ctr Autism & Dev Disabil, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Immunogenet Lab, Baltimore, MD 21205 USA. Univ Tennessee, Med Ctr, Dev & Genet Ctr, Knoxville, TN USA. Univ Tennessee, Med Ctr, Transplant Lab, Knoxville, TN USA. Kennedy Krieger Inst, Dept Neurol & Dev Med, Baltimore, MD USA. 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Susser, Ezra TI The National Children's Study: A 21-year prospective study of 100 000 American children SO PEDIATRICS LA English DT Review DE National Children's Study; epidemiology; asthma; attention-deficit/hyperactivity disorder; autism; schizophrenia; obesity ID CORONARY HEART-DISEASE; TESTICULAR DYSGENESIS SYNDROME; IMPAIRED GLUCOSE-TOLERANCE; ABDOMINAL-WALL DEFECTS; ADULT-BLOOD PRESSURE; INNER-CITY HOMES; BONE LEAD LEVELS; PHYSICAL-ACTIVITY; ENVIRONMENTAL-HEALTH; RISK-FACTORS AB Prospective, multiyear epidemiologic studies have proven to be highly effective in discovering preventable risk factors for chronic disease. Investigations such as the Framingham Heart Study have produced blueprints for disease prevention and saved millions of lives and billions of dollars. To discover preventable environmental risk factors for disease in children, the US Congress directed the National Institute of Child Health and Human Development, through the Children's Health Act of 2000, to conduct the National Children's Study. The National Children's Study is hypothesis-driven and will seek information on environmental risks and individual susceptibility factors for asthma, birth defects, dyslexia, attention-deficit/hyperactivity disorder, autism, schizophrenia, and obesity, as well as for adverse birth outcomes. It will be conducted in a nationally representative, prospective cohort of 100 000 US-born children. Children will be followed from conception to 21 years of age. Environmental exposures (chemical, physical, biological, and psychosocial) will be assessed repeatedly during pregnancy and throughout childhood in children's homes, schools, and communities. Chemical assays will be performed by the Centers for Disease Control and Prevention, and banks of biological and environmental samples will be established for future analyses. Genetic material will be collected on each mother and child and banked to permit study of gene-environment interactions. Recruitment is scheduled to begin in 2007 at 7 Vanguard Sites and will extend to 105 sites across the United States. The National Children's Study will generate multiple satellite studies that explore methodologic issues, etiologic questions, and potential interventions. It will provide training for the next generation of researchers and practitioners in environmental pediatrics and will link to planned and ongoing prospective birth cohort studies in other nations. Data from the National Children's Study will guide development of a comprehensive blueprint for disease prevention in children. 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Ala'i-Rosales, Shahla S. Glenn, Sigrid S. Rosales-Ruiz, Jesus Greenspoon, Joel TI The effects of graduated exposure, modeling, and contingent social attention on tolerance to skin care products with two children with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE skin care products; graduated exposure; autism; modeling ID TACTILE DEFENSIVENESS; BEHAVIOR ANALYSIS; REINFORCEMENT; PHOBIAS; SCALE AB Children with autism may display unusual or fearful responses to common stimuli, such as skin care products. Parents of children with autism have often reported that their children will not allow the application of these types of substances to their skin and if the parent persists, the children become extremely upset and anxious. Such responding can interfere with adaptive functioning. The purpose of this study was to evaluate the effects of a treatment package involving graduated exposure to steps in an avoidance hierarchy, modeling, and social attention on the responding of two children with autism who displayed fearful responses to skin care products. Both avoidance and acceptance responses to skin care products were measured. Both changing criteria and multiple baseline experimental designs were employed to assess the effects of the intervention package. The results suggest that the package was successful in teaching tolerance of skin products for both children. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ N Texas, Dept Behav Anal, Denton, TX 76203 USA. RP Ala'i-Rosales, SS (reprint author), Univ N Texas, Dept Behav Anal, POB 310919, Denton, TX 76203 USA. 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TI Overselective stimulus control in residential school students with intellectual disabilities SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE stimulus overselectivity; developmental disabilities; residential schools; discrimination learning; matching to sample; autism ID OVER-SELECTIVITY; MENTAL-RETARDATION; RETARDED-CHILDREN; YOUNG-CHILDREN; ATTENTION; AUTISM; ADULTS; ADOLESCENTS; SAMPLE AB Overselective stimulus control was assessed in 29 students at residential schools for individuals with developmental disabilities. Overselectivity testing included three different delayed identity matching-to-sample tasks. Sample stimuli for the Form/Color Test were nine possible combinations of three colors and three forms. On each trial, the S+ stimulus was identical to the sample, one S- was the same color as the sample but a different form, and the other S- was the same form but a different color. Sample stimuli for the Two-Sample Test were two alphanumeric characters. The S+ stimulus was identical to one of the sample stimuli, and two S- stimuli were characters different from both samples. Sample stimuli for the Faces Test were six digital images of adult faces. On each trial, the S+ stimulus was identical to the sample, one S-stimulus was a non-matching face to which one sample feature had been added (e.g., an identical hat or scarf), and the other S-stimulus was an unaltered non-matching face. All participants were also tested with the Peabody Picture Vocabulary Test HI (PPVT) and the Autism Diagnostic Observation Schedule (ADOS). Results indicated overselective stimulus control on at least one test for 18 of the 29 participants. Overselectivity (a) was distributed across a range of PPVT mental age equivalent scores from < 1.75 to 8.83; (b) was more likely in individuals with higher ADOS scores; (c) was most likely on the Two-Sample Test; and (d) was found in five individuals on more than one of the tests. 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Dev. Disabil. PD NOV-DEC PY 2006 VL 27 IS 6 BP 618 EP 631 DI 10.1016/j.ridd.2005.07.004 PG 14 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 097RC UT WOS:000241464900004 PM 16290082 ER PT J AU Sidener, TM Shabani, DB Carr, JE Roland, JP AF Sidener, Tina M. Shabani, Daniel B. Carr, James E. Roland, Jonathan P. TI An evaluation of strategies to maintain mands at practical levels SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE mands; developmental disabilities; autism; communication training; multiple schedules; stimuli; control; delayed reinforcement ID DELAYED REINFORCEMENT AB In order to teach individuals with developmental disabilities to request stimuli they are motivated to obtain (mand), it is often necessary to initially deliver the item requested immediately and frequently. This may result in an undesirably high rate of mands that is impractical to maintain. The purpose of the current investigation was to extend the findings of previous research on the maintenance of low-rate mands within a communication-training context for children diagnosed with autism by evaluating the efficacy of two procedures: (1) signaled del ay-to-reinforcement and (2) multiple schedules. The results of our evaluation of multiple schedules replicated those of previous research; this arrangement was found for all participants to be effective in maintaining mands, at low rates under multiple schedules with a 270-s extinction component and 30-s reinforcement component. For all participants, signaled delay-to-reinforcement was ineffective in maintaining mands at the terminal criterion, a 270-s delay. (c) 2005 Elsevier Ltd. All rights reserved. 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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L., 1998, TEACHING LANGUAGE CH Sundberg M L, 1991, Anal Verbal Behav, V9, P81 TARBOX J, 2003, COGNITIVE BEHAV THER, P129 Tiger JH, 2004, J APPL BEHAV ANAL, V37, P517, DOI 10.1901/jaba.2004.37-517 NR 20 TC 6 Z9 6 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 NOV-DEC PY 2006 VL 27 IS 6 BP 632 EP 644 DI 10.1016/j.ridd.2005.08.002 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 097RC UT WOS:000241464900005 PM 16298103 ER PT J AU Jesus, M Garcia, M Gomez-Becerra, I Chavez-Brown, M Greer, D AF Jesus, Maria Garcia, Martin Gomez-Becerra, Inmaculada Chavez-Brown, Mapy Greer, Douglas TI Perspective taking and theory of the mind: conceptual and empirical issues. A complementary and pragmatic proposal SO SALUD MENTAL LA Spanish DT Article DE perspective taking; theory of mind; concepts; evidence; etiology; functional-contextual analysis ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; CHILDS THEORY; MENTAL-RETARDATION; ASPERGER-SYNDROME; FALSE BELIEF; FACIAL EXPRESSIONS; EMPATHY QUOTIENT; INDIVIDUALS; REPRESENTATION AB The present work completes an exhaustive revision of the delimitation of the ability of perspective taking from different points of view. First, perspective taking is defined as the ability of an individual to interpret his/hers emotional and mental states and those of others. Additionally, the term has also been used in medical settings to refer to a tactic intended to stop certain limiting feeling and/or thoughts and instead move feelings and thoughts towards a different direction. At the same time, perspective taking is considered to be at the heart of psychological phenomena such as empathy, that is, the capacity to distinguish what individuals know about themselves in a certain situation (how someone thinks, feels and behaves), self-awareness, interpersonal relations, and various social skills deficits. Second, this ability is conceptualized as a meta-cognition and it is assumed that the object of study, is the theory of the mind. Third, from a developmental perspective, data have shown that children four to five years old, without any psychological disabilities, have the ability to take somebody else's perspective. We reviewed different studies regarding the development of the abilities to express and interpret emotions as precursors to perspective taking. Subsequently, we revised and analyzed the tests or strategies most commonly used to evaluate the ability of perspective taking. Typically, the capacity of an individual to have "a theory of the mind" is determined through tests of false beliefs (such as the classic test of Sally-Anne, the "Smarties" test, "M&M's" and the "Maxi's" Test). Multiple variations of the tests of false beliefs have been conducted with flashcards or photographs, with characters in oral stories, and through the use of games. Additionally, over the last few years the focus of this body of research has evolved towards the elaboration and validation instruments to measure empathy. Among them are the tests of Empathy Quotient (EQ), the Friendship Questionnaire (FQ), and reading the "mind" in the eyes. It is important to note that these efforts have been focused mostly on individuals with Asperger's Syndrome or those with higher verbal capabilities. From this latter perspective, we propose empirical evidence that points out to differences in the ability, of perspective taking between children with or without autism. This is also shown in the results of previous studies, in which different levels of perspective taking skills were seen between children diagnosed with autism, and those diagnosed with Down Syndrome. It is important to note that this was not true when their verbal skills were not considered as a variable. Like-wise, other studies showed that children with autism were not the only ones that failed the theory of the mind tests, but that these tests were also failed by those children with deficits in language and cognitive skills. In this article, we present the results of a study that replicates previous findings which show that typical developing children perform better in perspective taking tests, followed by children diagnosed with Down Syndrome, and subsequently by children with autism. It was also noted that the typical developing children showed the highest level of verbal discrimination, followed by the children diagnosed with Down Syndrome, and finally the children diagnosed with autism. One important finding in this study is that all children benefited from the use of contextual prompts, which improved the number of correct responses across all the theory of the mind tests. Additionally, the data varied depending on the type of tests utilized to measure perspective taking skills. In this article, we have also reviewed the different explanations for the origins and development of perspective taking, among which the theory of the mind prevails. The ability to take someone else's perspective is explained by the development or maturation of an innate and specialized module of representations and knowledge, and the formation of conceptual structures of a higher order or meta-representations. Additionally, the ability to ignore perceptual information, salient or not, and to combine simultaneously various contexts are considered prerequisites. In other words, perspective taking speaks to the relationship between psychological constructs such as perception and knowledge. Additionally, it has been hypothesized that shared, joint, or independent attention can be a prerequisite for conversation, and may be the basis of a theory of the mind. In any case, the origins of the development of such a theory have been especially ubiquitous in terms of the executive function and possible relations with cerebral lesions or alterations. However, some authors consider that the process of central coherence may be relatively independent of a theory of the mind. The research of Baron-Cohen et al. has concentrated on identifying existing neurological deficits or organic changes such as bilateral lesions or the role of testosterone on the quality of social interactions and the restrictive social interests of individuals with autism. A similar interest exists in researching the difference in perspective taking and empathy abilities exhibited by members of the opposite sex. Continuing with the neurological foundations of the empathy is of full present time the discoveries regarding <> and this recent study with monkeys proposes a specific cerebral area for the formation of the meta-representation. These neurons discharge both when the individual performs an action and when the individual observes another person performing the same action. Finally, even in the light of all the above, other sources point toward the social root of perspective taking skills. Additionally, as indicated by the research of Howlin, Baron-Cohen & Hadwin, it is considered perspective. taking includes five different levels: a) simple visual perspective taking, b) the knowledge that different individuals can have separately the same thoughts, and c) understanding that "seeing leads to learning," followed by d) the ability to predict actions based on valid beliefs, and finally e) the ability to predict false beliefs. In the light of all of the above, once the radical conclusions of these investigations are viewed critically, the theory of the mind is viewed as a disputable theory of the delimitation of the cause and development of such skills. In addition, to the perspective taking tests themselves, the prerequisite skills of perspective taking need to be extensively analyzed. In fact, it has been shown that, in order to have an adequate performance on these tests of false beliefs, individuals should be able: 1. to remember and adequately retell their own past desires, thoughts, and past actions; 2. to retain an object in their mind, perceive a second object, and form a relationship between the two, as in a "symbolic function"; 3. to demonstrate the ability to pretend; and 4. to identify the role of age and verbal abilities in children as pre-requisites for an accurate performance on tests of false beliefs, and interpretations of the world. Lastly, we propose a pragmatic and complementary analysis the Theory of Mind based in the functional-contextual analysis of behavior. First, it is considered that perspective taking requires or is closely related to other social behaviors (such as taking turns when talking, initiating verbal responses in interpersonal relations, and the capacity for empathy). In the same manner, theory of mind requires an adequate level of simple and complex conditional discriminations, and these should be analyzed in terms of stimulus control and equivalence relations. In other words, this ability to infer thoughts, feeling, and emotions of others exists if the following pre-requisites are present: 1. the processes of the classical conditioning of the emotions, 2. a generalized imitation, and 3. the development of functional classes. Without these experiences or the capability to be affected by them, children (i.e. children with generalized autism) do not develop language adequately. Second, perspective taking implies that an observer's previous experiences and observations with certain events determine his/her reaction to responses emitted by others in similar circumstances. Finally, from a contextual perspective, it is considered that a speaker's relational frames play a role in this proess (for the discriminations I/you, here/there, now/later). These relational properties are abstracted through multiple exemplars or multiple learning opportunities to speak from one's own perspective in relation to others. C1 Univ Almeria, Dept Personalidad Evaluac & Tratamiento Psicol, Almeria 04120, Spain. Wagner Coll, New York, NY USA. Columbia Univ, Coll Teachers, New York, NY 10027 USA. RP Gomez-Becerra, I (reprint author), Univ Almeria, Dept Personalidad Evaluac & Tratamiento Psicol, Ctra Sacramento S-N La Canada de San Urbano, Almeria 04120, Spain. 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TI Abnormal brain size effect on the thalamus in autism SO PSYCHIATRY RESEARCH-NEUROIMAGING LA English DT Article DE thalamus; autism; MRI; brain volume; structural neuroimaging ID MAGNETIC-RESONANCE; BASAL GANGLIA; MRI; VOLUME; ACTIVATION; INDIVIDUALS; TOMOGRAPHY; PATTERNS; DISORDER; PATHWAY AB This study was conducted to examine the volume of the thalamus in autism and to investigate the effect of brain size on this structure in an attempt to replicate, in a larger sample, findings from a previous study reporting the existence of a relationship between brain volume and thalamus in healthy controls but not in individuals with autism. Additionally, the relationships between thalamic volumes and clinical features were examined. Volumetric measurements of the right and left thalamic nuclei were performed on MRI scans obtained from 40 high-functioning individuals with autism (age range: 8-45 years) and 41 healthy controls (age range: 9-43 years). No differences were observed between the two groups for unadjusted thalamic volumes. However, the expected linear relationship between TBV and thalamic volume was not observed in individuals with autism. Furthermore, no correlations were observed between thalarnic volumes and clinical features. Findings from this larger study are consistent with the previous report of an abnormal brain size effect on the thalamus in autism and support the possibility of abnormal connections between cortical and subcortical structures in this disorder. (c) 2006 Elsevier Ireland Ltd. All rights reserved. C1 Univ Pittsburgh, Dept Psychiat, Western Psychiat Inst & Clin, Sch Med, Pittsburgh, PA 15213 USA. Columbia Univ, Coll Phys & Surg, Dept Psychiat, New York, NY 10027 USA. New York State Psychiat Inst & Hosp, New York, NY 10032 USA. Wayne State Univ, Dept Psychiat, Detroit, MI USA. RP Hardan, AY (reprint author), Univ Pittsburgh, Dept Psychiat, Western Psychiat Inst & Clin, Sch Med, 3811 OHara St, Pittsburgh, PA 15213 USA. 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Taylor, Palmer TI Gene selection, alternative splicing, and post-translational processing regulate neuroligin selectivity for beta-neurexins SO BIOCHEMISTRY LA English DT Article ID ADHESION MOLECULE; AUTISM REVEALS; LAMM EQUATION; LNS DOMAIN; BINDING; MUTATION; SYNAPSE; PROTEIN; NLGN4; ACETYLCHOLINESTERASE AB Neuroligins 1-4 are postsynaptic transmembrane proteins capable of initiating presynaptic maturation via interactions with beta-neurexin. Both neuroligins and beta-neurexins have alternatively spliced inserts in their extracellular domains. Using analytical ultracentrifugation, we determined that the extracellular domains of the neuroligins sediment as dimers, whereas the extracellular domains of the beta-neurexins appear monomeric. Sedimentation velocity experiments of titrated stoichiometry ratios of beta-neurexin and neuroligin suggested a 2: 2 complex formation. 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Only a few family studies on the heredity of facial expressions have been performed, none of which compared the gestalt of movements in various emotional states; they compared only a few movements in one or two emotional states. No studies, to our knowledge, have compared movements of congenitally blind subjects with their relatives to our knowledge. Using two types of analyses, we show a correlation between movements of congenitally blind subjects with those of their relatives in think-concentrate, sadness, anger, disgust, joy, and surprise and provide evidence for a unique family facial expression signature. In the analysis "in-out family test," a particular movement was compared each time across subjects. Results show that the frequency of occurrence of a movement of a congenitally blind subject in his family is significantly higher than that outside of his family in think-concentrate, sadness, and anger. 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TI En2 knockout mice display neurobehavioral and neurochemical alterations relevant to autism spectrum disorder SO BRAIN RESEARCH LA English DT Article DE autism; animal model; ENGRAILED-2; development; serotonin; social behavior; aggression ID HOMEOBOX-TRANSCRIPTION-FACTOR; EARLY INFANTILE-AUTISM; SEROTONIN TRANSPORTER; CEREBELLAR DEVELOPMENT; SUSCEPTIBILITY LOCUS; GENOMEWIDE SCREEN; ENGRAILED GENES; MUTANT MICE; BRAIN-STEM; CHILDREN AB Autism spectrum disorder (ASD) is a prevalent and inheritable neurodevelopmental disorder. Recent human genetic studies are consistent with the homeobox transcription factor, ENGRAILED 2 (EN2), being an ASD susceptibility gene. En2 knockout mice (En2(-/-)) display subtle cerebellar neuropathological changes similar to what has been observed in the ASD brain. To investigate whether En2(-/-) mice displayed abnormal behavior relevant to ASD, they were monitored in tasks designed to assess social maturation as well as learning and memory. Deficits in social behavior were detected in En2(-/-) mice across maturation that included decreased play, reduced social sniffing and allogrooming, and less aggressive behavior. Deficits in two spatial learning and memory tasks were also observed. Because locomotor activity was a component of many of the behavioral tasks, this was measured at various stages of development. Locomotor activity was not compromised in the knockout. However, a more thorough analysis of motor behavior in En2(-/-) mice revealed deficits in specific motor tasks. To determine whether neurochemical changes were associated with these behavioral phenotypes, monoamine levels in specific brain regions were assessed. A cerebellar-specific increase in serotonin and its metabolite was observed. Interestingly, several reports have suggested that the serotonin pathway is affected in ASD. 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B PD OCT 5 PY 2006 VL 141B IS 7 BP 703 EP 703 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700083 ER PT J AU Staal, W Franke, L Vorstman, J Hochstenbach, R van Daalen, E Wijmenga, C van Engeland, H AF Staal, Wouter Franke, Lude Vorstman, Jacob Hochstenbach, Ron van Daalen, Emma Wijmenga, Cisca van Engeland, Herman TI Autism candidate genes identified with a gene interaction network software-tool SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 UMC Utrecht, Utrecht, Netherlands. Dept Human Genet, Utrecht, Netherlands. Child & Adolescent Psychiat, Utrecht, Netherlands. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 703 EP 703 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700082 ER PT J AU Vincent, J Marsha, C Noor, A Windpassinger, C Horike, S Choufani, S Stachowiak, B Skaug, J Sloman, L Kroisel, P Petek, E Roberts, W Scherer, S AF Vincent, John Marshall, Christian Noor, Abdul Windpassinger, Christian Horike, Shin-ichi Choufani, Sanaa Stachowiak, Beata Skaug, Jennifer Sloman, Leon Kroisel, Peter Petek, Erwin Roberts, Wendy Scherer, Stephen TI Molecular analysis of 8 autism patients with cytogenetic abnormalities SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Ctr Addict & Mental Hlth, Toronto, ON, Canada. Hosp Sick Children, Toronto, ON M5G 1X8, Canada. Inst Human Genet, Graz, Austria. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 MA O141 BP 714 EP 714 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700131 ER PT J AU Ma, DQ Jaworski, J Skaar, DA Konidari, A Haynes, C Abramson, RK Wright, HH Cuccaro, ML Gilbert, JR Haines, JL Pericak-Vance, MA AF Ma, Deqiong Jaworski, J. Skaar, D. A. Konidari, A. Haynes, C. Abramson, R. K. Wright, H. H. Cuccaro, M. L. Gilbert, J. R. Haines, J. L. Pericak-Vance, M. A. TI 12q14: A novel linkage region in extended autism families SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Ctr Human Genet, Durham, NC USA. Univ S Carolina, Sch Med, Columbia, SC USA. Ctr Human Genet Res, Nashville, TN USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 MA O204 BP 723 EP 723 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700171 ER PT J AU Masetti, GG Bonati, MT Gessi, A Cavalleri, F Cogliati, F Marchi, M Lievers, LS Caffo, E Larizza, L Macciardi, F Russo, S AF Masetti, Guia Guffanti Bonati, M. T. Gessi, Alessandra Cavalleri, Florinda Cogliati, Francesca Marchi, Margherita Lievers, Luisa Strik Caffo, Ernesto Larizza, Lidia Macciardi, Fabio Russo, Silvia TI Putative identification of susceptibility genes for autism on 15q11-q13: Role of UBE3A and ATP10A SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Univ Studi Milano, Segrate, Italy. Ist Italiano Auxol, Milan, Italy. Univ Modena, I-41100 Modena, Italy. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 MA 0249 BP 730 EP 731 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700206 ER PT J AU Santangelo, S Haddad, S Santos, T Fagerness, J Moilanen, I Mattila, ML Jussila, K Kuusikko, S Ignatius, J Yamaki, L Moorjani, P Pauls, D Ramesh, V AF Santangelo, Susan Haddad, Stephen Santos, Tulio Fagerness, Jesen Moilanen, Irma Mattila, Marja-Leena Jussila, Katja Kuusikko, Sanna Ignatius, Jaakko Yamaki, Lesley Moorjani, Priya Pauls, David Ramesh, Vijaya TI Pam as a candidate gene for autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Boston, MA 02115 USA. CHGR, Psychiat Neurodev Genet Unit, Boston, MA USA. Massachusetts Gen Hosp, Ctr Human Genet Res, Boston, MA USA. Univ Oulu, Dept Child Psychiat, FIN-90570 Oulu, Finland. Univ Oulu, Genet Lab, FIN-90570 Oulu, Finland. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 735 EP 736 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700229 ER PT J AU Martins, M Correia, C Currais, A Coutinho, AM Marques, C Ataide, A Miguel, TS Almeida, J Bento, C Morgadinho, T Oliveira, G Vicente, AM AF Martins, Madalena Correia, Catarina Currais, Antonio Margarida Coutinho, Ana Marques, Carla Ataide, Assuncao Sao Miguel, Teresa Almeida, Joana Bento, Celeste Morgadinho, Teresa Oliveira, Guiomar Moura Vicente, Astrid TI Association of the GAD1 candidate gene with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Inst Gulbenkian Ciencias, Oeiras, Portugal. Inst Gulbenkian Ciencias, Lisbon, Portugal. Hosp Pediat Coimbra, Coimbra, Portugal. Univ Coimbra, Fac Med, Coimbra, Portugal. RI Oliveira, Guiomar/I-7255-2013 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 736 EP 736 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700231 ER PT J AU Sykes, N Lamb, J Maestrini, E Winchester, L Morris, A Butler, H Bacchelli, E Blasi, F Barnby, G Sousa, I Bailey, AJ Monaco, AP AF Sykes, Nuala Lamb, J. Maestrini, E. Winchester, L. Morris, A. Butler, H. Bacchelli, E. Blasi, F. Barnby, G. Sousa, I. Bailey, A. J. Monaco, A. P. TI High-density SNP association study of the autism susceptibility loci on chromosome 7q SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Univ Oxford, Oxford OX1 2JD, England. Wellcome Trust Ctr Human Genet, Oxford, England. Univ Bologna, I-40126 Bologna, Italy. Univ Oxford, Dept Psychiat, Oxford OX1 2JD, England. RI Bailey, Anthony/J-2860-2014 OI Bailey, Anthony/0000-0003-4257-972X NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 736 EP 736 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700230 ER PT J AU Castermans, D Freson, K De Vos, R Van de Ven, W Geet, CV Steyaert, J Creemers, J Devriendt, K AF Castermans, Dries Freson, Kathleen De Vos, Rita Van de Ven, Wim Geet, Christel Ven Steyaert, Jean Creemers, John Devriendt, Koen TI Amisyn, SCAMP5 and NBEA are candidate genesfor autism and suggest a role for neuron vesicle trafficking in the pathogenesis of autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Catholic Univ Leuven, Louvain, Belgium. RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 755 EP 755 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700315 ER PT J AU Curran, S Powell, J Pugliese, L Neale, BM Murphy, D Bolton, PF AF Curran, Sarah Powell, John Pugliese, Luca Neale, Ben M. Murphy, Declan Bolton, Patrick F. TI An association analysis of functional serotonin transporter polymorphisms in autism spectrum disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet RI Powell, John/G-4412-2011 OI Powell, John/0000-0001-6124-439X NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 758 EP 758 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700329 ER PT J AU Correia, CC Martins, M Coutinho, AM Marques, C Miguel, T Ataide, A Almeida, J Borges, L Gallagher, L Conroy, J Gill, M Oliveira, G Vicente, AM AF Correia, Catarina Catarina Martins, Madalena Coutinho, Ana Margarida Marques, Carla Miguel, Teresa Ataide, Assuncao Almeida, Joana Borges, Luis Gallagher, Louise Conroy, Judith Gill, Michael Oliveira, Guiomar Vicente, Astrid Moura TI Association of the beta-integrin subunit gene with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Gulbenkian Inst Sci, Oeiras, Portugal. Ctr Desenvolvimento Crianca, Coimbra, Portugal. Reg Educ Regiao, Coimbra, Portugal. Smurfit Inst, Dept Genet, Dublin, Ireland. RI Oliveira, Guiomar/I-7255-2013 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 759 EP 759 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700331 ER PT J AU Gauthier, J Drapeau, P Michaud, J Neri, C Dube, MP Cossette, P Bouvier, M Carbonetto, S Fombonne, E AF Gauthier, Julie Drapeau, Pierre Michaud, Jacques Neri, Christian Dube, Marie-Pierre Cossette, Patrick Bouvier, Michel Carbonetto, Savatore Fombonne, Eric TI High throughput strategy for the identification and characterization of genes involved in schizophrenia and autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 CHUM Res Ctr, Montreal, PQ, Canada. Univ Montreal, Montreal, PQ, Canada. INSERM, Paris, France. McGill Univ, Montreal, PQ, Canada. RI Neri, Christian/F-6729-2013; Dube, Marie-Pierre/B-9364-2008 OI Dube, Marie-Pierre/0000-0001-8442-4393 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 761 EP 761 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700341 ER PT J AU Cochrane, LE Conroy, J Anderson, G Gallagher, L Gill, M AF Cochrane, Lynne Elizabeth Conroy, Judith Anderson, George Gallagher, Louise Gill, Michael TI Four genes analysed for association with autism and DBH levels SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Univ Dublin Trinity Coll, Dublin 2, Ireland. Yale Univ, New Haven, CT 06520 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 766 EP 766 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700362 ER PT J AU Turunen, J Ylisaukko-oja, T Kilpinen, H Rehnstrom, K Kempas, E Vanhala, R Wendt, TNV von Wendt, L Peltonen, L AF Turunen, Joni Ylisaukko-oja, Tero Kilpinen, Helena Rehnstrom, Karola Kempas, Elli Vanhala, Raija Wendt, Taina Nieminen-von von Wendt, Lennart Peltonen, Leena TI Association analysis of SLC25A12 and EN2 in the Finnish families with autism-spectrum disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Natl Publ Hlth Inst, Helsinki, Finland. Hosp Children & Adolescents, Helsinki, Finland. NR 0 TC 1 Z9 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 766 EP 766 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700364 ER PT J AU Yang, MS Conroy, J Hawi, Z Gallagher, L Gill, M AF Yang, Mao-Shen Conroy, Judith Hawi, Ziarih Gallagher, Louise Gill, Michael TI PRKCB1 is not associated with autism in the Irish population SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Trinity Coll Dublin, Dublin, Ireland. NR 0 TC 1 Z9 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 766 EP 766 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700360 ER PT J AU Bacchelli, E Blasi, F Carone, S Toma, C Lamb, J Sykes, N Barnby, G Morris, A Winchester, L Butler, H Bailey, AJ Monaco, AP Maestrini, E AF Bacchelli, Elena Blasi, Francesca Carone, Simona Toma, Claudio Lamb, Janine Sykes, Nuala Barnby, Gabrielle Morris, Andrew Winchester, Laura Butler, Helen Bailey, Anthony J. Monaco, Anthony P. Maestrini, Elena CA Consortium IMGSAC TI A gene centric association study of 1500 SNPs in the chromosome 2q autism susceptibility locus SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Univ Bologna, I-40126 Bologna, Italy. Wellcome Trust Ctr Human Genet, Oxford, England. Pk Hosp Children, Oxford, England. RI Bolton, Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014 OI Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X NR 0 TC 1 Z9 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 767 EP 768 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700370 ER PT J AU Powell, J Curran, S Neal, B Dworzynski, K Bolton, P AF Powell, John Curran, Sarah Neal, Ben Dworzynski, Katharina Bolton, Patrick TI A positive haplotype association of the chromosome 15 gamma-amino butyric acid beta 3 subunit gene (GABRB3) with autism spectrum disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Kings Coll London, Inst Psychiat, London WC2R 2LS, England. RI Powell, John/G-4412-2011; Bolton, Patrick/E-8501-2010 OI Powell, John/0000-0001-6124-439X; Bolton, Patrick/0000-0002-5270-6262 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 767 EP 767 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700367 ER PT J AU Betancur, C Cai, GQ Chaste, P Nygren, G Goldsmith, J Reicher, J Anckarsater, H Rastam, M Leboyer, M Gillberg, C Verloes, A Buxbaum, JD AF Betancur, Catalina Cai, Guiquing Chaste, Pauline Nygren, Gudrun Goldsmith, Juliet Reicher, Jennifer Anckarsater, Henrik Rastam, Maria Leboyer, Marion Gillberg, Christopher Verloes, Alain Buxbaum, Joseph D. TI Mutation screening of the PTEN gene in patients with autism and macrocephaly SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 INSERM, U513, Creteil, France. Mt Sinai Sch Med, New York, NY USA. Univ Paris 12, INSERM, U513, Creteil, France. Dept Child & Adolescent Psych, Gothenburg, Sweden. Hop Robert Debre, Clin Genet Unit, F-75019 Paris, France. RI Anckarsater, Henrik/C-2244-2009 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 768 EP 768 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700371 ER PT J AU Vorsanova, S Iourov, I Voinova-Ulas, V Gorbachevskaya, N Kolotii, A Beresheva, A Demidova, I Ktavetz, V Monachov, V AF Vorsanova, Svetlana Iourov, Ivan Voinova-Ulas, Victoria Gorbachevskaya, Natalia Kolotii, Alexei Beresheva, Alphia Demidova, Irina Ktavetz, Viktor Monachov, Viktor TI Increased rate of low-level chromosomal mosaicism in autism: An interphase FISH survey SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 14th World Congress on Psychiatric Genetics CY OCT 28-NOV 01, 2006 CL Cagliari, ITALY SP Int Soc Psychiat Genet C1 Inst Pediat & Children Surg, Moscow, Russia. Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. RI Iourov, Ivan/O-7684-2014 OI Iourov, Ivan/0000-0002-4134-8367 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD OCT 5 PY 2006 VL 141B IS 7 BP 770 EP 770 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 089JW UT WOS:000240877700381 ER PT J AU Uhhaas, PJ Singer, W AF Uhhaas, Peter J. Singer, Wolf TI Neural synchrony in brain disorders: Relevance for cognitive dysfunctions and pathophysiology SO NEURON LA English DT Review ID HIGH-FREQUENCY OSCILLATIONS; HIGH-FUNCTIONING AUTISM; HIPPOCAMPUS IN-VITRO; WHITE-MATTER CHANGES; WORKING-MEMORY TASK; CAT VISUAL-CORTEX; ALZHEIMERS-DISEASE; EEG SYNCHRONIZATION; GAMMA ACTIVITY; GAP-JUNCTIONS AB Following the discovery of context-dependent synchronization of oscillatory neuronal responses in the visual system, novel methods of time series analysis have been developed for the examination of task- and performance-related oscillatory activity and its synchronization. Studies employing these advanced techniques revealed that synchronization of oscillatory responses in the beta- and gamma-band is involved in a variety of cognitive functions, such as perceptual grouping, attention-dependent stimulus selection, routing of signals across distributed cortical networks, sensory-motor integration, working memory, and perceptual awareness. Here, we review evidence that certain brain disorders, such as schizophrenia, epilepsy, autism, Alzheimer's disease, and Parkinson's are associated with abnormal neural synchronization. The data suggest close correlations between abnormalities in neuronal synchronization and cognitive dysfunctions, emphasizing the importance of temporal coordination. Thus, focused search for abnormalities in temporal patterning may be of considerable clinical relevance. C1 Max Planck Inst Brain Res, Dept Neurophysiol, D-60528 Frankfurt, Germany. Univ Frankfurt, Dept Psychiat, Lab Neurophysiol & Neuroimaging, D-60528 Frankfurt, Germany. Univ Frankfurt, Frankfurt Inst Adv Studies, D-60438 Frankfurt, Germany. RP Uhhaas, PJ (reprint author), Max Planck Inst Brain Res, Dept Neurophysiol, Deutschordenstr 46, D-60528 Frankfurt, Germany. 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Set shifting tasks are some of the best understood and widely used human neuropsychological tasks, with clinical relevance to traumatic brain injury, schizophrenia, autism, obsessive compulsive disorder, trichotillomania, and many other disorders. Here we report the first successful modification of a human set shifting neuropsychological task, the Intra-Dimensional Extra-Dimensional (IDED) task, for use with mice. We presented mice with a series of compound discrimination and reversal tasks where one stimulus dimension consistently cued reward. Task performance improved with a new set of compound stimuli, as did reversal performance-indicating the formation of a cognitive-attentional set. We then overtrained a subset of the mice, and presented control and overtrained mice with a new compound discrimination where a novel stimulus dimension cued reward. 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TI Today's epidemics in children: Possible relations to environmental pollution and suggested preventive measures SO ACTA PAEDIATRICA LA English DT Article DE children; environment; health; epidemic ID CHILDHOOD-CANCER INCIDENCE; PRENATAL EXPOSURE; DIABETES-MELLITUS; DIOXIN EXPOSURE; PREGNANCY; BRAIN; BIRTH; PRODUCTS; DISORDER; TRENDS AB Background: Facts and hypotheses on the relationship between some children's diseases or disorders and external stressors during the developmental stage of a child, both prenatally and postnatally are described in literature. In this paper the following changes in patterns and causes of the main childhood illnesses are summarized and recommendations for actions are made. Prematurity Intra-uterine growth restriction Testicular dysgenesis syndrome center dot Type I and Type II diabetes Asthma, atopy and hay fever Autism Attention deficit hyperactivity disorder (ADHD) Learning disabilities Cancer Obesity Hearing problems Results: Literature provides a growing amount of information on changing patterns in childhood diseases. Conclusions: The following recommendations for action are formulated Immediate research on endocrine disrupters in relation to prematurity Diabetes: avoid Maillard Compounds in liquid baby food and in food in general: promote breastfeeding Asthma: avoid exposure to smoking, the use of chemical household products, dioxin and dioxin-like chemicals, and avoid air pollution with high levels of particulate matter, especially around conception, during pregnancy and in the first years of life Autism: more research on incidence and causes ADHD and learning disabilities: more research on prevalence and causes. Preventions: 1) preconception counselling to avoid potentially harmful substances; 2) controlling and further lowering levels of polychlorinated biphenyls, lead and methyl mercury Cancer: promote breastfeeding, carry out research into effects of foetal exposure to internal fission-product radionuclides Obesity: stop smoking in pregnancy, avoid parental obesity, longer night sleep Hearing problems: lower noise levels in discotheques, promote the day-evening-night level to avoid noise (longer night sleep). C1 Ecobaby Fdn, NL-3634 AT Loenersloot, Netherlands. Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, NL-1105 AZ Amsterdam, Netherlands. Publ Hlth Serv Gelderland Midden, Arnhem, Netherlands. Fed Environm Agcy, Berlin, Germany. Natl Inst Publ Hlth, Copenhagen, Denmark. Bavarian Hlth & Food Safety Author, Dept Environm Hlth, Oberschleissheim, Germany. Univ Groningen, Groningen, Netherlands. Karolinska Inst, Div Toxicol & Neurotoxicol, Inst Environm Med, Stockholm, Sweden. Inst Med Res & Occupat Hlth, Zagreb 41000, Croatia. Med Univ Lodz, Dept Environm Epidemiol, PL-90131 Lodz, Poland. Med Univ Lodz, Dept Informat & Stat, PL-90131 Lodz, Poland. Norwegian Knowledge Ctr Hlth Serv, Oslo, Norway. Ullevaal Univ Hosp, Dept Neurol, Oslo, Norway. Med Univ Vienna, Ctr Publ Hlth, Inst Environm Hlth, Vienna, Austria. Kaunas Univ Med, Inst Biomed Res, Kaunas, Lithuania. Bristol Haematol & Oncol Ctr, Dept Med Phys, Bristol, Avon, England. Univ Roma La Sapienza, Sch Med 2, Dept Paediat, Rome, Italy. Inst Veille Sanit, St Maurice, France. Vlaamse Instelling Technol Onderzoek, Mol, Belgium. European Commiss, Joint Res Ctr, Ispra, Italy. Westfries Gasthuis, Dept Paediat & Neonatol, Hoorn, Netherlands. RP Koppe, JG (reprint author), Ecobaby Fdn, Hollandstr 6, NL-3634 AT Loenersloot, Netherlands. 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PD OCT PY 2006 VL 95 SU 453 BP 18 EP 25 DI 10.1080/08035320600885846 PG 8 WC Pediatrics SC Pediatrics GA 098DU UT WOS:000241502000004 PM 17000565 ER PT J AU Maimburg, RD Vaeth, M AF Maimburg, R. D. Vaeth, M. TI Perinatal risk factors and infantile autism SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE autistic disorders; pregnancy; asphyxia; abnormalities; foetal growth retardation ID OBSTETRIC COMPLICATIONS; NEONATAL COMPLICATIONS; POPULATION; DISORDER; PREGNANCY; CHILDREN; SPECTRUM; AGE AB Objective: Suboptimal conditions during pregnancy and birth have been suggested as a cause of infantile autism. We have studied the association between obstetric factors and infantile autism. Method: A population-based, matched case-control study of infantile autism. Conditional logistic regression was used to calculate odds ratios (OR) and 95% confidence intervals (CI). Results: The risk of infantile autism was increased for mothers aged > 35 years, with foreign citizenship, and mothers who used medicine during pregnancy. A higher risk of infantile autism was seen among children with low birth weight and with congenital malformations. Birth interventions, pathological cardiotocography, green amnion fluid and acidosis during delivery were not associated with increased risk for infantile autism. Conclusion: Our findings suggest that suboptimal birth conditions are not an independent risk factor for infantile autism. A high prevalence of low birth weight and birth defects among autism cases seems to explain the suboptimal birth outcome. C1 Aarhus Univ, Dept Epidemiol & Social Med, Inst Publ Hlth, DK-8000 Aarhus, Denmark. Univ Aarhus, Dept Biostat, Inst Publ Hlth, Aarhus, Denmark. RP Maimburg, RD (reprint author), Aarhus Univ, Dept Epidemiol & Social Med, Inst Publ Hlth, Vennelyst Blvd 6, DK-8000 Aarhus, Denmark. 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PD OCT PY 2006 VL 114 IS 4 BP 257 EP 264 DI 10.1111/j.1600-0447.2006.00805.x PG 8 WC Psychiatry SC Psychiatry GA 082DA UT WOS:000240365700006 PM 16968363 ER PT J AU Kodish, S Kulinna, PH Martin, J Pangrazi, R Darst, P AF Kodish, Stephen Kulinna, Pamela Hodges Martin, Jeffrey Pangrazi, Robert Darst, Paul TI Determinants of physical activity in an inclusive setting SO ADAPTED PHYSICAL ACTIVITY QUARTERLY LA English DT Article ID PLANNED BEHAVIOR; REASONED ACTION; EDUCATION CLASSES; CHILDREN; DISABILITIES; STUDENTS; PEDOMETERS; EFFICACY; HEALTH; ATTITUDES AB The purposes of this study included (a) to determine if the Theory of Planned Behavior (TPB) predicted intentions of individuals with and without disabilities to be physically active, (b) to determine if the TPB predicted behaviors of individuals with and without disabilities to be physically active, and (c) to determine if significant differences were present in physical activity opportunities between inclusive and non-inclusive elementary physical education classes taught by the same teacher. Students (N = 114, ages 10-13) completed questionnaires assessing the TPB constructs and had four days of PA evaluated through pedometer measurements. Analyses revealed that subjective norm and perceived behavioral control predicted students' intentions to be active, while behavioral intention was the only significant predictor of activity level by step count accrued in PE classes. Finally, the inclusion of students with autism did not significantly affect overall physical activity. C1 Arizona State Univ, Dept Kinesiol, Tempe, AZ 85287 USA. Arizona State Univ, Dept Phys Educ, Tempe, AZ USA. Wayne State Univ, Div Kinesiol Hlth & Sport Studies, Detroit, MI USA. RP Kodish, S (reprint author), Arizona State Univ, Dept Kinesiol, Tempe, AZ 85287 USA. 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TI Normal values for morphological abnormalities in school children SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE clinical morphology; phenotypic abnormality; congenital abnormality; minor anomaly; normal values; Caucasian; school children ID MINOR PHYSICAL ANOMALIES; ADOLESCENT ONSET SCHIZOPHRENIA; CONGENITAL-ANOMALIES; PERINATAL COMPLICATIONS; INCREASED PREVALENCE; DYSMORPHIC FEATURES; MENTAL-RETARDATION; CHILDHOOD AUTISM; CEREBRAL-PALSY; HIGH-RISK AB Clinical morphology has proven to be a strong tool in the delineation of many syndromes and a helpful instrument in molecular studies. Numerous studies have been performed investigating the prevalence of minor anomalies in various disorders; all concluding that minor anomalies can well be utilized as indicators of altered embryonic differentiation. However, for adequate evaluation, normal values for phenotypic abnormalities are essential. So far, only few studies on the frequency of phenotypic abnormalities in the normal population have been clone having one thing in common: all were performed in newborn infants. We studied morphological characteristics in a group of 1,007 school children, representative for the Dutch population, through a body Surface examination using detailed definitions for all morphological findings. The region of study and distribution of children over various school types was chosen in Such a way that it represented the general Dutch population. The median age of the studied children was 11 years (range 8-14 years), sex ratio (M:F) was 0.93. Nine hundred twenty-three children were of Caucasian descent, 84 others of mixed ethnic backgrounds. The reliability of the examinations was tested by independent scoring of 111 children by two observers, showing a kappa score of 0.85. Normal values for the morphological findings are presented together with their age-adjusted classification. These normal values provide a valuable source for validation of classifications of phenotypic abnormalities, especially those that are depending on frequency, that is, minor anomalies and common variants. Furthermore, they will allow a proper evaluation of patterns of phenotypic abnormalities found in patient groups with specific disorders. (c) 2006 Wiley-Liss, Inc. C1 Emma Childrens Hosp, Acad Med Ctr, Dept Pediat Oncol, NL-1105 AZ Amsterdam, Netherlands. Emma Childrens Hosp, Acad Med Ctr, Dept Pediat Genet, Amsterdam, Netherlands. Community Hlth Care Dept Kennemerland, Dept Epidemiol, Haarlem, Netherlands. Community Hlth Care Dept Kennemerland, Dept Youth Hlth Care, Haarlem, Netherlands. NCI, Dept Epidemiol, Amsterdam, Netherlands. UCL, Great Ormond St Hosp Children, Inst Child Hlth, London, England. RP Merks, JHM (reprint author), Emma Childrens Hosp, Acad Med Ctr, Dept Pediat Oncol, Floor F8-Room 245,Meibergdreef 9, NL-1105 AZ Amsterdam, Netherlands. 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J. Med. Genet. A PD OCT 1 PY 2006 VL 140A IS 19 BP 2091 EP 2109 DI 10.1002/ajmg.a.31355 PG 19 WC Genetics & Heredity SC Genetics & Heredity GA 091TM UT WOS:000241051200012 PM 16838341 ER PT J AU Kuhn, JC Carter, AS AF Kuhn, Jennifer C. Carter, Alice S. TI Maternal self-efficacy and associated parenting cognitions among mothers of children with autism SO AMERICAN JOURNAL OF ORTHOPSYCHIATRY LA English DT Article DE autism; maternal self-efficacy; parenting stress; depression; agency ID EARLY INTERVENTION; MEDIATIONAL ROLE; SOCIAL SUPPORT; YOUNG-CHILDREN; MENTAL-HEALTH; DEPRESSION; STRESS; DISABILITIES; BEHAVIORS; PROGRAM AB Feelings of competency in the parental role, termed parenting self-efficacy, have been associated with well-being and positive parenting outcomes. Given the unique stresses inherent in raising a child with autism, parents may find it challenging to maintain a positive sense of well-being and self-efficacy. Study aims were to investigate associations between maternal self-efficacy and parenting cognitions among mothers of children with autism. Mothers (n=170) completed questionnaires on paper or via the Internet. In a hierarchical linear regression, depression, parenting stress, agency, and guilt each accounted for unique variance in maternal self-efficacy when controlling for time since diagnosis and the presence of a second child with a disability. Autism knowledge was not associated with parenting self-efficacy. Self-efficacy appears to be associated with well-being, agency, and feelings of guilt among mothers of children with autism. Parent- and family-based interventions designed to support parental well-being and focusing on parenting cognitions may enhance parenting self-efficacy. C1 Univ Massachusetts, Dept Psychol, Boston, MA 02125 USA. RP Carter, AS (reprint author), Univ Massachusetts, Dept Psychol, 100 Morrissey Blvd, Boston, MA 02125 USA. 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J. Orthopsychiatr. PD OCT PY 2006 VL 76 IS 4 BP 564 EP 575 DI 10.1037/0002-9432.76.4.564 PG 12 WC Psychiatry; Social Work SC Psychiatry; Social Work GA 123FV UT WOS:000243282700017 PM 17209724 ER PT J AU Flusberg, S Tager-Flusberg, H AF Flusberg, Stephen Tager-Flusberg, Helen TI Autism, language, and the folk psychology of souls SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material AB Anecdotal evidence suggests that people with autism, with known impairments in mechanisms supporting a folk psychology of mind or souls, can hold a belief in an afterlife. We focus on the role language plays, not just in acquiring the specific content of beliefs, but more significantly, in the acquisition of the concept of life after death for all people. C1 Stanford Univ, Dept Psychol, Stanford, CA 94305 USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Flusberg, S (reprint author), Stanford Univ, Dept Psychol, Stanford, CA 94305 USA. EM sflus@stanford.edu; htagerf@bu.edu RI Tager-Flusberg, Helen/D-5265-2009 CR Baron-Cohen S., 2000, UNDERSTANDING OTHER, P3 Baron-Cohen Simon, 2000, UNDERSTANDING OTHER Castelli F, 2002, BRAIN, V125, P1839, DOI 10.1093/brain/awf189 Lakoff G., 1999, PHILOS FLESH EMBODIE Melser D., 2004, ACT THINKING Papineau David, 2002, THINKING CONSCIOUSNE Rutgers AH, 2004, J CHILD PSYCHOL PSYC, V45, P1123, DOI 10.1111/j.1469-7610.2004.t01-1-00305.x Ryle G., 1949, CONCEPT MIND TAGERFLUSBERG H, 2005, LANGUAGE MATTERS THE Wittgenstein Ludwig, 1953, PHILOS INVESTIGATION NR 10 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0140-525X J9 BEHAV BRAIN SCI JI Behav. Brain Sci. PD OCT PY 2006 VL 29 IS 5 BP 473 EP + PG 7 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 129EF UT WOS:000243710500013 ER PT J AU Bradley, E Bolton, P AF Bradley, Elspeth Bolton, Patrick TI Episodic psychiatric disorders in teenagers with learning disabilities with and without autism SO BRITISH JOURNAL OF PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; STRESSFUL LIFE EVENTS; DIAGNOSTIC INTERVIEW; SPECTRUM DISORDERS; YOUNG-ADULTS; FOLLOW-UP; CHILDREN; DEPRESSION; EPIDEMIOLOGY; ADOLESCENTS AB Background Mental health problems in people with learning disabilities and autism are poorly understood. Aims To investigate the prevalence of episodic psychiatric disorders in a sample of teenagers with learning disabilities with and without autism. Method Teenagers with learning disabilities living in one geographical area were identified. Those with autism were matched to those without. A semistructured investigator-based interview linked to Research Diagnostic Criteria was used to assess prevalence and type of episodic disorders. Results Significantly more individuals with autism had a lifetime episodic disorder, most commonly major depression. Two individuals with autism had bipolar affective disorder. Other episodic disorders with mood components and behaviour change were also evident, as were unclassifable disorders characterised by complex psychiatric symptoms, chronicity and general deterioration. Antipsychotics and stimulants were most frequently prescribed; the former associated with episodic disorder, the latter with autism. Conclusions Teenagers with learning disabilities and autism have higher rates of episodic psychiatric disorders than those with learning disabilities alone. C1 Surrey Pl Ctr, Toronto, ON M5S 2C2, Canada. Univ Toronto, Dept Psychiat, Toronto, ON, Canada. Inst Psychiat, MRC, Ctr Social Genet & Dev Psychiat, London, England. Inst Psychiat, Dept Child Psychiat, London, England. RP Bradley, E (reprint author), Surrey Pl Ctr, 2 Surrey Pl, Toronto, ON M5S 2C2, Canada. EM e.bradley@utoronto.ca RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bolton P. F., 1994, SCHEDULE ASSESSMENT Bradley EA, 2004, J AUTISM DEV DISORD, V34, P151, DOI 10.1023/B:JADD.0000022606.97580.19 BRADLEY EA, 1998, PSYCHIAT ILLNESS MEN Bradley EA, 2002, CAN J PSYCHIAT, V47, P652 BRADLEY EA, 2006, CANADIAN J PSYCHIAT, V51, P59 BRERETON V, 2006, J AUTISM DEV DISORD, DOI DOI 10.1007/S10803-006-0125-Y Brown G. 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J. Psychiatry PD OCT PY 2006 VL 189 BP 361 EP 366 DI 10.1192/bjp.bp.105.018127 PG 6 WC Psychiatry SC Psychiatry GA 099HV UT WOS:000241585100010 PM 17012660 ER PT J AU Lepisto, T Silokallio, S Nieminen-von Wendt, T Alku, P Naatanen, R Kujala, T AF Lepisto, T. Silokallio, S. Nieminen-von Wendt, T. Alku, P. Naatanen, R. Kujala, T. TI Auditory perception and attention as reflected by the brain event-related potentials in children with Asperger syndrome SO CLINICAL NEUROPHYSIOLOGY LA English DT Article DE Asperger syndrome; auditory processing; event-related potentials (ERP); mismatch negativity (MMN); P3a ID HIGH-FUNCTIONING AUTISM; MISMATCH NEGATIVITY; EVOKED POTENTIALS; JOINT ATTENTION; SPEECH; DISCRIMINATION; INDIVIDUALS; INFORMATION; DYSFUNCTION; IMPAIRMENT AB Objective: Language development is delayed and deviant in individuals with autism, but proceeds quite normally in those with Asperger syndrome (AS). We investigated auditory-discrimination and orienting in children with AS using an event-related potential (ERP) paradigm that was previously applied to children with autism. Methods: ERPs were measured to pitch, duration, and phonetic changes in vowels and to corresponding changes in non-speech sounds. Active sound discrimination was evaluated with a sound-identification task. Results: The mismatch negativity (MMN), indexing sound-discrimination accuracy, showed right-hemisphere dominance in the AS group, but not in the controls. Furthermore, the children with AS had diminished MMN-amplitudes and decreased hit rates for duration changes. In contrast, their MMN to speech pitch changes was parietally enhanced. The P3a, reflecting involuntary orienting to changes, was diminished in the children with AS for speech pitch and phoneme changes, but not for the corresponding non-speech changes. Conclusions: The children with AS differ from controls with respect to their sound-discrimination and orienting abilities. Significance: The results of the children with AS are relatively similar to those earlier obtained from children with autism using the same paradigm, although these clinical groups differ markedly in their language development. (c) 2006 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. C1 Univ Helsinki, Dept Psychol, Cognit Brain Res Unit, FIN-00014 Helsinki, Finland. Helsinki Brain Res Ctr, Helsinki, Finland. Univ Helsinki, Dept Child Neurol, Hosp Children & Adolescents, FIN-00014 Helsinki, Finland. Helsinki Asperger Ctr, Med Ctr Dextra, Helsinki, Finland. Helsinki Univ Technol, Lab Acoust & Audio Signal Proc, Helsinki, Finland. Univ Helsinki, Helsinki Coll Adv Studies, Helsinki, Finland. RP Lepisto, T (reprint author), Univ Helsinki, Dept Psychol, Cognit Brain Res Unit, POB 9, FIN-00014 Helsinki, Finland. 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PD OCT PY 2006 VL 6 IS 3-4 BP 111 EP 112 DI 10.1016/j.cnr.2006.09.001 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200001 ER PT J AU Folstein, SE AF Folstein, Susan E. TI The clinical spectrum of autism SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE clinical features; diagnosis; autism spectrum AB Autism, as defined by Kanner in 1943, required two features: the abnormal development of social relationships and the obsessive desire for the maintenance of sameness. This definition was applied only to children without dysmorphic features (except macrocephaly) and without profound mental retardation. This definition resulted in a strongly familial disorder. Family members of such cases have not only strictly defined autism but the milder Pervasive Developmental Disorder, Not Otherwise Specified (PDDNOS), and Asperger syndrome as well as milder social dysfunction, obsessional personality characteristics, language and reading disorders, and anxiety and depression. Some of these conditions have come to be called "autism spectrum disorders". Family members of strictly defined autism cases do not tend to have mental retardation, even when the proband with autism may have marked cognitive impairment and limited language. Another group of children that often meet modern criteria for autism and PDDNOS are those with profound mental retardation (IQ < 35 or 40), children with dysmorphic facial features, specific genetic conditions, such as tuberous sclerosis or Retts syndrome, and children who have suffered certain kinds of severe encephalitis at an early age. These children are etiologically very heterogeneous and need to be considered separately in studies of etiology and mechanism. (C) 2006 Association for Research in Nervous and Mental Disease. Published by Elsevier B.V. All rights reserved. C1 Johns Hopkins Sch Med, Baltimore, MD 21210 USA. RP Folstein, SE (reprint author), Johns Hopkins Sch Med, 111 Hamlet Hill Rd,406, Baltimore, MD 21210 USA. EM sfolstein@rcn.com CR Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 BAILEY A, 1995, PSYCHOL MED, V25, P63 Bleuler E., 1924, TXB PSYCHIAT Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 FREEMAN BJ, 1989, AM J PSYCHIAT, V146, P361 Kanner L, 1943, NERV CHILD, V2, P217 Kanner L., 1935, CHILD PSYCHIAT MANKOSKI R, 2006, IN PRESS J AUTISM DE Miles JH, 2005, AM J MED GENET A, V135A, P171, DOI 10.1002/ajmg.a.30590 PIVEN J, 1990, J AM ACAD CHILD PSY, V29, P177, DOI 10.1097/00004583-199003000-00004 Ssucharewa G E, 1996, Eur Child Adolesc Psychiatry, V5, P119 Ssucharewa GE, 1926, MON PSYCHIATR NEUROL, V60, P235 TADEVOSYANLEYFE.T, 2006, IN PRESS U AUTISM DE WING L, 1981, PSYCHOL MED, V11, P115 NR 15 TC 11 Z9 11 PU ELSEVIER SCI LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, OXON, ENGLAND SN 1566-2772 J9 CLIN NEUROSCI RES JI Clin. Neurosci. Res. PD OCT PY 2006 VL 6 IS 3-4 BP 113 EP 117 DI 10.1016/j.cnr.2006.06.008 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200002 ER PT J AU Grether, JK AF Grether, Judith K. TI Epidemiology of autism: Current controversies and research directions SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE autism epidemiology; autism prevalence; autism surveillance; autism risk factors; early biologic markers ID SHORT INTERPREGNANCY INTERVALS; PERINATAL RISK-FACTORS; SPECTRUM DISORDERS; PATERNAL AGE; NEUROANATOMICAL OBSERVATIONS; CHANGING PREVALENCE; NEUROTROPHIC FACTOR; INFANTILE-AUTISM; NEONATAL BLOOD; UNITED-STATES AB In many respects, the epidemiology of autism is still in its infancy. Although important questions remain unanswered, epidemiologists are making significant progress in several areas of inquiry that will be addressed in this presentation: How common is autism? Has the prevalence changed over time? What demographic and environmental risk factors have been identified that may provide clues to underlying etiology? What research is being done to search for early biologic markers for autism and related disorders? Epidemiologists like to count "cases" to estimate the frequency with which autism occurs in a population. However, prevalence estimates are heavily influenced by the methodology used for identification of affected individuals, making it difficult to compare prevalence across different time periods or populations. Current estimates of autism prevalence based on different methodologies and factors contributing to observed time trends will be provided for consideration. The tools of epidemiology are also useful for identifying demographic and environmental risk factors that may provide clues to underlying etiology. Preliminary data will be presented from large California studies on characteristics of parents and newborns that are associated with risk of autism. Finally, in collaboration with basic scientists, slow progress is being made in identifying and evaluating early biologic markers for autism. Current studies will be described and preliminary data on newborns presented. Published by Elsevier B.V. on behalf of Association for Research in Nervous and Mental Disease. C1 Calif Dept Hlth Serv, Environm Hlth Invest Branch, Calif CADDRE, Richmond, CA 94804 USA. RP Grether, JK (reprint author), Calif Dept Hlth Serv, Environm Hlth Invest Branch, Calif CADDRE, 850 Marina Bay,Pkwy Bldg P,3rd Floor, Richmond, CA 94804 USA. 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TI Abnormalities of cortical minicolumnar organization in the prefrontal lobes of autistic patients SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE minicolumns; autism; pervasive developmental disorders of childhood (PDD); neocortex; neuropathology; prefrontal cortex ID HIGH-FUNCTIONING AUTISM; CHILDHOOD AUTISM; MAJOR DETERMINANT; CEREBRAL-CORTEX; FRONTAL-CORTEX; BRAIN; CONNECTIVITY; INDIVIDUALS; HYPOTHESIS; EVOLUTION AB Recent functional imaging studies suggest deficits in connectivity between disparate and distant regions in the brains of autistic individuals. One possible explanation to these findings is the presence of modular abnormalities in the neocortex of autistic patients: a change in neuronal specialization within minicolumns that emphasizes short connecting fibers. In this study, we expand on previous findings by exploring the topography of minicolumnar abnormalities in autism. Our postmortem study included six patients with autism (DSM-IV-TR and ADI-R diagnosed) and six age-matched controls. Entire brain hemispheres were celloidin embedded, serially sectioned, and stained with gallocyanin. Digital photomicrographs of n = 9 cortical areas (including paralimbic, heteromodal association, unimodal association, and primary areas) obtained at high magnification were assembled into montages covering the entire cortical thickness. Stained cell somata were segmented from neuropil by thresholding. Computer image analysis clustered neurons into minicolumnar fragments. The full width of the image region nearest each fragment and the width of the cell-dense core of the fragment were estimated. The difference between these two quantities can be used as a measure of the peripheral neuropil space of minicolumns. 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PD OCT PY 2006 VL 6 IS 3-4 BP 127 EP 133 DI 10.1016/j.cnr.2006.06.003 PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200004 ER PT J AU Mosconi, M Zwaigenbaum, L Piven, J AF Mosconi, Matthew Zwaigenbaum, Lonnie Piven, Joseph TI Structural MRI in autism: Findings and future directions SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis ID MAGNETIC-RESONANCE IMAGES; HIGH-FUNCTIONING AUTISM; MATTER VOLUME INCREASE; CORPUS-CALLOSUM; HUMAN BRAIN; HEAD CIRCUMFERENCE; POSTERIOR-FOSSA; SPECTRUM DISORDERS; INFANTILE-AUTISM; YOUNG-CHILDREN AB Structural MRI studies of the brain in autism have yielded inconsistent results until recent years. Studies over the past decade have revealed several exciting new findings and have fostered novel hypotheses about the onset and etiology of this disorder. The most consistent MRI finding in autism is that the brain is enlarged. Studies have suggested that brain overgrowth may be most robust early in development, but increased brain volume has been observed throughout adolescence and early adult life. Retrospective head circumference studies have indicated that the onset of brain enlargement may occur during the latter part of the first year of life and does not appear to be present at birth. Recent studies of infant siblings of children with autism suggest that the onset of the core behavioral features of autism also occur during the latter part of the first year of life and may not be present by 6 months of age. The coincident timing of the onset of brain and behavioral abnormalities in autism suggests that these features may be related. Future longitudinal MRI studies of infant siblings of children with autism will help elucidate this relationship and potentially delineate the pathogenesis of this disorder. Additional findings from structural MRI studies of autism have begun to map patterns of brain overgrowth across cortical lobes and tissue types (gray and white matter). These studies are somewhat inconsistent, but suggest generalized overgrowth affecting both cortical gray and cortical white matter, as well as several subcortical structures. The diffuse network of regions affected has shifted research attention from hypotheses about specific regions and structures to more widespread mechanisms involving neural circuits and diffuse mechanisms at the neuronal level. These findings, their implications for our understanding of the pathogenesis of autism, and future directions for structural MRI studies of autism are discussed. (C) 2006 Association for Research in Nervous and Mental Disease. Published by Elsevier B.V. All rights reserved. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychol, Chapel Hill, NC USA. Glenrose Rehabil Hosp, Capital Hlth, Edmonton, AB, Canada. Univ Alberta, Dept Pediat, Edmonton, AB, Canada. RP Piven, J (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. 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A large body of evidence suggests that several aspects of face processing are impaired in autism, including anomalies in gaze processing, memory for facial identity and recognition of facial expressions of emotion. In search of neural markers of anomalous face processing in autism, much interest has focused on a network of brain regions that are implicated in social cognition and face processing. In this review, we will focus on three such regions, namely the STS for its role in processing gaze and facial movements, the FFA in face detection and identification and the amygdala in processing facial expressions of emotion. Much evidence suggests that a better understanding of the normal development of these specialized regions is essential for discovering the neural bases of face processing anomalies in autism. Thus, we will also examine the available literature on the normal development of face processing. Key unknowns in this research area are the neuro-developmental processes, the role of experience and the interactions among components of the face processing system in shaping each of the specialized regions for processing faces during normal development and in autism. C1 Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. Stanford Univ, Dept Psychol, Stanford, CA 94305 USA. Stanford Univ, Program Neurosci, Stanford, CA 94305 USA. RP Golarai, G (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. 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Neurosci. Res. PD OCT PY 2006 VL 6 IS 3-4 BP 145 EP 160 DI 10.1016/j.cnr.2006.08.001 PG 16 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200006 ER PT J AU Grice, DE Buxbaum, JD AF Grice, D. E. Buxbaum, J. D. TI The genetic architecture of autism and related disorders SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE pervasive developmental disorders; autism spectrum disorders; genetics; linkage; association; susceptibility locus ID HOMEOBOX-TRANSCRIPTION-FACTOR; AFFECTED SIBLING PAIRS; CARRIER SLC25A12 GENE; INFANTILE-AUTISM; SPECTRUM-DISORDER; BROADER PHENOTYPE; GLUTAMATE CARRIER; RETT-SYNDROME; ASSOCIATION; TWIN AB Epidemiological twin studies demonstrate that autism spectrum disorders (ASDs) represent genetic disorders. Subsequent analyses indicate that the causes of ASDs include rarer single gene mutations and chromosomal abnormalities, as well as ASDs caused by multiple interacting genes of weak effect. Genome-wide linkage analysis has identified several susceptibility loci for the ASDs, and positional and functional candidate genes have been identified that may represent susceptibility genes for the ASDs. Analysis of additional larger samples, and the use of genome-wide association and high-throughput variant detection will lead to the identification of further genes for ASDs. (C) 2006 Association for Research in Nervous and Mental Disease. Published by Elsevier B.V. All rights reserved. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, New York, NY 10029 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Psychiat, Newark, NJ 07103 USA. CUNY Mt Sinai Sch Med, Dept Neurosci, Lab Mol Neuropsychiat, New York, NY 10029 USA. 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Neurosci. Res. PD OCT PY 2006 VL 6 IS 3-4 BP 161 EP 168 DI 10.1016/j.cnr.2006.06.004 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200007 ER PT J AU McDougle, CJ Stigler, KA Erickson, CA Posey, DJ AF McDougle, Christopher J. Stigler, Kimberly A. Erickson, Craig A. Posey, David J. TI Pharmacology of autism SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE autism; psychopharmacology; aggression; dopamine; serotonin; glutamate ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; RETROSPECTIVE ANALYSIS; REPETITIVE THOUGHTS; INFANTILE-AUTISM; CROSSOVER TRIAL; CASE SERIES; CHILDREN; PLACEBO; RISPERIDONE AB The purpose of this review is to discuss the pharmacology of autistic disorder (autism) and other pervasive developmental disorders (PDDs) from the perspective of specific target symptom domains of behavior. Drug treatment strategies directed toward the following target symptom domains are included: motor hyperactivity and inattention; interfering stereotypical and repetitive behavior; aggression and self-injurious behavior (SIB); and the core social impairment of autism and other PDDs. For motor hyperactivity and inattention, studies have indicated that the alpha(2) adrenergic agonists, clonidine and guanfacine, are useful. A placebo-controlled study by the Research Units on Pediatric Psychopharmacology (RUPP) Autism Network found methylphenidate to be efficacious in 49% of subjects with various PDDs for these target symptoms. Preliminary data with the norepinephrine reuptake inhibitor atomoxetine are encouraging. For interfering stereotypical and repetitive behavior, controlled studies of the selective serotonin reuptake inhibitor fluvoxamine found the drug to be more efficacious and better tolerated in adults than children with autism and other PDDs. A recent controlled study of low-dose liquid fluoxetine found the drug more efficacious than placebo for interfering repetitive behavior and well tolerated. A large placebo-controlled study of the atypical antipsychotic risperidone found the drug to be efficacious for reducing aggression, SIB and tantrumming in 70% of children with autism and that the response was maintained for up to 6 months. Open-label studies of other atypical antipsychotics are generally encouraging. A small, single-blind study of the glutamatergic agent D-cycloserine showed significant benefit for the social withdrawal of autism. Future directions include studying coactive pharmacological treatment strategies utilizing more than one drug to target more than one target symptom domain in individuals with autism and other PDDs. (C) 2006 Association for Research in Nervous and Mental Disease. Published by Elsevier B.V. All rights reserved. C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), Indiana Univ, Sch Med, Dept Psychiat, 1111 W 10th St,PB A305, Indianapolis, IN 46202 USA. 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Neurosci. Res. PD OCT PY 2006 VL 6 IS 3-4 BP 179 EP 188 DI 10.1016/j.cnr.2006.06.012 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200009 ER PT J AU Lord, C Luyster, R AF Lord, Catherine Luyster, Rhiannon TI Early diagnosis of children with autism spectrum disorders SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE autistic disorder; longitudinal studies; early diagnosis; early development; communication; social development ID FOLLOW-UP; DEVELOPMENTAL DISORDERS; OBSERVATION SCHEDULE; AGE; IDENTIFICATION; INDIVIDUALS; OUTCOMES; DELAYS; LIFE AB Research focusing on early development in children with Autism Spectrum Disorders (ASD) has been of particular interest in recent years. A greater understanding of the accuracy of early diagnosis, as well as the developmental pathways that are observed in young children with ASD, is of both theoretical and practical importance. In accordance with these concerns, this review addresses questions about three topics: the reliability of early diagnosis, the validity of using narrow versus broad diagnostic categories, and trajectories of development in children with ASD. Findings from two prospective longitudinal studies are reviewed. The first investigation included children referred for ASD at age 2 who were followed for one year. The second study followed children referred for ASD at age 2 until age 9. Results suggested that early diagnoses can be made reliably, that there is no empirical evidence for using narrowly defined diagnostic categories within ASD and that trajectories of development showed considerable heterogeneity. (C) 2006 Association for Research in Nervous and Mental Disease. Published by Elsevier B.V. All rights reserved. C1 Univ Michigan, Autism & Commun Disorders Ctr, Ann Arbor, MI 48104 USA. RP Lord, C (reprint author), Univ Michigan, Autism & Commun Disorders Ctr, 1111 E Catherine St, Ann Arbor, MI 48104 USA. EM celord@umich.edu CR ANDERSON D, 2006, UNPUB J CONSULT CLIN Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x BERNARDOPITZ V, 1982, J SPEECH HEAR DISORD, V47, P99 BISHOP SL, 2006, IN PRESS CHILD NEURO Charman T, 2005, J CHILD PSYCHOL PSYC, V46, P500, DOI 10.1111/j.1469-7610.2004.00377.x Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Eaves LC, 2004, J AUTISM DEV DISORD, V34, P367, DOI 10.1023/B:JADD.0000037414.33270.a8 GOTHAM K, 2006, IN PRESS J AUTISM DE Greenspan S. 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Neurosci. Res. PD OCT PY 2006 VL 6 IS 3-4 BP 189 EP 194 DI 10.1016/j.cnr.2006.06.005 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200010 ER PT J AU Allen, G AF Allen, Greg TI Cerebellar contributions to autism spectrum disorders SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE autism; cerebellum; connectivity; development; FMRI; MRI; Purkinje cells ID FUNCTIONAL MAGNETIC-RESONANCE; POSITRON-EMISSION-TOMOGRAPHY; HOMEOBOX-TRANSCRIPTION-FACTOR; COGNITIVE-AFFECTIVE SYNDROME; POSTERIOR-FOSSA STRUCTURES; VOXEL-BASED MORPHOMETRY; INFANTILE-AUTISM; MOTOR CONTROL; SELECTIVE VULNERABILITY; SHIFTING ATTENTION AB The pathophysiology of autism appears to encompass a number of different brain structures and systems. However, the most consistent site of neural abnormality in autism is the cerebellum. Postmortem investigations have reported a variety of anomalies, most notably a reduction in the number of Purkinje neurons. Additionally, structural neuroimaging studies have shown volumetric changes in the cerebellum, including decreases in gray matter and increases in white matter. Emerging evidence for cerebellar abnormality in autism was paralleled by a revolution in our understanding of normal cerebellar function and cerebellar connectivity, such that the importance of elucidating the contributions of the cerebellum to autism is now clear. In fact, recent brain-behavior correlation studies suggest that cerebellar abnormality may play a more central role in autism than previously thought. At present, it is crucial that we increase our understanding of cerebellar functioning in autism, and functional neuroimaging studies are just beginning to reveal the possible role(s) of cerebellar dysfunction in this disorder. In this review, evidence for cerebellar anatomic and functional abnormality in autism will be delineated. This will be followed by consideration of the implications of cerebellar abnormality in autism. Two major questions will be addressed: (1) how might dysfunction of the cerebellum impact the development of connectivity between the cerebellum and other brain systems, and (2) how might cerebellar dysfunction impact behavior and the symptoms of autism. The paper concludes with a discussion of how cerebellar abnormalities might inform our understanding of the etiology of autism spectrum disorders. (C) 2006 Association for Research in Nervous and Mental Disease. Published by Elsevier B.V. All rights reserved. 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Neurosci. Res. PD OCT PY 2006 VL 6 IS 3-4 BP 195 EP 207 DI 10.1016/j.cnr.2006.06.002 PG 13 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200011 ER PT J AU Rapin, I AF Rapin, Isabelle TI Language heterogeneity and regression in the autism spectrum disorders - Overlaps with other childhood language regression syndromes SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE autism; autism spectrum disorders; language regression; epilepsy; Landau-Kleffner syndrome; immunology; disintegrative disorder; Rolandic epilepsy; children ID LANDAU-KLEFFNER-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; VERBAL AUDITORY AGNOSIA; PURE WORD DEAFNESS; TERM-FOLLOW-UP; CONVULSIVE DISORDER; ACQUIRED APHASIA; TEMPORAL-LOBE; DISINTEGRATIVE DISORDER; EPILEPTIFORM ACTIVITY AB Some third of parents of children on the autism spectrum report that their toddler's language regressed, usually insidiously, or stagnated during a prolonged plateau. Regression was associated with loss of sociability, interest in toys, and other behavioral skills, without motor regression. After months or longer, language usually returns, but variably severe autistic features persist. Nonverbal cognitive skills may or may not be affected. Some parents recall some antecedent nonspecific illness or stressor like the absence of a parent, a move, or the birth of a sibling. Occasionally, regression seems temporally related to an epileptic seizure, suggesting an overlap with acquired epileptic aphasia (Landau-Kleffner syndrome-LKS) in which language regression is associated with either clinical seizures or subclinical perisylvian temporo-parietal epileptiform EEG activity. LKS onset peaks at 4-6 years, autistic regression before age 2 years and is infrequently associated with seizures or an epileptiform EEG, except in the rare case of disintegrative disorder, a late global autistic regression which, like LKS, may be associated with electrical status epilepticus in slow wave sleep. Mute or dysfluent children with LKS, autism, or developmental language disorders are unable to decode or have difficulty decoding acoustically presented language (speech). They are at higher risk for epilepsy than fluent children with the typically aberrant language of verbal children with autism. The pathogenesis of language regression remains unknown because autistic toddlers are rarely studied at the time of language regression so that no empirically validated effective treatment has yet been devised. (C) 2006 Association for Research in Nervous and Mental Disease. Published by Elsevier B.V. All rights reserved. C1 Albert Einstein Coll Med, Rose F Kennedy Ctr Res Mental Retardat & Human De, Dept Pediat, Saul R Korey Dept Neurol, Bronx, NY 10467 USA. RP Rapin, I (reprint author), Albert Einstein Coll Med, Rose F Kennedy Ctr Res Mental Retardat & Human De, Dept Pediat, Saul R Korey Dept Neurol, Bronx, NY 10467 USA. 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Neurosci. Res. PD OCT PY 2006 VL 6 IS 3-4 BP 209 EP 218 DI 10.1016/j.cnr.2006.06.011 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 111WJ UT WOS:000242486200012 ER PT J AU Tager-Flusberg, H AF Tager-Flusberg, Helen TI Defining language phenotypes in autism SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Article; Proceedings Paper CT 85th Annual Conference of the Association-for-Reseach-in-Nervous-and-Mental-Disease CY DEC 01-02, 2005 CL New York, NY SP Assoc Res Nervous & Mental Dis DE autism; language; phonological processing; grammar ID NONWORD REPETITION; ASSOCIATION CORTEX; PLANUM TEMPORALE; GENETIC-BASIS; IMPAIRMENT; CHILDREN; DISORDERS; ASYMMETRY; TWIN; SPEECH AB All children with autism spectrum disorders have deficits in pragmatic aspects of communication; however, formal language abilities are extremely heterogeneous, ranging from nonverbal to superior linguistic skills. Recent studies have focused on defining different language phenotypes among verbal children. One subtype has been compared to specific language impairment (SLI), a language disorder that is diagnosed on the basis of delays and deficits in language acquisition in the absence of hearing impairment, frank neurological damage or co-morbid psychopathology. Two behavioral studies address the question of whether children with autism and language impairment have specific language deficits that are similar to those found in SLI. These experiments focused on phonological processing in a nonsense word repetition task, and use of grammatical morphology in conversational speech. The findings from these studies are discussed in the context of recent neuroimaging and genetic studies of autism. (C) 2006 Association for Research in Nervous and Mental Disease. Published by Elsevier B.V. All rights reserved. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. 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PD OCT PY 2006 VL 11 IS 10 BP 741 EP 741 PG 1 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 097KU UT WOS:000241447100012 ER PT J AU Rinehart, NJ Tonge, BJ Iansek, R McGinley, J Brereton, AV Enticott, PG Bradshaw, JL AF Rinehart, Nicole J. Tonge, Bruce J. Iansek, Robert McGinley, Jenny Brereton, Avril V. Enticott, Peter G. Bradshaw, John L. TI Gait function in newly diagnosed children with autism: cerebellar and basal ganglia related motor disorder SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PARKINSONS-DISEASE; CHILDHOOD AUTISM; STRIDE LENGTH; INDIVIDUALS; MOVEMENTS AB We investigated gait in newly diagnosed children with autism. From our previous study with 6- to 14-year-olds, we hypothesized that motor symptoms indicative of basal ganglia and cerebellar dysfunction would appear across the developmental trajectory of autism. Two groups were recruited children with autism (eight males, three females; moan age 5y 10mo [SD 9mo]; range 4y 4mo-6y 9mo) and a comparison group of typically developing children (eight males, three females; mean age 5y 9mo [SD 1y 1mo]; range 4y 3mo-1y 2mo). The GAITRite Walkway was used to gather data from average gait and intra-walk measurements. Experienced physiotherapists analyzed gait qualitatively. Groups were matched according to age, height, weight, and IQ; although not statistically significant, IQ was lower in the group with autism. Spatiotemporal gait data for children with autism were compatible with findings from patients with cerebellar ataxia: specifically, greater difficulty walking along a straight line, and the coexistence of variable stride length and duration. Children with autism were also less coordinated and rated as more variable and inconsistent (i.e. reduced smoothness) relative to the comparison group. Postural abnormalities in the head and trunk suggest additional involvement of the fronto-striatal basal ganglia region. Abnormal gait features are stable across key developmental periods and are, therefore, promising for use in clinical screening for autism. C1 Monash Univ, Dept Psychol Med, Monash Med Ctr, Clayton, Vic 3168, Australia. Monash Univ, Ctr Dev Psychiat, Sch Psychol Psychiat & Psychol Med, Clayton, Vic 3168, Australia. Monash Ageing Res Ctr, Geriatr Res Unit, Kingston Ctr, Cheltenham, Glos, England. Murdoch Childrens Res Inst, Parkville, Vic, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Dept Psychol Med, Monash Med Ctr, Level 3,Block P, Clayton, Vic 3168, Australia. 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Although MECP2 coding mutations are a rare cause of autism, MeCP2 expression defects were previously found in autism brain. To further study the role of MeCP2 in autism spectrum disorders (ASDs), we determined the frequency of MeCP2 expression defects in brain samples from autism and other ASDs. We also tested the hypotheses that MECP2 promoter mutations or aberrant promoter methylation correlate with reduced expression in cases of idiopathic autism. MeCP2 immunofluorescence in autism and other neurodevelopmental disorders was quantified by laser scanning cytometry and compared with control postmortem cerebral cortex samples on a large tissue microarray. A significant reduction in MeCP2 expression compared to age-matched controls was found in 11/14 autism (79%), 9/9 RTT (100%), 4/4 Angelman syndrome (100%), 3/4 Prader-Willi syndrome (75%), 3/5 Down syndrome (60%), and 2/2 attention deficit hyperactivity disorder (100%) frontal cortex samples. One autism female was heterozygous for a rare MECP2 promoter variant that correlated with reduced MeCP2 expression. A more frequent occurrence was significantly increased MECP2 promoter methylation in autism male frontal cortex compared to controls. Furthermore, percent promoter methylation of MECP2 significantly correlated with reduced MeCP2 protein expression. These results suggest that both genetic and epigenetic defects lead to reduced MeCP2 expression and may be important in the complex etiology of autism. C1 [Nagarajan, Raman P.; Hogart, Amber R.; Gwye, Ynnez; Martin, Michelle R.; LaSalle, Janine M.] Univ Calif Davis, Sch Med, Rowe Program Human Genet, Davis, CA 95616 USA. RP LaSalle, JM (reprint author), 1 Shields Ave, Davis, CA 95616 USA. EM jmlasalle@ucdavis.edu FU NIH [1R01HD048799]; predoctoral fellowship (RN) from the U.C. Davis M.I.N.D. Institute; Harvard Brain Tissue Resource Center [R24MH-068855] FX We thank Dr. Paul Hagerman for Fragile X brain and critical review of the manuscript. We also thank D. Yasui, S. Swanberg, S. Peddada, K. Thatcher, and M. Baerwald for manuscript review. Human brain tissue samples were generously provided by the Autism Tissue Program, The University of Maryland Brain and Tissue Bank for Developmental Disorders, The University of Miami Brain and Tissue Bank for Developmental Disorders, and the Harvard Brain Tissue Resource Center (supported in part by NIH R24MH-068855). This work was supported in part by NIH 1R01HD048799 and a predoctoral fellowship (RN) from the U.C. Davis M.I.N.D. Institute. 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We investigated the extent to which this visuomotor priming effect is mediated by bottom-up or top-down processing. The bottom-up hypothesis suggests that robotic movements are less effective in activating the 'mirror system' via pathways from visual areas via the superior temporal sulcus to parietal and premotor cortices. The top-down hypothesis postulates that beliefs about the animacy of a movement stimulus modulate mirror system activity via descending pathways from areas such as the temporal pole and prefrontal cortex. In an automatic imitation task, subjects performed a prespecified movement (e.g. hand opening) on presentation of a human or robotic hand making a compatible (opening) or incompatible (closing) movement. The speed of responding on compatible trials, compared with incompatible trials, indexed visuomotor priming. In the first experiment, robotic stimuli were constructed by adding a metal and wire 'wrist' to a human hand. Questionnaire data indicated that subjects believed these movements to be less animate than those of the human stimuli but the visuomotor priming effects of the human and robotic stimuli did not differ. In the second experiment, when the robotic stimuli were more angular and symmetrical than the human stimuli, human movements elicited more visuomotor priming than the robotic movements. However, the subjects' beliefs about the animacy of the stimuli did not affect their performance. These results suggest that bottom-up processing is primarily responsible for the visuomotor priming advantage of human stimuli. C1 UCL, Dept Psychol, London WC1H 0AP, England. RP Press, C (reprint author), UCL, Dept Psychol, Gower St, London WC1H 0AP, England. 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PD OCT PY 2006 VL 24 IS 8 BP 2415 EP 2419 DI 10.1111/j.1460-9568.2006.05115.x PG 5 WC Neurosciences SC Neurosciences & Neurology GA 098FL UT WOS:000241506300031 PM 17042792 ER PT J AU Toro, J Mur, M Canto, T AF Toro, Josep Mur, Maria Canto, Tomas TI Psychiatric treatments for children and adolescents preferred by Spanish psychiatrists SO EUROPEAN JOURNAL OF PSYCHIATRY LA English DT Article DE nationwide cross-sectional survey; medication; psychotherapy; children; adolescents ID OBSESSIVE-COMPULSIVE DISORDER; RANDOMIZED CONTROLLED-TRIAL; ANXIETY DISORDERS; MEDICATION; ANTIDEPRESSANTS; COMBINATION; FLUOXETINE; PATTERNS; YOUTHS AB Objectives: To study the prescription criteria of Spanish psychiatrists treating children and adolescents. Methods: a survey was designed to record their first choice and complementary preferences for pharmacological, psychotherapeutic and psychoeducational interventions in five disorders: autism, depression, separation anxiety, obsessive compulsive and attention-deficit/hyperactivity disorders. Results: One hundred and nine psychiatrists responded. No distinction was made between children and adolescents. Around 90% recommended all three types of intervention in the five disorders. Only 2-10% would use only one treatment. Antidepressants were the most frequently prescribed drugs (recommended by 58%), followed by anxiolytics (33%), antipsychotics (24%), stimulants (20%), beta-blockers (19%), mood stabilizers (10%) and alpha-adrenergics (4%). Cognitive-behavioral therapy was the most popular approach, recommended by 66%; a third of the interviewees recommended family, support, interpersonal and dynamic psychotherapy. 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They are of low molecular weight (6-7 kDa) and of the 60+ amino acid residues, 20 are cysteines. Functions attributed to MTs include the sequestration and dispersal of metal ions, primarily in zinc and copper homeostasis; regulation of the biosynthesis and activity of zinc metalloproteins, most notably zinc-dependent transcription factors; and cellular cytoprotection from reactive oxygen species, ionizing radiation, electrophilic anticancer drugs and mutagens, and metals. Observations on the abundance of MTs within the central nervous system (CNS) and the identification of a brain-specific isoform, MT-III, suggest that it might have important neurophysiological and neuromodulatory functions. Reinforced by the potential involvement of MT-III in a number of neurodegenerative disorders, the role of MTs in the CNS has become an intense focus of scientific pursuit. 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This article reviews 77 clinical trials published in the last 10 years, investigating their efficacy, effectiveness, safety and pharmacokinetic data in paediatric populations. The diagnostic categories in which the antipsychotics are commonly used (schizophrenia, pervasive developmental disorders, Tourette's disorder, mental retardation/subaverage intelligence, mood disorders and disruptive behaviour disorders) were used in order to review the evidence and effectiveness. All randomised, double-blind, placebo-controlled trials from the past decade are also summarised. This review refers to recent relevant practice parameters, guidelines and reviews throughout the text Consistent with previous reviews, it is concluded that the recent trend of increased use of antipsychotics in children and adolescents is not adequately supported by evidence. Specific suggestions have been provided on how to. incorporate the existing evidence base into clinical decision making. 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Pharmacother. PD OCT PY 2006 VL 7 IS 14 BP 1871 EP 1885 DI 10.1517/14656566.7.14.1871 PG 15 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 091GN UT WOS:000241015200003 PM 17020414 ER PT J AU Hviid, A AF Hviid, Anders TI Postlicensure epidemiology of childhood vaccination: the Danish experience SO EXPERT REVIEW OF VACCINES LA English DT Review DE epidemiology; immunization; postlicensure; vaccines ID RUBELLA VACCINATION; ROUTINE VACCINATION; DIABETES-MELLITUS; UNITED-STATES; PERTUSSIS; MEASLES; MUMPS; IMMUNIZATION; AUTISM; CHILDREN AB The efficacy, the ability to confer protection against a target disease and the safety of a vaccine are assessed in great detail before licensure. However, inherent limitations in the prelicensure assessment necessitate continued epidemiological evaluations of efficacy and safety issues after the introduction of vaccines into use. In Denmark, the opportunities available for epidemiological research are unique. In 2001, an initiative was undertaken to take advantage of these opportunities to study the postlicensure epidemiology of childhood vaccination with respect to effectiveness and safety. First, we describe the unique opportunities for postlicensure research in Denmark with respect to the data sources available and the epidemiological and statistical methods used. We then describe a number of recent postlicensure studies of effectiveness and safety that took advantage of these opportunities. Specifically, studies on the effectiveness of Hoemophilus influenzoe type b vaccination, the effectiveness of pertussis vaccination, the impact of a preschool pertussis booster on infant pertussis, measles-mumps-rubella vaccine and autism, thimerosal-containing vaccine and autism, measles-mumps-rubella vaccine and febrile seizures, childhood vaccination and Type I diabetes, and childhood vaccination and nontargeted infectious disease are discussed. 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Notably, musical stimuli have been shown to activate specific pathways in several brain areas associated with emotional behaviours, such as the insular and cingulate cortex, hypothalamus, hippocampus, amygdala, and prefrontal cortex. In addition, neurochemical studies have suggested that several biochemical mediators, such as endorphins, endocannabinoids, dopamine and nitric oxide, may play a role in the musical experience. A growing body of evidence also indicates that music therapy could be useful in the clinical management of numerous neurological and psychiatric disorders. Indeed, music therapy could be effective in patients with neurodegenerative disorders, such as Alzheimer's dementia and Parkinson's disease, as well as in psychiatric illnesses, such as schizophrenia, depression, anxiety and autism spectrum disorders. 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Neurol. PD OCT-DEC PY 2006 VL 21 IS 4 BP 187 EP 191 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 162HQ UT WOS:000246078000003 PM 17367577 ER PT J AU Lane, AE AF Lane, Alison E. TI The science and fiction of autism SO HEALTH LA English DT Book Review C1 Univ S Australia, Sch Hlth Sci, Adelaide, SA 5001, Australia. Univ S Australia, Sansom Inst, Adelaide, SA 5001, Australia. RP Lane, AE (reprint author), Univ S Australia, Sch Hlth Sci, Adelaide, SA 5001, Australia. 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TI Tourette syndrome in infancy and early childhood SO INFANTS & YOUNG CHILDREN LA English DT Article DE attention deficit/hyperactivity disorder; basal ganglia; blinking; child; comorbidity; learning disability; obsessive-compulsive disorder; social support; tics; Tourette syndrome ID DEFICIT HYPERACTIVITY DISORDER; OBSESSIVE-COMPULSIVE DISORDER; MONOZYGOTIC TWINS; TIC SEVERITY; CHILDREN; PREVALENCE; EXPRESSION; ETIOLOGY; BEHAVIOR; AUTISM AB Although it is the presence of motor and phonic tics that defines Tourette syndrome (TS), explorations over the past two decades have uncovered a complex and multidimensional nature of this genetic-based neurological disorder. Tics customarily first become apparent during the latter half of the first decade of life, although they may occur earlier, including during infancy. However, associated "comorbid" conditions, rather than tics, usually determine the functional and qualitative experiences for the child with TS. These conditions often become problematic prior to tic onset. Misconceptions regarding the nature of tics and the varied associated conditions are common, placing children with TS at significant risk for underdiagnosis, mismanagement, and missed opportunities for prevention. This article will consider risk factors and associated behaviors, both subtle and more obvious, that can alert the clinician to infants and young children with tics or who are at increased risk to develop TS. Themes in management strategies include interdisciplinary participation, "Medical Home" foundation, and ongoing monitoring and support. C1 Univ Washington, Dept Pediat, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. RP Zinner, SH (reprint author), Univ Washington, Dept Pediat, Ctr Human Dev & Disabil, Box 357920, Seattle, WA 98195 USA. 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PD OCT-DEC PY 2006 VL 19 IS 4 BP 353 EP 370 PG 18 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 087RK UT WOS:000240759700007 ER PT J AU James, IA Mukaetova-Ladinska, E Reichelt, FK Briel, R Scully, A AF James, Ian Andrew Mukaetova-Ladinska, Elizabeta Reichelt, F. Katharina Briel, Ruth Scully, Ann TI Diagnosing Aspergers syndrome in the elderly: a series of case presentations SO INTERNATIONAL JOURNAL OF GERIATRIC PSYCHIATRY LA English DT Article DE Aspergers syndrome; older adult; diagnosis; case report; assessment tool ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; DEPRESSION; QUOTIENT; CHILDREN; ADULTS AB Background There are over 200000 people in the UK diagnosed with Aspergers Syndrome (AS). Most of these are children and young adults, owing to the fact the disorder was established relatively recently. It can be argued, therefore, that there are many older adults who may have met the criteria for AS as children, but never received such a diagnosis due to the fact it had yet to be established. What happended to these people as they aged? Method This paper examines this issue in detail and presents five case studies of elderly individuals who the authors believe meet the criteria of AS. Results The work illustrates AS presentation in old age, the assessment problems and tools required to assess older people, and the implications of such formulations for clinical practice. Conclusion Older patients with undiagnosed AS may currently be receiving inappropriate treatments. Greater awareness of AS in the older population would enable better management of such patients. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 Univ Newcastle Upon Tyne, Inst Ageing & Hlth, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. Newcastle N Tyneside & Northumberland Mental Hlth, Newcastle Upon Tyne, Tyne & Wear, England. RP James, IA (reprint author), Newcastle Gen Hosp, Ctr Hlth Elderly, Westgate Rd, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England. 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E., 1982, NATL ADULT READING T Psychological Corporation, 2001, WECHSL TEST AD READ Schopler E., 1986, CHILDHOOD AUTISM RAT Wechsler D., 1987, WECHSLER MEMORY SCAL Wechsler D, 1997, WECHSLER ADULT INTEL, V3rd Wilson B.A., 1996, BEHAV ASSESSMENT DYS WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1994, INT STAT CLASS DIS R YESAVAGE JA, 1983, J PSYCHIAT RES, V17, P37, DOI 10.1016/0022-3956(82)90033-4 NR 26 TC 11 Z9 12 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 0885-6230 J9 INT J GERIATR PSYCH JI Int. J. Geriatr. Psychiatr. PD OCT PY 2006 VL 21 IS 10 BP 951 EP 960 DI 10.1002/gps.1588 PG 10 WC Geriatrics & Gerontology; Gerontology; Psychiatry SC Geriatrics & Gerontology; Psychiatry GA 101AW UT WOS:000241712300007 PM 16927399 ER PT J AU Ventola, PE Kleinman, J Pandey, J Barton, M Allen, S Green, J Robins, D Fein, D AF Ventola, Pamela E. Kleinman, Jamie Pandey, Juhi Barton, Marianne Allen, Sarah Green, James Robins, Diana Fein, Deborah TI Agreement among four diagnostic instruments for autism spectrum disorders in toddlers SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; ASD; diagnostic instruments; toddlers ID PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIORAL TREATMENT; CHILDHOOD AUTISM; YOUNG-CHILDREN; RATING-SCALE; FIELD TRIAL; ADI-R; AGE; COMMUNICATION; SYMPTOMS AB Autistic spectrum disorders (ASD) can be difficult to diagnose in toddlers. This study compared diagnostic measures (ADOS-G, ADI-R, CARS, and clinical judgment using DSM-IV criteria) applied to toddlers. Results indicated that the ADOS-G, CARS, and clinical judgment agreed with each other but not with the ADI-R. Many of the children classified with ASD by the other measures were not classified with autism by the ADI-R because they did not display enough repetitive behaviors and stereotyped interests. These results indicate that young children with ASD may not display repetitive behaviors and stereotyped interests, and for toddlers, the ADI-R would have a higher sensitivity if revised to include a diagnosis of PDD-NOS, for which the requirement of repetitive behaviors is less stringent. C1 Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA. Georgia State Univ, Atlanta, GA 30303 USA. RP Ventola, PE (reprint author), Univ Connecticut, Dept Psychol, 406 Babbidge Rd, Storrs, CT 06269 USA. 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Autism Dev. Disord. PD OCT PY 2006 VL 36 IS 7 BP 839 EP 847 DI 10.1007/s10803-006-0128-8 PG 9 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600002 PM 16897398 ER PT J AU Leyfer, OT Folstein, SE Bacalman, S Davis, NO Dinh, E Morgan, J Tager-Flusberg, H Lainhart, JE AF Leyfer, Ovsanna T. Folstein, Susan E. Bacalman, Susan Davis, Naomi O. Dinh, Elena Morgan, Jubel Tager-Flusberg, Helen Lainhart, Janet E. TI Comorbid psychiatric disorders in children with autism: Interview development and rates of disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE psychopathology; autism; psychiatric interview; comorbidity ID SCHOOL-AGE-CHILDREN; ABERRANT BEHAVIOR CHECKLIST; MENTALLY-RETARDED CHILDREN; INTELLECTUAL DISABILITY; DIAGNOSTIC INTERVIEW; EXECUTIVE FUNCTION; COMMUNICATION DEFICITS; POPULATION PREVALENCE; PROBLEMS-INVENTORY; K-SADS AB The Kiddie Schedule for Affective Disorders and Schizophrenia was modified for use in children and adolescents with autism by developing additional screening questions and coding options that reflect the presentation of psychiatric disorders in autism spectrum disorders. The modified instrument, the Autism Comorbidity Interview-Present and Lifetime Version (ACI-PL), was piloted and frequently diagnosed disorders, depression, ADHD, and OCD, were tested for reliability and validity. The ACI-PL provides reliable DSM diagnoses that are valid based on clinical psychiatric diagnosis and treatment history. The sample demonstrated a high prevalence of specific phobia, obsessive compulsive disorder, and ADHD. The rates of psychiatric disorder in autism are high and are associated with functional impairment. C1 Utah Autism Res Program, Salt Lake City, UT 84108 USA. Univ Louisville, Dept Psychol & Brain Sci, Louisville, KY 40292 USA. Johns Hopkins Univ, Dept Psychiat, Baltimore, MD USA. Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Univ Massachusetts, Dept Psychol, Boston, MA 02125 USA. Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02215 USA. Univ Utah, Sch Med, Dept Psychiat, Salt Lake City, UT 84112 USA. RP Lainhart, JE (reprint author), Utah Autism Res Program, 421 Wakara Way,Suite 143, Salt Lake City, UT 84108 USA. 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Autism Dev. Disord. PD OCT PY 2006 VL 36 IS 7 BP 849 EP 861 DI 10.1007/s10803-006-0123-0 PG 13 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600003 PM 16845581 ER PT J AU Brereton, AV Tonge, BJ Einfeld, SL AF Brereton, Avril V. Tonge, Bruce J. Einfeld, Stewart L. TI Psychopathology in children and adolescents with autism compared to young people with intellectual disability SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; psychopathology; intellectual disability; comorbidity ID DEVELOPMENTAL BEHAVIOR CHECKLIST; EMOTIONAL DISTURBANCE; MENTAL-RETARDATION; POPULATION PREVALENCE; AFFECTIVE-DISORDERS; WILLIAMS-SYNDROME; INFANTILE-AUTISM; SEX-DIFFERENCES; INDIVIDUALS; PATTERNS AB Autism is a neurodevelopmental disorder with a specific pattern of behavioural, communication and social problems. Additional mental health problems are often poorly understood and undetected. This study investigates the level and pattern of emotional and behavioural problems in young people with autism compared with children with intellectual disability (ID). Subjects were 381 young people with autism and a representative group of 581 Australian young people with ID aged 4-18 years. Parents/carers provided details of the emotional and behavioural problems of their child using the Developmental Behaviour Checklist (DBC-P). Young people with autism were found to suffer from significantly higher levels of psychopathology than young people with ID. The implications of this finding are discussed. C1 Monash Univ, Ctr Dev Psychiat & Psychol, Monash Med Ctr, Clayton, Vic 3168, Australia. Univ New S Wales, Sch Psychiat, Sydney, NSW, Australia. RP Brereton, AV (reprint author), Monash Univ, Ctr Dev Psychiat & Psychol, Monash Med Ctr, 246 Clayton Rd, Clayton, Vic 3168, Australia. 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Stuart, Tami Auinger, Peggy TI Health care utilization and expenditures for children with autism: Data from US national samples SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; health services; mental retardation; depressive disorder ID MENTAL-RETARDATION; SPECTRUM DISORDER; ASPERGER-SYNDROME; DIAGNOSIS; DISABILITIES; PREVALENCE; COSTS; NEEDS AB Little is known about the use of medical services by children who have autism (ASD). Provide nationally representative data for health service utilization and expenditures of children with ASD. Cross-sectional survey using the Medical Expenditure Panel (MEPS), and National (Hospital) Ambulatory Medical Care Surveys (N(H)AMCS). A total of 80 children with ASD were identified from N(H)AMCS (weighted sample size (wss) 186,281), and 31 (wss 340,158) from MEPS. They had more outpatient visits, physician visits, and medications prescribed than children in general. They spent more time during physician visits than other children. Annual expenses for children with autism spectrum disorder ($6,132) were more than for other children ($860). Children with ASD have a substantial burden of medical illness. C1 Univ Rochester, Med Ctr, Rochester, NY 14642 USA. RP Liptak, GS (reprint author), Univ Rochester, Med Ctr, 601 Elmwood Ave,POB 671, Rochester, NY 14642 USA. 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Autism Dev. Disord. PD OCT PY 2006 VL 36 IS 7 BP 871 EP 879 DI 10.1007/s10803-006-0119-9 PG 9 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600005 PM 16855879 ER PT J AU Webb, SJ Dawson, G Bernier, R Panagiotides, H AF Webb, Sara J. Dawson, Geraldine Bernier, Raphael Panagiotides, Heracles TI ERP evidence of atypical face processing in young children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; event-related potentials; faces; N170; children ID VISUAL RECOGNITION MEMORY; SPECTRUM DISORDER; 6-MONTH-OLD INFANTS; FACIAL EXPRESSIONS; FAMILIAR FACE; MOTHERS FACE; POTENTIALS; PERCEPTION; STIMULI; SPECIALIZATION AB Autism involves a basic impairment in social cognition. This study investigated early stage face processing in young children with autism by examining the face-sensitive early negative event-related brain potential component in 3-4 year old children with autism spectrum disorder (ASD), typical development, and developmental delay. Results indicated that children with ASD showed a slower electrical brain response to faces and a larger amplitude response to objects compared to children with typical development and developmental delay. These findings indicate that children with ASD have a disordered pattern of brain responses to faces and objects at an early age. C1 CHDD, Psychiat & Behav Sci, Seattle, WA 98195 USA. Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. RP Webb, SJ (reprint author), CHDD, Psychiat & Behav Sci, Box 357920, Seattle, WA 98195 USA. 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Autism Dev. Disord. PD OCT PY 2006 VL 36 IS 7 BP 881 EP 890 DI 10.1007/s10803-006-0126-x PG 10 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600006 PM 16897400 ER PT J AU Jansen, LMC Gispen-de Wied, CC Wiegant, VM Westenberg, HGM Lahuis, BE van Engeland, H AF Jansen, Lucres M. C. Gispen-de Wied, Christine C. Wiegant, Victor M. Westenberg, Herman G. M. Lahuis, Bertine E. van Engeland, Herman TI Autonomic and neuroendocrine responses to a psychosocial stressor in adults with autistic spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; adults; stress; physiology; autonomic; neuroendocrine ID INFANTILE-AUTISM; DEVELOPMENTAL DISORDER; SOCIAL ATTACHMENT; NERVOUS-SYSTEM; DOUBLE-BLIND; OXYTOCIN; CHILDREN; VASOPRESSIN; CATECHOLAMINES; INVOLVEMENT AB Objective of the study was to replicate in adults our previous findings of decreased heart rate and normal endocrine responses to stress in autistic children and to elucidate the discrepancy between autonomic and endocrine stress responses by including epinephrine, norepinephrine, oxytocin and vasopressin measurements. Ten autistic spectrum disorder (ASD) adults were compared to 14 healthy controls in their response to a psychosocial stressor (public speaking). ASD patients showed decreased heart rate, but normal cortisol responses, consistent with our prior findings in children. No differences in norepinephrine, epinephrine, oxytocin or vasopressin responses to stress were found. However, in contrast to previous findings in low functioning, autistic children, ASD adults showed increased basal oxytocin levels, which may be related to developmental factors. C1 VU Univ, Med Ctr, Dept Child & Adolescent Psychiat, NL-1115 ZG Duivendrecht, Netherlands. Univ Utrecht, Med Ctr, Rudolf Magnus Inst Neurosci, Dept Child & Adolescent Psychiat, Utrecht, Netherlands. RP Jansen, LMC (reprint author), VU Univ, Med Ctr, Dept Child & Adolescent Psychiat, P-A De Bascule,POB 303, NL-1115 ZG Duivendrecht, Netherlands. EM l.nauta@debascule.com RI Jansen, Lucres/D-7754-2015 CR Althaus M, 1999, BIOL PSYCHIAT, V46, P799, DOI 10.1016/S0006-3223(98)00374-6 BOUVARD MP, 1995, PSYCHIAT RES, V58, P191, DOI 10.1016/0165-1781(95)02601-R Carter CS, 1998, PSYCHONEUROENDOCRINO, V23, P779 Cohen S, 2000, ANN BEHAV MED, V22, P171, DOI 10.1007/BF02895111 Corona R, 1998, CHILD DEV, V69, P1494, DOI 10.1111/j.1467-8624.1998.tb06172.x Croonenberghs J, 2000, NEUROPSYCHOPHARMACOL, V22, P275, DOI 10.1016/S0893-133X(99)00131-1 DEWIED D, 1993, FRONT NEUROENDOCRIN, V14, P251, DOI 10.1006/frne.1993.1009 DIMSDALE JE, 1980, PSYCHOSOM MED, V42, P493 Green LA, 2001, BIOL PSYCHIAT, V50, P609, DOI 10.1016/S0006-3223(01)01139-8 GRODEN J, 1994, CURR I AUT, P177 Hollander E, 2003, NEUROPSYCHOPHARMACOL, V28, P193, DOI 10.1038/sj.npp.1300021 Insel TR, 1999, BIOL PSYCHIAT, V45, P145, DOI 10.1016/S0006-3223(98)00142-5 Insel TR, 2000, CURR OPIN NEUROBIOL, V10, P784, DOI 10.1016/S0959-4388(00)00146-X Insel TR, 1997, AM J PSYCHIAT, V154, P726 Jansen LMC, 2003, NEUROPSYCHOPHARMACOL, V28, P582, DOI 10.1038/sj.npp.1300046 LAKE CR, 1977, ARCH GEN PSYCHIAT, V34, P553 LAUNAY JM, 1987, J AUTISM DEV DISORD, V17, P333, DOI 10.1007/BF01487064 LEBOYER M, 1992, J AUTISM DEV DISORD, V22, P309, DOI 10.1007/BF01058158 Legros JJ, 2001, PSYCHONEUROENDOCRINO, V26, P649, DOI 10.1016/S0306-4530(01)00018-X MAHER KR, 1975, J NERV MENT DIS, V161, P180, DOI 10.1097/00005053-197509000-00005 MARTINEAU J, 1992, DEV MED CHILD NEUROL, V34, P593 MARTINEAU J, 1994, DEV MED CHILD NEUROL, V36, P688 MINDERAA RB, 1994, BIOL PSYCHIAT, V36, P237, DOI 10.1016/0006-3223(94)90605-X Modahl C, 1998, BIOL PSYCHIAT, V43, P270, DOI 10.1016/S0006-3223(97)00439-3 Neumann ID, 2000, REGUL PEPTIDES, V96, P31, DOI 10.1016/S0167-0115(00)00197-X Nijsen MJMA, 1998, EUR J PHARMACOL, V350, P211, DOI 10.1016/S0014-2999(98)00261-1 Novotny SL, 2000, BIOL PSYCHIAT, V47, p159S, DOI 10.1016/S0006-3223(00)00793-9 Porges SW, 2001, INT J PSYCHOPHYSIOL, V42, P123, DOI 10.1016/S0167-8760(01)00162-3 Romero LM, 1996, J NEUROENDOCRINOL, V8, P243, DOI 10.1046/j.1365-2826.1996.04441.x Sheehan DV, 2001, J CLIN PSYCHIAT S20, V59, P20 Tordjman S, 1997, J CHILD PSYCHOL PSYC, V38, P705, DOI 10.1111/j.1469-7610.1997.tb01697.x VANDAMBAGGEN CMJ, 1987, 10A INVENTARISATIELI VANDERPLOG HM, 1981, HANDLEIDING BIJ ZELF Van Londen L, 1998, PSYCHOL MED, V28, P275, DOI 10.1017/S0033291797006284 Wechsler D., 1986, WECHSLER INTELLIGENC YAMAZAKI K, 1975, J AUTISM CHILD SCHIZ, V5, P323, DOI 10.1007/BF01540679 NR 36 TC 63 Z9 63 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 OCT PY 2006 VL 36 IS 7 BP 891 EP 899 DI 10.1007/s10803-006-0124-z PG 9 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600007 PM 16865550 ER PT J AU Wong, HHL Smith, RG AF Wong, Helen H. L. Smith, Ronald G. TI Patterns of complementary and alternative medical therapy use in children diagnosed with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE supplements; complementary; alternative; diets; children; autism ID UNITED-STATES; PEDIATRICIANS; POPULATION; CHALLENGES; PREVALENCE; CANCER; TRENDS AB Previous studies suggest that complementary and alternative medical (CAM) therapy use in children with chronic illnesses is higher than in children in the general population. In this study, we investigated patterns of CAM therapy use in children diagnosed with autism spectrum disorders (ASD, n = 50) as compared to a control population of children with no ASD (n = 50). Over half of the parents in the ASD group reported using, or had used at least one CAM therapy for their child (52%) as compared to 28% of the control group (P = 0.024). Seventy percent of therapies used in the ASD group were biologically based therapies comprised of special diets or supplements, and parents felt that 75% of the therapies used were beneficial. C1 Hop Hotel Dieu, Child Dev Ctr, Kingston, ON K7L 5G2, Canada. Queens Univ, Fac Med, Kingston, ON, Canada. RP Smith, RG (reprint author), Hop Hotel Dieu, Child Dev Ctr, 166 Brock St, Kingston, ON K7L 5G2, Canada. EM gs3@post.queensu.ca CR Angell M, 1998, NEW ENGL J MED, V339, P839, DOI 10.1056/NEJM199809173391210 [Anonymous], 2004, WHAT IS COMPL ALT ME Barnard L, 2002, J PSYCHOPHARMACOL, V16, P93 Beigel Y, 1998, NEW ENGL J MED, V339, P827, DOI 10.1056/NEJM199809173391208 Charman T, 2002, EUR CHILD ADOLES PSY, V11, P249, DOI 10.1007/s00787-002-0297-8 Cuzzolin L, 2003, EUR J PEDIATR, V162, P820, DOI 10.1007/s00431-003-1313-9 Davis MP, 2003, ARCH PEDIAT ADOL MED, V157, P393, DOI 10.1001/archpedi.157.4.393 EISENBERG DM, 1993, NEW ENGL J MED, V328, P246, DOI 10.1056/NEJM199301283280406 Eisenberg DM, 1998, JAMA-J AM MED ASSOC, V280, P1569, DOI 10.1001/jama.280.18.1569 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Friedman T, 1997, PEDIATRICS, V100, part. no., DOI 10.1542/peds.100.6.e1 Hagen LEM, 2003, ARTHRIT RHEUM-ARTHR, V49, P3, DOI 10.1002/art.10931 Kelly KM, 2004, EUR J CANCER, V40, P2041, DOI 10.1016/j.ejca.2004.05.012 Kessler RC, 2001, ANN INTERN MED, V135, P262 Lanski SL, 2003, PEDIATRICS, V111, P981, DOI 10.1542/peds.111.5.981 Levy SE, 2003, J DEV BEHAV PEDIATR, V24, P418, DOI 10.1097/00004703-200312000-00003 Markowitz JE, 2004, INFLAMM BOWEL DIS, V10, P599, DOI 10.1097/00054725-200409000-00015 Millar W J, 2001, Health Rep, V13, P9 Mitzdorf U, 1999, J ALTERN COMPLEM MED, V5, P463, DOI 10.1089/acm.1999.5.463 Moore ML, 2004, ANN PHARMACOTHER, V38, P1515, DOI 10.1345/aph.1D543 Owley T, 2001, J AM ACAD CHILD PSY, V40, P1293, DOI 10.1097/00004583-200111000-00009 Pitetti R, 2001, PEDIATR EMERG CARE, V17, P165, DOI 10.1097/00006565-200106000-00004 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Richardson MA, 2002, SEMIN ONCOL, V29, P531, DOI 10.1053/sonc.2002.50002 Sandler AD, 2001, PEDIATRICS, V107, P598 Sibinga EMS, 2004, CLIN PEDIATR, V43, P367, DOI 10.1177/000992280404300408 Sikand A, 1998, ARCH PEDIAT ADOL MED, V152, P1059 SPIGELBLATT L, 1994, PEDIATRICS, V94, P811 Sterba JA, 2002, DEV MED CHILD NEUROL, V44, P301 Volkmar FR, 2003, LANCET, V362, P1133, DOI 10.1016/S0140-6736(03)14471-6 Weinstein M, 2003, CAN MED ASSOC J, V168, P201 WHIPPLE J, 2000, J MUSIC THER, V41, P90 Yussman SM, 2004, AMBUL PEDIATR, V4, P429, DOI 10.1367/A03-091R1.1 NR 33 TC 77 Z9 78 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 OCT PY 2006 VL 36 IS 7 BP 901 EP 909 DI 10.1007/s10803-006-0131-0 PG 9 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600008 PM 16897395 ER PT J AU Nation, K Clarke, P Wright, B Williams, C AF Nation, Kate Clarke, Paula Wright, Barry Williams, Christine TI Patterns of reading ability in children with autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE reading; language; comprehension; autism; hyperlexia ID LANGUAGE IMPAIRMENT; DEVELOPMENTAL DYSLEXIA; HYPERLEXIC CHILDREN; COMPREHENSION; DIFFICULTIES; INDIVIDUALS; LITERACY; READERS AB This study investigated reading skills in 41 children with autism spectrum disorder. Four components of reading skill were assessed: word recognition, nonword decoding, text reading accuracy and text comprehension. Overall. levels of word and nonword reading and text reading accuracy fell within average range although reading comprehension was impaired. However, there was considerable variability across the sample with performance on most tests ranging from floor to ceiling levels. Some children read accurately but showed very poor comprehension, consistent with a hyperlexia reading profile; some children were poor at reading words and nonwords whereas others were unable to decode nonwords, despite a reasonable level of word reading skill. These findings demonstrate the heterogeneous nature of reading skills in children with ASD. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. Univ York, Dept Psychol, York YO10 5DD, N Yorkshire, England. Selby & York Primary Care Trust, Child & Adolescent Mental Hlth, York, N Yorkshire, England. RP Nation, K (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. EM kate.nation@psy.ox.ac.uk RI Nation, Kate/F-8228-2014 CR AARON PG, 1990, READ WRIT, V2, P243, DOI 10.1007/BF00257974 BISHOP DVM, 1990, J CHILD PSYCHOL PSYC, V31, P1027, DOI 10.1111/j.1469-7610.1990.tb00844.x Bishop DVM, 2004, AM J MED GENET B, V129B, P94, DOI 10.1002/ajmg.b.30065 Bishop DVM, 2004, PSYCHOL BULL, V130, P858, DOI 10.1037/0033-2909.130.6.858 Briscoe J, 2001, J CHILD PSYCHOL PSYC, V42, P329, DOI 10.1017/S0021963001007041 Catts H. W., 2005, CONNECTIONS LANGUAGE Dunn L. M., 1997, BRIT PICTURE VOCABUL, V2nd Elliot C. 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TI Assessing need for social support in parents of children with autism and Down syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism spectrum disorder; social support; Down syndrome; autism; adaptation; Family Needs Questionnaire ID TRAUMATIC BRAIN INJURY; FAMILY NEEDS; SCREENING QUESTIONNAIRE; BEHAVIORAL TREATMENT; SPECTRUM DISORDERS; ASPERGER-SYNDROME; STRESS; ADAPTATION; INDIVIDUALS; PERSPECTIVE AB Parents of children with autism frequently turn to the service delivery system to access supports designed to help adapt to the challenges of having a child with a life-long impairment. Although studies have suggested various supports and coping strategies that are effective for adapting, few studies have examined parents' own perceptions of needs.. and whether parents felt their needs were being met. In the present study the Family Needs Questionnaire (FNQ, Waaland et al., 1993) was modified to address needs for children with developmental disorders. A sample of fifty-six parents of children with autism and a comparison group of thirty-two parents of children with Down syndrome completed the FNQ. The groups did not differ significantly on the number of important needs reported nor the number of important needs being met. However, the two groups differed in the types of supports they most frequently endorsed as Important or Unmet. C1 Univ Victoria, Dept Psychol, Victoria, BC V8W 3P5, Canada. RP Kerns, KA (reprint author), Univ Victoria, Dept Psychol, POB 3050, Victoria, BC V8W 3P5, Canada. 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Autism Dev. Disord. PD OCT PY 2006 VL 36 IS 7 BP 921 EP 933 DI 10.1007/s10803-006-0129-7 PG 13 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600010 PM 16897397 ER PT J AU Hall, S DeBernardis, M Reiss, A AF Hall, Scott DeBernardis, Marie Reiss, Allan TI Social escape behaviors in children with fragile X syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT 30th Annual Convention of the Association for Applied Behavior Analysis CY 2004 CL Boston, MA DE social escape; eye contact; fragile X syndrome; cortisol ID SELF-INJURIOUS-BEHAVIOR; LESCH-NYHAN DISEASE; FUNCTIONAL-ANALYSIS; AVOIDANCE; CORTISOL; CHOICE; AUTISM; MALES AB Social escape behavior is a common behavioral feature of individuals with fragile X syndrome (fraX). In this observational study, we examined the effect of antecedent social and performance demands on problem behaviors in four conditions: face-to-face interview, silent reading, oral reading and a singing task. Results showed that problem behaviors were significantly more likely to occur during the interview and singing conditions. Higher levels of salivary cortisol were predictive of higher levels of fidgeting behavior and lower levels of eye contact in male participants. There were no associations between level of FMRP expression and social escape behaviors. These data suo-est that specific antecedent biological and environmental factors evoke social escape behaviors in fragile X syndrome. C1 Stanford Univ, Behav Neurogenet Res Ctr, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. RP Hall, S (reprint author), Stanford Univ, Behav Neurogenet Res Ctr, Dept Psychiat & Behav Sci, Rm 1367,401 Quarry Rd, Stanford, CA 94305 USA. 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Autism Dev. Disord. PD OCT PY 2006 VL 36 IS 7 BP 935 EP 947 DI 10.1007/s10803-006-0132-z PG 13 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600011 PM 16897394 ER PT J AU Carroll, JM Yung, CK AF Carroll, Julia M. Yung, Chiew Kin TI Sex and discipline differences in empathising, systemising and autistic symptomatology: Evidence from a student population SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE empathising; systemising; extreme male brain; gender; central coherence; theory of mind ID WEAK CENTRAL COHERENCE; FUNCTIONING AUTISM; ASPERGER-SYNDROME; MIND; ADULTS AB Baron-Cohen's [(2002) Trends in Cognitive Sciences, 6, 248-255] 'extreme male brain' theory of autism is investigated by examining the relationships between theory of mind, central coherence, empathising, systemising and autistic-like symptomatology in typical undergraduates. There were sex differences in the expected directions on all tasks. Differences according to discipline were found only in central coherence. There was no evidence of an association between empathising and systemising. In the second study, performance on the Mechanical Reasoning task was compared with Systemising quotient and the Social Skills Inventory was compared with the Empathising Quotient. Moderate, but not high correlations were found. Findings are broadly consistent with the distinction between empathising and systemising but cast some doubt on the tasks used to measure these abilities. C1 Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. Univ York, Dept Psychol, York YO10 5DD, N Yorkshire, England. RP Carroll, JM (reprint author), Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. EM J.M.Carroll@warwick.ac.uk RI Carroll, Julia/D-6259-2011 OI Carroll, Julia/0000-0002-3614-6883 CR Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE BARONCOHEN S, 1997, ADV INFANCY RES, V11, P196 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S., 1998, AUTISM, V2, P296, DOI 10.1177/1362361398023008 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1997, AUTISM, V1, P101, DOI 10.1177/1362361397011010 BENNETT GK, 1974, DIFFERENTIAL APTITUE Briskman J, 2001, J CHILD PSYCHOL PSYC, V42, P309, DOI 10.1111/1469-7610.00724 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Frith U., 2003, AUTISM EXPLAINING EN HOFFMAN ML, 1977, PSYCHOL BULL, V84, P712, DOI 10.1037//0033-2909.84.4.712 Jarrold C, 2000, DEV PSYCHOL, V36, P126, DOI 10.1037/0012-1649.36.1.126 Lawson J, 2004, J AUTISM DEV DISORD, V34, P301, DOI 10.1023/B:JADD.0000029552.42724.1b Morgan B, 2003, DEV PSYCHOL, V39, P646, DOI 10.1037/0012-1649.39.4.646 Riggio R. E., 1989, SOCIAL SKILLS INVENT VOYER D, 1995, PSYCHOL BULL, V117, P250, DOI 10.1037/0033-2909.117.2.250 Wechsler D, 1999, WECHSLER ABBREVIATED Witkin HA, 1971, MANUAL EMBEDDED FIGU NR 20 TC 37 Z9 37 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 OCT PY 2006 VL 36 IS 7 BP 949 EP 957 DI 10.1007/s10803-006-0127-9 PG 9 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600012 PM 16897399 ER PT J AU Delmolino, LM AF Delmolino, Lara M. TI Brief report: Use of DQ for estimating cognitive ability in young children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; assessment; intelligence; development; testing ID PRESCHOOL-CHILDREN; INTERVENTION; IQ AB The utility of Developmental Quotients (DQ) from the Psychoeducational Profile-Revised (PEP-R) to estimate cognitive ability in young children with autism was assessed. DQ scores were compared to scores from the Stanford-Binet Intelligence Scales-Fourth Edition (SB-FE) for 27 preschool students with autism. Overall and domain DQ's on the PEP-R were significantly correlated with SB-FE composite IQ and Verbal Reasoning scores. Additional analyses with rank scores from each instrument confirmed these results. Results indicate that DQ scores obtained by the PEP-R are reasonable estimates of cognitive ability in this sample as measured by the SB-FE. Some administration advantages suggest that the PEP-R may be a viable alternative to the SB-FE (for estimating cognitive skills) under some conditions. C1 Rutgers State Univ, Div Res & Training, Douglass Dev Disabil Ctr, New Brunswick, NJ 08901 USA. RP Delmolino, LM (reprint author), Rutgers State Univ, Div Res & Training, Douglass Dev Disabil Ctr, 25 Gibbons Circle, New Brunswick, NJ 08901 USA. EM delmolin@rci.rutgers.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bayley N., 1969, BAYLEY SCALES INFANT Doll E. A., 1965, VINELAND SOCIAL MATU Dunn LM, 1965, PEABODY PICTURE VOCA Harris SL, 1990, SPECIAL SERVICES SCH, V6, P135 HARRIS SL, 1991, J AUTISM DEV DISORD, V21, P281, DOI 10.1007/BF02207325 Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 KLIN A, 1997, HDB AUTISM PERVASIVE, P418 Koegel LK, 1997, J AUTISM DEV DISORD, V27, P233, DOI 10.1023/A:1025894213424 Kurita H, 2003, PSYCHIAT CLIN NEUROS, V57, P231, DOI 10.1046/j.1440-1819.2003.01106.x Leiter R. 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PD OCT PY 2006 VL 36 IS 7 BP 959 EP 963 DI 10.1007/s10803-006-0133-y PG 5 WC Psychology, Developmental SC Psychology GA 093ME UT WOS:000241171600013 PM 16897393 ER PT J AU Owley, T Salt, J Salt, J Guter, S Grieve, A Walton, L Ayuyao, N Leventhal, BL Cook, EH AF Owley, Thomas Salt, Jeff Salt, Jeff Guter, Stephen Grieve, Adam Walton, Laura Ayuyao, Nelson Leventhal, Bennett L. Cook, Edwin H., Jr. TI A prospective, open-label trial of memantine in the treatment of cognitive, behavioral, and memory dysfunction in pervasive developmental disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID RETT-SYNDROME; AUTISM; GLUTAMATE; CHILDREN; RECEPTORS AB Background: This pilot study examined the effectiveness of memantine hydrochloride in improving cognitive functioning and behavioral symptoms in children with pervasive developmental disorders (PDDs). Method: Subjects aged 3-12 years inclusive were enrolled in this 8-week, open-label study. Expressive and receptive language, nonverbal IQ, and nonverbal memory measures were administered at baseline and after 8 weeks of treatment with 0.4 mg/kg of memantine hydrochloride. Throughout the study, the Aberrant Behavior Checklist (ABC) was sent in weekly by parents as a measure of behavioral change. Results: Twelve of 14 subjects completed the study. Significant improvement from baseline was noted on the memory test (Children's Memory Scale Dot Learning Subtest). There were no significant differences from baseline on measures of expressive or receptive language or nonverbal IQ. There were significant improvements on a number of ABC subscales, including hyperactivity, lethargy, and irritability. There were no overall significant statistical differences from baseline on the Clinical Global Improvement-Severity (CGI-S) scale. On the Clinical Global Improvement-Improvement (CGI-I), 4 of 14 subjects showed minimal improvement, and none was deemed "much-improved" or "very much improved." Conclusions: This small, prospective, open-label study suggests that memantine may be useful in the treatment of memory functioning and some behavioral symptoms in PDDs. The investigators did not see the same degree of change as endorsed by caretakers. Controlled studies are needed to substantiate and clarify these preliminary findings. C1 Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA. RP Owley, T (reprint author), Univ Illinois, Dept Psychiat MC 747, Inst Juvenile Res, 1747 W Roosevelt Rd,Room 155, Chicago, IL 60608 USA. 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Hagerman, Randi TI Effect of CX516, an AMPA-modulating compound, on cognition and behavior in fragile X syndrome: A controlled trial SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID MENTAL-RETARDATION PROTEIN; SYNAPTIC PLASTICITY; AUTISM; MEMORY; HIPPOCAMPAL; EXPRESSION; CHILDREN; CURRENTS; DRUG AB A Phase II, 4-week randomized, double-blind, placebo-controlled clinical trial was conducted to evaluate the safety and efficacy of the Ampakine compound CX516 as a potential treatment for the underlying disorder in fragile X syndrome (FXS). After baseline screening, subjects with FXS (n = 49) underwent a 1-week placebo lead-in and then were randomized to study drug or placebo for a 4-week period. Cognitive and behavioral outcome measures were administered prior to treatment, at the end of treatment, and 2 weeks posttreatment. There were minimal side effects, no significant changes in safety parameters, and no serious adverse events. There was a 12.5% frequency of allergic rash in the CX516 group and 1 subject developed a substantial rash. There was also no significant improvement in memory, the primary outcome measure, or in secondary measures of language, attention/executive function, behavior, and overall functioning in CX516-treated subjects compared to placebo. This study did demonstrate that many outcome measures were reproducible in this test-retest setting for the FXS population, yet some were too difficult or variable. Adult subjects with FXS were able to complete an intensive clinical trial, and some valid outcome measures were identified for future FXS trial design. Problems with potency of CX516 in other studies have suggested dosing may have been inadequate for therapeutic effect and thus it remains unclear whether modulation of AMPA-mediated neurotransmission is a viable therapeutic strategy for the treatment of FXS. C1 Rush Univ, Med Ctr, Dept Pediat, Chicago, IL 60612 USA. 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PD OCT PY 2006 VL 16 IS 5 BP 525 EP 540 DI 10.1089/cap.2006.16.525 PG 16 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600004 PM 17069542 ER PT J AU Hollander, E Wasserman, S Swanson, EN Chaplin, W Schapiro, ML Zagursky, K Novotny, S AF Hollander, Eric Wasserman, Stacey Swanson, Erika N. Chaplin, William Schapiro, Melissa L. Zagursky, Karen Novotny, Sherie TI A double-blind placebo-controlled pilot study of olanzapine in childhood/adolescent pervasive developmental disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID AUTISTIC-CHILDREN; ATYPICAL ANTIPSYCHOTICS; BEHAVIORAL SYMPTOMS; RATING-SCALE; OPEN-LABEL; HALOPERIDOL; RISPERIDONE; ADOLESCENTS; WEIGHT; DESIGN AB Atypical antipsychotics have been shown to improve disruptive and repetitive behaviors in pervasive developmental disorders (PDDs), but they require assessment of potential side effects. This is the first placebo-controlled trial of olanzapine in the treatment of children and adolescents with PDD. Eleven patients with a diagnosis of either autism, Asperger's syndrome, or PDD not otherwise specified (PDD-NOS) and aged 6-14 years were randomized into an 8-week double-blind, placebo-controlled, parallel treatment study with olanzapine. There was a significant linear trend X group interaction on the Clinical Global Impressions-Improvement (CGI-I) and 50% on olanzapine versus 20% on placebo were responders. Olanzapine was associated with significant weight gain (7.5 +/- 4.8 lbs vs. 1.5 +/- 1.5 lbs on placebo). Olanzapine may be a promising treatment for improving global functioning of PDDs, but the risk of significant weight gain remains a concern. Additional studies are needed to determine the efficacy and safety of olanzapine in the treatment of children with PDD. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, Seaver & NY Autism Ctr Excellence, New York, NY 10029 USA. RP Hollander, E (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, Seaver & NY Autism Ctr Excellence, 1 Gustave L Levy Pl,Box 1230, New York, NY 10029 USA. 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Child Adolesc. Psychopharmacol. PD OCT PY 2006 VL 16 IS 5 BP 541 EP 548 DI 10.1089/cap.2006.16.541 PG 8 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600005 PM 17069543 ER PT J AU Valicenti-McDermott, MR Demb, H AF Valicenti-McDermott, Maria R. Demb, Howard TI Clinical effects and adverse reactions of off-label use of aripiprazole in children and adolescents with developmental disabilities SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID SUBAVERAGE INTELLIGENCE; DOUBLE-BLIND; RISPERIDONE; DISORDERS; SCHIZOPHRENIA; PLACEBO; AUTISM; TOLERABILITY; RECEPTORS; SYMPTOMS AB Objective: The aim of this study was to report on the clinical efficacy and side effects of aripiprazole in treating behavioral symptoms of children with a developmental disability (DDs). Design/methods: A retrospective chart review of the first 32 children treated with aripiprazole at an urban clinic for children with DD was conducted. Results: Ages ranged from 5 to 19 years; 9 (28%) were female. Twenty four had diagnoses within the autistic spectrum and 18 had mental retardation (MR). Other disorders included: attention-deficit/hyperactivity disorder/disruptive behavior disorders (n = 13), mood disorders (n = 7), reactive attachment (n = 2), and sleep disorders (n = 2). Target symptoms included aggression, hyperactivity, impulsivity and, self-injurious behaviors. Twenty eight of the children were switched from another antipsychotic. The mean daily aripiprazole starting dose was 7.1 +/- 0.32 mg (0.17 mg/kg/day) and the mean daily maintenance dose was 10.55 +/- 6.9 mg (0.27mg/kg/day). Aripiprazole had been used for a period between 6 and 15 months. Improvement in target symptoms was found in 56%. When treating a child with MR, the concomitant presence of an autistic spectrum diagnosis predicted a worse outcome. Side effects were reported in 16 (50%), with the most frequent being sleepiness (n = 6). Mean body mass index (BMI) rose from 22.5 to 24.1 (p = 0.003) over the follow up period, with changes in the BMI z scores. These changes were more pronounced in children younger than 12 years. Conclusions: These results with aripiprazole in this difficult-to-treat population suggest that this medication warrants controlled studies of its effectiveness and safety. C1 Albert Einstein Coll Med, RF Kennedy Ctr Excellence Dev Disabil, Childrens Evaluat & Rehabil Ctr, Bronx, NY 10467 USA. RP Valicenti-McDermott, MR (reprint author), 1410 Pelham Pkwy S, Bronx, NY 10461 USA. EM rvalicenti@hotmail.com CR AMAN MG, 2005, AM J PSYCHIAT, V162, P1367 Aman MG, 2002, AM J PSYCHIAT, V159, P1337, DOI 10.1176/appi.ajp.159.8.1337 American Psychiatric Association, 2000, DIAGN STAT MAN MENT AMES D, 1996, ESSENT PSYCHOPHARMAC, V1, P5 Barzman DH, 2004, J CHILD ADOL PSYCHOP, V14, P593, DOI 10.1089/cap.2004.14.593 Burris KD, 2002, J PHARMACOL EXP THER, V302, P381, DOI 10.1124/jpet.102.033175 COHEN DJ, 1986, J AM ACAD CHILD PSY, V25, P213, DOI 10.1016/S0002-7138(09)60228-4 CONNOR DF, 1998, MENTAL HLTH ASPECTS, V1, P93 Croonenberghs J, 2005, J AM ACAD CHILD PSY, V44, P64, DOI 10.1097/01.chi.0000145805.24274.09 DURKIN JP, 2004, J CHILD ADOL PSYCHOP, V14, P5005 Findling RL, 2000, J AM ACAD CHILD PSY, V39, P509, DOI 10.1097/00004583-200004000-00021 GALLUCCI G, 2004, MENT HLTH ASPECT DEV, V7, P53 Guy W, 1976, US DHEW PUBLICATION, V76-338, P218 Hollander E, 2003, LANCET, V362, P732, DOI 10.1016/S0140-6736(03)14236-5 JIBSON MD, 1996, ESSENTIAL PSYCHOPHAR, V1, P27 Kemner C, 2002, J CLIN PSYCHOPHARM, V22, P455, DOI 10.1097/01.jcp.0000033400.43191.6f LEONARD H, 2003, BROWN U CHILD ADOLES, V5, P1 Lindsey RL, 2003, J AM ACAD CHILD PSY, V42, P1268, DOI 10.1097/01.chi.0000095540.18151.b0 MADRID AL, 2000, CHILD ADOL PSYCH CL, P225 Marder SR, 2003, SCHIZOPHR RES, V61, P123, DOI 10.1016/S0920-9964(03)00050-1 Masi G, 2003, J CLIN PSYCHIAT, V64, P1039 McDougle CJ, 2002, J AM ACAD CHILD PSY, V41, P921, DOI 10.1097/00004583-200208000-00010 McRae A., 2003, INTERN DRUG THER NEW, V38, P25 Ogden CL, 2002, PEDIATRICS, V109, P45, DOI 10.1542/peds.109.1.45 OREN DA, 2003, ARIPIPRAZOLE PEDIAT Potkin SG, 2003, ARCH GEN PSYCHIAT, V60, P681, DOI 10.1001/archpsyc.60.7.681 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 RIFKIN A, 1999, NADD B, V2, P27 Spalding S, 2004, J AM ACAD CHILD PSY, V43, P1457, DOI 10.1097/01.chi.0000142277.95052.94 Spreat S, 2004, AM J MENT RETARD, V109, P322, DOI 10.1352/0895-8017(2004)109<322:SLSOPM>2.0.CO;2 Stahl SM, 2001, J CLIN PSYCHIAT, V62, P841 STEELE J, 2002, EXCEP PARENT, P58 Stigler K. A., 2003, CHILD ADOL PSYCH CL, V8, P6, DOI 10.1521/capn.8.7.6.24962 Stigler KA, 2004, J CHILD ADOL PSYCHOP, V14, P455 TOWBIN KE, 1993, J AM ACAD CHILD PSY, V32, P775, DOI 10.1097/00004583-199307000-00011 NR 35 TC 44 Z9 45 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 OCT PY 2006 VL 16 IS 5 BP 549 EP 560 DI 10.1089/cap.2006.16.549 PG 12 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600006 PM 17069544 ER PT J AU Troost, PW Althaus, M Lahuis, BE Buitelaar, JK Minderaa, RB Hoekstra, PJ AF Troost, Pieter W. Althaus, Monika Lahuis, Bertine E. Buitelaar, Jan K. Minderaa, Ruud B. Hoekstra, Pieter J. TI Neuropsychological effects of risperidone in children with pervasive developmental disorders: A blinded discontinuation study SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID AUTISM SPECTRUM DISORDERS; HIGH-FUNCTIONING AUTISM; LONG-TERM SAFETY; EXECUTIVE FUNCTIONS; ATTENTION; SCALE AB Objective: Little is known about the neuropsychological effects of risperidone in children with pervasive developmental disorders. Method: Twenty-four children (aged 5-17 years) with pervasive developmental disorders and co-morbid disruptive behavior who responded favorably to open-label treatment with risperidone as part of a previously described controlled discontinuation study completed two different computerized attention tasks at baseline, weeks 4, 8, and 24 of open-label treatment, and, at 8 weeks after random assignment to either placebo or risperidone. The primary efficacy measures were response latencies to visually presented stimuli requiring two different types of attention-controlled processing, i.e., focused and divided attention. Results: About half of the clinical responders did not produce valid performance measures. These could be shown to be of younger mental age and less adaptive as measured by the Vineland Behavior Scales. For the valid task performers divided attention (serial search in working memory) was shown to regress in the placebo group (n = 7), while in the risperidone group (n = 7) there was further improvement. No such group difference was found for focused attention. Conclusions: The study suggests a beneficial effect of risperidone after several months of treatment, enhancing divided attention in children with pervasive developmental disorders. C1 Univ Groningen, Univ Med Ctr Groningen, Dept Psychiat, NL-9700 AB Groningen, Netherlands. Univ Med Ctr Utrecht, Dept Child Psychiat, Utrecht, Netherlands. Univ Med Ctr Utrecht, Rudolf Magnus Inst Neurosci, Utrecht, Netherlands. Univ Med Ctr, Dept Psychiat, Nijmegen, Netherlands. RP Troost, PW (reprint author), Child & Adolescent Psychiat Ctr, POB 660, NL-9700 AR Groningen, Netherlands. EM p.troost@accare.nl RI Buitelaar, Jan/E-4584-2012; Hoekstra, Pieter/O-4396-2014 OI Buitelaar, Jan/0000-0001-8288-7757; CR Althaus M, 1999, BIOL PSYCHIAT, V46, P799, DOI 10.1016/S0006-3223(98)00374-6 Althaus M, 1996, CHILD NEUROPSYCHOL, V2, P17, DOI 10.1080/09297049608401347 Aman MG, 2005, J CHILD ADOL PSYCHOP, V15, P869, DOI 10.1089/cap.2005.15.869 AMAN MG, 1985, AM J MENT DEF, V89, P485 American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x DESONNEVILLE LMJ, 1993, COMP PSYCH, V4, P168 Findling RL, 2004, AM J PSYCHIAT, V161, P677, DOI 10.1176/appi.ajp.161.4.677 Guy W, 1976, ASSESSMENT MANUAL PS Harvey PD, 2003, PSYCHOPHARMACOLOGY, V169, P404, DOI 10.1007/s00213-002-1342-5 Haznedar MM, 2000, AM J PSYCHIAT, V157, P1994, DOI 10.1176/appi.ajp.157.12.1994 Haznedar MM, 1997, AM J PSYCHIAT, V154, P1047 Keefe RSE, 1999, SCHIZOPHRENIA BULL, V25, P201 Koshino H, 2005, NEUROIMAGE, V24, P810, DOI 10.1016/j.neuroimage.2004.09.028 Landa RJ, 2005, J AUTISM DEV DISORD, V35, P557, DOI 10.1007/s10803-005-0001-1 Levitt JG, 2003, CEREB CORTEX, V13, P728, DOI 10.1093/cercor/13.7.728 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Luna B, 2002, NEUROLOGY, V59, P834 McDougle CJ, 2005, AM J PSYCHIAT, V162, P1142, DOI 10.1176/appi.ajp.162.6.1142 Ozonoff S, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Patel NC, 2005, J AM ACAD CHILD PSY, V44, P548, DOI 10.1097/01.chi.0000157543.74509.c8 Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x Pierce K, 1997, J AUTISM DEV DISORD, V27, P265, DOI 10.1023/A:1025898314332 PIVEN J, 1991, J AUTISM DEV DISORD, V21, P51, DOI 10.1007/BF02206997 POSNER MI, 1994, IMAGES MIND, P153 Mccracken JT, 2005, AM J PSYCHIAT, V162, P1361 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 SCHNEIDER W, 1977, PSYCHOL REV, V84, P1, DOI 10.1037/0033-295X.84.1.1 SHIFFRIN RM, 1977, PSYCHOL REV, V84, P127, DOI 10.1037/0033-295X.84.2.127 Stevens J, 2002, APPL MULTIVARIATE ST, P197 Troost PW, 2005, J AM ACAD CHILD PSY, V44, P1137, DOI 10.1097/01.chi.0000177055.11229.76 Turgay A, 2002, PEDIATRICS, V110, DOI 10.1542/peds.110.3.e34 Zarahn E, 2005, CEREB CORTEX, V15, P303, DOI 10.1093/cercor/bhh132 NR 33 TC 14 Z9 14 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 OCT PY 2006 VL 16 IS 5 BP 561 EP 573 DI 10.1089/cap.2006.16.561 PG 13 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600007 PM 17069545 ER PT J AU Luby, J Mrakotsky, C Stalets, MM Belden, A Heffelfinger, A Williams, M Spitznagel, E AF Luby, Joan Mrakotsky, Christine Stalets, Melissa Meade Belden, Andy Heffelfinger, Amy Williams, Meghan Spitznagel, Edward TI Risperidone in preschool children with autistic spectrum disorders: An investigation of safety and efficacy SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PEDIATRIC PSYCHOPHARMACOLOGY; DISCONTINUATION; ADOLESCENTS; BRAIN AB Introduction: Early intervention in autism spectrum disorders (ASDs) appears promising and may represent a window of opportunity for more effective treatment. Whereas the safety and efficacy of risperidone have been established for children aged 5 and older, they has not been adequately tested in preschool children. Methods: A randomized placebo-controlled study of risperidone in preschool children was conducted in a sample of young children, most of whom were also undergoing intensive behavioral treatment. Results: Preschool children tolerated low-dose risperidone well with no serious adverse effects observed over a 6-month treatment period. Weight gain and hypersalivation were the most common side effects reported, and hyperprolactinemia without lactation or related signs was observed. Significant differences between groups found at baseline complicated the analyses; however, controlling for some of these differences revealed that preschoolers on risperidone demonstrated greater improvements in autism severity. The change in autism severity scores from baseline to 6-month follow up for the risperidone group was 8% compared to 3% for the placebo group. Notably, both groups significantly improved over the 6-month treatment period. Conclusions: Study findings suggest that risperidone is well tolerated in preschoolers over a 6-month period, but that only minimally greater improvement in target symptoms was evident in the risperidone group, possibly due to the differences between groups at baseline or due to the small sample size. Although these findings are not sufficient to direct treatment, they suggest that larger-scale, double-blind, placebo-controlled investigations of risperidone in preschoolers with ASDs should now be conducted. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63117 USA. Harvard Univ, Sch Med, Childrens Hosp, Dept Psychiat, Boston, MA USA. Med Coll Wisconsin, Dept Neurol, Milwaukee, WI 53226 USA. Washington Univ, Dept Math, St Louis, MO 63130 USA. 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Child Adolesc. Psychopharmacol. PD OCT PY 2006 VL 16 IS 5 BP 575 EP 587 DI 10.1089/cap.2006.16.575 PG 13 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600008 PM 17069546 ER PT J AU Scahill, L Aman, MG McDougle, CJ McCracken, JT Tierney, E Dziura, J Arnold, E Posey, D Young, C Shah, B Ghuman, J Ritz, L Vitiello, B AF Scahill, Lawrence Aman, Michael G. McDougle, Christopher J. McCracken, James T. Tierney, Elaine Dziura, James Arnold, Eugene Posey, David Young, Christopher Shah, Bhavik Ghuman, Jaswinder Ritz, Louise Vitiello, Benedetto TI A prospective open trial of guanfacine in children with pervasive developmental disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID ABERRANT BEHAVIOR CHECKLIST; DEFICIT HYPERACTIVITY DISORDER; METHYLPHENIDATE; ADHD; ATOMOXETINE; COMMUNITY; AUTISM; NORMS; MTA AB Objective: A common complaint for children with pervasive developmental disorder (PDD) is hyperactivity. The purpose of this pilot study was to gather preliminary information on the efficacy of guanfacine in children with PDD and hyperactivity. Methods: Children with PDD accompanied by hyperactivity entered the open-label trial if there was a recent history of failed treatment with methylphenidate or the child did not improve on methylphenidate in a multisite, placebo-controlled trial. Results: Children (23 boys and 2 girls) with a mean age of 9.03 (+/- 3.14) years entered the open-label trial. After 8 weeks of treatment, the parent-rated Hyperactivity subscale of the Aberrant Behavior Checklist (ABC) went from a mean of 31.3 (+/- 8.89) at baseline to 18.9 (+/- 10.37) (effect size = 1.4; p < 0.001). The teacher-rated Hyperactivity subscale decreased from a mean of 29.9 (+/-\9.12) at baseline to 22.3 (+/- 9.44) (effect size = 0.83; p < 0.01). Twelve children (48%) were rated as Much Improved or Very Much Improved on the Clinical Global Impressions-Improvement. Doses ranged from 1.0 to 3.0 mg/day in two or three divided doses. Common adverse effects included irritability, sedation, sleep disturbance (insomnia or midsleep awakening), and constipation. Irritability led to discontinuation in 3 subjects. There were no significant changes in pulse, blood pressure, or electrocardiogram. Conclusions: Guanfacine may be useful for the treatment of hyperactivity in children with PDD. Placebo-controlled studies are needed to guide clinical practice. C1 Yale Univ, Yale Child Study Ctr, New Haven, CT 06520 USA. Ohio State Univ, Columbus, OH 43210 USA. Indiana Univ, Bloomington, IN 47405 USA. Univ Calif Los Angeles, Los Angeles, CA USA. Kennedy Krieger Inst, Baltimore, MD USA. NIMH, Bethesda, MD 20892 USA. RP Scahill, L (reprint author), Yale Univ, Yale Child Study Ctr, POB 207900, New Haven, CT 06520 USA. EM lawrence.scahill@yale.edu CR AMAN MG, 1985, AM J MENT DEF, V89, P485 American Psychiatric Association, 2000, DIAGN STAT MAN MENT Arnold L. E., 2003, J CHILD ADOL PSYCHOP, V13, P27 ARNSTEN AFT, 2004, NEUROBIOLOGY EXECUTI Avery RA, 2000, NEUROPSYCHOPHARMACOL, V23, P240, DOI 10.1016/S0893-133X(00)00111-1 Brown EC, 2002, RES DEV DISABIL, V23, P45, DOI 10.1016/S0891-4222(01)00091-9 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Cummings DD, 2002, CLIN NEUROPHARMACOL, V25, P325, DOI 10.1097/00002826-200211000-00009 Greenhill LL, 2001, J AM ACAD CHILD PSY, V40, P180, DOI 10.1097/00004583-200102000-00012 JASELSKIS CA, 1992, J CLIN PSYCHOPHARM, V12, P322 Kratochvil CJ, 2002, J AM ACAD CHILD PSY, V41, DOI 10.1097/00004583-200207000-00008 LECAVALIER L, 2006, J AUTISM DEV DI 0802 Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 MARSHBURN EC, 1992, J AUTISM DEV DISORD, V22, P357, DOI 10.1007/BF01048240 Michelson D, 2002, AM J PSYCHIAT, V159, P1896, DOI 10.1176/appi.ajp.159.11.1896 Jensen PS, 1999, ARCH GEN PSYCHIAT, V56, P1073 Mullen E, 1995, MULLEN SCALES EARLY NEWCORN JH, 2003, PEDIAT PSYCHOPHARMAC, P264 Posey DJ, 2004, J CHILD ADOL PSYCHOP, V14, P233, DOI 10.1089/1044546041649084 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Aman MG, 2005, ARCH GEN PSYCHIAT, V62, P1266 Roid G., 1997, LEITER INT PERFORMAN Rush A. J., 2000, AM J MENT RETARD, V105, P159 Scahill L, 2001, AM J PSYCHIAT, V158, P1067, DOI 10.1176/appi.ajp.158.7.1067 Slosson R. L., 1983, SLOSSON INTELLIGENCE Swanson JM, 2001, J AM ACAD CHILD PSY, V40, P168, DOI 10.1097/00004583-200102000-00011 Wechsler D., 1991, MANUAL WECHSLER INTE Wechsler D., 1989, MANUAL WECHSLER PRES NR 28 TC 51 Z9 52 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 OCT PY 2006 VL 16 IS 5 BP 589 EP 598 DI 10.1089/cap.2006.16.589 PG 10 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600009 PM 17069547 ER PT J AU Troost, PW Steenhuis, MP Tuynman-Qua, HG Kalverdijk, LJ Buitelaar, JK Minderaa, RB Hoekstra, PJ AF Troost, Pieter W. Steenhuis, Mark-Peter Tuynman-Qua, Hanneke G. Kalverdijk, Luuk J. Buitelaar, Jan K. Minderaa, Ruud B. Hoekstra, Pieter J. TI Atomoxetine for attention-deficit/hyperactivity disorder symptoms in children with pervasive developmental disorders: A pilot study SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; DOUBLE-BLIND; SPECTRUM DISORDERS; PLACEBO; AUTISM; ADOLESCENTS; METHYLPHENIDATE; ADHD; DESIPRAMINE; RISPERIDONE AB Objective: This pilot study examined the effects of atomoxetine on attention-deficit/hyperactivity disorder (ADHD) symptoms and autistic features in children with pervasive developmental disorders (PDD). Method: Twelve children (aged 6-14 years) with PDD accompanied by ADHD symptoms entered a 10-week open-label study with atomoxetine (1.19 +/- 0.41 mg/kg/day). Response was assessed by using parent and clinician rating scales with change in the ADHD-Rating Scale (ADHDRS) as primary outcome measure. Results: Atomoxetine reduced ADHD-symptoms as measured by the ADHDRS (44% decrease vs. baseline, p < 0.003), the Conners' Parent Rating Scale-R:S (CPRS-R) (25% in the subscale "Cognitive Problems," p < 0.028; 32% in "Hyperactivity," p < 0.030; and 23% in "ADHD index," p < 0.023). We found a reduction of 21% (p = 0.071) for changes in the subscale "Hyperactivity" of the Aberrant Behavior Checklist (ABC). No change was found in any of the other ABC subscales, nor in the subscale "Oppositional" of the CPRS-R. Five patients (42%) discontinued because of side effects. Gastrointestinal symptoms, irritability, sleep problems, and fatigue were the most frequent side effects. Conclusions: These preliminary findings indicate that atomoxetine may be a promising new agent in the treatment of ADHD symptoms in children with PDD. However, children with PDD may have a higher vulnerability for some of the known side-effects of atomoxetine. C1 Univ Groningen, Univ Med Ctr Groningen, Dept Psychiat, NL-9700 AB Groningen, Netherlands. Eli Lilly & Co, Indianapolis, IN 46285 USA. Univ Med Ctr, Dept Psychiat, Nijmegen, Netherlands. RP Troost, PW (reprint author), Child & Adolescent Psychiat Ctr, POB 660, NL-9700 AR Groningen, Netherlands. EM p.troost@accare.nl RI Buitelaar, Jan/E-4584-2012; Hoekstra, Pieter/O-4396-2014 OI Buitelaar, Jan/0000-0001-8288-7757; CR Aman Michael G, 2004, Semin Pediatr Neurol, V11, P225, DOI 10.1016/j.spen.2004.07.006 Aman MG, 1996, J DEV PHYS DISABIL, V8, P347, DOI 10.1007/BF02578400 AMAN MG, 1985, AM J MENT DEF, V89, P485 AMAN MG, 1993, J AUTISM DEV DISORD, V23, P491, DOI 10.1007/BF01046052 AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 American Psychiatric Association, 2000, DIAGN STAT MAN MENT ANDERSON LT, 1989, J AUTISM DEV DISORD, V19, P227, DOI 10.1007/BF02211843 BIEDERMAN J, 2000, EUR CHILD ADOLESC S1, V9, P151 Biederman J, 1999, J CHILD ADOL PSYCHOP, V9, P233, DOI 10.1089/cap.1999.9.233 BIEDERMAN J, 1989, J AM ACAD CHILD PSY, V28, P777, DOI 10.1097/00004583-198909000-00022 Buitelaar JK, 2000, EUR CHILD ADOLES PSY, V9, P85 Buitelaar JK, 2004, EUR CHILD ADOLES PSY, V13, P249, DOI 10.1007/s00787-004-0401-3 Cohen J., 1988, STAT POWER ANAL BEHA, V2nd Conners C. K., 1997, CONNERS RATING SCALE Conners CK, 1996, J AM ACAD CHILD PSY, V35, P1314, DOI 10.1097/00004583-199610000-00018 DuPaul G. J., 1998, ADHD RATING SCALE, VIV GILLBERG C, 2003, ATOMOXETINE VERSUS M Handen BL, 2000, J AUTISM DEV DISORD, V30, P245, DOI 10.1023/A:1005548619694 JASELSKIS CA, 1992, J CLIN PSYCHOPHARM, V12, P322 Jou RJ, 2005, J CHILD ADOL PSYCHOP, V15, P325, DOI 10.1089/cap.2005.15.325 Kratochvil CJ, 2002, J AM ACAD CHILD PSY, V41, DOI 10.1097/00004583-200207000-00008 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Michelson D, 2001, PEDIATRICS, V108, DOI 10.1542/peds.108.5.e83 Michelson D, 2004, J AM ACAD CHILD PSY, V43, P896, DOI 10.1097/01.chi.0000125089.35109.81 Pliszka SR, 1996, J AM ACAD CHILD PSY, V35, P264, DOI 10.1097/00004583-199603000-00006 Posey DJ, 2004, J CHILD ADOL PSYCHOP, V14, P233, DOI 10.1089/1044546041649084 Prince JB, 2000, J CHILD ADOL PSYCHOP, V10, P193, DOI 10.1089/10445460050167304 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Aman MG, 2005, ARCH GEN PSYCHIAT, V62, P1266 RUTTER M, 2003, AUTISM DIAGNOSTIC IN Scahill L, 2001, AM J PSYCHIAT, V158, P1067, DOI 10.1176/appi.ajp.158.7.1067 Spencer T, 2002, ARCH GEN PSYCHIAT, V59, P649, DOI 10.1001/archpsyc.59.7.649 Spencer T, 1998, J CLIN PSYCHIAT, V59, P59 Troost PW, 2005, J AM ACAD CHILD PSY, V44, P1137, DOI 10.1097/01.chi.0000177055.11229.76 Tse WS, 2002, PSYCHOPHARMACOLOGY, V159, P216, DOI 10.1007/s00213-001-0926-9 Volkmar FR, 2004, J CHILD PSYCHOL PSYC, V45, P135, DOI 10.1046/j.0021-9630.2003.00317.x Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd NR 37 TC 42 Z9 42 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 OCT PY 2006 VL 16 IS 5 BP 611 EP 619 DI 10.1089/cap.2006.16.611 PG 9 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600011 PM 17069549 ER PT J AU Nicolson, R Craven-Thuss, B Smith, J AF Nicolson, Rob Craven-Thuss, Beth Smith, Judy TI A prospective, open-label trial of galantamine in autistic disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID DEFICIT HYPERACTIVITY DISORDER; RATING-SCALE; ADJUNCTIVE DONEPEZIL; CHILDREN; ABNORMALITIES; CORTEX AB Objective: Post-mortem studies have reported abnormalities of the cholinergic system in autism. The purpose of this study was to assess the use of galantamine, an acetylcholinesterase inhibitor and nicotinic receptor modulator, in the treatment of interfering behaviors in children with autism. Methods: Thirteen medication-free children with autism (mean age, 8.8 +/- 3.5 years) participated in a 12-week, open-label trial of galantamine. Patients were rated monthly by parents on the Aberrant Behavior Checklist (ABC) and the Conners' Parent Rating Scale-Revised, and by a physician using the Children's Psychiatric Rating Scale and the Clinical Global Impressions scale. Results: Patients showed a significant reduction in parent-rated irritability and social withdrawal on the ABC as well as significant improvements in emotional lability and inattention on the Conners' Parent Rating Scale-Revised. Similarly, clinician ratings showed reductions in the anger subscale of the Children's Psychiatric Rating Scale. Eight of 13 participants were rated as responders on the basis of their improvement scores on the Clinical Global Impressions scale. Overall, galantamine was well-tolerated, with no significant adverse effects apart from headaches in one patient. Conclusion: In this open trial, galantamine was well-tolerated and appeared to be beneficial for the treatment of interfering behaviors in children with autism, particularly aggression, behavioral dyscontrol, and inattention. Further controlled trials are warranted. C1 Univ Western Ontario, Dept Psychiat, London, ON N6A 3K7, Canada. RP Nicolson, R (reprint author), 800 Commissioners Rd E,E2-601, London, ON N6C 2V5, Canada. EM Rnicolso@uwo.ca RI Nicolson, Robert/E-4797-2011 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Arnold LE, 2000, J AUTISM DEV DISORD, V30, P99, DOI 10.1023/A:1005451304303 Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 Brown EC, 2002, RES DEV DISABIL, V23, P45, DOI 10.1016/S0891-4222(01)00091-9 CHEZ M, 2001, ANN NEUROL, V49, pS95 Chez MG, 2004, J CHILD NEUROL, V19, P165 Conners CK, 1998, J ABNORM CHILD PSYCH, V26, P257, DOI 10.1023/A:1022602400621 FISH B, 1985, PSYCHOPHARMACOL BULL, V21, P753 Frazier J. A., 2001, J ATTEN DISORD, V4, P203, DOI DOI 10.1177/108705470100400402 Guy W., 1976, ECDEU ASSESSMENT MAN Hardan AY, 2002, J CHILD ADOL PSYCHOP, V12, P237, DOI 10.1089/104454602760386923 King BH, 2001, J AM ACAD CHILD PSY, V40, P658, DOI 10.1097/00004583-200106000-00010 Lee M, 2002, BRAIN, V125, P1483, DOI 10.1093/brain/awf160 Maelicke A, 2001, BIOL PSYCHIAT, V49, P279, DOI 10.1016/S0006-3223(00)01109-4 CAMPBELL M, 1985, PSYCHOPHARMACOL BULL, V21, P1063 Niederhofer H, 2002, BRIT MED J, V325, P1422 OVERALL JE, 1988, J CLIN PSYCHOL, V44, P708, DOI 10.1002/1097-4679(198809)44:5<708::AID-JCLP2270440507>3.0.CO;2-T PERRY E, 2005, NEUROBIOLOGY AUTISM, P331 Perry EK, 2001, AM J PSYCHIAT, V158, P1058, DOI 10.1176/appi.ajp.158.7.1058 Posey D J, 2001, Expert Opin Pharmacother, V2, P587, DOI 10.1517/14656566.2.4.587 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Wilens TE, 1999, AM J PSYCHIAT, V156, P1931 Wilens TE, 2000, J CHILD ADOL PSYCHOP, V10, P217, DOI 10.1089/10445460050167322 NR 24 TC 28 Z9 28 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 OCT PY 2006 VL 16 IS 5 BP 621 EP 629 DI 10.1089/cap.2006.16.621 PG 9 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600012 PM 17069550 ER PT J AU Stigler, KA Posey, DJ McDougle, CJ AF Stigler, Kimberly A. Posey, David J. McDougle, Christopher J. TI Ramelteon for insomnia in two youths with autistic disorder SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID SLEEP PROBLEMS; ASPERGERS-DISORDER; MENTAL-RETARDATION; CHILDREN; MELATONIN; DISTURBANCES; PATTERNS; TAK-375; AGONIST AB Objective: The aim of this study was to report preliminary data on the effectiveness and tolerability of ramelteon for the treatment of insomnia in youth with autistic disorder (autism). Method: Two youths, ages 7 and 18 years, with autism and significant insomnia characterized by problems with sleep onset and maintenance received an open-label trial of ramelteon (4-8 mg) over a duration of 16-18 weeks. Results: Target symptoms of delayed sleep onset and/or frequent nocturnal awakening improved significantly, as determined by Clinical Global Impressions-Improvement (CGI-I) scale ratings of either "much improved" or "very much improved." Ramelteon was well tolerated. No daytime sedation was reported. Conclusions: This case report illustrates the potential effectiveness and tolerability of ramelteon for sleep disturbances in 2 patients with autism. Further research is needed to verify its safety, tolerability, and efficacy in children and adolescents with autism. C1 Indiana Univ, Sch Med, James Whitcomb Riley Hosp Children, Dept Psychiat, Indianapolis, IN 46202 USA. James Whitcomb Riley Hosp Children, Christian Sarkine Autism Treatment Ctr, Indianapolis, IN 46202 USA. RP Stigler, KA (reprint author), Indiana Univ, Sch Med, James Whitcomb Riley Hosp Children, Dept Psychiat, Room 4300, Indianapolis, IN 46202 USA. EM kstigler@iupui.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Corkum P, 1998, J AM ACAD CHILD PSY, V37, P637, DOI 10.1097/00004583-199806000-00014 Diomedi M, 1999, BRAIN DEV-JPN, V21, P548, DOI 10.1016/S0387-7604(99)00077-7 Elia M, 2000, BRAIN DEV-JPN, V22, P88, DOI 10.1016/S0387-7604(99)00119-9 Erman M, 2006, SLEEP MED, V7, P17, DOI 10.1016/j.sleep.2005.09.004 Guy W., 1976, ECDEU ASSESSMENT MAN Hayashi E, 2000, PSYCHIAT CLIN NEUROS, V54, P383, DOI 10.1046/j.1440-1819.2000.00725.x Hering E, 1999, J AUTISM DEV DISORD, V29, P143, DOI 10.1023/A:1023092627223 Honomichl RD, 2002, J AUTISM DEV DISORD, V32, P553, DOI 10.1023/A:1021254914276 Horrigan JP, 1997, J AM ACAD CHILD PSY, V36, P1014, DOI 10.1097/00004583-199708000-00002 HOSHINO Y, 1984, FOLIA PSYCHIAT NEU J, V38, P45 Kato K, 2005, NEUROPHARMACOLOGY, V48, P301, DOI 10.1016/j.neuropharm.2004.09.007 Kulman G, 2000, NEUROENDOCRINOL LETT, V21, P31 Lancioni GE, 1999, AM J MENT RETARD, V104, P170, DOI 10.1352/0895-8017(1999)104<0170:ROSFTS>2.0.CO;2 Malow BA, 2004, MENT RETARD DEV D R, V10, P122, DOI 10.1002/mrdd.20023 McDougle CJ, 2005, J CLIN PSYCHIAT, V66, P9 Nir I, 1995, J AUTISM DEV DISORD, V25, P641, DOI 10.1007/BF02178193 Paavonen EJ, 2003, J CHILD ADOL PSYCHOP, V13, P83, DOI 10.1089/104454603321666225 Patzold LM, 1998, J PAEDIATR CHILD H, V34, P528 Polimeni MA, 2005, J INTELL DISABIL RES, V49, P260, DOI 10.1111/j.1365-2788.2005.00642.x Richdale A., 2001, SLEEP DISTURBANCE CH, P181 Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 Roth T, 2005, SLEEP, V28, P303 Stigler Kimberly A, 2002, Expert Rev Neurother, V2, P499, DOI 10.1002/1615-9861(200205)2:5&lt;499::AID-PROT499&gt;3.0.CO;2-H TIARA M, 1998, PSYCHIAT CLIN NEUROS, V52, P182 Tordjman S, 2005, BIOL PSYCHIAT, V57, P134, DOI 10.1016/j.biopsych.2004.11.003 Wiggs L, 1996, J INTELL DISABIL RES, V40, P518, DOI 10.1046/j.1365-2788.1996.799799.x NR 27 TC 15 Z9 15 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 OCT PY 2006 VL 16 IS 5 BP 631 EP 636 DI 10.1089/cap.2006.16.631 PG 6 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 109KT UT WOS:000242307600013 PM 17069551 ER PT J AU Knickmeyer, RC Baron-Cohen, S AF Knickmeyer, Rebecca Christine Baron-Cohen, Simon TI Fetal testosterone and sex differences in typical social development and in autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Review ID CONGENITAL ADRENAL-HYPERPLASIA; HIGH-FUNCTIONING AUTISM; ANDROGEN-INSENSITIVITY SYNDROME; CENTRAL NERVOUS-SYSTEM; GENDER-ROLE-BEHAVIOR; TYPED TOY PLAY; TURNER-SYNDROME; ASPERGER-SYNDROME; DIETHYLSTILBESTROL DES; PRENATAL EXPOSURE AB Experiments in animals leave no doubt that androgens, including testosterone, produced by the testes in fetal and/or neonatal life act on the brain to induce sex differences in neural structure and function. In human beings, there is evidence supporting a female superiority in the ability to read nonverbal signals, specific language-related skills, and theory of mind. Even more striking than the sex differences seen in the typical population is the elevated occurrence of social and communicative difficulties in human males. One such condition, autism, occurs four times more frequently in boys than in girls. Recently, a novel theory known as the "extreme male brain" has been proposed. It suggests that the behaviors seen in autism are an exaggeration of typical sex differences and that exposure to high levels of prenatal testosterone might be a risk factor. In this article, we argue that prenatal and neonatal testosterone exposures are strong candidates for having a causal role in sexual dimorphism in human behavior, including social development, and as risk factors for conditions characterized by social impairments, particularly autism spectrum conditions. 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PD OCT PY 2006 VL 21 IS 10 BP 825 EP 845 DI 10.2310/7010.2006.00213 PG 21 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 122DU UT WOS:000243206700001 PM 17005117 ER PT J AU Eluvathingal, TJ Behen, ME Chugani, HT Janisse, J Bernardi, B Chakraborty, P Juhasz, C Muzik, O Chugani, DC AF Eluvathingal, Thomas J. Behen, Michael E. Chugani, Harry T. Janisse, James Bernardi, Bruno Chakraborty, Pulak Juhasz, Csaba Muzik, Otto Chugani, Diane C. TI Cerebellar lesions in tuberous sclerosis complex: Neurobehavioral and neuroimaging correlates SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID POSITRON-EMISSION-TOMOGRAPHY; SEROTONIN SYNTHESIS CAPACITY; INFANTILE-AUTISM; CLINICORADIOLOGICAL EVALUATION; ATTENTION DEFICITS; BRAIN; DISORDERS; CHILDREN; PET; ABNORMALITIES AB We assessed the structural and functional imaging features of cerebellar lesions and their neurobehavioral correlates in a large cohort of patients with tuberous sclerosis complex. A consecutive series of 78 patients with tuberous sclerosis complex underwent magnetic resonance imaging (MRI) and positron emission tomography (PET) studies with [F-18]fluorodeoxyglucose (FDG) and alpha-[C-11]methyl-L-tryptophan (AMT) as part of their evaluation for epilepsy surgery. Neurobehavioral assessment included the Gilliam Autism Rating Scales (GARS) and the Vineland Adaptive Behavior Scales (VABS). Twenty-one patients (27%) had cerebellar lesions (10 boys; mean age 9 +/- 8 years; 9 had right-sided, 10 had left-sided, and 2 had bilateral cerebellar lesions). The lesions showed decreased glucose metabolism (0.79 +/- 0.10) and increased (1.04 +/- 0.10) AMT uptake compared with the normal (nonlesional) cerebellar cortex. Comparisons between patients with (n = 20) and without (n = 57) a cerebellar lesion on neurobehavioral functioning, controlling for the number and location of cortical tubers, revealed that the cerebellar lesion group had higher overall autistic symptomatology. Within-group analyses of the cerebellar lesion group revealed that children with right-sided cerebellar lesions had higher social isolation and communicative and developmental disturbance compared with children with left-sided cerebellar lesions. The side of the cerebellar lesion was not related to adaptive behavior functioning. These findings provide additional empiric support for a role of the cerebellum in autistic symptomatology. Further investigation of the potential role of the right cerebellum in autism, particularly with regard to the dentatothalamofrontal circuit, is warranted. C1 Wayne State Univ, Dept Pediat, Childrens Hosp Michigan, PET Ctr, Detroit, MI 48201 USA. Wayne State Univ, Dept Neurol, Childrens Hosp Michigan, Detroit, MI 48201 USA. Wayne State Univ, Dept Radiol, Childrens Hosp Michigan, Detroit, MI 48201 USA. Wayne State Univ, Ctr Hlth Effectiveness Res, Childrens Hosp Michigan, Detroit, MI 48201 USA. RP Chugani, DC (reprint author), Wayne State Univ, Dept Pediat, Childrens Hosp Michigan, PET Ctr, 3901 Beaubien Blvd, Detroit, MI 48201 USA. 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Child Neurol. PD OCT PY 2006 VL 21 IS 10 BP 846 EP 851 DI 10.2310/7010.2006.00192 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 122DU UT WOS:000243206700003 PM 17005099 ER PT J AU Hardan, AY Girgis, RR Lacerda, ALT Yorbik, O Kilpatiick, M Keshavan, MS Minshew, NJ AF Hardan, Antonio Y. Girgis, Ragy R. Lacerda, Acioly L. T. Yorbik, Ozgur Kilpatiick, Megan Keshavan, Matcheri S. Minshew, Nancy J. TI Magnetic resonance imaging study of the orbitofrontal cortex in autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; PROGRESSIVE SUPRANUCLEAR PALSY; CEREBRAL-BLOOD-FLOW; CORTICOBASAL DEGENERATION; BASAL GANGLIA; POSTERIOR-FOSSA; VOLUMETRIC MRI; BRAIN VOLUME; MIND; CHILDREN AB The orbitofrontal cortex is involved in multiple psychologic functions, such as emotional and cognitive processing, learning, and social behavior. These functions are variably impaired in individuals with autism. The present study examined the size of the orbitofrontal cortex, and its medial and lateral subdivisions, using magnetic resonance imaging (MRI) scans obtained from 40 non-mentally retarded individuals with autism and 41 healthy controls. No differences were observed between the two groups on any of the orbitofrontal cortex measurements. However, when compared with controls, a smaller right lateral orbitofrontal cortex was observed in children and adolescents with autism, whereas a larger right lateral orbitofrontal cortex was found in adult patients. Interestingly, a positive relationship was found in the patient group between circumscribed interests and all orbitofrontal cortex structures. The present study suggests the absence of global volumetric abnormalities in the orbitofrontal cortex in autism and indicates that the functional disturbances in this structure might not be related to anatomic alterations. C1 Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. 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Child Psychol. Psychiatry PD OCT PY 2006 VL 47 IS 10 BP 979 EP 982 DI 10.1111/j.1469-7610.2006.01690.x PG 4 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 099VL UT WOS:000241625200001 PM 17073975 ER PT J AU Kemner, C Schuller, AM van Engeland, H AF Kemner, C. Schuller, A-M. van Engeland, H. TI Electrocortical reflections of face and gaze processing in children with pervasive developmental disorder SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE pervasive developmental disorder; face; eye gaze; cueing; N170; ERP ID AUTISM SPECTRUM DISORDER; EYE GAZE; VISUOSPATIAL ATTENTION; SPATIAL-FREQUENCY; ASPERGER-SYNDROME; BRAIN POTENTIALS; NEURAL BASIS; PERCEPTION; INDIVIDUALS; DEFICITS AB Background: Children with pervasive developmental disorder (PDD) show behavioral abnormalities in gaze and face processing, but recent studies have indicated that normal activation of face-specific brain areas in response to faces is possible in this group. It is not clear whether the brain activity related to gaze processing is also normal in children with PDD. Methods: Event-related brain potentials (ERPs) were measured during two spatial attention tasks in which a centrally presented stimulus served as cue for the location of a forthcoming target. In one task faces were used as cues, and in the other arrows. Seventeen children with PDD and 18 age- and IQ-matched control children were tested. Results: Face stimuli elicited the same specific ERP activity in both groups. Also, both children with PDD and controls showed shorter reaction times as well as larger amplitudes and shorter latency times of several ERP peaks to congruently cued targets than to incongruently cued targets in both tasks. However, children with PDD showed abnormally small occipital ERPs in response to both face and arrow stimuli. Conclusion: The results provide evidence for the capability of normal processing of face and gaze change in children with PDD. The smaller occipital activity might be related to more general abnormalities in perception. C1 Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, Rudolf Magnus Inst Neurosci, NL-3508 TC Utrecht, Netherlands. Maastricht Univ, Fac Psychol, Dept Neurocognit, Maastricht, Netherlands. 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Child Psychol. Psychiatry PD OCT PY 2006 VL 47 IS 10 BP 1063 EP 1072 DI 10.1111/j.1469-7610.2006.01678.x PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 099VL UT WOS:000241625200011 PM 17073985 ER PT J AU Anderson, CJ Colombo, J Shaddy, DJ AF Anderson, Christa J. Colombo, John Shaddy, D. Jill TI Visual scanning and pupillary responses in young children with autism spectrum disorder SO JOURNAL OF CLINICAL AND EXPERIMENTAL NEUROPSYCHOLOGY LA English DT Article ID HOME VIDEOTAPES; STIMULI; AGE; INDIVIDUALS; RECOGNITION; PERFORMANCE; RESOURCES; ATTENTION; INFANCY; TASK AB Using eye-tracking technology we investigated visual scanning and pupillary responses to face and non-face stimuli in nine children (M = 49.6 months) with Autism Spectrum Disorder (ASD) compared to six mental-age and nine chronological-age matched children. The results revealed a significant decrease in visual scanning to landscapes. In addition, the ASD group showed pupillary constriction to children's faces, while control groups showed pupillary dilation. Visual scanning responses to landscapes had a negative correlation with the Behavior subscale of the Autism Diagnostic Observation Schedule-Generic for the ASD group. Potential use of these measures as early indicators of ASD is discussed. C1 Univ Kansas, Dept Psychol, Lawrence, KS 66045 USA. RP Anderson, CJ (reprint author), Univ Kansas, Dept Psychol, 1415 Jayhawk Blvd, Lawrence, KS 66045 USA. 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Clin. Exp. Neuropsychol. PD OCT PY 2006 VL 28 IS 7 BP 1238 EP 1256 DI 10.1080/13803390500376790 PG 19 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA 064KV UT WOS:000239089300014 PM 16840248 ER PT J AU Montes, G Halterman, JS AF Montes, Guillermo Halterman, Jill S. TI Characteristics of school-age children with autism SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism; prevalence; schools; epidemiology; comorbidity; children ID PERVASIVE DEVELOPMENTAL DISORDERS; EARLY INTERVENTION; YOUNG-CHILDREN; PREVALENCE; HEALTH; POPULATION; RATES AB The objectives of this study were to provide a national profile of children with autism, to describe the impact of autism on school functioning, and to describe the utilization of services among children with autism. We performed a cross-sectional descriptive analysis of 9583 children (grades K-8) from the 2001 National Household Education Survey Before and After School Survey. We used parent-reported information to determine the prevalence of autism, and children with autism were compared to children without autism on sociodemographic measures and several measures of school functioning and utilization of services. The prevalence of autism in this sample was 66 per 10,000. Children with autism were proportionately represented in all communities and all regions of the country. While children with autism were equally likely to attend public schools compared to children without autism, they were significantly more likely to have learning difficulties and to carry multiple diagnoses, including attention deficit disorder and learning disability. Most of these children received services for their disability through the school district. 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This ability has fascinated scientists for many years because it is predominantly observed in people with limited intelligence and may appear very early in life. Exceptional visual memory, exceptional concentration abilities, or privileged access to lower levels of information not normally available through introspection have been advanced to explain such phenomena. In the present article, the authors show that a simple cognitive model can explain all aspects of the performance of Donny, a young autistic savant who is possibly the fastest and most accurate calendar prodigy ever described. C1 Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. RP Thioux, M (reprint author), Univ Groningen, Med Ctr, Neuro Imaging Ctr, Antonius Deusinglaan 2, NL-9713 AW Groningen, Netherlands. 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TI Prevalence of gastrointestinal disorders in adult clients with pervasive developmental disorders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE behavioural disorders; gastrointestinal disorders; intellectual disability; neuro-organic comorbidity; pervasive developmental disorders (PDD) ID INTELLECTUALLY DISABLED INDIVIDUALS; GASTROESOPHAGEAL-REFLUX DISEASE; HELICOBACTER-PYLORI INFECTION; HIRSCHSPRUNG-DISEASE; BRAIN-STEM; AUTISM; CHILDREN; DISABILITY; ABNORMALITIES; MMR AB Background: In clients with pervasive developmental disorders (PDD), some authors have noticed the presence of gastrointestinal disorders and behavioural disorders. An augmented prevalence of different histological anomalies has also been reported. The aim of our study is to highlight the prevalence of gastrointestinal disorders in this adult with PDD sample and to demonstrate the importance of accurate evaluation of gastrointestinal disorders in clients with PDD. Methods: The present comparative study involved 118 clients. Our research was motivated by the clinical observation that behavioural disorders sometimes disappeared with administration of anti-gastric acid or anti-ulcerous medications. It focused on two samples of clients with intellectual disability - those with associated PDD and those without. The presence of gastrointestinal disorders was assessed retrospectively on the basis of hospital records. Results: The prevalence of gastrointestinal disorders reported in clinical files was 48.8% in clients with PDD, as compared with 8.0% in non-PDD clients (P < 0.00001). Conclusion: Gastrointestinal disorders, and especially gastro-oesophageal reflux, if neglected, may contribute to behavioural disorders in PDD clients. Moreover, gastrointestinal disorders may be considered as a feature of PDD. We highlight the fact that somatic disorders may coexist in persons with PDD. 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CHO cells transfected with constructs encompassing the RELN 5'UTR with 4-to-13 GGC repeats upstream of the luciferase reporter gene show declining luciferase activity with increasing GGC repeat number (P < 0.005), as predicted by computer-based simulations. Conversely, RELN 5'UTR sequences boost reporter gene expression above control levels in neuronal SN56 and N2A cell lines, but 12- and 13-repeat alleles still yield 50-60% less luciferase activity compared to the more common 8- and 10-repeat alleles (P < 0.0001). RELN "long" GGC alleles significantly blunt gene expression and may, through this effect, confer vulnerability to human disorders, such as schizophrenia and autism. C1 Univ Rome, Lab Mol Psychiat & Neurogenet, I-00155 Rome, Italy. IRCCS, Fdn S Lucia, Rome, Italy. Vanderbilt Univ, Vanderbilt Kennedy Ctr Res Human Dev, Nashville, TN USA. Vanderbilt Univ, Dept Pharmacol, Nashville, TN USA. RP Persico, AM (reprint author), Univ Rome, Lab Mol Psychiat & Neurogenet, Campus Biomed,Via Emilio Longoni 83, I-00155 Rome, Italy. 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Neural Transm. PD OCT PY 2006 VL 113 IS 10 BP 1373 EP 1382 DI 10.1007/s00702-006-0441-6 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 088FP UT WOS:000240797700003 PM 16604303 ER PT J AU Wilson, D Wharton, T AF Wilson, Deirdre Wharton, Tim TI Relevance and prosody SO JOURNAL OF PRAGMATICS LA English DT Article; Proceedings Paper CT Conference on Prosody and Pragmatics CY NOV, 2003 CL Preston, ENGLAND SP Univ Cent Lancashire, N West Ctr Linguist, Linguist Assoc Great Britain, British Assoc Acad Phonet DE prosody; pragmatics; relevance theory; signs; signals; inference ID FACIAL EXPRESSIONS; MIND; INTENTIONS; MODULARITY; PRAGMATICS; EMOTION; AUTISM; COMMUNICATION; LANGUAGE; VOICE AB Prosodic elements such as stress and intonation are generally seen as providing both 'natural' and properly linguistic input to utterance comprehension. They contribute not only to overt communication but to more covert or accidental forms of information transmission. They typically create impressions, convey information about emotions or attitudes, or alter the salience of linguistically-possible interpretations rather than conveying distinct propositions or concepts in their own right. These aspects of communication present a challenge to pragmatic theory: how should they be described and explained? This paper is an attempt to explore how the wealth of insights provided by the literature on the interpretation of prosody might be integrated into the relevance-theoretic framework (Sperber and Wilson, 1986/1995; Blakemore, 2002; Carston, 2002). We will focus on four main issues. First, how should the communication of emotions, attitudes and impressions be analysed? Second, how might prosodic elements function as 'natural' communicative devices? Third, what (if anything) do prosodic elements encode? Fourth, what light can the study of prosody shed on the place of pragmatics in the architecture of the mind? 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Pragmat. PD OCT PY 2006 VL 38 IS 10 BP 1559 EP 1579 DI 10.1016/j.pragma.2005.04.012 PG 21 WC Linguistics; Language & Linguistics SC Linguistics GA 087PV UT WOS:000240755300003 ER PT J AU Peppe, S McCann, J Gibbon, F O'Hare, A Rutherford, M AF Peppe, Sue McCann, Joanne Gibbon, Fiona O'Hare, Anne Rutherford, Marion TI Assessing prosodic and pragmatic ability in children with high-functioning autism SO JOURNAL OF PRAGMATICS LA English DT Article; Proceedings Paper CT Conference on Prosody and Pragmatics CY NOV, 2003 CL Preston, ENGLAND SP Univ Cent Lancashire, N West Ctr Linguist, Linguist Assoc Great Britain, British Assoc Acad Phonet DE prosody; intonation; autism; pragmatic; assessment ID LANGUAGE IMPAIRMENTS; ASPERGER-SYNDROME; INTONATION; STRESS; SPEECH; ADULTS; VOICE; MIND AB Children with high-functioning autism are widely reported to show deficits in both prosodic and pragmatic ability. New procedures for assessing both of these are now available and have been used in a study of 31 children with high-functioning autism and 72 controls. Some of the findings from a review of the literature on prosodic skills in individuals with autism are presented, and it is shown how these skills are addressed in a new prosodic assessment procedure, PEPS-C. A case study of a child with high-functioning autism shows how his prosodic skills can be evaluated on the prosody assessment procedure, and how his skills compare with those of controls. He is also assessed for pragmatic ability. Results of both assessments are considered together to show how, in the case of this child, specific prosodic skill-levels can affect pragmatic ability. (c) 2006 Elsevier B.V. All rights reserved. C1 Queen Margaret Univ Coll, Speech & Hearing Sci, Edinburgh EH12 8TS, Midlothian, Scotland. Univ Edinburgh, Royal Hosp Sick Children, Edinburgh EH10 5HF, Midlothian, Scotland. 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Cook, Amelia M. Witwer, Andrea N. Hall, Kristy L. Thompson, Susan Ramadan, Yaser TI Atomoxetine for hyperactivity in autism spectrum disorders: Placebo-controlled crossover pilot trial SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE attention-deficit/hyperactivity disorder; autism; treatment; atomoxetine; clinical trial ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; ABERRANT BEHAVIOR CHECKLIST; MENTAL-RETARDATION; METHYLPHENIDATE TREATMENT; SCHIZOPHRENIC CHILDREN; RELAPSE PREVENTION; DOUBLE-BLIND; ADHD; ADOLESCENTS AB Objective: To explore placebo-controlled efficacy and safety of atomoxetine (ATX) for attention-deficit/hyper-activity disorder (ADHD) symptoms in children with autism spectrum disorders (ASD). Method: Children ages 5 to 15 with ASD and prominent ADHD symptoms were randomly assigned to order in a crossover of clinically titrated ATX and placebo, 6 weeks each, separated by 1-week washout. Slopes for each condition were compared by paired t test. Results: In 2004-2005, 12 boys and 4 girls (7 with autistic disorder, 1 Asperger's, 8 pervasive developmental disorder not otherwise specified) all completed at least 3 weeks of each condition. On the primary outcome, the Hyperactivity subscale of the Aberrant Behavior Checklist, ATX was superior to placebo (p=.043, effect size d=0.90). It was also superior on a 0 to 3 rating of nine DSM-IV ADHD hyperactive/impulsive symptoms (p = .005, d = 1.27), but missed significance on nine inattentive symptoms (p = .053, d = 0.89). Nine subjects responded to ATX, four to placebo (25% improvement on the Hyperactivity subscale plus Clinical Global Impressions-improvement of 1-2. One Was rehospitalized for recurrent violence on ATX. Adverse events were otherwise tolerable, with no tendency to stereotypy. Conclusions: ATX appears safe and effective for treating hyperactivity in some children with autism spectrum disorders. 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Am. Acad. Child Adolesc. Psychiatr. PD OCT PY 2006 VL 45 IS 10 BP 1196 EP 1205 DI 10.1097/01.chi.0000231976.28719.2a PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 087MP UT WOS:000240746800007 PM 17003665 ER PT J AU Ronald, A Happe, F Price, TS Baron-Cohen, S Plomin, R AF Ronald, Angelica Happe, Francesca Price, Thomas S. Baron-Cohen, Simon Plomin, Robert TI Phenotypic and genetic overlap between autistic traits at the extremes of the general population SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE twins; genetics; autism; autistic traits ID INDIVIDUAL-DIFFERENCES; BEHAVIOR PROBLEMS; ASPERGER-SYNDROME; TWIN DATA; CHILDREN; COMORBIDITY; CHILDHOOD; RELATIVES; ETIOLOGY; DISABILITIES AB Objective: To investigate children selected from a community sample for showing extreme autistic-like traits and to assess the degree to which these individual traits-social impairments (SIs), communication impairments (CIs), and restricted repetitive behaviors and interests (RRBIs)-are caused by genes and environments, whether all of them are caused by the same genes and environments, and how often they occur together (as required by an autism diagnosis). Method: The most extreme-scoring 5% were selected from 3,419 8-year-old pairs in the Twins Early Development Study assessed on the Childhood Asperger Syndrome Test. Phenotypic associations between extreme traits were compared with associations among the full-scale scores. Genetic associations between extreme traits were quantified using bivariate DeFries-Fulker extremes analysis. Results: Phenotypic relationships between extreme SIs, CIs, and RRBIs were modest. There was a degree of genetic overlap between them, but also substantial genetic specificity. Conclusions: This first twin study assessing the links between extreme individual autistic-like traits (SIs, CIs, and RRBIs) found that all are highly heritable but show modest phenotypic and genetic overlap. This finding concurs with that of an earlier study from the same cohort that showed that a total autistic symptoms score at the extreme showed high heritability and that SIs, CIs, and RRBIs show weak links in the general population. This new finding has relevance for both clinical models and future molecular genetic studies. C1 Kings Coll London, Social Genet & Dev Psychiat Ctr, Inst Psychiat, London SE5 8AF, England. Univ Penn, Sch Med, Inst Translat Med & Therapeut, Philadelphia, PA 19104 USA. Univ Cambridge, Autism Res Ctr, Cambridge, England. RP Ronald, A (reprint author), Kings Coll London, Social Genet & Dev Psychiat Ctr, Inst Psychiat, De Crespigny Pk, London SE5 8AF, England. 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PD OCT PY 2006 VL 45 IS 10 BP 1206 EP 1214 DI 10.1097/01.chi.0000230165.54117.41 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 087MP UT WOS:000240746800008 PM 17003666 ER PT J AU Azar, M Badr, LK AF Azar, Mathilde Badr, Lina Kurdahi TI The adaptation of mothers of children with intellectual disability in Lebanon SO JOURNAL OF TRANSCULTURAL NURSING LA English DT Article; Proceedings Paper CT International Scientific Conference on One Hundred Years of Nursing Education at American-University-of-Beirut CY JUN 30-JUL 02, 2005 CL Beirut, LEBANON HO Amer Univ Beirut Sch Nursing DE intellectual disability; developmentally disabled; developmentally impaired; mental retardation; coping; adaptation ID DOUBLE ABCX MODEL; PARENTAL STRESS; MENTAL-RETARDATION; SOCIAL SUPPORT; FAMILIES; FATHERS; DEPRESSION; AUTISM AB In many Middle Eastern countries, including Lebanon, there is a stigma attached to families who have an intellectually impaired child. These families complain of isolation and lack of community resources that could help them cope with their circumstances to optimize the child's abilities. Health professionals and researchers should be cognizant of factors related to the process of stress adaptation to help families cope with their circumstances. The aim of this cross-sectional study was to identify factors that play a role in mothers' adaptation to the care of their intellectually impaired children. The results, based on a sample of 127 mothers from Lebanon, reveal that a high percentage of mothers had depressive symptoms. Multiple regression analysis demonstrates that by order of importance, the factors that determine maternal depression are family strain, parental stress, and family income. The conclusions about nursing implications from a cultural perspective are discussed and recommendations proposed. C1 Univ Balamand, Nursing Program, French Sect, Fac Hlth Sci, Beirut, Lebanon. 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TI Obsessive-compulsive disorder as a disturbance of security motivation: Constraints on comorbidity SO NEUROTOXICITY RESEARCH LA English DT Article; Proceedings Paper CT Meeting of the Fundacion-Cerebro-and-Mente CY 2005 CL SPAIN SP Fund Cerebro Mente DE anxiety disorders; negative feedback; security motivation; yedasentience ID AFFECTIVE NEUROSCIENCE; ANTIPREDATOR BEHAVIOR; POLYVAGAL THEORY; COGNITIVE THEORY; ANXIETY; AUTISM; FEAR; PERSPECTIVES; ORGANIZATION; STIMULATION AB Patients with OCD often meet criteria for additional psychiatric disorders, with the incidence of comorbidity being as high as 75% in some studies. Here we examine the theoretical plausibility that in OCD much of the domain of co-morbid presentations encompasses related perturbations of the security motivation system. 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Res. PD OCT PY 2006 VL 10 IS 2 BP 103 EP 112 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 104XM UT WOS:000241993900004 PM 17062372 ER PT J AU D'Souza, Y Fombonne, E Ward, BJ AF D'Souza, Yasmin Fombonne, Eric Ward, Brian J. TI No evidence of persisting measles virus in peripheral blood mononuclear cells from children with autism spectrum disorder SO PEDIATRICS LA English DT Article DE measles; MMR; autism; autistic spectrum disorder; real-time PCR ID SUBACUTE SCLEROSING PANENCEPHALITIS; INFLAMMATORY-BOWEL-DISEASE; POLYMERASE CHAIN-REACTION; PERVASIVE DEVELOPMENTAL DISORDERS; IMMUNOGOLD ELECTRON-MICROSCOPY; LYMPHOID-NODULAR HYPERPLASIA; MUMPS-RUBELLA VACCINATION; CROHNS-DISEASE; EPIDEMIOLOGIC EVIDENCE; CAUSAL ASSOCIATION AB OBJECTIVES. Despite epidemiologic evidence to the contrary, claims of an association between measles-mumps-rubella vaccination and the development of autism have persisted. Such claims are based primarily on the identification of measles virus nucleic acids in tissues and body fluids by polymerase chain reaction. We sought to determine whether measles virus nucleic acids persist in children with autism spectrum disorder compared with control children. PATIENTS AND METHODS. Peripheral blood mononuclear cells were isolated from 54 children with autism spectrum disorder and 34 developmentally normal children, and up to 4 real-time polymerase chain reaction assays and 2 nested polymerase chain reaction assays were performed. These assays targeted the nucleoprotein, fusion, and hemagglutinin genes of measles virus using previously published primer pairs with detection by SYBR green I. Our own real-time assay targeted the fusion gene using novel primers and an internal fluorescent probe. Positive reactions were evaluated rigorously, and amplicons were sequenced. Finally, antimeasles antibody titers were measured by enzyme immunoassay. RESULTS. The real-time assays based on previously published primers gave rise to a large number of positive reactions in both autism spectrum disorder and control samples. Almost all of the positive reactions in these assays were eliminated by evaluation of melting curves and amplicon band size. The amplicons for the remaining positive reactions were cloned and sequenced. No sample from either autism spectrum disorder or control groups was found to contain nucleic acids from any measles virus gene. In the nested polymerase chain reaction and in-house assays, none of the samples yielded positive results. Furthermore, there was no difference in anti-measles antibody titers between the autism and control groups. INTERPRETATION. There is no evidence of measles virus persistence in the peripheral blood mononuclear cells of children with autism spectrum disorder. C1 McGill Univ, Montreal Gen Hosp, Dept Psychiat, Montreal, PQ H3G 1A4, Canada. 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TI Has the measles-mumps-rubella vaccine been fully exonerated? SO PEDIATRICS LA English DT Editorial Material ID CHILDREN; VIRUS; ELIMINATION; AUTISM C1 Duke Univ, Med Ctr, Div Pediat Infect Dis, Durham, NC 27710 USA. RP Katz, SL (reprint author), Duke Univ, Med Ctr, Div Pediat Infect Dis, Box 2925, Durham, NC 27710 USA. EM katz0004@mc.duke.edu CR Afzal MA, 2006, J MED VIROL, V78, P623, DOI 10.1002/jmv.20585 D'Souza Y, 2006, PEDIATRICS, V118, P1664, DOI 10.1542/peds.2006-1262 GERSHON MD, 2001, 107 C 1 SESS, P74 HALSEY NA, 2001, PEDIATRICS, P107 *I MED, 2004, IMM SAF REV MEASL MU Katz SL, 2004, J INFECT DIS, V189, pS43, DOI 10.1086/377696 Kawashima H, 2000, DIGEST DIS SCI, V45, P723, DOI 10.1023/A:1005443726670 Martin CM, 2002, MOL PSYCHIATR, V7, pS47, DOI 10.1038/sj.mp.4001179 OLDSTONE MBA, 2001, 107 C 1 SESS, V29, P193 Parker AA, 2006, NEW ENGL J MED, V355, P447, DOI 10.1056/NEJMoa060775 Singh VK, 2003, PEDIATR NEUROL, V28, P292, DOI 10.1016/S0887-8994(02)00627-6 Uhlmann V., 2002, Molecular Pathology, V55, P84, DOI 10.1136/mp.55.2.84 WAKEFIELD AJ, 2000, ADVERSE DRUG REACT T, V19, P1 Wakefield AJ, 2004, LANCET, V363, P750 NR 14 TC 7 Z9 8 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 OCT PY 2006 VL 118 IS 4 BP 1744 EP 1745 DI 10.1542/ped.2006-2252 PG 2 WC Pediatrics SC Pediatrics GA 090NZ UT WOS:000240959300050 PM 17015569 ER PT J AU Croen, LA Najjar, DV Ray, GT Lotspeich, L Bernal, P AF Croen, Lisa A. Najjar, Daniel V. Ray, G. Thomas Lotspeich, Linda Bernal, Pilar TI A comparison of health care utilization and costs of children with and without autism spectrum disorders in a large group-model health plan SO PEDIATRICS LA English DT Article DE medical costs; ASD; autism; pervasive; developmental disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHOPHARMACOLOGY; EXPENDITURES; POPULATION; PREVALENCE; CALIFORNIA; ANXIETY; UPDATE AB OBJECTIVE. Data on the current costs of medical services for children with autism spectrum disorders are lacking. Our purpose for this study was to compare health care utilization and costs of children with and without autism spectrum disorders in the same health plan. PATIENTS AND METHODS. Participants included all 2- to 18-year-old children with autism spectrum disorders (n = 3053) and a random sample of children without autism spectrum disorders (n = 30 529) who were continuously enrolled in the Kaiser Permanente Medical Care Program in northern California between July 1, 2003, and June 30, 2004. Data on health care utilization and costs were derived from health plan administrative databases. MAIN OUTCOME MEASURES. Outcome measures included mean annual utilization and costs of health services per child. RESULTS. Children with autism spectrum disorders had a higher annual mean number of total clinic (5.6 vs 2.8), pediatric (2.3 vs 1.6), and psychiatric (2.2 vs 0.3) outpatient visits. A higher percentage of children with autism spectrum disorders experienced inpatient (3% vs 1%) and outpatient (5% vs 2%) hospitalizations. Children with autism spectrum disorders were nearly 9 times more likely to use psychotherapeutic medications and twice as likely to use gastrointestinal agents than children without autism spectrum disorders. Mean annual member costs for hospitalizations ($550 vs $208), clinic visits ($ 1373 vs $540), and prescription medications ($724 vs $96) were more than double for children with autism spectrum disorders compared with children without autism spectrum disorders. The mean annual age- and gender-adjusted total cost per member was more than threefold higher for children with autism spectrum disorders ($2757 vs $892). Among the subgroup of children with other psychiatric conditions, total mean annual costs were 45% higher for children with autism spectrum disorders compared with children without autism spectrum disorders; excess costs were largely explained by the increased use of psychotherapeutic medications. CONCLUSIONS. The utilization and costs of health care are substantially higher for children with autism spectrum disorders compared with children without autism spectrum disorders. Research is needed to evaluate the impact of improvements in the management of children with autism spectrum disorders on health care utilization and costs. C1 Kaiser Permanente, Div Res, Kaiser Fdn Res Inst, Oakland, CA 94612 USA. Kaiser Permanente Santa Teresa Med Ctr, Dept Psychiat, San Jose, CA USA. RP Croen, LA (reprint author), Kaiser Permanente, Div Res, Kaiser Fdn Res Inst, 2000 Broadway, Oakland, CA 94612 USA. 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A study of the Autism-Spectrum Quotient (AQ) and the NEO-PI-R SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE Autism-Spectrum Quotient; Big Five model; the NEO-PI-R; autistic traits AB This study examines the relation between autistic traits and the personality dimensions of the Big Five model in a sample of 320 university students. We administered the Autism-Spectrum Questionnaire (AQ) and the NEO-PI-R. Results showed the AQ correlated with Extraversion and Conscientiousness negatively, and Neuroticism positively. Results of multiple regression analyses suggested the NEO-PI-R did not predict AQ score. Joint factor analyses also suggested autistic traits are independent of the big five personality dimensions. High AQ scorers, who are an analogue model of autism spectrum conditions, showed a profile of high Neuroticism, low Extraversion and low Conscientiousness. Results are discussed in terms of autistic traits representing a sixth factor of personality. (c) 2006 Elsevier Ltd. All rights reserved. C1 Chiba Univ, Dept Psychol, Chiba 2638522, Japan. Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 2AH, England. RP Wakabayashi, A (reprint author), Chiba Univ, Dept Psychol, 1-33 Yayoi Cho, Chiba 2638522, Japan. EM akiowcam@mac.com CR ALVAREZ A, 1999, AUTISM PERSONALITY F American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Austin EJ, 2005, PERS INDIV DIFFER, V38, P451, DOI 10.1016/j.paid.2004.04.022 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Costa Jr P. T., 1992, NEO PI R PROFESSIONA Frith U, 1991, AUTISM ASPERGERS SYN Murphy M, 2000, PSYCHOL MED, V30, P1411, DOI 10.1017/S0033291799002949 Pervin L., 1994, PSYCHOL INQ, V5, P103, DOI 10.1207/s15327965p1i0502_1 SAUCIER G, 1994, J PERS ASSESS, V63, P506, DOI 10.1207/s15327752jpa6303_8 Shimonaka Y., 1999, NEO PI R NEO FFI MAN WAKABAYASHI A, IN PRESS J AUTISM DE Wakabayashi A, 2004, JAPANESE J PSYCHOL, V75, P78 Wing L, 1988, ASPECTS AUTISM BIOL WING L, 1981, PSYCHOL MED, V11, P115 NR 15 TC 40 Z9 41 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0191-8869 J9 PERS INDIV DIFFER JI Pers. Individ. Differ. PD OCT PY 2006 VL 41 IS 5 BP 873 EP 883 DI 10.1016/j.paid.2006.04.003 PG 11 WC Psychology, Social SC Psychology GA 087OI UT WOS:000240751300008 ER PT J AU Wakabayashi, A Baron-Cohen, S Wheelwright, S Goldenfeld, N Delaney, J Fine, D Smith, R Weil, L AF Wakabayashi, Akio Baron-Cohen, Simon Wheelwright, Sally Goldenfeld, Nigel Delaney, Joe Fine, Debra Smith, Richard Weil, Leonora TI Development of short forms of the Empathy Quotient (EQ-Short) and the Systemizing Quotient (SQ-Short) SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE empathizing; systemizing; E-S theory; EQ-Short; SQ-Short; cognitive style ID SEX-DIFFERENCES; FUNCTIONING AUTISM; ASPERGER-SYNDROME; ADULTS AB The empathizing-systemizing (E-S) theory has been tested using the Empathy Quotient (EQ) and the Systemizing Quotient (SQ). The present study tested n = 1761 students with these instruments, to determine if short versions of these scales could be constructed. This would be desirable both for faster assessment and to establish which are the key items on each scale. Principal component analysis and factor analysis suggested that a 22-item version of the EQ (EQ-Short) and a 25-item version of the SQ (SQ-Short) were highly correlated with the full scale versions. The reliability of each short scale was reasonable. Results showed that females scored significantly higher than males on the EQ-Short, whilst males scored higher than females on the SQ-Short. Additionally, scores were analyzed according to the degree the student was studying. On the EQ-Short, students studying humanities scored higher than students studying sciences, whereas on the SQ-Short, the results were the opposite. Finally, distributions of the population who showed 'brain types' based on the scores on two scales were examined. The pattern of distribution of the brain types was consistent with the E-S theory. These results suggest that the EQ-Short and SQ-Short are useful instruments for measuring fundamental cognitive styles. (c) 2006 Elsevier Ltd. All rights reserved. C1 Chiba Univ, Dept Psychol, Chiba 2638522, Japan. Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 2AH, England. Univ Illinois, Dept Phys, Urbana, IL 61801 USA. RP Wakabayashi, A (reprint author), Chiba Univ, Dept Psychol, 1-33 Yayoi Cho, Chiba 2638522, Japan. EM akiowcam@mac.com CR Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S., 2003, AUTISM MIND BRAIN, P161 Baron-Cohen S, 2004, J AUTISM DEV DISORD, V34, P163, DOI 10.1023/B:JADD.0000022607.19833.00 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 BARONCOHEN S, 1997, EMERGENCE CORE DOMAI, P45 BENBOW CP, 1988, BEHAV BRAIN SCI, V11, P169 BILLINGTON J, UNPUB SYSTEMIZING QU Geary DC, 1996, BEHAV BRAIN SCI, V19, P229 GOLDENFELD N, IN PRESS CLIN NEUROP, V2 HALL JA, 1978, PSYCHOL BULL, V85, P845, DOI 10.1037//0033-2909.85.4.845 Lawson J, 2004, J AUTISM DEV DISORD, V34, P301, DOI 10.1023/B:JADD.0000029552.42724.1b Leslie A.M., 1994, MAPPING MIND DOMAIN, P119, DOI DOI 10.1017/CBO9780511752902.006 Premack David, 1995, CAUSAL COGNITION Tomasello M., 1999, CULTURAL ORIGINS HUM WAKABAYASHI A, IN PRESS J AUTISM DE NR 15 TC 62 Z9 64 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0191-8869 J9 PERS INDIV DIFFER JI Pers. Individ. Differ. PD OCT PY 2006 VL 41 IS 5 BP 929 EP 940 DI 10.1016/j.paid.2006.03.017 PG 12 WC Psychology, Social SC Psychology GA 087OI UT WOS:000240751300013 ER PT J AU Cholbi, M AF Cholbi, Michael TI Moral belief attribution: A reply to Roskies SO PHILOSOPHICAL PSYCHOLOGY LA English DT Editorial Material DE Donald Davidson; emotion; moral belief; moral motivation; motive internalism; theory of mind ID ASPERGER-SYNDROME; AUTISM; BRAIN; PSYCHOLOGY; CHILDREN; EMPATHY AB I here defend my earlier doubts that VM patients serve as counterexamples to motivational internalism by highlighting the difficulties of belief attribution in light of holism about the mental and by suggesting that a better understanding of the role of emotions in the self- attribution of moral belief places my earlier Davidsonian "theory of mind'' argument in a clearer light. C1 Calif State Polytech Univ Pomona, Dept Philosophy, Pomona, CA 91768 USA. RP Cholbi, M (reprint author), Calif State Polytech Univ Pomona, Dept Philosophy, 3801 W Temple Ave, Pomona, CA 91768 USA. EM mjcholbi@csupomona.edu CR Asch Solomon, 1951, GROUPS LEADERSHIP ME, P177 Banks C., 1973, INT J CRIMINOLOGY PE, V1, P69 Baron-Cohen S, 2004, J AUTISM DEV DISORD, V34, P163, DOI 10.1023/B:JADD.0000022607.19833.00 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x BLOCK N, 1998, ROUTLEDGE ENCY PHILO, V4, P488 Brink DO, 1997, ETHICS, V108, P4, DOI 10.1086/233786 Castelli F, 2002, BRAIN, V125, P1839, DOI 10.1093/brain/awf189 Cholbi M, 2006, PHILOS PSYCHOL, V19, P607, DOI 10.1080/09515080600901939 Darwall Stephen, 1997, MORAL DISCOURSE PRAC, P305 Dennis M, 2000, AUTISM, V4, P370, DOI DOI 10.1177/1362361300004004003 Doris JM, 1998, NOUS, V32, P504, DOI 10.1111/0029-4624.00136 DREIER J, 1990, ETHICS, V101, P6, DOI 10.1086/293257 FRITH U, 2000, CHILDHOOD COGNITIVE, P324 Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 Harman Gilbert, 1999, P ARISTOTELIAN SOC, V99, P315, DOI DOI 10.1111/1467-9264.00062 KAUPINNEN A, 2004, UNPUB EMPIRICAL EVID KORSGAARD CM, 1986, J PHILOS, V83, P5, DOI 10.2307/2026464 Milgram S., 1974, OBEDIENCE AUTHORITY Nagel T, 1970, POSSIBILITY ALTRUISM Nisbett R., 1980, HUMAN INFERENCE STRA Nussbaum M., 2001, UPHEAVALS THOUGHT Parfit Derek, 1997, P ARISTOTELIAN SOC S, V71, P99, DOI DOI 10.1111/1467-8349.00021 Rieffe C, 2000, J AUTISM DEV DISORD, V30, P195, DOI 10.1023/A:1005540417877 Roskies A, 2003, PHILOS PSYCHOL, V16, P51, DOI 10.1080/0951508032000067743 Roskies A, 2006, PHILOS PSYCHOL, V19, P617, DOI 10.1080/09515080600901947 Smith Michael, 1994, MORAL PROBLEM Stone T, 1997, MIND LANG, V12, P327, DOI 10.1111/1468-0017.00051 Williams B., 1973, PROBLEMS SELF, P207, DOI 10.1017/CBO9780511621253.015 YIRMIYA N, 1992, CHILD DEV, V63, P150, DOI 10.1111/j.1467-8624.1992.tb03603.x NR 29 TC 1 Z9 1 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 0951-5089 J9 PHILOS PSYCHOL JI Philos. Psychol. PD OCT PY 2006 VL 19 IS 5 BP 629 EP 638 DI 10.1080/09515080600901954 PG 10 WC Ethics; Psychology, Multidisciplinary SC Social Sciences - Other Topics; Psychology GA 085DR UT WOS:000240584000005 ER PT J AU Bouma, HK AF Bouma, Hanni K. TI Radical interpretation and high-functioning autistic speakers: a Defense of Davidson on thought and language SO PHILOSOPHICAL PSYCHOLOGY LA English DT Editorial Material DE Donald Davidson; radical interpretation; theory of mind; thought ID FALSE BELIEF; MIND; CHILDREN; INTENTION; DEFICIT AB Donald Davidson argues in "Thought and Talk'' that all speakers must be interpreters of other speakers: linguistic competence requires the possession of intentional concepts and the ability to attribute intentional states to other people. Kristin Andrews ( in Philosophical Psychology, 15) has argued that empirical evidence about autism undermines this theoretical claim, for some individuals with autism lack the requisite "theory of mind'' skills to be able to interpret, yet are competent speakers. In this paper, Davidson is defended on the grounds that the high- functioning autistic individuals in question have a more robust theory of mind than has been acknowledged, and that this is sufficient for them to be interpreters of other speakers. It is argued, further, that Davidson's theory would remain intact even if one or more autistic speakers lacking a theory of mind were to exist, as he makes conceptual claims about thought and language that are not vulnerable to empirical counterexamples. C1 Mem Univ Newfoundland, Sch Med, St John, NF A1C 5S7, Canada. RP Bouma, HK (reprint author), 56 Belvedere St, St John, NF A1C 3Y2, Canada. EM hannibouma@hotmail.com CR Andrews K, 2002, PHILOS PSYCHOL, V15, P317, DOI 10.1080/09515080210000061111 BALTAXE CAM, 1988, LANGUAGE TREATMENT A, P155 Baron- Cohen S., 1989, DEV PSYCHOPATHOL, V1, P185, DOI 10.1017/ S0954579400000377 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BARONCOHEN S, 1991, BRIT J DEV PSYCHOL, V9, P301 BARONCOHEN S, 1991, CHILD DEV, V62, P385, DOI 10.1111/j.1467-8624.1991.tb01539.x BaronCohen S, 1997, ISRAEL J PSYCHIAT, V34, P174 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Davidson D., 2001, ESSAYS ACTIONS EVENT, P261 Davidson D., 1991, AJ AYER MEMORIAL ESS, P153 Davidson D., 2001, SUBJECTIVE INTERSUBJ, P107 Davidson D., 1985, ESSAYS DAVIDSON ACTI, P242 DAVIDSON D, 1999, PHILOS D DAVIDSON, P305 Davidson D., 2001, SUBJECTIVE INTERSUBJ, P95 Davidson D., 2001, SUBJECTIVE INTERSUBJ, P123 Davidson Donald, 2001, INQUIRIES TRUTH INTE, P155 Davies N M, 2001, Expert Opin Pharmacother, V2, P139, DOI 10.1517/14656566.2.1.139 Evnine S., 1991, D DAVIDSON FRITH U, 1994, PHILOS T ROY SOC B, V346, P97, DOI 10.1098/rstb.1994.0133 Garfield JL, 2001, MIND LANG, V16, P494, DOI 10.1111/1468-0017.00180 Gluer K, 2003, MIND LANG, V18, P23, DOI 10.1111/1468-0017.00213 Grandin T., 1996, EMERGENCE LABELED AU HANSEN SOLES Deborah, 1999, PHILOS D DAVIDSON, P311 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x HEWETSON A, 2002, STOLEN CHILD ASPECTS Leslie A. M., 1993, UNDERSTANDING OTHER, P83 LESLIE AM, 1988, BRIT J DEV PSYCHOL, V6, P315 Lewis D, 1983, PHILOS PAPERS, V1, P108, DOI 10.1093/0195032047.003.0008 MCALPINE LM, 1995, J VISUAL IMPAIR BLIN, V89, P349 Minter M, 1998, BRIT J DEV PSYCHOL, V16, P183 Mundy P, 1993, UNDERSTANDING OTHER, P181 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x PERNER J, 1987, BRIT J DEV PSYCHOL, V5, P125 PERNER J, 1993, UNDERSTANDING OTHER, P112 Phillips W, 1998, BRIT J DEV PSYCHOL, V16, P337 Russell J, 2001, J CHILD PSYCHOL PSYC, V42, P317, DOI 10.1017/S0021963001006874 Russell J, 1999, J CHILD PSYCHOL PSYC, V40, P859, DOI 10.1017/S0021963099004229 Russell J., 1997, AUTISM EXECUTIVE DIS Siegel B., 1996, WORLD AUTISTIC CHILD Tager-Flusberg H., 1993, UNDERSTANDING OTHER, P138 Tager-Flusberg H, 1989, AUTISM NATURE DIAGNO, P92 Tan J., 1991, DEV PSYCHOPATHOL, V3, P163, DOI 10.1017/S0954579400000055 TANTAM D, 1992, ACTA PAEDOPSYCHIATR, V55, P88 NR 43 TC 2 Z9 2 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 0951-5089 J9 PHILOS PSYCHOL JI Philos. Psychol. PD OCT PY 2006 VL 19 IS 5 BP 639 EP 662 DI 10.1080/09515080600904370 PG 24 WC Ethics; Psychology, Multidisciplinary SC Social Sciences - Other Topics; Psychology GA 085DR UT WOS:000240584000006 ER PT J AU Andrews, K Radenovic, L AF Andrews, Kristin Radenovic, Ljiljana TI Speaking without interpreting: a reply to Bouma on autism and Davidsonian interpretation SO PHILOSOPHICAL PSYCHOLOGY LA English DT Editorial Material DE autism; belief; Donald Davidson; interpretation; joint attention; theory of mind; triangulation ID TEACHING THEORY; MIND; CHILDREN; BEHAVIOR; LANGUAGE; ABILITY AB We clarify some points previously made by Andrews, and defend the claim that Davidson's account of belief can be and is challenged by the existence of some people with autism. We argue that both Bouma and Andrews ( Philosophical Psychology, 15) blurred the subtle distinctions between the psychological concepts of theory of mind and joint attention and the Davidsonian concepts of interpretation and triangulation. And we accept that appeal to control group studies is not the appropriate place to look for an individual who can speak but who has significant problems with interpretation. In this paper we argue that by turning to the clinical literature we can more readily find such a challenge to Davidson's account. C1 York Univ, Dept Philosophy, N York, ON M3J 1P3, Canada. RP Andrews, K (reprint author), York Univ, Dept Philosophy, 4700 Keele St, N York, ON M3J 1P3, Canada. EM andrewsk@yorku.ca CR Andrews K, 2002, PHILOS PSYCHOL, V15, P317, DOI 10.1080/09515080210000061111 BALDWIN DA, 1993, J CHILD LANG, V20, P395 BALDWIN DA, 1991, CHILD DEV, V62, P875, DOI 10.2307/1131140 Baron-Cohen S., 1991, NATURAL THEORIES MIN, P233 Bauminger N, 2002, J AUTISM DEV DISORD, V32, P283, DOI 10.1023/A:1016378718278 BONDY A, 1996, LEARNING COGNITION A Bouma HK, 2006, PHILOS PSYCHOL, V19, P639, DOI 10.1080/09515080600904370 Bruner Jerome, 1983, CHILDS TALK Davidson D., 1991, AJ AYER MEMORIAL ESS, P153 Davidson Donald, 1975, MIND LANG, P7 Davies N M, 2001, Expert Opin Pharmacother, V2, P139, DOI 10.1517/14656566.2.1.139 Frith U., 1994, SOCIAL DEV, V3, P108, DOI DOI 10.1111/J.1467-9507.1994.TB00031.X Garfield JL, 2001, MIND LANG, V16, P494, DOI 10.1111/1468-0017.00180 Gluer K, 2003, MIND LANG, V18, P23, DOI 10.1111/1468-0017.00213 Gray C., 2000, WRITING SOCIAL STORI Gray C. A., 1993, FOCUS AUTISTIC BEHAV, V8, P1, DOI DOI 10.1177/108835769300800101 Hadwin J, 1997, J AUTISM DEV DISORD, V27, P519, DOI 10.1023/A:1025826009731 Happe F., 1994, AUTISM INTRO PSYCHOL Happe F. G. E., 2000, UNDERSTANDING OTHER, P203 HOBSON P, 2002, CARDLE THOUGHT EXPLO Howlin P, 1998, J CHILD PSYCHOL PSYC, V39, P307, DOI 10.1017/S0021963097002138 Klinger LG, 2001, DEV PSYCHOPATHOL, V13, P111, DOI 10.1017/S0954579401001080 KLINNERT MD, 1984, INFANT BEHAV DEV, V7, P447, DOI 10.1016/S0163-6383(84)80005-3 LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 Plaisted KC, 2000, UNDERSTANDING OTHER, P222 PREMACK D, 1978, BEHAV BRAIN SCI, V1, P515 Quill K. A., 1995, TEACHING CHILDREN AU SCHWITZGEBEL E, 1997, THESIS UC BERKELEY B SORCE JF, 1985, DEV PSYCHOL, V21, P195, DOI 10.1037//0012-1649.21.1.195 Swettenham J, 1996, J CHILD PSYCHOL PSYC, V37, P157, DOI 10.1111/j.1469-7610.1996.tb01387.x TOMASELLO M, 1992, J CHILD LANG, V19, P311 Tomasello M., 1999, CULTURAL ORIGINS HUM Tomasello Michael, 2003, CONSTRUCTING LANGUAG Walker M., 1980, MAKATON VOCABULARY Wittgenstein Ludwig, 1953, PHILOS INVESTIGATION NR 36 TC 4 Z9 4 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 0951-5089 J9 PHILOS PSYCHOL JI Philos. Psychol. PD OCT PY 2006 VL 19 IS 5 BP 663 EP 678 DI 10.1080/09515080600904404 PG 16 WC Ethics; Psychology, Multidisciplinary SC Social Sciences - Other Topics; Psychology GA 085DR UT WOS:000240584000007 ER PT J AU Bouma, HK AF Bouma, Hanni K. TI High-functioning autistic speakers as Davidsonian interpreters: a reply to Andrews and Radenovic SO PHILOSOPHICAL PSYCHOLOGY LA English DT Editorial Material DE autism; Donald Davidson; language; radical interpretation; theory of mind; thought AB In this paper, I provide further support for my earlier claim that the existence of high-functioning autistic speakers does not undermine Davidson's theory of radical interpretation. Andrews and Radenovic, in criticizing my arguments for this position, have presented fresh evidence from the clinical literature on autism for the existence of an individual who speaks but does not interpret, and maintain that the existence of such an individual seriously challenges Davidson's theory. I counter this claim by showing that the evidence they point to in fact better supports the conclusion that this autistic speaker, and others like him, are Davidsonian interpreters. C1 Mem Univ Newfoundland, Sch Med, St John, NF A1C 5S7, Canada. RP Bouma, HK (reprint author), 56 Belvedere St, St John, NF A1C 3Y2, Canada. EM hannibouma@hotmail.com CR Andrews K, 2006, PHILOS PSYCHOL, V19, P663, DOI 10.1080/09515080600904404 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bouma HK, 2006, PHILOS PSYCHOL, V19, P639, DOI 10.1080/09515080600904370 Davidson D., 2001, INQUIRIES TRUTH INTE, P141 Davidson Donald, 2001, INQUIRIES TRUTH INTE, P155 Davies N M, 2001, Expert Opin Pharmacother, V2, P139, DOI 10.1517/14656566.2.1.139 Gluer K, 2003, MIND LANG, V18, P23, DOI 10.1111/1468-0017.00213 MACASKILL E, 2005, GUARDIAN 1007 NR 8 TC 1 Z9 1 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 0951-5089 J9 PHILOS PSYCHOL JI Philos. Psychol. PD OCT PY 2006 VL 19 IS 5 BP 679 EP 690 DI 10.1080/09515080600904412 PG 12 WC Ethics; Psychology, Multidisciplinary SC Social Sciences - Other Topics; Psychology GA 085DR UT WOS:000240584000008 ER PT J AU Herrera, G Jordan, R Vera, L AF Herrera, Gerardo Jordan, Rita Vera, Lucia TI Agency and presence: A common dependence on subjectivity? SO PRESENCE-TELEOPERATORS AND VIRTUAL ENVIRONMENTS LA English DT Article; Proceedings Paper CT 8th Annual International Workshop on Presence CY SEP 21-23, 2005 CL London, ENGLAND HO Univ Coll London ID AUTISTIC SPECTRUM DISORDERS; VIRTUAL-REALITY; IMITATION; CHILDREN; PLAY; TOOL AB This paper argues that presence, as shown in virtual environments, can usefully be seen as comprising various subtypes and that these in turn may have common conceptual and ontological features with a sense of agency as defined by Russell ( 1996, Agency: Its Role in Mental Development, Erlbaum.). Furthermore, an analysis of Russell's characterization of the concept of agency may be useful for acquiring insight into the sense of presence itself and the variables affecting it. Empirical evidence from cognitive developmental research and the positive results of attempts to develop symbolic understanding in people with autism spectrum disorders (ASD) in virtual environments suggest that presence may be more about experiencing agency than either pretending to be there or constructing and reconstructing mental models in real time. This analysis is used to shed some light on the current issues of presence research and to open up new philosophical and psychological aspects, in relation to both presence and ASD. C1 Univ Valencia, Inst Robot, Autism & Learning Difficulties Grp, Valencia, Spain. Univ Birmingham, Sch Educ, Autism Team, Birmingham B15 2TT, W Midlands, England. RP Herrera, G (reprint author), Univ Valencia, Inst Robot, Autism & Learning Difficulties Grp, Valencia, Spain. 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Virtual Env. PD OCT PY 2006 VL 15 IS 5 BP 539 EP 552 DI 10.1162/pres.15.5.539 PG 14 WC Computer Science, Cybernetics; Computer Science, Software Engineering SC Computer Science GA 109XB UT WOS:000242341800006 ER PT J AU Kumar, S Kim, YS Oh, KS AF Kumar, Surender Kim, Yong Seob Oh, Kun Seok TI Development of a social interaction questionnaire for the trainers and mothers of children with disabilities participating in Dousa-hou (Japanese psycho-rehabilitation) camps SO PSYCHOLOGICAL REPORTS LA English DT Article AB A 12-item Social Interaction Questionnaire was developed to measure the social interactions among trainers and mothers of children with disabilities in Dousa-hou camps. Dousa-hou is a Japanese psychological rehabilitation method which is widely used for children with mental retardation, cerebral palsy, and autism in Japan and other Asian countries. The primary focus of the rehabilitation method is to improve bodily movements, posture, and social support to patients and their first-degree relatives as well as promoting social interaction among participants. Two factors of interaction, (1) educational and daily life matters and (2) health and care matters, emerged through factor analysis. Cronbach coefficient alpha of the questionnaire was .91. The back-translated version of the Social Interaction Questionnaire also yielded two factors and Cronbach coefficient alpha of .87. It was found that mothers or first degree relatives (N = 13 8; M = 43.5 yr., SD = 12.3) of the patients reported more social interaction than trainers when interacting with their child's trainer, supervisor, other trainers, and other mothers during six-day Dousa-hou camps. C1 Chikushi Womens Univ, Dept Preschool Educ, Dazaifu, Fukuoka 8180192, Japan. Chosun Univ, Div Publ Adm & Social Welf, Coll Social Sci, Seoul, South Korea. Dept Hosp Informat Management, Kwangju Hlth Coll, Kwangju, South Korea. RP Kumar, S (reprint author), Chikushi Womens Univ, Dept Preschool Educ, Ishizaka 2-12-1, Dazaifu, Fukuoka 8180192, Japan. EM kumar@chikushi-u.ac.jp CR Barron F, 1963, CREATIVITY PSYCHOL H HARIZUKA S, 1992, J REHABILITATION PSY, V19, P27 Kim YS, 2004, PSYCHOL REP, V95, P1050 Kinnear PR, 2000, SPSS WINDOWS MADE SI KLINE P, 1994, EASY GUIDE FACTOR AN KONNO Y, 1993, P 57 ANN CONV JAP PS, P235 KUMAR S, 2001, KOREAN J REHABILITAT, V2, P1 KUMAR S, 2005, DOUSA HOU JAPANESE P LEON GD, 1997, THERAPEUTIC COMMUNIT Murphy K. 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PD OCT PY 2006 VL 99 IS 2 BP 591 EP 598 DI 10.2466/PR0.99.2.591-598 PG 8 WC Psychology, Multidisciplinary SC Psychology GA 107UZ UT WOS:000242197800034 PM 17153831 ER PT J AU Fuentes-Biggi, J Ferrari-Arroyo, MJ Boada-Munoz, L Tourino-Aguilera, E Artigas-Pallares, J Belinchon-Carmona, M Munoz-Yunta, JA Hervas-Zuniga, A Canal-Bedia, R Hernandez, JM Diez-Cuervo, A Idiazabal-Aletxa, MA Mulas, E Palacios, S Tamarit, J Martos-Perez, J Posada-De La Paz, M AF Fuentes-Biggi, J. Ferrari-Arroyo, M. J. Boada-Munoz, L. Tourino-Aguilera, E. Artigas-Pallares, J. Belinchon-Carmona, M. Munoz-Yunta, J. A. Hervas-Zuniga, A. Canal-Bedia, R. Hernandez, J. M. Diez-Cuervo, A. Idiazabal-Aletxa, M. A. Mulas, E. Palacios, S. Tamarit, J. Martos-Perez, J. Posada-De la Paz, M. CA Grp Estudios Trastornos Espectro TI Good practice guidelines for the treatment of autistic spectrum disorders SO REVISTA DE NEUROLOGIA LA English DT Review DE Asperger disorder; autism spectrum disorders; autistic disorder; evidence; practice guidelines; recommendations; services; support; treatment ID PERVASIVE DEVELOPMENTAL DISORDERS; ATYPICAL ANTIPSYCHOTICS; DOUBLE-BLIND; CHILDREN; INTERVENTIONS; VITAMIN-B6; DIAGNOSIS; CROSSOVER; EFFICACY; OUTCOMES AB Introduction. Due to the inexistence of an aetiology-based intervention for autistic spectrum disorders (ASD) families and professionals are exposed to diverse and sometimes conflictive recommendations when they have to decide the most adequate alternative for treatment. Aim. To elaborate treatment guidelines agreed by consensus at the ASD Study Group of the (National) Institute of Health Carlos III. Development. Information about treatment of ASD was searched and gathered through available evidence based medical (EBM) databases. The data generated was complemented with practice parameters published elsewhere, reports from prestigious international institutions, focus oriented searches in PubMed and, finally, the opinion and experience of a multidisciplinary Study Group with extensive experience in treating ASD in Spain. Most popular treatment methods were reviewed as well as the common elements to be considered in successful support programs. Conclusion. No simple treatment algorithm can be produced at this time, and the level of available evidence based recommendations are in the weaker degrees of EBM classifications. Nevertheless, there is widespread agreement to stress that education, with special incidence in the development of communication and social competence, with the addition of community support are the main means of treatment. They can be complemented, depending on individual needs, with medication, behavioural approaches and cognitive-behavioural therapy for associated psychological problems in persons with higher cognitive level. Support to families and community empowerment are essential elements for the quality of life of persons with ASD. C1 Inst Salud Carlos III, IIER, Unidad Sindrome Aceito Tox, E-28029 Madrid, Spain. Policlin Gipuzkoa, Serv Psiquiatria Infanto Juvenil, San Sebastian, Spain. GAUTENA, San Sebastian, Spain. Hosp Sabadell, Corp Sanit Parc Tauli, Unidad Neuropediat, Barcelona, Spain. Univ Autonoma Madrid, Dept Psicol Basica, Fac Psicol, Madrid, Spain. Univ Autonoma Madrid, Ctr Psicol Aplicada, Madrid, Spain. Hosp del Mar, Secc Neuropediat, Barcelona, Spain. Ctr Neuropsicobiol, Barcelona, Spain. Hosp Mutua Terrassa, Ctr Salud Mental Infanto Juvenil, Barcelona, Spain. Clin Univ Dexeus, Barcelona, Spain. Univ Salamanca, Fac Educ, Dept Personalidad Evaluac & Tratamiento Psicol, E-37008 Salamanca, Spain. Consejeria Educac Comunidad Autonoma Madrid, Equipo Especif Alterac Graves Desarrollo, Madrid, Spain. Inst Neurocognit Incia & Clin Ntra Sra Pilar, Barcelona, Spain. FESPAU, Asesor Med Asociaciones, PAUTA, JARES, Barcelona, Spain. FESPAU, APNA, Barcelona, Spain. Hop La Fe Valencia, Serv Neuropediat, Valencia, Spain. Asociac Autismo Burgos, Burgos, Spain. FEAPS, Dept Calidad, Madrid, Spain. APNA, Serv Diagnost, Madrid, Spain. Ctr Leo Kanner, Madrid, Spain. RP Ferrari-Arroyo, MJ (reprint author), Inst Salud Carlos III, IIER, Unidad Sindrome Aceito Tox, Pabellon 11,Sinesio Delgado 6, E-28029 Madrid, Spain. 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Neurologia PD OCT 1 PY 2006 VL 43 IS 7 BP 425 EP 438 PG 14 WC Clinical Neurology SC Neurosciences & Neurology GA 092ZD UT WOS:000241135700008 PM 17006862 ER PT J AU Zaroff, CM Barr, WB Carlson, C LaJoie, J Madhavan, D Miles, DK Nass, R Devinsky, O AF Zaroff, Charles M. Barr, William B. Carlson, Chad LaJoie, Josiane Madhavan, Deepak Miles, Daniel K. Nass, Ruth Devinsky, Orrin TI Mental retardation and relation to seizure and tuber burden in tuberous sclerosis complex SO SEIZURE-EUROPEAN JOURNAL OF EPILEPSY LA English DT Article DE tuberous sclerosis complex; tubers-epilepsy; mental retardation; autism; infantile spasms; bilateral; neuropsychology ID INFANTILE SPASMS; EPILEPSY; AUTISM; IMPAIRMENT; TSC1 AB In patients with tuberous sclerosis complex (TSC), the high rates of mental retardation are associated with cortical tubers, seizure activity, and genetic factors. The goat of the study was to investigate the relationship between bilateral cortical tubers and seizure variables and mental retardation in individuals with TSC. The records of 27 patients with TSC (age 6 months to 33 years) undergoing neuropsychological assessment and the following clinical variables were examined: bilateral versus non-bilateral cortical tubers, the age of seizure onset, and presence of infantile spasms. Results were statistically analyzed. Bilateral cortical tubers (p = 0.02) and early age of seizure onset (p = 0.04) were significantly related to impaired cognitive functioning. Only one of the seven patients with normal cognitive functioning had bilateral tubers, whereas 13/21 patients with intellectual impairment had bilateral tubers. Patients with normal cognitive functioning experienced a mean age of seizure onset after 6 years. A trend was observed between infantile spasms and cognitive functioning (p = 0.06); the lack of statistical significance likely reflects the small sample size. Neither age nor gender was related to cognitive status. Further investigation incorporating additional neuroimaging factors, antiepileptic treatment effects, and genetic variables, is needed. (C) 2006 British Epilepsy Association. Published by Elsevier Ltd. All rights reserved. C1 NYU, Med Ctr, New York, NY 10016 USA. RP Zaroff, CM (reprint author), NYU, Med Ctr, 403 E 34th St,4th Floor, New York, NY 10016 USA. EM chartes.zaroff@med.nyu.edu CR (APA) APA, 2000, DIAGN STAT MAN MENT Curatolo P, 2004, EUR J PAEDIATR NEURO, V8, P327, DOI 10.1016/j.ejpn.2004.08.005 De Vries P J, 2000, J Med Genet, V37, pE3, DOI 10.1136/jmg.37.5.e3 Goh S, 2005, NEUROLOGY, V65, P235, DOI 10.1212/01.wnl.0000168908.78118.99 Gomez M. 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During cognitive tasks, cortical areas known as the 'default state' network - areas that have been implicated in both self-referential processing and processing of socially relevant information - typically reduce their brain activity. In patients with autism, such a reduction was not observed. This new finding indicates that a core deficit in autism might be related to the construal of a sense of self in its relationship with others and will certainly generate exciting new research on the neurobiology of autism. C1 Univ Calif Los Angeles, David Geffen Sch Med, Brain Res Inst,Atmanson Lovelace Brain Mapping Ct, Dept Psychiat & Biobehav Sci,Neuropsychiat Inst, Los Angeles, CA 90095 USA. RP Iacoboni, M (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Brain Res Inst,Atmanson Lovelace Brain Mapping Ct, Dept Psychiat & Biobehav Sci,Neuropsychiat Inst, Los Angeles, CA 90095 USA. 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SCI. PD OCT PY 2006 VL 10 IS 10 BP 431 EP 433 DI 10.1016/j.tics.2006.08.002 PG 3 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 097XL UT WOS:000241482900001 PM 16934520 ER PT J AU Striano, T Reid, VM AF Striano, Tricia Reid, Vincent M. TI Social cognition in the first year SO TRENDS IN COGNITIVE SCIENCES LA English DT Review ID EVENT-RELATED POTENTIALS; JOINT ATTENTION; BIOLOGICAL MOTION; DEVELOPMENTAL-CHANGES; 4-MONTH-OLD INFANTS; INTENTIONAL ACTION; VOCAL CUES; STILL-FACE; AUTISM; GAZE AB Although the study of infancy has answered many important questions about the human capacity for social cognition, the relatively young field of developmental social cognition is far from reaching its adulthood. With the merging of developmental, behavioral and neuro-cognitive sciences, some growing pains are in store. New work demonstrates that research into early social cognitive development must integrate various research fields and methods in order to achieve a more robust understanding of the nature and parameters of human social cognition. C1 Vanderbilt Univ, Dept Pediat, Nashville, TN 37203 USA. Vanderbilt Univ, Kennedy Ctr Human Dev, Nashville, TN 37203 USA. Univ Leipzig, Ctr Adv Studies, Neurocognit & Dev Grp, D-04109 Leipzig, Germany. Max Planck Inst Human Cognit & Brain Sci, D-04103 Leipzig, Germany. RP Striano, T (reprint author), Vanderbilt Univ, Dept Pediat, Nashville, TN 37203 USA. 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SCI. PD OCT PY 2006 VL 10 IS 10 BP 471 EP 476 DI 10.1016/j.tics.2006.08.006 PG 6 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 097XL UT WOS:000241482900007 PM 16942896 ER PT J AU Fischer, C Probst, P AF Fischer, Christian Probst, Paul TI Obsessive-compulsive phenomena in Asperger's disorder and high-functioning-autism SO ZEITSCHRIFT FUR PSYCHIATRIE PSYCHOLOGIE UND PSYCHOTHERAPIE LA German DT Article DE autistic disorders; obsessive-compulsive phenomena; Asperger's disorder; high-functioning autism; special interests; obsessions; compulsions ID REPETITIVE BEHAVIORS; CHILDHOOD AUTISM; CHILDREN; AMYGDALA; PARENTS; SYMPTOMS; ANXIETY; ADOLESCENTS; HIPPOCAMPUS; VOLUMES AB Although obsessive-compulsive, ritualistic and stereotyped behaviors are a core feature of autistic disorders, substantial data related to those phenomena are lacking. Ritualistic and stereotyped behavior can be found in almost all autistic patients. Additionally, cognitive able individuals with Asperger's disorder and high-functioning autism mostly develop circumscribed, often called << obsessional >> interests and preoccupations. Results from recent research indicate that autistic individuals frequently suffer from OCD-typical obsessions and compulsions associated with marked distress and interference with daily life. Results from recent research indicate phenomenological similarities between OCD and autism. Etiologic overlap between the disorders becomes especially evident when focussing cognitive, neurobiological and genetic aspects. Autism-related obsessive-compulsive phenomena have generally to be differentiated from OCD-symptoms, although there is no sharp borderline. Further research will be necessary to determine if obsessive-compulsive symptoms in autistic disorders should be regarded as an integral part of those disorders or if they are to be diagnosed as symptoms of a distinct condition which is comorbid obsessive-compulsive-disorder. C1 Univ Hamburg, Fachbereich Psychol, D-20146 Hamburg, Germany. RP Probst, P (reprint author), Univ Hamburg, Fachbereich Psychol, Melle Pk 5, D-20146 Hamburg, Germany. 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Lawrie, Stephen TI A neuropsychological investigation into 'Theory of Mind' and enhanced risk of schizophrenia SO PSYCHIATRY RESEARCH LA English DT Article DE Theory of Mind; state; trait; schizophrenia liability; Edinburgh high risk study ID EDINBURGH HIGH-RISK; RELATIVES; SYMPTOMS; PEOPLE; METAANALYSIS; AUTISM; MEMORY; ADULTS AB Theory of Mind (ToM) is the ability to correctly determine the intentions and behaviours of others. it is known that this capability is compromised in individuals with schizophrenia. It is has not been fully elucidated whether this observed phenomenon is of a state or trait nature. This study investigated whether ToM impairments could be linked to schizophrenia liability. A battery of ToM tests (the Hinting Task, a Self-Monitoring drawing task and cartoon picture stories) were used to compare healthy controls (n = 13) with relatives of individuals with schizophrenia who had experienced psychotic symptoms (HR+, n = 12) and those relatives who had not (HR-, n = 13). All participants belonged to the Edinburgh High Risk Study. Significant group differences were seen on the Self-Monitoring and cartoon tasks for the HR+ group, particularly those who had experienced symptoms at or around the time of testing. The observed ToM deficits measured by this battery of ToM tasks appeared to be related to state effects rather than enhanced risk of schizophrenia. (c) 2006 Elsevier Ireland Ltd. All rights reserved. C1 Univ Edinburgh, Sackler Suite Imaging Lab, Royal Edinburgh Hosp, Div Psychiat, Edinburgh EH10 5HF, Midlothian, Scotland. RP Marjoram, D (reprint author), Univ Edinburgh, Sackler Suite Imaging Lab, Royal Edinburgh Hosp, Div Psychiat, Floor 7 Kennedy Tower,Morningside Pk, Edinburgh EH10 5HF, Midlothian, Scotland. 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PD SEP 30 PY 2006 VL 144 IS 1 BP 29 EP 37 DI 10.1016/j.psychres.2006.01.008 PG 9 WC Psychiatry SC Psychiatry GA 093MD UT WOS:000241171500003 PM 16904190 ER PT J AU Hallene, KL Oby, E Lee, BJ Santaguida, S Bassanini, S Cipolla, M Marchi, N Hossain, M Battaglia, G Janigro, D AF Hallene, K. L. Oby, E. Lee, B. J. Santaguida, S. Bassanini, S. Cipolla, M. Marchi, N. Hossain, M. Battaglia, G. Janigro, D. TI Prenatal exposure to thalidomide, altered vasculogenesis, and CNS malformations SO NEUROSCIENCE LA English DT Article DE cortical dysplasia; angiogenesis; brain development; vasculogenesis; blood-brain barrier; endothelium ID BLOOD-BRAIN-BARRIER; CENTRAL-NERVOUS-SYSTEM; METHYLAZOXYMETHANOL ACETATE; CEREBRAL HETEROTOPIA; CORTICAL DYSPLASIA; HIPPOCAMPAL SLICES; WATER TRANSPORT; ANIMAL-MODELS; RADIAL GLIA; ANGIOGENESIS AB Malformations of cortical development (MCD) result from abnormal neuronal positioning during corticogenesis. MCD are believed to be the morphological and perhaps physiological bases of several neurological diseases, spanning from mental retardation to autism and epilepsy. In view of the fact that during development, an appropriate blood supply is necessary to drive organogenesis in other organs, we hypothesized that vasculogenesis plays an important role in brain development and that E15 exposure in rats to the angiogenesis inhibitor thalidomide would cause postnatal MCD. Our results demonstrate that thalidomide inhibits angiogenesis in vitro at concentrations that result in significant morphological alterations in cortical and hippocampal regions of rats prenatally exposed to this vasculotoxin. Abnormal neuronal development was associated with vascular malformations and a leaky blood-brain barrier. Protein extravasation and uptake of fluorescent albumin by neurons, but not glia, was commonly associated with abnormal cortical development. Neuronal hyperexcitability was also a hallmark of these abnormal cortical regions. Our results suggest that prenatal vasculogenesis is required to support normal neuronal migration and maturation. Altering this process leads to failure of normal cerebrovascular development and may have a profound implication for CNS maturation. (c) 2006 IBRO. Published by Elsevier Ltd. All rights reserved. C1 Cleveland Clin Fdn, Dept Cerebrovasc Res, Cleveland, OH 44195 USA. Cleveland Clin Fdn, Dept Mol Med, Cleveland, OH 44195 USA. Cleveland Clin Fdn, Dept Neurosurg, Cleveland, OH 44195 USA. Neurol Inst C Besta, Dept Expt Neurophysiol, Milan, Italy. Univ Vermont, Coll Med, Dept Neurol, Burlington, VT USA. RP Janigro, D (reprint author), Cleveland Clin Fdn, Dept Cerebrovasc Res, 9500 Euclid Ave,NB-20 LRI, Cleveland, OH 44195 USA. 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While neonatal disorders, diarrhoea, pneumonia, and malaria as well as being underweight account for most of the child deaths worldwide, children's health discussions in Europe and the USA focus on other issues such as asthma, neurodevelopmental disorders, male genital malformations, and childhood cancer. There is clear evidence of increasing rates of asthma in various countries during the last decades, although rates in some countries may now have stabilised or even decline as recent UK data indicate. Although an increase in the frequency of neurodevelopmental disorders such as autism and attention deficit disorder has frequently been discussed, the limited data in this field does not justify such a conclusion. While geographic heterogeneity regarding reproductive outcomes is apparent, global trends have not been identified. Interpretation of the available information on asthma, neurodevelopmental disorders and reproductive outcomes is hampered by inconstant diagnostic criteria over place and time and the lack of good and comprehensive population-based surveillance data, which makes it impossible to ascertain trends in actual disease frequency. Data indicate that developed countries have a gradually increasing incidence in leukaemia with a corresponding drop in the incidence of lymphoma. Increases in brain tumour frequency may be related to the development and wide application of new diagnostic capabilities, rather than a true change in the incidence of malignant disease. With a better prognosis for childhood cancer survival, secondary cancers following chemotherapy appear to be increasing. A wide range of environmental factors is thought to have an impact on children's health. These factors include nutrition (protein, vitamins, antioxidants), lifestyle and behaviour choices such as tobacco and alcohol use, parental health, socio-economic status, choice of living environment (urban versus rural, etc.),and parent-sibling behaviour. From the available data, no general conclusions on the contribution of specific chemicals can be drawn. (c) 2006 Elsevier B.V. All rights reserved. C1 BASF AG, GOA, D-67056 Ludwigshafen, Germany. RP Pallapies, D (reprint author), BASF AG, GOA, CP-H308,Carl Bosch Str 38, D-67056 Ludwigshafen, Germany. 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Res. Genet. Toxicol. Environ. Mutagen. PD SEP 28 PY 2006 VL 608 IS 2 SI SI BP 100 EP 111 DI 10.1016/j.mrgentox.2006.03.007 PG 12 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology SC Biotechnology & Applied Microbiology; Genetics & Heredity; Toxicology GA 088TY UT WOS:000240835200002 PM 16854614 ER PT J AU Kuwabara, H Kasai, K Takizawa, R Kawakubo, Y Yamasue, H Rogers, MA Ishijima, M Watanabe, K Kato, N AF Kuwabara, Hitoshi Kasai, Kiyoto Takizawa, Ryu Kawakubo, Yuki Yamasue, Hidenori Rogers, Mark A. Ishijima, Michiko Watanabe, Keiichiro Kato, Nobumasa TI Decreased prefrontal activation during letter fluency task in adults with pervasive developmental disorders: A near-infrared spectroscopy study SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE pervasive developmental disorders (PDD); near-infrared spectroscopy (NIRS); letter fluency task; prefrontal cortex ID AUTISM RATING-SCALE; CHILDHOOD AUTISM; HEMODYNAMIC-RESPONSE; WORKING-MEMORY; BRAIN; PERFORMANCE; CHILDREN; FMRI; CORTEX; CARS AB Functional neuroimaging studies have suggested that dysfunction of prefrontal cortex (PFC) is present in persons with pervasive developmental disorders (PDD). Recently, the development of near-infrared spectroscopy (NIRS) has enabled noninvasive bedside measurement of regional cerebral blood volume. Although NIRS enables the noninvasive clarification of brain functions in many psychiatric disorders, it has not yet been used to examine subjects with PDD. The aim of our study was to conduct an NIRS cognitive activation study to verify PFC dysfunction in PDD. The subjects were 10 adults with PDD and 10 age- and gender-matched healthy subjects. Hemoglobin concentration changes were measured with a 24-channel NIRS machine during the letter fluency task. While the number of words generated during the letter fluency task did not differ significantly between groups, the analysis of covariance including IQ as a confounding covariate showed that the PDD group was associated with bilateral reduction in oxy-hemoglobin concentration change as compared with the control group. The statistical results did not change when only IQ-matched high-functioning subjects (N=7) were included. Moreover, reduced oxy-hemoglobin concentration change for the right PFC was significantly correlated with verbal communication deficits within the PDD group. The present findings are consistent with proposed prefrontal dysfunction in PDD subjects identified by other neuroimaging modalities. The present results may be also potentially useful for applying NIRS to clinical settings,of child psychiatry. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, Tokyo 1138655, Japan. Tokyo Metropolitan Umegaoka Hosp, Dept Psychiat, Tokyo, Japan. RP Kuwabara, H (reprint author), Univ Tokyo, Grad Sch Med, Dept Neuropsychiat, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1138655, Japan. 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Brain Res. PD SEP 25 PY 2006 VL 172 IS 2 BP 272 EP 277 DI 10.1016/j.bbr.2006.05.020 PG 6 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 080IO UT WOS:000240241300012 PM 16806521 ER PT J AU Branchi, I Alleva, E AF Branchi, Igor Alleva, Enrico TI Communal nesting, an early social enrichment, increases the adult anxiety-like response and shapes the role of social context in modulating the emotional behavior SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE communal nesting; social context; anxiety-like behavior; early experiences; plus-maze; openfield ID NEONATAL MATERNAL SEPARATION; ELEVATED PLUS-MAZE; LONG-EVANS RATS; CORTICOSTERONE RESPONSE; INDIVIDUAL-DIFFERENCES; LABORATORY MICE; RHESUS-MONKEYS; MUS-MUSCULUS; STRESS; BRAIN AB Early experiences affect brain function and behavior at adulthood. Being reared in a communal nest (CN), consisting in a single nest where three mothers keep their pups together and share care-giving behavior from birth to weaning (postnatal day 25), provides a highly stimulating social environment to the developing pup. CN characterizes the natural ecological niche of many rodent species including the mouse. Here we show that, at adulthood, compared to mice reared in standard laboratory conditions (SN), CN reared mice displayed increased anxiety-like behavior, performing more thigmotaxis in the open field and spending less time in the open arms of the plus-maze. Furthermore, we showed that social context (being alone or with a familiar conspecific in the test apparatus) affects the emotional response in both the plus-maze and open field test and that the relevance of social context changes according to the early social experiences. In particular, CN mice display higher levels of anxiety-like behavior, compared to SN mice, only when alone but not in the presence of a familiar conspecific. Overall, in line with previous findings, the present study suggests that CN mice have a more elaborate social and emotional behavior compared to SN mice and thus may be more appropriate to investigate socio-emotional impairments, in particular in the case of mouse models of neurodevelopmental disorders, such as autism, or anxiety and mood disorders. (c) 2006 Elsevier B.V. All rights reserved. C1 Ist Super Sanita, Sect Behav Neurosci, Dept Cell Biol & Neurosci, I-00161 Rome, Italy. RP Branchi, I (reprint author), Ist Super Sanita, Sect Behav Neurosci, Dept Cell Biol & Neurosci, Viale Regina Elena 299, I-00161 Rome, Italy. 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Using two-dimensional gel and MALDI-TOF analysis, we detected 20 proteins that were differentially regulated by over-expression of human UBE3A in Drosophila heads. One protein responsive to UBE3A was the Rho-GEF pebble (pbl). Here, we present three lines of evidence suggesting that UBE3A regulates Pbl. First, we show genetic evidence that UBE3A and the Drosophila de-ubiquitinase fat facets (faf) exert opposing effects on Pbl function. Secondly, we find that both Pbl and ECT2, the mammalian orthologue of Pbl called epithelial cell transforming sequence 2 oncogene, physically interact with their respective ubiquitin E3 ligases. Finally, we show that Ect2 expression is regulated by Ube3a in mouse neurons as the pattern of Ect2 expression is dramatically altered in the hippocampus and cerebellum of Ube3a null mice. These results suggest that an orthologous UBE3A post-translational regulatory pathway regulates neuronal outgrowth in the mammalian brain and that dysregulation of this pathway may result in neurological phenotypes including AS and possibly other autism spectrum disorders. C1 Univ Calif San Diego, Sect Cell & Dev Biol, La Jolla, CA 92093 USA. Univ Tennessee, Ctr Hlth Sci, Dept Pathol, Memphis, TN 38163 USA. Univ Tennessee, Ctr Hlth Sci, Dept Neurol, Memphis, TN 38163 USA. RP Bier, E (reprint author), Univ Calif San Diego, Sect Cell & Dev Biol, 9500 Gilman Dr,Bonner Hall,Room 4221, La Jolla, CA 92093 USA. 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Mol. Genet. PD SEP 15 PY 2006 VL 15 IS 18 BP 2825 EP 2835 DI 10.1093/hmg/ddl225 PG 11 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 085FZ UT WOS:000240590400017 PM 16905559 ER PT J AU Di Bella, MA Cali, F Seidita, G Mirisola, M Ragusa, A Ragalmuto, A Galesi, O Elia, M Greco, D Zingale, M Gambino, G D'Anna, RP Regan, R Carbone, MC Gallo, A Romano, V AF Di Bella, Maria Antonietta Cali, Francesco Seidita, Gregorio Mirisola, Mario Ragusa, Angela Ragalmuto, Alda Galesi, Ornella Elia, Maurizio Greco, Donatella Zingale, Marinella Gambino, Giovanna D'Anna, Rosalba P. Regan, Regina Carbone, Maria Carmela Gallo, Alessia Romano, Valentino TI Screening of subtelomeric rearrangements in autistic disorder: Identification of a partial trisomy of 13q34 in a patient bearing a 13q;21p translocation SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; frontal bossing; gene dosage ID PERVASIVE DEVELOPMENTAL DISORDERS; IN-SITU HYBRIDIZATION; CHROMOSOMAL-ABNORMALITIES; COMPLEX; INDIVIDUALS; CHILDREN; GENE; DELETIONS; SPECTRUM; CLASSIFICATION AB Within the framework of a FISH screening protocol to detect cryptic subtelomeric rearrangements in autistic disorder (AD), a patient bearing three copies of the subtelomeric portion of the q arm of chromosome 13 has been identified. Beside AD, the patient also has severe mental retardation and displays several dysmorphic features. Further FISH analyses revealed that the trisomy was caused by the translocation. of a 13q subtelomeric fragment to the acrocentric tip of one chromosome 21 [46,X-Y.ish der(21) t(13;21) (q34;p13) (D13S1825+)]. Gene dosage experiments carried out with three multiallelic polymorphisms of the subtelomeric region of chromosome 13q showed that the putative length of the triplicate region does not exceed 300 kb about, that is, the distance from telomere to the first normally inherited marker. In addition, gene dosage analysis performed on the derivative chromosome 21, did not reveal loss of the most telomerie protein-encoding genes on 21p. The potential relationship between a postulated increased expression of genes on 13q34 and the complex phenotype in this trisomic patient is discussed. (c) 2006 Wiley-Liss, Inc. C1 Univ Palermo, Dipartimento Biopatol & Metodol Biomed, I-90133 Palermo, Italy. Univ Palermo, Ctr Interdipartimentale Ricerca Clin & Sperimenta, I-90133 Palermo, Italy. IRCCS, Assoc OASI Maria SS, Troina, EN, Italy. Osped Vittorio Emanuele, Lab Genet Umana, Catania, Italy. PO Aiuto Materno, Palermo, Italy. Wellcome Trust Res Labs, Ctr Human Genet, Oxford, England. RP Romano, V (reprint author), Univ Palermo, Dipartimento Biopatol & Metodol Biomed, Via Divisi 83, I-90133 Palermo, Italy. 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J. Med. Genet. B PD SEP 5 PY 2006 VL 141B IS 6 BP 584 EP 590 DI 10.1002/ajmg.b.30328 PG 7 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 077RZ UT WOS:000240049100005 PM 16823807 ER PT J AU Spence, SJ Cantor, RM Chung, L Kim, S Geschwind, DH Alarcon, M AF Spence, Sarah J. Cantor, Rita M. Chung, Lien Kim, Sharon Geschwind, Daniel H. Alarcon, Maricela TI Stratification based on language-related endophenotypes in autism: Attempt to replicate reported linkage SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; linkage; endophenotypes; language; AGRE ID GENOMEWIDE SCREEN; GENOMIC SCREEN; CHROMOSOME 7Q; SUSCEPTIBILITY LOCUS; DISORDER; FAMILIES; SPECTRUM; GENE; ASSOCIATION; SUPPORT AB The identification of autism susceptibility genes has been hampered by phenotypic heterogeneity of autism, among other factors. However, the use of endophenotypes has shown preliminary success in reducing heterogeneity and identifying potential autism-related susceptibility regions. To further explore the utility of using language-related endophenotypes, we performed linkage analysis on multiplex autism families stratified according to delayed expressive speech and also assessed the extent to which parental phenotype information would aid in identifying regions of linkage. A whole genome scan using a multipoint non-parametric linkage approach was performed in 133 families, stratifying the sample by phrase speech delay and word delay (WD). None of the regions reached suggested genome-wide or replication significance thresholds. However, several loci on chromosomes 1, 2,4,6,7,8,9,10,12,15, and 19 yielded nominally higher linkage signals in the delayed groups. The results did not support reported linkage findings for loci on chromosomes 7 or 13 that were a result of stratification based on the language delay endophenotype. In addition, inclusion of information on parental history of language delay did not appreciably affect the linkage results. The nominal increase in NPL scores across several regions using language delay endophenotypes for stratification suggests that this strategy may be useful in attenuating heterogeneity. However, the inconsistencies in regions identified across studies highlight the importance of increasing sample sizes to provide adequate power dent samples. to test replications in independent (c) 2006 Wiley-Liss, Inc. C1 Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Pediat, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Program Neurogenet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Reed Neurol Res Ctr, Dept Neurol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Ctr Autism Res & Treatment, Semel Inst Neurosci & Human Behav, Los Angeles, CA 90095 USA. RP Geschwind, DH (reprint author), Univ Calif Los Angeles, Reed Neurol Res Ctr, Dept Neurol, 710 Westwood Plaza, Los Angeles, CA 90095 USA. 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J. Med. Genet. B PD SEP 5 PY 2006 VL 141B IS 6 BP 591 EP 598 DI 10.1002/ajmg.b.30329 PG 8 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 077RZ UT WOS:000240049100006 PM 16752361 ER PT J AU Zandi, PP Kalaydjian, A Avramopoulos, D Shao, HB Fallin, MD Newschaffer, CJ AF Zandi, Peter P. Kalaydjian, Amanda Avramopoulos, Dimitrios Shao, Huibo Fallin, M. Daniele Newschaffer, Craig J. TI Rh and ABO maternal-fetal incompatibility and risk of autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; immune incompatibility; antibodies; log-linear model; genotype ID UNITED-STATES; ANTI-D; DISEASE AB We hypothesized that maternal-fetal incompatibility at the Rh or ABO loci may contribute to the risk of autism. There are biologically plausible reasons to believe such effects may play a role, and two previous epidemiologic studies have provided suggestive evidence. To further test this hypothesis, we genotyped the Rh and ABO loci in a sample of 389 independent case-parent trios from the AGRE repository and analyzed the data using a modification of the log-linear model for case-parent trios in which the effects of maternal-fetal genotype incompatibility are modeled jointly with the effects of the affected child's or mother's genotypes. We did not find any evidence that incompatibility at the Rh or ABO loci increases the risk of autism. Furthermore, we did not find any evidence for the presence of a high-risk susceptibility allele at or near these two loci operating either through the mother or child. (c) 2006 Wiley-Liss, Inc. C1 Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mental Hlth, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Baltimore, MD 21205 USA. RP Zandi, PP (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Mental Hlth, Hampton House,Room 857,624 N Broadway, Baltimore, MD 21205 USA. 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