FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Klin, A AF Klin, A TI Social neuroscience of autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 61st Annual Convention of the Society-of-Biological-Psychiatry CY MAY 18-20, 2006 CL Toronto, CANADA SP Soc Biol Psychiat C1 Yale Univ, New Haven, CT USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2006 VL 59 IS 8 SU S MA 627 BP 192S EP 192S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 032IE UT WOS:000236767301199 ER PT J AU DeVito, T Drost, D Rajakumar, N Pavlosky, W Williamson, P Nicolson, R AF DeVito, T Drost, D Rajakumar, N Pavlosky, W Williamson, P Nicolson, R TI Gray matter glutamatergic deficits in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 61st Annual Convention of the Society-of-Biological-Psychiatry CY MAY 18-20, 2006 CL Toronto, CANADA SP Soc Biol Psychiat C1 Univ Western Ontario, London, ON N6A 3K7, Canada. RI Nicolson, Robert/E-4797-2011 NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2006 VL 59 IS 8 SU S MA 700 BP 214S EP 214S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 032IE UT WOS:000236767301272 ER PT J AU Pandina, GJ Bossie, CA Zhu, Y Flanders, S AF Pandina, GJ Bossie, CA Zhu, Y Flanders, S TI The aberrant behavior checklist: Use in clinical trials of pediatric autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract CT 61st Annual Convention of the Society-of-Biological-Psychiatry CY MAY 18-20, 2006 CL Toronto, CANADA SP Soc Biol Psychiat C1 Janssen Pharmaceut Inc, Med Affairs, Titusville, NJ USA. Janssen Sci Affairs, LLC, Ortho McNeil, Qualitat Methodol, Titusville, NJ USA. Janssen Sci Affairs, LLC, Ortho McNeil, Outcomes Res, Titusville, NJ USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2006 VL 59 IS 8 SU S MA 761 BP 233S EP 233S PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 032IE UT WOS:000236767301333 ER PT J AU Anckarsater, H AF Anckarsater, H TI Central nervous changes in social dysfunction: Autism, aggression, and psychopathy SO BRAIN RESEARCH BULLETIN LA English DT Review DE antisocial personality disorder; violence; neurotransmitter; brain imaging; empathy ID POSITRON-EMISSION-TOMOGRAPHY; ANTISOCIAL PERSONALITY-DISORDER; DEFICIT HYPERACTIVITY DISORDER; WEAK CENTRAL COHERENCE; CEREBRAL-BLOOD-FLOW; VIOLENT OFFENDERS; CEREBROSPINAL-FLUID; CONDUCT DISORDER; MONOAMINE METABOLITES; CRIMINAL PSYCHOPATHS AB Neurodevelopmental disorders such as autism and schizophrenia involve social interaction problems and poor mentalizing abilities, associated with abnormal regional cerebral activity. Similar problems may be present in aggressive personality disorders and psychopathy. This paper reviews brain imaging data from research aiming at establishing possible central nervous correlates to aggression and psychopathy. Studies in this field are associated with a range of method problems. Differences between criminal offenders and controls may be confounded by a number of factors unrelated to personality traits or aggression per se. Phenotypical characterisation varies between Studies as do the laboratory methods and their interpretation. In spite of these problems, there are some recurrent findings in the present literature. Hypoactivity or structural reduction of the prefrontal cortex is a consistent finding in violent offenders or subjects with antisocial personality disorder. When defined as a personality disorder of social interaction and empathy, psychopathy seems to be associated rather with central abnormalities in the limbic circuitry. Indications of ail increased dopaminergic neurotransmission relative to the serotonergic have also been connected to such personality traits, especially to the AD/HD-related behavioural aspects. Further studies using strict phenotypical definitions or experimental models are clearly warranted to establish a pathophysiological background to destructive personality traits and the propensity to violent acting out. (c) 2006 Elsevier Inc. All rights reserved. C1 Lund Univ, Malmo Univ Hosp, Inst Clin Sci, Forens Psychiat Clin, S-20502 Malmo, Sweden. RP Anckarsater, H (reprint author), Lund Univ, Malmo Univ Hosp, Inst Clin Sci, Forens Psychiat Clin, Sege Pk 8A, S-20502 Malmo, Sweden. 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Bull. PD APR 14 PY 2006 VL 69 IS 3 BP 259 EP 265 DI 10.1016/j.brainresbull.2006.01.008 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 030UQ UT WOS:000236660900003 PM 16564420 ER PT J AU De Jaco, A Comoletti, D Kovarik, Z Gaietta, G Radic, Z Lockridge, O Ellisman, MH Taylor, P AF De Jaco, A Comoletti, D Kovarik, Z Gaietta, G Radic, Z Lockridge, O Ellisman, MH Taylor, P TI A mutation linked with autism reveals a common mechanism of endoplasmic reticulum retention for the alpha,beta-hydrolase fold protein family SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID RECOMBINANT HUMAN ACETYLCHOLINESTERASE; HUMAN BUTYRYLCHOLINESTERASE; MASS-SPECTROMETRY; DISULFIDE BONDS; C-TERMINUS; BCHE GENE; NEUROLIGINS; TORPEDO; CHOLINESTERASE; EXPRESSION AB A mutation linked to autistic spectrum disorders encodes an Arg to Cys replacement in the C-terminal portion of the extracellular domain of neuroligin-3. The solvent-exposed Cys causes virtually complete retention of the protein in the endoplasmic reticulum when the protein is expressed in transfected cells. An identical Cys substitution was reported for butyrylcholinesterase through genotyping patients with post-succinylcholine apnea. Neuroligin, butyrylcholinesterase, and acetylcholinesterase are members of the alpha,beta-hydrolase fold family of proteins sharing sequence similarity and common tertiary structures. Although these proteins have distinct oligomeric assemblies and cellular dispositions, homologous Arg residues in neuroligin-3 (Arg-451), in butyrylcholinesterase (Arg-386), and in acetylcholinesterase (Arg-395) are conserved in all studied mammalian species. To examine whether an homologous Arg to Cys mutation affects related proteins similarly despite their differing capacities to oligomerize, we inserted homologous mutations in the acetylcholinesterase and butyrylcholinesterase cDNAs. Using confocal fluorescence microscopy and analysis of oligosaccharide processing, we find that the homologous Arg to Cys mutation also results in endoplasmic reticulum retention of the two cholinesterases. Small quantities of mutated acetylcholinesterase exported from the cell retain activity but show a greater K-m, a much smaller k(cat), and altered substrate inhibition. The nascent proteins associate with chaperones during processing, but the mutation presumably restricts processing through the endoplasmic reticulum and Golgi apparatus, because of local protein misfolding and inability to oligomerize. The mutation may alter the capacity of these proteins to dissociate from their chaperone prior to oligomerization and processing for export. C1 Univ Calif San Diego, Dept Pharmacol, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Natl Ctr Microscopy & Imaging Res, La Jolla, CA 92093 USA. 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Biol. Chem. PD APR 7 PY 2006 VL 281 IS 14 BP 9667 EP 9676 DI 10.1074/jbc.M510262200 PG 10 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 027HB UT WOS:000236404700079 PM 16434405 ER PT J AU Blasi, F Bacchelli, E Pesaresi, G Carone, S Bailey, AJ Maestrini, E AF Blasi, F Bacchelli, E Pesaresi, G Carone, S Bailey, AJ Maestrini, E CA Int Molecular Genetic Study Autism TI Absence of coding mutations in the X-linked genes neuroligin 3 and neuroligin 4 in individuals with autism from the IMGSAC collection SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; neuroligin; chromosome X; mutation screening; synaptogenesis ID NLGN4 AB Neuroligin abnormalities have been recently implicated in the actiology of autism spectrum disorders (ASD), given the finding of point mutations in the two X-linked genes NLGN3 and NLGN4X and the important role of neuroligins in synaptogenesis. 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J. Med. Genet. B PD APR 5 PY 2006 VL 141B IS 3 BP 220 EP 221 DI 10.1002/ajmg.b.30287 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 031BL UT WOS:000236679000004 PM 16508939 ER PT J AU Pasca, SP Nemes, B Vlase, L Gagyi, CE Dronca, E Miu, AC Dronca, M AF Pasca, SP Nemes, B Vlase, L Gagyi, CE Dronca, E Miu, AC Dronca, M TI High levels of homocysteine and low serum paraoxonase 1 arylesterase activity in children with autism SO LIFE SCIENCES LA English DT Article DE autism; homocysteine; paraoxonase 1; glutathione peroxidase; B-12 ID PERVASIVE DEVELOPMENTAL DISORDERS; GROWTH-FACTOR-I; GLUTATHIONE-PEROXIDASE; OXIDATIVE STRESS; FOLATE; PREVALENCE; PHENOTYPE; ENZYMES; ACID AB Autism is a behaviorally defined disorder of unknown etiology that is thought to be influenced by genetic and environmental factors. High levels of homocysteine and oxidative stress are generally associated with neuropsychiatric disorders. The purpose of this study was to compare the level of homocysteine and other biomarkers in children with autism to corresponding values in age-matched healthy children. We measured total homocysteine (tHcy), vitamin B-12, paraoxonase and arylesterase activities of human paraoxonase 1 (PON1) in plasma and glutathione peroxidase (GPx) activity in erythrocytes from 21 children: 12 with autism (age: 8.29 +/- 2.76 years) and 9 controls (age: 8.33 +/- 1.82 years). We found statistically significant differences in tHcy levels and in arylesterase activity of PON1 in children with autism compared to the control group: 9.83 +/- 2.75 vs. 7.51 +/- 0.93 mu mol/L (P <= 0.01) and 72.57 +/- 11.73 vs. 81.83 +/- 7.39 kU/L (P <= 0.005). In the autistic group there was a strong negative correlation between tHcy and GPx activity and the vitamin 1312 level was low or suboptimal. In conclusion, our study shows that in children with autism there are higher levels of tHcy, which is negatively correlated with GPx activity, low PON1 arylesterase activity and suboptimal levels of vitamin B-12. (c) 2005 Elsevier Inc. All rights reserved. C1 Iuliu Hajtieganu Univ Med & Pharm, Fac Med, Cluj Napoca 400023, Romania. Ctr Cognit & Neural Studies Coneural, Cluj Napoca 4000504, Romania. Iuliu Hajtieganu Univ Med & Pharm, Fac Pharm, Cluj Napoca 400023, Romania. Univ Babes Bolyai, Dept Psychol, Program Cognit Neurosci, Cluj Napoca 400015, Romania. RP Dronca, M (reprint author), Iuliu Hajtieganu Univ Med & Pharm, Fac Med, Cluj Napoca 400023, Romania. 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TI The neuroscience of observing consciousness & mirror neurons in therapeutic hypnosis SO AMERICAN JOURNAL OF CLINICAL HYPNOSIS LA English DT Article DE brain plasticity; creative; empathy; gene expression/protein synthesis; activity-dependent hypnotic induction; ideodynamic; implicit processing heuristics; mind-body; mirror neurons; psychosomatic; rapport zone; rehabilitation; segmentalized trance; skill sets ID CHILDREN; IMITATION; OTHERS; FMRI AB Neuroscience documents the activity of "mirror neurons" in the human brain as a mechanism whereby we experience empathy and recognize the intentions of others by observing their behavior and automatically matching their brain activity. This neural basis of empathy finds support in research on dysfunctions in the mirror systems of humans with autism and fMRI research on normal subjects designed to assess intentionality, emotions, and complex cognition. 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PD APR PY 2006 VL 48 IS 4 BP 263 EP 278 PG 16 WC Psychology, Clinical SC Psychology GA 068WW UT WOS:000239406300006 PM 16696558 ER PT J AU Suresh, R Ambrose, N Roe, C Pluzhnikov, A Wittke-Thompson, JK Ng, MCY Wu, XL Cook, EH Lundstrom, C Garsten, M Ezrati, R Yairi, E Cox, NJ AF Suresh, R Ambrose, N Roe, C Pluzhnikov, A Wittke-Thompson, JK Ng, MCY Wu, XL Cook, EH Lundstrom, C Garsten, M Ezrati, R Yairi, E Cox, NJ TI New complexities in the genetics of stuttering: Significant sex-specific linkage signals SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID AUTISM SPECTRUM DISORDER; LANGUAGE DISORDER; GENOME SCAN; CHROMOSOME-2; GUIDELINES; RECOVERY; PROGRAM; SUPPORT; DISEASE; MARKERS AB Stuttering is a speech disorder long recognized to have a genetic component. Recent linkage studies mapped a susceptibility locus for stuttering to chromosome 12 in 46 highly inbred families ascertained in Pakistan. We report here on linkage studies in 100 families of European descent ascertained in the United States, Sweden, and Israel. These families included 252 individuals exhibiting persistent stuttering, 45 individuals classified as recovered from stuttering, and 19 individuals too young to classify. Primary analyses identified moderate evidence for linkage of the broader diagnosis of "ever stuttered" ( including both persistent and recovered stuttering) on chromosome 9 ( LOD p 2.3 at 60 cM) and of the narrower diagnosis of persistent stuttering on chromosome 15 ( LOD p 1.95 at 23 cM). In contrast, sex-specific evidence for linkage on chromosome 7 at 153 cM in the male-only data subset ( LOD p 2.99) and on chromosome 21 at 34 cM in the female-only data subset ( LOD p 4.5) met genomewide criteria for significance. Secondary analyses revealed a significant increase in the evidence for linkage on chromosome 12, conditional on the evidence for linkage at chromosome 7, with the location of the increased signal congruent with the previously reported signal in families ascertained in Pakistan. In addition, a region on chromosome 2 ( 193 cM) showed a significant increase in the evidence for linkage conditional on either chromosome 9 ( positive) or chromosome 7 ( negative); this chromosome 2 region has been implicated elsewhere in studies on autism, with increased evidence for linkage observed when the sample is restricted to those with delayed onset of phrase speech. Our results support the hypothesis that the genetic component to stuttering has significant sex effects. C1 Univ Chicago, Dept Med, Med Genet Sect, Chicago, IL 60637 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ Illinois, Dept Speech & Hearing Sci, Urbana, IL 61801 USA. Columbia Univ, Dept Genet & Dev, New York, NY USA. 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J. Hum. Genet. PD APR PY 2006 VL 78 IS 4 BP 554 EP 563 DI 10.1086/501370 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 032EE UT WOS:000236755900003 PM 16532387 ER PT J AU Archer, HL Evans, JC Millar, DS Thompson, PW Kerr, AM Leonard, H Christodoulou, J Ravine, D Lazarou, L Grove, L Verity, C Whatley, SD Pitz, DT Sampson, JR Clarke, AJ AF Archer, HL Evans, JC Millar, DS Thompson, PW Kerr, AM Leonard, H Christodoulou, J Ravine, D Lazarou, L Grove, L Verity, C Whatley, SD Pitz, DT Sampson, JR Clarke, AJ TI NTNG1 mutations are a rare cause of Rett syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE Rett syndrome; netrin G1; autism; NMDA receptor ID RECEPTOR EXPRESSION; INFANTILE SPASMS; BASAL GANGLIA; NETRIN-G1; MECP2; CDKL5; GENE; SCHIZOPHRENIA; RETARDATION; PHENOTYPE AB A translatin that disrupted the netrin G1 gene (NTNG1) was recently reported in a patient with an early seizure variant of Rett syndrome (RTT). The Netrin G1 protein (NTNG1) has an important in the developing central nervous system, particularly in axonal guidance, signalling and NMDA receptor function and awas a good candidate gene for RTT. We recruited 115 patients with RTT (females: 25 classic and 84 atypical; 6 males) but no mutation in the MECP2 gene. For those 52 patienta with epileptic seizure onset in the first 6 months of life. CDKL5 mutations were also excluded. We aimed to determine whether mutations in NTNG1 accounted for a sifgnificant subset of patients with RTT, particularly those with the early onset seizure variant and other atypical presentations. We sequenced the nine coding exons of NTNG1 and identified four sequence variants, none of which were likely to be pathogenic. Mutations in the NTNG1 function demands further investigation in relation to the central nervous system pathophysiology of the disorder. (c) 2006 Wiley-Liss, Inc. 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J. Med. Genet. A PD APR 1 PY 2006 VL 140A IS 7 BP 691 EP 694 DI 10.1002/ajmg.a.31133 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 031BN UT WOS:000236679200006 PM 16502428 ER PT J AU Baghdadli, A Beuzon, S Bursztejn, C Constant, J Desguerre, I Roge, B Squillante, M Voisin, J Aussilloux, C AF Baghdadli, A Beuzon, S Bursztejn, C Constant, J Desguerre, I Roge, B Squillante, M Voisin, J Aussilloux, C TI Clinical guidelines for the screening and the diagnosis of autism and pervasive developmental disorders SO ARCHIVES DE PEDIATRIE LA French DT Review DE autistic disorder; autism, early infantile; practice guidelines; screening; early diagnosis ID SPECTRUM DISORDERS; CHILDREN; RECOGNITION; PREVALENCE; AGE AB Autism is the best defined category among PDD. Its high prevalence, its onset in very young children and its persistence in adulthood arise many questions about early screening and early diagnosis. The aim of the study was to identify professional best practices about screening and diagnosis of autism in order to propose clinical guidelines and actions for the future. Scientific experts and parents take part to this procedure. Literature and previous guidelines were analyzed, experts in various fields were interviewed, a national study about the medical practices of the diagnosis of autism was made and questionnaires were send to 1600 psychiatrists and pediatricians. Guidelines built around 2 levels were proposed about screening and diagnosis. Conclusion. - Diagnosis needs a multidisciplinary approach, validated instruments and more communication between professionals and parents. Finally one of the more important aims of the diagnosis of autism is to facilitate intervention program. (c) 2006 Elsevier SAS. Tous droits rerserves. C1 CHU Montpellier, Hop Colombiere, Ctr Ressources Autisme, F-34295 Montpellier 05, France. Hop St Anne, Fed Francaise Psychiat, F-75674 Paris, France. Haute Autorite Sante, F-93218 La Plaine St Denis, France. Hop La Pitie Salpetriere, Soc Francaise Psychiat Enfant & Adolescent, AP HP, F-75651 Paris 13, France. Hop Necker Enfants Malad, Soc Francaise Pediat, AP HP, F-75015 Paris, France. Assoc Rech Autisme & Prevent Inadaptat, F-37016 Tours, France. CMP Ferrie, Assoc Psychiat Intersecteurs, F-34100 Montpellier, France. Assoc Natl Equipes Contribuant Act Medicosociale, F-75012 Paris, France. RP Baghdadli, A (reprint author), CHU Montpellier, Hop Colombiere, Ctr Ressources Autisme, F-34295 Montpellier 05, France. EM cent-ress-autisme@chu-montpellier.fr CR ALLEN DA, 1988, J CHILD NEUROL, V3, pS48 *AM AC PED COMM CH, 2001, PEDIATRICS Baghdadli A, 2003, EUR CHILD ADOLES PSY, V12, P122, DOI 10.1007/s00787-003-0314-6 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Bursztejn C, 2003, ARCH PEDIATRIE, V10, p129S, DOI 10.1016/S0929-693X(03)90410-6 Cohen D. J, 1997, HDB AUTISM PERVASIVE De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 Filipek PA, 2000, NEUROLOGY, V55, P468 FILIPEK PA, 1999, J AM ACAD CHILD PSY, V38, pS32 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Kanner L, 1943, NERV CHILD, V2, P217 Le Couteur A. 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PD APR PY 2006 VL 13 IS 4 BP 373 EP 378 DI 10.1016/j.arcped.2005.12.011 PG 6 WC Pediatrics SC Pediatrics GA 033GV UT WOS:000236836000011 PM 16423515 ER PT J AU Perry, A Prichard, EA Penn, HE AF Perry, A Prichard, EA Penn, HE TI Indicators of quality teaching in intensive behavioral intervention: A survey of parents and professionals SO BEHAVIORAL INTERVENTIONS LA English DT Article; Proceedings Paper CT 30th Annual Meeting of the Association-for-Behavior-Analysis CY MAY, 2004 CL Boston, MA SP Assoc Behav Anal ID AUTISTIC-CHILDREN; YOUNG-CHILDREN AB Intensive Behavioral Intervention (IBI) is being used extensively with children with autism. it is widely accepted that a large quantity of IBI is necessary to maximize children's outcomes, but outcomes remain variable and one reason for this is likely related to the quality of intervention children are receiving. There is little empirical evidence regarding the nature and measurement of quality IBI. This paper presents results of a survey examining the views of parents and professionals about quality IBI and how it should be measured. Parents rated the importance of 11 IBI characteristics and professionals indicated whether these characteristics should be measured objectively or subjectively. All respondents selected three characteristics they thought most important and answered open-ended questions about: additional quality indicators and IBI programming issues for which empirical evidence is needed. Parental ratings supported the importance of virtually all the suggested characteristics. Professional results emphasized the importance of objective measurement. The most frequently selected indicators of high quality teaching across groups were: creating generalization opportunities, administering reinforcers of the appropriate type, and using effective/appropriate behavior management strategies. There were interesting differences across groups and many valuable suggestions about additional indicators of quality and empirical questions of interest. Copyright (c) 2006 John Wiley & Sons, Ltd. C1 York Univ, Dept Psychol BS 219, Clin Dev Pychol Program, N York, ON M3J 1P3, Canada. RP Perry, A (reprint author), York Univ, Dept Psychol BS 219, Clin Dev Pychol Program, 4700 Keele St, N York, ON M3J 1P3, Canada. 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Intervent. PD APR PY 2006 VL 21 IS 2 BP 85 EP 96 DI 10.1002/bin.212 PG 12 WC Psychology, Clinical SC Psychology GA 038PZ UT WOS:000237236400002 ER PT J AU Wang, AT Lee, SS Sigman, M Dapretto, M AF Wang, AT Lee, SS Sigman, M Dapretto, M TI Neural basis of irony comprehension in children with autism: the role of prosody and context SO BRAIN LA English DT Article DE autism; brain development; fMRI; language pragmatics; social cognition ID AUTOMATED IMAGE REGISTRATION; HIGH-FUNCTIONING ADULTS; CEREBRAL-BLOOD-FLOW; ASPERGER-SYNDROME; LISTENING PREFERENCES; UNDERSTANDING SARCASM; DIAGNOSTIC INTERVIEW; EMOTIONAL PROSODY; HEMISPHERE DAMAGE; CENTRAL COHERENCE AB While individuals with autism spectrum disorders (ASD) are typically impaired in interpreting the communicative intent of others, little is known about the neural bases of higher-level pragmatic impairments. Here, we used functional MRI (fMRI) to examine the neural circuitry underlying deficits in understanding irony in high-functioning children with ASD. Participants listened to short scenarios and decided whether the speaker was sincere or ironic. Three types of scenarios were used in which we varied the information available to guide this decision. Scenarios included (i) both knowledge of the event outcome and strong prosodic cues (sincere or sarcastic intonation), (ii) prosodic cues only or (iii) knowledge of the event outcome only. Although children with ASD performed well above chance, they were less accurate than typically developing (TD) children at interpreting the communicative intent behind a potentially ironic remark, particularly with regard to taking advantage of available contextual information. In contrast to prior research showing hypoactivation of regions involved in understanding the mental states of others, children with ASD showed significantly greater activity than TD children in the right inferior frontal gyrus (IFG) as well as in bilateral temporal regions. Increased activity in the ASD group fell within the network recruited in the TD group and may reflect more effortful processing needed to interpret the intended meaning of an utterance. These results confirm that children with ASD have difficulty interpreting the communicative intent of others and suggest that these individuals can recruit regions activated as part of the normative neural circuitry when task demands require explicit attention to socially relevant cues. C1 Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Ahmanson Lovelace Brain Mapping Ctr, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. RP Dapretto, M (reprint author), Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, Ahmanson Lovelace Brain Mapping Ctr, Room 101,660 Charles E Young Dr S, Los Angeles, CA 90095 USA. 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NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0278-2626 J9 BRAIN COGNITION JI Brain Cogn. PD APR PY 2006 VL 60 IS 3 BP 318 EP 318 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 028XG UT WOS:000236521500065 ER PT J AU Vermeiren, R Jespers, I Moffitt, T AF Vermeiren, R Jespers, I Moffitt, T TI Mental health problems in juvenile justice populations SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID POSTTRAUMATIC-STRESS-DISORDER; SUBSTANCE USE DISORDERS; FLEMISH DELINQUENT ADOLESCENTS; VOICE DISC-IV; AGE-OF-ONSET; PSYCHIATRIC-DISORDERS; FOLLOW-UP; CONDUCT DISORDER; INCARCERATED DELINQUENTS; REPRESENTATIVE SAMPLE AB The limited literature on mental health problems in juvenile justice population has reported that most youth in juvenile justice hold psychiatric pathology. 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Psychiatr. N. Am. PD APR PY 2006 VL 15 IS 2 BP 333 EP + DI 10.1016/j.chc.2005.11.008 PG 21 WC Psychiatry SC Psychiatry GA 028YE UT WOS:000236523900005 PM 16527659 ER PT J AU Salman, M Blaser, SE Sharpe, JA Dennis, M AF Salman, M Blaser, SE Sharpe, JA Dennis, M TI Cerebellar vermis morphology in children with spina bifida and Chiari type II malformation SO CHILDS NERVOUS SYSTEM LA English DT Article DE cerebellar malformation; vermis morphology; children; spina bifida; MRI; midsagittal area ID DEFICIT HYPERACTIVITY DISORDER; POSTERIOR-FOSSA STRUCTURES; MRI; AUTISM; SIZE; AGE; MYELOMENINGOCELE; SCHIZOPHRENIA; AREA AB Posterior fossa size and cerebellar weight and volume are reduced in Chiari type II malformation (CII). This is assumed to affect the cerebellum uniformly. We quantified the presumed reduction in vermis size on magnetic resonance imaging (MRI). A midsagittal brain MRI slice was selected from each of 68 participants with CII (mean age 13 years). Control participants were 28 typically developing children (mean age 14.1 years). Midsagittal surface areas occupied by the intracranial fossa, posterior fossa, vermis, and its lobules were measured. Mean posterior fossa area was significantly smaller (P < 0.003), although mean vermis area was significantly larger (P < 0.0001), in participants with CII than in control participants. This expansion involved vermis lobules I-V and VI-VII areas (P < 0.0001). The midsagittal vermis was expanded and not reduced in size in participants with CII. This is attributed to compressive displacement of midline structures within the confines of a small posterior fossa. C1 Childrens Hosp, Sect Paediat Neurol, Winnipeg, MB R3A 1R9, Canada. Hosp Sick Children, Div Neurol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Toronto Western Hosp, Div Neurol, Toronto, ON M5T 2S8, Canada. Hosp Sick Children, Div Radiol, Toronto, ON M5G 1X8, Canada. Hosp Sick Children, Div Psychol, Toronto, ON M5G 1X8, Canada. 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Delatycki, Martin B. TI Long-term survival in a child with severe congenital contractural arachnodactyly, autism and severe intellectual disability SO CLINICAL DYSMORPHOLOGY LA English DT Article DE Beals syndrome; lehal disorder; neonatal Marfan syndrome ID MARFAN-SYNDROME; BEALS-SYNDROME; NEVO-SYNDROME; MUTATIONS; PHENOTYPE; ANOMALIES; INFANT AB The severe form of congenital contractural arachnoclactyly is usually associated with early mortality due to multisystem complications. Here, we report a 9-year-old male child with severe skeletal manifestations of congenital contractural arachnodactyly. He had none of the cardiovascular or gastrointestinal features that have been described in severe congenital contractural arachnodactyly. He had profound intellectual disability with autism. All exons of FBN2, the gene associated with congenital contractural arachnodactyly, were sequenced and no disease-causing mutation was found. When severe congenital contractural arachnoclactyly is diagnosed in the newborn period, parents need to be aware that long-term survival is possible, particularly if no significant extraskeletal complications are present, and that significant neurodevelopmental delay may occur. C1 [Snape, Katie M. G.; Fahey, Michael C.; Delatycki, Martin B.] Bruce Lefroy Ctr Genet, Murdoch Childrens Res Inst, Parkville, Vic 3052, Australia. [Fahey, Michael C.; Delatycki, Martin B.] Univ Melbourne, Dept Paediat, Parkville, Vic 3052, Australia. [McGillivray, George; Delatycki, Martin B.] Royal Childrens Hosp, Gen Hlth Serv Victoria, Parkville, Vic 3052, Australia. [Gupta, Prateek; Milewicz, Dianna M.] Univ Texas Houston, Sch Med, Dept Internal Med, Houston, TX USA. RP Delatycki, MB (reprint author), Royal Childrens Hosp, Murdoch Childrens Res Inst, Bruce Lefroy Ctr Genet Hlth Res, Flemington Rd, Parkville, Vic 3052, Australia. 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Dysmorphol. PD APR PY 2006 VL 15 IS 2 BP 95 EP 99 DI 10.1097/01.mcd.0000203633.86190.2d PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 248LL UT WOS:000252154700009 PM 16531736 ER PT J AU Li, BB Huang, XN AF Li, BB Huang, XN TI Existence and uniqueness of relative incidence estimates in case-series analysis SO COMPUTATIONAL STATISTICS & DATA ANALYSIS LA English DT Article DE case-series analysis; existence and uniqueness; maximum likelihood estimate; nonlinear programming; relative incidence ID LOGISTIC-REGRESSION; CAUSAL ASSOCIATION; VACCINE; MEASLES; AUTISM; MODELS; MUMPS AB Case-series analysis is used to estimate relative incidences of clinical events in defined time intervals after vaccination compared to a control period. It has advantages, in terms of both a reduction in data collection effort, because it uses only data on cases, and a reduction in the resultant variances of estimates, due to individuals being self-controlled. The existence and uniqueness of relative incidence estimates in case-series analysis are investigated. For the relative incidence of a clinical event, a simple condition for existence and uniqueness of the estimate of the parameter vector in a case-series model is established. An algorithm is developed to examine the established condition, which provides a clue for remedy when the condition for existence and uniqueness is not satisfied. (C) 2005 Elsevier B.V. All rights reserved. C1 Univ Loughborough, Sch Business, Loughborough LE11 3TU, Leics, England. Pfizer Global Res & Dev, Sandwich CT13 9NJ, Kent, England. RP Li, BB (reprint author), Univ Loughborough, Sch Business, Ashby Rd, Loughborough LE11 3TU, Leics, England. EM b.li2@lboro.ac.uk CR ALBERT A, 1984, BIOMETRIKA, V71, P1 BEGG N, 1990, VACCINE, V8, P180, DOI 10.1016/0264-410X(90)90042-K Corwin L.J., 1982, MULTIVARIABLE CALCUL Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 FARRINGTON CP, 1995, BIOMETRICS, V51, P228, DOI 10.2307/2533328 FARRINGTON P, 1995, LANCET, V345, P567, DOI 10.1016/S0140-6736(95)90471-9 Fiacco AV, 1968, NONLINEAR PROGRAMMIN Heinze G, 2002, STAT MED, V21, P2409, DOI 10.1002/sim.1047 Kim I, 2004, COMPUT STAT DATA AN, V46, P631, DOI 10.1016/j.csda.2003.09.002 Mitrinovic D.S, 1970, ANAL INEQUALITIES Murphy TV, 2001, NEW ENGL J MED, V344, P564, DOI 10.1056/NEJM200102223440804 SILVAPULLE MJ, 1986, J ROY STAT SOC B MET, V48, P100 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 NR 13 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-9473 J9 COMPUT STAT DATA AN JI Comput. Stat. Data Anal. PD APR 1 PY 2006 VL 50 IS 7 BP 1807 EP 1817 DI 10.1016/j.csda.2005.02.002 PG 11 WC Computer Science, Interdisciplinary Applications; Statistics & Probability SC Computer Science; Mathematics GA 008FP UT WOS:000235025900009 ER PT J AU Curatolo, P Bombardieri, R Cerminara, C AF Curatolo, P Bombardieri, R Cerminara, C TI Current management for epilepsy in tuberous sclerosis complex SO CURRENT OPINION IN NEUROLOGY LA English DT Article DE intractable seizures; outcome; surgery; tuberous sclerosis ID MOLECULAR PATHOGENESIS; INFANTILE SPASMS; SURGERY; CHILDREN; AUTISM AB Purpose of review This article reviews the most significant advances in the field of epilepsy associated with tuberous sclerosis complex, with emphasis on new advances in the knowledge of the pathophysiological mechanisms of epileptogenicity, progress in identifying the epileptogenic zone, and the rationale for surgical management in individuals with intractable seizures. Recent findings Advances in our understanding of the mechanisms and genetics underlying infantile spasms and catastrophic epilepsy associated with tuberous sclerosis complex may facilitate more effective interventions. Early effective seizure control could significantly reduce the adverse developmental effects of chronic epilepsy in tuberous sclerosis. Vigabatrin is the first choice in the short-term treatment of infantile spasms. Some individuals, however, develop seizures that remain highly intractable. The factors that influence the intractability of epilepsy associated with tuberous sclerosis complex remain poorly understood. Multimodality neuroimaging has improved detection of epileptogenic foci, allowing an increased number of individuals to be evaluated for resective surgery. Epilepsy surgery is often associated with significant improvement of the neurologic outcome. Summary Epilepsy in tuberous sclerosis seems to arise from the interaction between multiple areas, all of which have increased excitability and reduced inhibition. Understanding the mechanisms of epileptogenesis might increase the availability of development of a more specific and efficacious treatment. New evidence suggests that it is possible to noninvasively identify children with tuberous sclerosis who are highly likely to become seizure free following surgical treatment. C1 Univ Roma Tor Vergata, Dept Neurosci, Pediat Neurol Unit, I-00133 Rome, Italy. RP Curatolo, P (reprint author), Univ Roma Tor Vergata, Dept Neurosci, Pediat Neurol Unit, Via Montpellier 1, I-00133 Rome, Italy. 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Opin. Neurol. PD APR PY 2006 VL 19 IS 2 BP 119 EP 123 DI 10.1097/01.wco.0000218225.50807.12 PG 5 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 031SH UT WOS:000236723800002 PM 16538083 ER PT J AU Rinehart, NJ Tonge, BJ Bradshaw, JL Iansek, R Enticott, PG Johnson, KA AF Rinehart, NJ Tonge, BJ Bradshaw, JL Iansek, R Enticott, PG Johnson, KA TI Movement-related potentials in high-functioning autism and Asperger's disorder SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PARKINSONS-DISEASE; CHILDHOOD AUTISM; MOTOR AREA; CHILDREN; INDIVIDUALS; STRATEGIES; CORTEX; MODEL AB Autism and Asperger's disorder (AD) are neurodevelopmental conditions that affect cognitive and social-communicative function. Using a movement-related potential (MRP) paradigm, we investigated the clinical and neurobiological issue of 'disorder separateness' versus 'disorder variance' in autism and AD. This paradigm has been used to assess basal ganglia/supplementary motor functioning in Parkinson's disease. Three groups (high functioning autism [HFA]: 16 males, 1 female; mean age 12y 5mo [SD 4y 4mo]; AD: 11 males, 2 females; mean age 13y 5mo [SD 3y 8mo]; comparison group: 13 males, 8 females; mean age 13y 10mo, [SD 3y 11 mo]) completed a cued motor task during electroencephalogram recording of MRPs. The HFA group showed reduced peak amplitude at Cz, indicating less activity over the supplementary motor area during movement preparation. Although an overall significant between-group effect was found for early slope and peak amplitude, subanalysis revealed that the group with AD did not differ significantly from either group. However, it is suggested that autism and AD may be dissociated on the basis of brain-behaviour correlations of IQ with specific neurobiological measures. The overlap between MRP traces for autism and Parkinson's disease suggests that the neurobiological wiring of motor functioning in autism may bypass the supplementary motor area/primary motor cortex pathway. C1 Monash Univ, Ctr Dev Psychiat & Psychol, Clayton, Vic 3168, Australia. Monash Univ, Expt Neuropsychol Res Unit, Sch Psychol Psychiat & Psychol Med, Clayton, Vic 3168, Australia. RP Rinehart, NJ (reprint author), Monash Med Ctr, Dept Med Psychol, 246 Clayton Rd, Clayton, Vic 3168, Australia. 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PD APR PY 2006 VL 48 IS 4 BP 272 EP 277 DI 10.1017/S0012162206000594 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 028CY UT WOS:000236465400007 PM 16542514 ER PT J AU Livet, MO Villeneuve, N Daquin, G Cournelle, MA Mancini, J Moncla, A AF Livet, Marie-Odile Villeneuve, Nathalie Daquin, Geraldine Cournelle, Marie-Anne Mancini, Joselle Moncla, Anne TI Epilepsy and mental retardation: genetic syndromes SO EPILEPTIC DISORDERS LA English DT Article; Proceedings Paper CT Annual Epilepsy Teaching Course CY 2003 CL Talmont, FRANCE DE Angelman syndrome; ring chromosome 20; Wolf-Hirschorn; genetic syndromes and epilepsy ID FRAGILE-X-SYNDROME; ANGELMAN-SYNDROME; RING CHROMOSOME-20; GENERALIZED EPILEPSY; EEG; UBE3A; ABNORMALITIES; DUPLICATION; CHILDREN; AUTISM AB The identification of an etiology in children and adults with mental deficiency is a major challenge and needs a comprehensive clinical approach and multidisciplinary collaborations. Some genetic syndromes with intellectual disability may also be associated with specific dysmorphic features, behavioural patterns or electro-clinically recognizable epilepsy syndromes. Identifying the epilepsy syndrome may prove to be an important clue for the diagnosis of the associated genetic syndrome. Moreover, the implicated chromosomal regions may be useful targets when searching for epilepsy genes. We review and discuss available data on some genetic syndromes (Angelman syndrome, duplication of the 15q11-q13 region, Wolf-Hirschorn syndrome, ring chromosome 20, fragile X syndrome) also presenting specific epilepsy features. C1 Ctr Hosp Pays dAix, F-13616 Aix En Provence 1, France. Hop La Timone, Marseille, France. Hop Henri Gastaut, Ctr St Paul, Marseille, France. RP Livet, MO (reprint author), Ctr Hosp Pays dAix, Aile Cezanne,Ave Tamaris, F-13616 Aix En Provence 1, France. 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PD APR PY 2006 VL 8 SU 1 BP S23 EP S32 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA 063JS UT WOS:000239015100003 ER PT J AU Hwang, JW Lee, JB Kim, BN Lee, HY Lee, DS Shin, MS Cho, SC AF Hwang, JW Lee, JB Kim, BN Lee, HY Lee, DS Shin, MS Cho, SC TI Regional cerebral perfusion abnormalities in developmental language disorder SO EUROPEAN ARCHIVES OF PSYCHIATRY AND CLINICAL NEUROSCIENCE LA English DT Article DE developmental language disorder; SPECT; statistical parametric mapping ID PARKINSONS-DISEASE; LEARNING-DISABILITIES; COMPUTED-TOMOGRAPHY; INHERITED SPEECH; BLOOD-FLOW; PET IMAGES; CHILDREN; BRAIN; IMPAIRMENT; AUTISM AB Objective A voxel based investigation of cerebral blood flow was conducted to identify brain functional differences during resting state between children with developmental language disorder ( DLD) and normal controls. Method Using DSM-IV criteria, we selected 21 children with DLD. All children were examined by technetium-99m-HMPAO Brain SPECT. Using SPM analyses, we compared the SPECT images of children with DLD and those of 17 control subjects on a voxel by voxel basis using ANCOVA covarying for age. Results Reduced cerebral blood flow in the right putamen, the right inferior parietal cortex, and the left globus pallidus were found in children with DLD versus the controls. However, no area of increased cerebral blood flow was observed in children with DLD compared to the controls. Conclusion Though results should be interpreted cautiously, this study confirms the presence of functional defects in the basal ganglia and the inferior parietal lobe during the resting state of the brains of children with DLD. It also gives further evidence for functional deficits in basal ganglia as an important factor in the etiology of DLD. C1 Seoul Natl Univ Hosp, Dept Neuropsychiat, Div Child & Adolescent Psychiat, Seoul 110744, South Korea. Seoul Natl Univ Hosp, Dept Nucl Med, Seoul 110744, South Korea. 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The cannabinoid receptor 1 (CNR1) is the best-characterized molecule of the endocannabinoid system, involved in processing rewards. We hypothesized that genetic variation in human CNR1 gene would predict differences in the striatal response to happy faces. In a 3T functional magnetic resonance imaging (fMRI) scanning study on 19 Caucasian volunteers, we report that four single nucleotide polymorphisms (SNPs) in the CNR1 locus modulate differential striatal response to happy but not to disgust faces. This suggests a role for the variations of the CNR1 gene in underlying social reward responsivity. Future studies should aim to replicate this finding with a balanced design in a larger sample, but these preliminary results suggest neural responsivity to emotional and socially rewarding stimuli varies as a function of CNR1 genotype. This has implications for medical conditions involving hypo-responsivity to emotional and social stimuli, such as autism. 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J. Neurosci. PD APR PY 2006 VL 23 IS 7 BP 1944 EP 1948 DI 10.1111/j.1460-9568.2006.04697.x PG 5 WC Neurosciences SC Neurosciences & Neurology GA 028AK UT WOS:000236457500028 PM 16623851 ER PT J AU Wright, JA Polack, C AF Wright, JA Polack, C TI Understanding variation in measles-mumps-rubella immunization coverage-a population-based study SO EUROPEAN JOURNAL OF PUBLIC HEALTH LA English DT Article DE censuses; geographic information systems; immunization; measles ID AUTISTIC SPECTRUM DISORDER; MMR VACCINATION; PARENTS; CHILDREN; BELIEFS; DISEASE; HEALTH AB Background: Coverage of the Measles-Mumps-Rubella combined vaccine ( MMR) has declined in recent years in the UK, following adverse publicity about possible links between the vaccine, autism, and Crohn's disease. The objectives of this study were to assess geographical variation in trends in MMR coverage and to identify the factors affecting MMR uptake at population level. Methods: We conducted an ecological study of immunization coverage by second birthday, based on routinely collected data from 1993 - 2004 for England. Trends in MMR uptake were assessed in 95 District Health Authorities in England over the study period. We investigated the relationship between MMR immunization uptake and deprivation, ethnicity, education, population density, rurality, and socioeconomic class. Results: Since 2000, MMR coverage has declined significantly in virtually all areas of England. Population density and deprivation were both strongly correlated with low MMR uptake. The decline in coverage since 1993 - 94 was significantly related to the proportion of educated population and was greater in densely populated areas. Conclusion: Decline in MMR coverage now affects most areas of England. The lowest rates of MMR coverage remain in urban areas, particularly in inner cities, which also tend to show high levels of deprivation. 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J. Public Health PD APR PY 2006 VL 16 IS 2 BP 137 EP 142 DI 10.1093/eurpub/cki194 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 027SG UT WOS:000236435100009 PM 16207728 ER PT J AU Canitano, R Zappella, M AF Canitano, Roberto Zappella, Michele TI Autistic epileptiform regression SO FUNCTIONAL NEUROLOGY LA English DT Article DE autism; pervasive developmental disorders; regression ID LANDAU-KLEFFNER-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; SEIZURE DISORDERS; CHILDREN; CHILDHOOD; CLASSIFICATION; ABNORMALITIES; EPILEPSY AB Autistic regression is a well known condition that occurs in one third of children with pervasive developmental disorders, who, after normal development in the first year of life, undergo a global regression during the second year that encompasses language, social skills and play. In a portion of these subjects, epileptiform abnormalities are present with or without seizures, resembling, in some respects, other epileptiform regressions of language and behaviour such as Landau-Kleffner syndrome. In these cases, for a more accurate definition of the clinical entity, the term autistic epileptifom regression has been suggested. As in other epileptic syndromes with regression, the relationships between EEG abnormalities, language and behaviour, in autism, are still unclear. We describe two cases of autistic epileptiform regression selected from a larger group of children with autistic spectrum disorders, with the aim of discussing the clinical features of the condition, the therapeutic approach and the outcome. C1 Gen Univ Hosp Siena, Div Child & Adolescent Neuropsychiat, Siena, Italy. RP Canitano, R (reprint author), Viale Bracci 1, I-53100 Siena, Italy. 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Neurol. PD APR-JUN PY 2006 VL 21 IS 2 BP 97 EP 101 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 077XZ UT WOS:000240066400007 PM 16796825 ER PT J AU Torres, AR Sweeten, TL Cutler, A Bedke, BJ Fillmore, M Stubbs, EG Odell, D AF Torres, AR Sweeten, TL Cutler, A Bedke, BJ Fillmore, M Stubbs, EG Odell, D TI The association and linkage of the HLA-A2 class I allele with autism SO HUMAN IMMUNOLOGY LA English DT Article DE autism; HLA; HLA-A2; class I; immune ID MAJOR HISTOCOMPATIBILITY COMPLEX; SYSTEMIC-LUPUS-ERYTHEMATOSUS; CENTRAL-NERVOUS-SYSTEM; SYNAPTIC PLASTICITY; INCREASED FREQUENCY; DISEASE; GENES; SUSCEPTIBILITY; REGION; MHC AB Previous research has revealed associations between autism and immune genes located in the human leukocyte antigen (HLA). To better understand which HLA genetic loci may be associated with autism, we compared the class I HLA-A and -B alleles in autistic probands with case control subjects from Caucasian families. The frequency of HLA-A2 alleles was significantly increased in autistic subjects compared with normal allelic frequencies from the National Marrow Donors Program (NMDP) (p = 0.0043 after allelic correction). The transmission disequilibrium test for the A2 allele revealed an increased frequency of inheritance for autistic children (P = 0.033). There were no significant associations of autism with HLA-B alleles; however, the A2-B44 and A2-B51 haplotypes were two times more frequent in autistic subjects. The association and linkage of the class I HLA-A2 allele with autism suggests its involvement in the etiology of autism. Possible roles are discussed for the HLA-A2 association in the presentation of microbial antigen within the central nervous system and/or in the establishment of synaptic and neuronal circuits in the developing brain. C1 Utah State Univ, Ctr Persons & Disabil, Logan, UT 84322 USA. Utah State Univ, Dept Math & Stat, Logan, UT 84322 USA. Oregon Hlth Sci Univ, Portland, OR 97201 USA. RP Torres, AR (reprint author), Utah State Univ, Ctr Persons & Disabil, 6895 Old Main Hill, Logan, UT 84322 USA. 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Immunol. PD APR-MAY PY 2006 VL 67 IS 4-5 BP 346 EP 351 DI 10.1016/j.humimm.2006.01.001 PG 6 WC Immunology SC Immunology GA 050QE UT WOS:000238102200013 PM 16720216 ER PT J AU Rappley, MD AF Rappley, MD TI Actual psychotropic medication use in preschool children SO INFANTS AND YOUNG CHILDREN LA English DT Article DE clonidine; mental health; methylphenidate; preschool; psychotropic medications; riperidone ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PERVASIVE DEVELOPMENTAL DISORDERS; DISRUPTIVE BEHAVIOR DISORDERS; AUTISTIC DISORDER; YOUNG-CHILDREN; OPEN-LABEL; RISPERIDONE; SYMPTOMS; PSYCHOPATHOLOGY; ADOLESCENTS AB Preschool children who receive psychotropic medications are a special and vulnerable group of children. They have a wide range of mental health and other medical diagnoses. Their families face challenges in parenting as well as social and mental health issues. These children receive a very large spectrum of psychotropic medications. The issue of safe and appropriate use of such medication is of concern within the context of increased diagnosis of mental health conditions, especially attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorders, and the increased use of psychotropic medications for all children and adults. Stimulants, risperidone, and clonidine are the few medications studied in this age group. A national registry or other large-scale organized approach is likely the best method to gather information related to indications and long-term management of psychotropic medications for preschool-aged children. An approach is suggested to allow treatment while specific guidance is formulated at the national C1 Michigan State Univ, Coll Human Med, E Lansing, MI 48824 USA. RP Rappley, MD (reprint author), Michigan State Univ, Coll Human Med, A118 E Fee Hall, E Lansing, MI 48824 USA. 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PD APR-JUN PY 2006 VL 19 IS 2 BP 154 EP 163 PG 10 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 028XC UT WOS:000236521100008 ER PT J AU Hollander, E Soorya, L Wasserman, S Esposito, K Chaplin, W Anagnostou, E AF Hollander, E Soorya, L Wasserman, S Esposito, K Chaplin, W Anagnostou, E TI Divalproex sodium vs. placebo in the treatment of repetitive behaviours in autism spectrum disorder SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Article DE autism; valproate; divalproex; repetitive behaviours ID PRADER-WILLI-SYNDROME; BORDERLINE PERSONALITY-DISORDER; TOPIRAMATE; AGGRESSION; TRIAL AB Autism is a neurodevelopmental disorder characterized by impairment in three core symptom domains: socialization, communication, and repetitive/stereotyped behaviours. Other associated symptom domains are also affected including impulsivity/aggression, self-injury, anxiety, and mood lability. Divalproex has been shown to have efficacy in treating epilepsy, bipolar disorder, mood lability, and impulsive aggression. The present study evaluated the use of divalproex in the treatment of repetitive, compulsive-like symptoms of autism spectrum disorder (ASD). Thirteen individuals with ASD participated in an 8-wk, double-blind, placebo-controlled trial of divalproex sodium vs. placebo. There was a significant group difference on improvement in repetitive behaviours as measured by file Children's Yale-Brown Obsessive Compulsive Scale (C-YBOCS) (p = 0.037) and a large effect size (d = 1.616). This Study provides preliminary Support for the use of divalproex in treating repetitive behaviours in ASD. Further research is needed to evaluate the specificity and mechanism of action of these findings. C1 CUNY Mt Sinai Sch Med, Seaver & NY Autism Ctr Excellence, Dept Psychiat, New York, NY 10029 USA. St Johns Univ, Dept Psychol, New York, NY USA. RP Hollander, E (reprint author), CUNY Mt Sinai Sch Med, Seaver & NY Autism Ctr Excellence, Dept Psychiat, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA. EM eric.hollander@mssm.edu CR Costa Erminio, 2003, Mol Interv, V3, P220, DOI 10.1124/mi.3.4.220 Dimitropoulos A, 2000, MENT RETARD DEV D R, V6, P125, DOI 10.1002/1098-2779(2000)6:2<125::AID-MRDD6>3.0.CO;2-T Goodman WK, 1991, CHILDRENS YALE BROWN Hollander E, 2005, AM J PSYCHIAT, V162, P621, DOI 10.1176/appi.ajp.162.3.621 Hollander E, 2003, NEUROPSYCHOPHARMACOL, V28, P1186, DOI 10.1038/sj.npp.1300153 Hollander E, 2001, J CLIN PSYCHIAT, V62, P530 Hollander E, 1999, J CLIN PSYCHIAT, V60, P38 HOLLANDER E, 2002, AM PSYCHIAT PRESS TX, P579 Johnson BA, 2003, LANCET, V361, P1677, DOI 10.1016/S0140-6736(03)13370-3 McElroy SL, 2004, J CLIN PSYCHIAT, V65, P1463 Pallanti S, 2002, J CLIN PSYCHIAT, V63, P559 Smathers SA, 2003, PEDIATR NEUROL, V28, P130, DOI 10.1016/S0887-8994(02)00490-3 Soderpalm B, 2002, EUR J PAIN-LONDON, V6, P3, DOI 10.1053/eujp.2001.0315 Veltman MWM, 2004, EUR CHILD ADOLES PSY, V13, P42, DOI 10.1007/s00787-004-0354-6 Yang P, 2000, BRAIN RES, V887, P276, DOI 10.1016/S0006-8993(00)02996-6 NR 15 TC 49 Z9 50 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 1461-1457 J9 INT J NEUROPSYCHOPH JI Int. J. Neuropsychopharmacol. PD APR PY 2006 VL 9 IS 2 BP 209 EP 213 DI 10.1017/S1461145705005791 PG 5 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 020KQ UT WOS:000235908300008 PM 16316486 ER PT J AU Fonseca, VRJRM Bussab, BSR AF Fonseca, VRJRM Bussab, BSR TI Self, other and dialogical space in autistic disorders SO INTERNATIONAL JOURNAL OF PSYCHOANALYSIS LA English DT Article DE autism; dialogism; pervasive developmental disorders AB The authors propose to re-evaluate Tustin's thesis using both the extensive clinical material of a child with an autistic disorder [PDD], and current research on infant development. Beebe's concept of 'interaction structure' that could be inferred from the fifth month of life using face-to-face research data is used for postulating a dialogic space that would be generated inside such structure, allowing for definition of self and other in a relationship. If such space is collapsed, the other would be a threat of annihilation for the self thus it should be avoided or merged with, which could explain the systematic avoidance of the not-me in autistic states. The authors stress that these ideas are just one alternate model, among several, that seems to be able to explain the patient deviant development. RP Fonseca, VRJRM (reprint author), Rua Paulo IV 292, BR-05657130 Sao Paulo, Brazil. EM verareg@ajato.com.br; vsbussab@usp.br CR Aitken KJ, 1997, DEV PSYCHOPATHOL, V9, P653 Alvarez A, 1992, LIVE CO PSYCHOANALYT Beebe B., 1997, PSYCHOANALYTIC DIALO, V7, P133 Bion W. R., 1967, 2 THOUGHTS SELECTED BRATEN S, 2003, CULT PSYCHOL, V9, P61 BRITTON R, 1997, CONT KLEINIANS LONDO, P239 Fonseca VRJRM, 1999, INT J PSYCHOANAL, V80, P885, DOI 10.1516/0020757991599133 Freud Sigmund, 1952, STANDARD EDITION, V17, P219 Gergely G, 1996, INT J PSYCHOANAL, V77, P1181 Green A, 1998, INT J PSYCHOANAL, V79, P649 GROTSTEIN J, 1997, ENCOUNTERS AUTISTIC, P257 Haag G, 1997, ENCOUNTERS AUTISTIC, P355 HAAG G, 1990, J PSYCHOANAL ENFANT, V8, P19 HOBSON P, 2002, CRADLE THOUGHT CHALL Holquist Michael, 1990, DIALOGISM BAKHTIN HI Klein M., 1952, DEV PSYCHOANALYSIS, P198 Meltzer D., 1975, EXPLORATIONS AUTISM Meltzer D, 1992, CLAUSTRUM INVESTIGAT MITRANI J, 1997, ENCOUNTERS AUTISTIC, P23 Schore A, 1994, AFFECT REGULATION Shuttleworth J., 1989, CLOSELY OBSERVED INF, P22 Stern D., 1985, INTERPERSONAL WORLD TREVARTHEN C, 1996, HILDREN AUTISM DIAGN, P93 TUSTIN F, 1981, AUTISTIC STTAES CHIL Tustin F, 1972, AUTISM CHILDHOOD PSY TUSTIN F, 1991, INT J PSYCHOANAL, V72, P585 Tustin F, 1990, PROTECTIVE SHELL CHI Winnicott D. W., 1958, COLLECTED PAPERS THR Winnicott D. W., 1971, PLAYING REALITY WINNICOTT DW, 1960, INT J PSYCHOANAL, V41, P585 NR 30 TC 2 Z9 2 PU INST PSYCHO-ANALYSIS PI LONDON PA BYRON HOUSE, 112A-114 SHIRLAND RD, LONDON W9 2EQD, ENGLAND SN 0020-7578 J9 INT J PSYCHOANAL JI Int. J. Psychoanal. PD APR PY 2006 VL 87 BP 439 EP 455 DI 10.1516/6CN4-9C1H-G6PL-HMPK PN 2 PG 17 WC Psychology, Psychoanalysis SC Psychology GA 033SR UT WOS:000236870000010 PM 16581585 ER PT J AU Deruelle, C Rondan, C Gepner, B Fagot, J AF Deruelle, C Rondan, C Gepner, B Fagot, J TI Processing of compound visual stimuli by children with autism and Asperger syndrome SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; FACE RECOGNITION; PERCEPTION; DISCRIMINATION; INDIVIDUALS; INFORMATION; PERFORMANCE; PRECEDENCE; ABILITIES; DISORDER AB A typical modes of visual processing are common in individuals with autism. In particular, and unlike typically developing children, children with autism tend to process the parts of a complex object as a priority, rather than attending to the object as a whole. This bias for local processing is likely to be due to difficulties in assembling subparts into a coherent whole, as proposed by Frith (1989) using the term "weak central coherence'' or WCC. This study was aimed to better characterize the processing of complex visual stimuli by children with autism. Thirteen children with autistic spectrum disorders were individually paired with children of two control groups, one matched on verbal mental age (VMA) and one matched on chronological age (CA). Participants from the three groups were tested in two tasks. The first task involved hierarchical global/local stimuli, inspired by Navon (1977). The second task employed compound face-like or geometrical stimuli. This task emphasized the processing of configural properties of the stimuli (i.e., spatial relationships). Children from the three groups showed a perceptual bias favouring the global dimension of the stimuli in the first task. By contrast, children with autism were deficient compared to normal children for the processing of the configural dimensions of the stimuli in the second task. These results suggest that visual cognition of children with autism is characterized by a dissociation between global and configural processing, with global processing being preserved and configural processing being altered in these children, therefore delineating the extents and limits of the WCC theory (Frith, 1989). C1 CNRS, INCM, F-13402 Marseille 20, France. Montperrin Hosp, Aix En Provence, France. RP Deruelle, C (reprint author), CNRS, INCM, 31Chemin Joseph Aiguier, F-13402 Marseille 20, France. 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J. Psychol. PD APR PY 2006 VL 41 IS 2 BP 97 EP 106 DI 10.1080/00207590500184610 PG 10 WC Psychology, Multidisciplinary SC Psychology GA 045SM UT WOS:000237762500003 ER PT J AU Richardson, AJ AF Richardson, AJ TI Omega-3 fatty acids in ADHD and related neurodevelopmental disorders SO INTERNATIONAL REVIEW OF PSYCHIATRY LA English DT Review ID DEFICIT-HYPERACTIVITY-DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; ESSENTIAL FATTY-ACIDS; PLACEBO-CONTROLLED TRIAL; ALPHA-LINOLENIC ACID; DEVELOPMENTAL COORDINATION DISORDER; PRELIMINARY DOUBLE-BLIND; RANDOMIZED DOUBLE-BLIND; DOCOSAHEXAENOIC ACID; PSYCHIATRIC-DISORDERS AB Omega-3 fatty acids are dietary essentials, and are critical to brain development and function. Increasing evidence suggests that a relative lack of omega-3 may contribute to many psychiatric and neurodevelopmental disorders. This review focuses on the possible role of omega-3 in attention-deficit/hyperactivity disorder ( ADHD) and related childhood developmental disorders, evaluating the existing evidence from both research and clinical perspectives. Theory and experimental evidence support a role for omega-3 in ADHD, dyslexia, developmental coordination disorder ( DCD) and autism. Results from controlled treatment trials are mixed, but the few studies in this area have involved different populations and treatment formulations. Dietary supplementation with fish oils ( providing EPA and DHA) appears to alleviate ADHD-related symptoms in at least some children, and one study of DCD children also found benefits for academic achievement. Larger trials are now needed to confirm these findings, and to establish the specificity and durability of any treatment effects as well as optimal formulations and dosages. Omega-3 is not supported by current evidence as a primary treatment for ADHD or related conditions, but further research in this area is clearly warranted. Given their relative safety and general health benefits, omega-3 fatty acids offer a promising complementary approach to standard treatments. C1 Univ Oxford, Physiol Lab, Dept Physiol Human Anat & Genet, Oxford OX1 3PT, England. RP Richardson, AJ (reprint author), Univ Oxford, Physiol Lab, Dept Physiol Human Anat & Genet, Parks Rd, Oxford OX1 3PT, England. 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Rev. Psych. PD APR PY 2006 VL 18 IS 2 BP 155 EP 172 DI 10.1080/09540260600583031 PG 18 WC Psychiatry SC Psychiatry GA 050HF UT WOS:000238077400009 PM 16777670 ER PT J AU de Bruin, EI Verheij, F Ferdinand, RF AF de Bruin, EI Verheij, F Ferdinand, RF TI WISC-R subtest but no overall VIQ-PIQ difference in Dutch children with PDD-NOS SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article DE pervasive developmental disorders; autism; asperger syndrome; PDD-NOS; intelligence; WISC-R ID COGNITIVE PROFILES; AUTISM; AGE; INTELLIGENCE; DISORDERS; IV AB VIQ-PIQ differences have been studied in children with autism and Asperger syndrome but have not been studied in a separate group of children with PDD-NO, although, PDD-NOS has a much higher prevalence rate than autism and deficits in communication and social interaction are severe. The Wechsler Intelligence Scale for Children-Revised (WISC-R) was administered to 100 children, aged 6-12 years, with PDD-NOS (n = 76), autism (n = 13), and Asperger syndrome (n = 11). PDD-NOS was diagnosed using explicit research criteria. No overall differences between VIQ and PIQ were found in PDD-NOS and autism. Peaks in the subtest scores on Information, Similarities, Picture Arrangement, and Mazes, and troughs in the subtest scores on Comprehension, Digit Span, and Coding were demonstrated in children with PDD-NOS. Their score on the Freedom from Distractibility factor was lower than the scores on the Verbal Comprehension factor and the Perceptual Organization factor. Children with PDD-NOS seemed to have a similar VIQ-PIQ profile as children with autism, and on the subtest level children with PDD-NOS showed some similarities to children with Asperger syndrome or autism. It was not possible to distinguish PDD-NOS from autism or Asperger syndrome by using IQ scores. C1 Sophia Childrens Univ Hosp, Erasmus Med Ctr Rotterdam, Dept Child & Adolescent Psychiat, NL-3015 GJ Rotterdam, Netherlands. RP Ferdinand, RF (reprint author), Sophia Childrens Univ Hosp, Erasmus Med Ctr Rotterdam, Dept Child & Adolescent Psychiat, NL-3015 GJ Rotterdam, Netherlands. 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PD APR PY 2006 VL 34 IS 2 BP 263 EP 271 DI 10.1007/s10802-005-9018-3 PG 9 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 049NC UT WOS:000238022300010 PM 16485174 ER PT J AU Richler, J Luyster, R Risi, S Hsu, WL Dawson, G Bernier, R Dunn, M Hepburn, S Hyman, SL McMahon, WM Goudie-Nice, J Minshew, N Rogers, S Sigman, M Spence, MA Goldberg, WA Tager-Flusberg, H Volkmar, FR Lord, C AF Richler, J Luyster, R Risi, S Hsu, WL Dawson, G Bernier, R Dunn, M Hepburn, S Hyman, SL McMahon, WM Goudie-Nice, J Minshew, N Rogers, S Sigman, M Spence, MA Goldberg, WA Tager-Flusberg, H Volkmar, FR Lord, C TI Is there a 'regressive phenotype' of autism spectrum disorder associated with the measles-mumps-rubella vaccine? A CPEA study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism spectrum disorder; language development; regression; Autism Diagnostic Interview - Revised (ADI-R); measles-mumps-rubella (MMR) vaccine; gastrointestinal disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; INFLAMMATORY-BOWEL-DISEASE; INFANTILE-AUTISM; SPEECH LOSS; NO EVIDENCE; CHILDREN; POPULATION; LANGUAGE; AGE; INDIVIDUALS AB A multi-site study of 351 children with Autism Spectrum Disorders (ASD) and 31 typically developing children used caregiver interviews to describe the children's early acquisition and loss of social-communication milestones. For the majority of children with ASD who had experienced a regression, pre-loss development was clearly atypical. Children who had lost skills also showed slightly poorer outcomes in verbal IQ and social reciprocity, a later mean age of onset of autistic symptoms, and more gastrointestinal symptoms than children with ASD and no regression. There was no evidence that onset of autistic symptoms or of regression was related to measles-mumps-rubella vaccination. The implications of these findings for the existence of a 'regressive phenotype' of ASD are discussed. C1 Univ Michigan, Autism & Commun Disorders Ctr, Ann Arbor, MI 48109 USA. Univ Washington, Seattle, WA 98195 USA. Albert Einstein Coll Med, Bronx, NY 10467 USA. Univ Colorado, Hlth Sci Ctr, Aurora, CO USA. Univ Rochester, Rochester, NY USA. Univ Utah, Salt Lake City, UT USA. Univ Pittsburgh, Pittsburgh, PA USA. Univ Calif Davis, Davis, CA 95616 USA. Univ Calif Los Angeles, Los Angeles, CA USA. Univ Calif Irvine, Irvine, CA USA. Boston Univ, Boston, MA 02215 USA. Yale Univ, New Haven, CT USA. RP Lord, C (reprint author), Univ Michigan, Autism & Commun Disorders Ctr, 1111 E Catherine St, Ann Arbor, MI 48109 USA. 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Autism Dev. Disord. PD APR PY 2006 VL 36 IS 3 BP 299 EP 316 DI 10.1007/s10803-005-0070-1 PG 18 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400002 PM 16729252 ER PT J AU Molloy, CA Morrow, AL Meinzen-Derr, J Dawson, G Bernier, R Dunn, M Hyman, SL McMahon, WM Goudie-Nice, J Hepburn, S Minshew, N Rogers, S Sigman, M Spence, MA Tager-Flusberg, H Volkmar, FR Lord, C AF Molloy, CA Morrow, AL Meinzen-Derr, J Dawson, G Bernier, R Dunn, M Hyman, SL McMahon, WM Goudie-Nice, J Hepburn, S Minshew, N Rogers, S Sigman, M Spence, MA Tager-Flusberg, H Volkmar, FR Lord, C TI Familial autoimmune thyroid disease as a risk factor for regression in children with autism spectrum disorder: A CPEA study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; ASD; family history; autoimmune; regression ID PERVASIVE DEVELOPMENTAL DISORDERS; RHEUMATOID-ARTHRITIS; INCREASED PREVALENCE; CYTOKINE PRODUCTION; INFANTILE-AUTISM; IMMUNE-SYSTEM; LANGUAGE; AUTOANTIBODIES; COMMUNICATION; PHENOTYPES AB A multicenter study of 308 children with Autism Spectrum Disorder (ASD) was conducted through the Collaborative Programs of Excellence in Autism (CPEA), sponsored by the National Institute of Child Health and Human Development, to compare the family history of autoimmune disorders in children with ASD with and without a history of regression. A history of regression was determined from the results of the Autism Diagnostic Interview-Revised (ADI-R). Family history of autoimmune disorders was obtained by telephone interview. Regression was significantly associated with a family history of autoimmune disorders (adjusted OR=1.89; 95% CI: 1.17, 3.10). The only specific autoimmune disorder found to be associated with regression was autoimmune thyroid disease (adjusted OR=2.09; 95% CI: 1.28, 3.41). C1 Univ Cincinnati, Coll Med, Ctr Biostat & Epidemiol, Cincinnati Childrens Hosp Med Ctr, Cincinnati, OH 45229 USA. Univ Washington, Seattle, WA 98195 USA. Yeshiva Univ, Albert Einstein Coll Med, Bronx, NY USA. Univ Rochester, Sch Med & Dent, Rochester, NY USA. Univ Utah, Sch Med, Salt Lake City, UT USA. Univ Colorado, Hlth Sci Ctr, Denver, CO USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA USA. Univ Calif Davis, Davis, CA 95616 USA. Univ Calif Los Angeles, Los Angeles, CA USA. Univ Calif Irvine, Irvine, CA USA. Boston Univ, Boston, MA 02215 USA. Yale Univ, New Haven, CT USA. Univ Michigan, Ann Arbor, MI 48109 USA. RP Molloy, CA (reprint author), Univ Cincinnati, Coll Med, Ctr Biostat & Epidemiol, Cincinnati Childrens Hosp Med Ctr, 3333 Burnet Ave,MLC 4051, Cincinnati, OH 45229 USA. 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Autism Dev. Disord. PD APR PY 2006 VL 36 IS 3 BP 317 EP 324 DI 10.1007/s10803-005-0071-0 PG 8 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400003 PM 16598435 ER PT J AU Baron-Cohen, S Hoekstra, RA Knickmeyer, R Wheelwright, S AF Baron-Cohen, S Hoekstra, RA Knickmeyer, R Wheelwright, S TI The autism-spectrum quotient (AQ)-adolescent version SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE AQ; adolescents; screening; autistic spectrum; Asperger Syndrome ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; SCHOOL-AGE-CHILDREN; ASPERGER-SYNDROME; ADULTS; QUESTIONNAIRE; CHILDHOOD; VALIDITY; AQ AB The Autism Spectrum Quotient (AQ) quantifies autistic traits in adults. This paper adapted the AQ for children (age 9.8-15.4 years). Three groups of participants were assessed: Group 1: n=52 adolescents with Asperger Syndrome (AS) or high-functioning autism (HFA); Group 2: n=79 adolescents with classic autism; and Group 3, n=50 controls. The adolescents with AS/HFA did not differ significantly from the adolescents with autism but both clinical groups scored higher than controls. Approximately 90% of the adolescents with AS/HFA and autism scored 30+, vs. none of the controls. Among the controls, boys scored higher than girls. The AQ can rapidly quantify where an adolescent is situated on the continuum from autism to normality. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. EM sb205@cam.ac.uk RI Hoekstra, Rosa/G-2410-2011; Knickmeyer, Rebecca/G-8128-2014 OI Knickmeyer, Rebecca/0000-0001-7708-1388 CR American Psychiatric Association [APA], 1994, DSM 4 DIAGN STAT MAN Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Attwood T, 1997, ASPERGERS SYNDROME Baron-Cohen S, 1997, ADV INFANCY RES, V11, P193 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S, 2003, J AUTISM DEV DISORD, V33, P509, DOI 10.1023/A:1025879411971 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 Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206 Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Scott FJ, 2002, AUTISM, V6, P9, DOI 10.1177/1362361302006001003 Wakabayashi A, 2004, JAPANESE J PSYCHOL, V75, P78 WECHSLER D, 1958, SEX DIFFERENCES INTE WING L, 1981, PSYCHOL MED, V11, P115 Woodbury-Smith MR, 2005, J AUTISM DEV DISORD, V35, P331, DOI 10.1007/s10803-005-3300-7 NR 16 TC 100 Z9 102 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 APR PY 2006 VL 36 IS 3 BP 343 EP 350 DI 10.1007/s10803-006-0073-6 PG 8 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400005 PM 16552625 ER PT J AU Verte, S Geurts, HM Roeyers, H Oosterlaan, J Sergeant, JA AF Verte, S Geurts, HM Roeyers, H Oosterlaan, J Sergeant, JA TI Executive functioning in children with an autism spectrum disorder: Can we differentiate within the spectrum? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE high-functioning autism; Asperger's syndrome; pervasive developmental disorder not otherwise specified (PDD-NOS); executive functioning ID PERVASIVE DEVELOPMENTAL DISORDER; DEFICIT HYPERACTIVITY DISORDER; CARD-SORTING-TEST; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; TEMPORAL-LOBE LESIONS; ASPERGER-SYNDROME; FRONTAL-LOBE; DSM-IV; COMMUNICATION CHECKLIST; DIAGNOSTIC INTERVIEW AB The aim of this study was to investigate whether children with high-functioning autism (HFA), Asperger's syndrome (AS), and pervasive developmental disorder not otherwise specified (PDDNOS) can be differentiated from each other and from normal controls on their neurocognitive executive functioning (EF) profile. Children with HFA and AS showed the most EF deficits. The EF profile of the PDDNOS group was more disturbed that the normal control group, but was less disturbed than the profile of the HFA and AS groups. 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PD APR PY 2006 VL 36 IS 3 BP 351 EP 372 DI 10.1007/s10803-006-0074-5 PG 22 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400006 PM 16575542 ER PT J AU Koyama, T Tachimori, H Osada, H Kurita, H AF Koyama, T Tachimori, H Osada, H Kurita, H TI Cognitive and symptom profiles in high-functioning pervasive developmental disorder not otherwise specified and attention-deficit/hyperactivity disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE attention-deficit; hyperactivity disorder (ADHD); autism; high-functioning; pervasive developmental disorder not otherwise specified (PDDNOS); Wechsler Intelligence Scale for Children Third Edition (WISC-III) ID AUTISM RATING-SCALE; DEFICIT-HYPERACTIVITY DISORDER; ASPERGER-SYNDROME; CHILDHOOD AUTISM; TOKYO VERSION; WISC-III; PDD-NOS; CHILDREN; ADHD; COMORBIDITY AB Age- and IQ-balanced 27 children with high-functioning (IQ >= 70) pervasive developmental disorder not otherwise specified (HPDDNOS) and 27 children with attention-deficit/hyperactivity disorder (ADHD) were compared on the Japanese version of Wechsler Intelligence Scale for Children Third Edition (WISC-III) and the Childhood Autism Rating Scale-Tokyo Version (CARS-TV). Compared with the ADHD children, the HPDDNOS children scored significantly lower on verbal comprehension, vocabulary, and comprehension, but significantly higher on block design. After controlling for the total CARS-TV score, the HPDDNOS children were significantly more abnormal on "relationships with people," "nonverbal communication," and "general impressions," but less abnormal on "near receptor responsiveness" and "activity level." These differences in cognitive and autistic symptom profiles may help professionals to distinguish clinically between both conditions. C1 NIMH, Dept Mental Hlth Adm, Natl Ctr Neurol & Psychiat, Kodaira, Tokyo 1878553, Japan. Univ Tokyo, Dept Mental Hlth, Grad Sch Med, Tokyo, Japan. Univ Tokyo, Fac Law, Tokyo 113, Japan. RP Koyama, T (reprint author), NIMH, Dept Mental Hlth Adm, Natl Ctr Neurol & Psychiat, 4-1-1 Ogawa Higashi, Kodaira, Tokyo 1878553, Japan. 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Autism Dev. Disord. PD APR PY 2006 VL 36 IS 3 BP 373 EP 380 DI 10.1007/s10803-006-0075-4 PG 8 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400007 PM 16568358 ER PT J AU Sasson, NJ AF Sasson, NJ TI The development of face processing in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE face processing; autism; development ID SPECTRUM DISORDER; OBJECT RECOGNITION; SOCIAL INFORMATION; YOUNG-CHILDREN; MOTHERS FACE; PERCEPTION; INFANTS; FUSIFORM; AREA; STIMULI AB Both behavioral and neuroimaging evidence indicate that individuals with autism demonstrate marked abnormalities in the processing of faces. These abnormalities are often explained as either the result of an innate impairment to specialized neural systems or as a secondary consequence of reduced levels of social interest. A review of the developmental literature on typical and atypical face processing supports a synthesis of these two hypotheses by demonstrating that face processing is an emergent and developmental skill that is heavily mediated by early experience with faces. Individuals with autism may possess central nervous system irregularities that fail to attribute special status to faces, thereby limiting the visual input required for the development of neural regions specialized for face processing. C1 Univ N Carolina, Dept Psychol, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. RP Sasson, NJ (reprint author), Univ N Carolina, Dept Psychol, Neurodev Disorders Res Ctr, CB 3270, Chapel Hill, NC 27599 USA. 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Autism Dev. Disord. PD APR PY 2006 VL 36 IS 3 BP 381 EP 394 DI 10.1007/s10803-006-0076-3 PG 14 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400008 PM 16572261 ER PT J AU Ben Shalom, D Mostofsky, SH Hazlett, RL Goldberg, MC Landa, RJ Faran, Y McLeod, DR Hoehn-Saric, R AF Ben Shalom, D Mostofsky, SH Hazlett, RL Goldberg, MC Landa, RJ Faran, Y McLeod, DR Hoehn-Saric, R TI Normal physiological emotions but differences in expression of conscious feelings in children with high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE amygdala; conscious feelings; physiological emotions; prefrontal cortex ID DIAGNOSTIC-INTERVIEW; INDIVIDUALS; DEFICITS AB To provide insight into what aspects of the emotional circuit might be affected in high-functioning autism, we measured indices of physiological emotions and of the expression of conscious feelings in 10 children with high-functioning autism or Asperger syndrome and 10 comparison participants. Pleasant, unpleasant, and neutral pictures were presented while skin conductance responses were measured. Self-report ratings of pleasantness and interestingness were taken between pictures. Skin conductance responses did not differ between the groups. Self report ratings were different, with the children with autism giving more similar answers to the two questions than the comparison children. Impairments in socio-emotional expression in autism may be related to deficits in perception and/or expression of conscious feelings; physiological emotions may be relatively preserved. C1 Ben Gurion Univ Negev, Dept Foreign Literatures & Linguist, Zlotowski Ctr Neurosci, IL-84105 Beer Sheva, Israel. Kennedy Krieger Inst, Dept Dev Cognit Neurol, Baltimore, MD USA. Johns Hopkins Sch Med, Dept Neurol, Baltimore, MD USA. Johns Hopkins Sch Med, Dept Psychiat, Baltimore, MD USA. Kennedy Krieger Inst, Ctr Autism & Related Disorders, Baltimore, MD USA. RP Ben Shalom, D (reprint author), Ben Gurion Univ Negev, Dept Foreign Literatures & Linguist, Zlotowski Ctr Neurosci, POB 653, IL-84105 Beer Sheva, Israel. 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Autism Dev. Disord. PD APR PY 2006 VL 36 IS 3 BP 395 EP 400 DI 10.1007/s10803-006-0077-2 PG 6 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400009 PM 16565884 ER PT J AU Hellings, JA Zarcone, JR Reese, RM Valdovinos, MG Marquis, JG Fleming, KK Schroeder, SR AF Hellings, JA Zarcone, JR Reese, RM Valdovinos, MG Marquis, JG Fleming, KK Schroeder, SR TI A crossover study of risperidone in children, adolescents and adults with mental retardation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE risperidone; mental retardation; aggression; weight gain ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISTIC DISORDER; DOUBLE-BLIND; SEROTONIN TRANSPORTER; BEHAVIORAL SYMPTOMS; ABERRANT BEHAVIOR; PLACEBO; HALOPERIDOL; SCALE AB Risperidone has shown safety and efficacy for aggressive and destructive behaviors in short-term studies. This longer-duration study includes a broad sample. Forty subjects, aged 8-56 years (mean=22), all with mental retardation and 36 with autism spectrum disorders participated in this 22-week crossover study, with 24 weeks of open maintenance thereafter. Of 40 subjects, 23 (57.5%) responded fully (50% decrease in Aberrant Behavior Checklist-Community Irritability subscale score), while 35 subjects (87.5%) showed a 25% decrease. Gender, mood disorder, and antiseizure medications did not alter response. Increased appetite and weight gain were common. Low dose risperidone was effective for aggressive behavior in persons with MR. More long-term studies are needed, incorporating weight control interventions. C1 Univ Kansas, Med Ctr, Dept Psychiat, Kansas City, KS 66103 USA. Vanderbilt Univ, Nashville, TN USA. Univ Kansas, Lawrence, KS 66045 USA. RP Hellings, JA (reprint author), Univ Kansas, Med Ctr, Dept Psychiat, Kansas City, KS 66103 USA. 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PD APR PY 2006 VL 36 IS 3 BP 401 EP 411 DI 10.1007/s10803-006-0078-1 PG 11 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400010 PM 16596465 ER PT J AU Elder, JH Shankar, M Shuster, J Theriaque, D Burns, S Sherrill, L AF Elder, JH Shankar, M Shuster, J Theriaque, D Burns, S Sherrill, L TI The gluten-free, casein-free diet in autism: Results of a preliminary double blind clinical trial SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; diet; gluten; casein; GFCF diet ID CHILDREN; BEHAVIOR AB This study tested the efficacy of a gluten-free and casein-free (GFCF) diet in treating autism using a randomized, double blind repeated measures crossover design. The sample included 15 children aged 2-16 years with autism spectrum disorder. Data on autistic symptoms and urinary peptide levels were collected in the subjects' homes over the 12 weeks that they were on the diet. Group data indicated no statistically significant findings even though several parents reported improvement in their children. Although preliminary, this study demonstrates how a controlled clinical trial of the GFCF diet can be conducted, and suggests directions for future research. C1 Univ Florida, Coll Nursing, Gainesville, FL 32610 USA. Univ Florida, Gen Clin Res Ctr, Gainesville, FL 32610 USA. RP Elder, JH (reprint author), Univ Florida, Coll Nursing, HPNP Bldg,Box 100187, Gainesville, FL 32610 USA. EM elderjh@nursing.ufl.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Arnold GL, 2003, J AUTISM DEV DISORD, V33, P449, DOI 10.1023/A:1025071014191 BZOCH K, 1970, RECEPTIVE EXPRESIVE CADE R, 1999, NUTR NEUROSCI, V3, P57 CARR EG, 1985, COMMUNICATIVE PROBLE DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x DOHAN FC, 1966, ACTA PSYCHIAT SCAND, V42, P125, DOI 10.1111/j.1600-0447.1966.tb01920.x Elder J., 1996, ISSUES COMPREHENSIVE, V19, P246 Elder Jennifer H, 2003, Issues Ment Health Nurs, V24, P273, DOI 10.1080/01612840305276 Elder J H, 1995, Sch Inq Nurs Pract, V9, P71 Feingold BF., 1975, WHY YOUR CHILD HYPER Fombonne E., 2003, JAMA-J AM MED ASSOC, V289, P1 HAGMAN B, 1990, GLUTEN FREE GOURMET Hastings RP, 2002, AM J MENT RETARD, V107, P222, DOI 10.1352/0895-8017(2002)107<0222:BPOCWA>2.0.CO;2 HOOVER DW, 1994, J ABNORM CHILD PSYCH, V22, P501, DOI 10.1007/BF02168088 Kanner L, 1943, NERV CHILD, V2, P217 KIDDER B, 1988, MILK FREE KITCHEN LI Knivsberg AM, 2002, NUTR NEUROSCI, V5, P251, DOI 10.1080/10281450290028945 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MCDONALD JD, 1989, ECO SCALES MANUAL PRINZ RJ, 1980, J CONSULT CLIN PSYCH, V48, P760, DOI 10.1037//0022-006X.48.6.760 Rutter M., 1978, AUTISM REAPPRAISAL C SCHAKEL SF, 1988, J AM DIET ASSOC, V88, P1268 SCHOPLER E, 1986, CHIDHOOD AUTISM RATI SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Shannon WR, 1922, AM J DIS CHILD, V24, P89 Sun Z, 1999, AUTISM, V3, P67, DOI 10.1177/1362361399003001006 Sun Z., 1999, AUTISM, V3, P85, DOI 10.1177/1362361399003001007 TAPP J, 1996, MOOSES LODGE Vojdani A, 2003, INT J IMMUNOPATH PH, V16, P189 WOLRAICH ML, 1986, J AM DIET ASSOC, V86, P500 Wolraich ML, 1996, CONT PEDIAT, V13, P29 NR 32 TC 84 Z9 85 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 APR PY 2006 VL 36 IS 3 BP 413 EP 420 DI 10.1007/s10803-006-0079-0 PG 8 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400011 PM 16555138 ER PT J AU Lee, R Sturmey, P AF Lee, R Sturmey, P TI The effects of lag schedules and preferred materials on variable responding in students with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE behavioral variability; lag reinforcement schedules; stimulus preference; language training ID VARIABILITY; INDIVIDUALS AB Effects of a Lag 1 reinforcement schedule on appropriate and varied responding to the social question, "What do you like to do?" and effects of the proportion of preferred stimuli present during training on the amount of varied responding in each session were investigated with students with autism. An ABAB reversal design and a multielement design were used to evaluate the effects of the Lag schedule and proportion of preferred stimuli, respectively. Results showed that a Lag 1 schedule was effective at increasing varied vocal responding for 2 of 3 participants. The proportion of stimuli that were preferred did not affect the amount of varied responding emitted. C1 CUNY Queens Coll, New York, NY USA. CUNY, Grad Sch, New York, NY USA. CUNY, Univ Ctr, New York, NY 10021 USA. RP Lee, R (reprint author), QSAC Day Sch, 12-10 150th St, Whitestone, NY 11357 USA. EM norpsy@ix.netcom.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th DeLeon IG, 1996, J APPL BEHAV ANAL, V29, P519, DOI 10.1901/jaba.1996.29-519 DUKER PC, 1991, J APPL BEHAV ANAL, V24, P379, DOI 10.1901/jaba.1991.24-379 GOETZ EM, 1973, J APPL BEHAV ANAL, V6, P209, DOI 10.1901/jaba.1973.6-209 JONES RSP, 1990, J MENT DEFIC RES, V34, P261 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 LALLI JS, 1994, J APPL BEHAV ANAL, V33, P151 Lee R, 2002, J APPL BEHAV ANAL, V35, P391, DOI 10.1901/jaba.2002.35-391 Miller N, 2000, J APPL BEHAV ANAL, V33, P151, DOI 10.1901/jaba.2000.33-151 PAGE S, 1985, J EXP PSYCHOL ANIM B, V11, P429, DOI 10.1037//0097-7403.11.3.429 SCHWARTZ B, 1982, J EXP PSYCHOL GEN, V111, P23, DOI 10.1037//0096-3445.111.1.23 NR 11 TC 12 Z9 12 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 APR PY 2006 VL 36 IS 3 BP 421 EP 428 DI 10.1007/s10803-006-0080-7 PG 8 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400012 PM 16568357 ER PT J AU Gillberg, C Cederlund, M Lamberg, K Zeijlon, L AF Gillberg, C Cederlund, M Lamberg, K Zeijlon, L TI Brief report: "The autism epidemic". The registered prevalence of autism in a swedish urban area SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; autism spectrum disorder; prevalence. Autism; Asperger syndrome; autism spectrum disorder; prevalence ID ASPERGER-SYNDROME; DIAGNOSTIC INTERVIEW; CHILDHOOD AUTISM; CHANGING PREVALENCE; RATING-SCALE; DISORDER AB The objective of this study was to establish rates of diagnosed autism spectrum disorders (ASDs) in a circumscribed geographical region. The total population born in 1977-1994, living in Goteborg Sweden in 2001, was screened for ASD in registers of the Child Neuropsychiatry Clinic. The minimum registered rate of autistic disorder was 20.5 in 10,000. Other ASDs were 32.9 in 10,000, including 9.2 in 10,000 with Asperger syndrome. Males predominated. In the youngest group (7-12 years), 1.23% had a registered diagnosis of ASD. There was an increase in the rate of diagnosed registered ASD over time; the cause was not determined. The increase tended to level off in the younger age cohort, perhaps due to Asperger syndrome cases missed in screening. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, S-41119 Gothenburg, Sweden. Nordhem Sch, Gothenburg, Sweden. St Georges Hosp Med Sch, Dept Child & Adolescent Psychiat, London, England. RP Gillberg, C (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Kungsgatan 12, S-41119 Gothenburg, Sweden. EM christopher.gillberg@pediat.gu.se CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association (APA), 1980, DIAGN STAT MAN MENT APA, 1987, DIAGN STAT MAN MENT Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Cederlund M, 2004, DEV MED CHILD NEUROL, V46, P652 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Frith U, 2004, J CHILD PSYCHOL PSYC, V45, P672, DOI 10.1111/j.1469-7610.2004.00262.x GILLBERG C, 1983, J CHILD PSYCHOL PSYC, V24, P377, DOI 10.1111/j.1469-7610.1983.tb00116.x Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 GILLBERG C, 1984, J CHILD PSYCHOL PSYC, V25, P35, DOI 10.1111/j.1469-7610.1984.tb01717.x GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Kanner L, 1943, NERV CHILD, V2, P217 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Leekam SR, 2002, J CHILD PSYCHOL PSYC, V43, P327, DOI 10.1111/1469-7610.00024 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 Nordin V, 1998, J AUTISM DEV DISORD, V28, P69, DOI 10.1023/A:1026067104198 Rutter M., 1994, CHILD ADOL PSYCH CL, P569 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 STEFFENBURG S, 1986, BRIT J PSYCHIAT, V149, P81, DOI 10.1192/bjp.149.1.81 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Webb EVJ, 1997, DEV MED CHILD NEUROL, V39, P150 Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 Wing L, 1996, AUTISM SPECTRUM WING L, 1981, PSYCHOL MED, V11, P115 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 33 TC 83 Z9 86 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 APR PY 2006 VL 36 IS 3 BP 429 EP 435 DI 10.1007/s10803-006-0081-6 PG 7 WC Psychology, Developmental SC Psychology GA 047EA UT WOS:000237861400013 PM 16568356 ER PT J AU Baron-Cohen, S Scott, F Wheelwright, S Johnson, M Bisarya, D Desai, A Ahluwalia, J AF Baron-Cohen, S Scott, F Wheelwright, S Johnson, M Bisarya, D Desai, A Ahluwalia, J TI Can Asperger syndrome be diagnosed at 26 months old? A genetic high-risk single-case study SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; NORMAL ADULTS; SPECTRUM QUOTIENT; REVISED VERSION; CHILDREN; BRAIN; MIND; CAREGIVERS; DISORDERS; PHENOTYPE AB Asperger syndrome, a heritable condition entailing empathy deficits together with unusually narrow interests in individuals of normal or even above-average intelligence, was recognized only recently. Here we report the first-ever prospective study of a child born to two adults with a formal diagnosis of Asperger syndrome. The child's parents are both scientists (a mathematician and a chemist). The aim of study 1 was to test if the child also developed Asperger syndrome, given the heritability of the condition, and if Asperger syndrome can be detected at 26 months. At 18 months, the child was given the Checklist for Autism in Toddlers, and at 26 months, she was assessed diagnostically for autism spectrum conditions using the Autism Diagnostic Interview-Revised and the Autism Diagnostic Observational Scale. The child failed the Checklist for Autism in Toddlers at 18 months and met the criteria for Asperger syndrome at 26 months. This single case is consistent with the hypersystemizing, assortative mating theory of autism. This theory requires further testing with large samples. This study also demonstrates that Asperger syndrome can be diagnosed by age 26 months. The aim of study 2 was to test if dyadic eye contact in infancy is intact in a child later diagnosed with Asperger syndrome. The same child's eye contact was measured at three time points (3, 6, and 9 months) over her first year of life and compared with that of age-matched controls. Although the child had low rates of eye contact at 6 months, it was within the normal range at all three points in the first year of life. We conclude that low levels of eye contact are not predictive of later development of Asperger syndrome. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. Univ London, Birkbeck Coll, Neurocognit Dev Unit, London, England. Rosie Hosp, Dept Neonatol, Cambridge, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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Child Neurol. PD APR PY 2006 VL 21 IS 4 BP 351 EP 356 DI 10.2310/7010.2006.00072 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 049GA UT WOS:000238002800019 PM 16900937 ER PT J AU Christison, GW Ivany, K AF Christison, GW Ivany, K TI Elimination diets in autism spectrum disorders: Any wheat amidst the chaff? SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism spectrum disorder; elimination diets; complementary; alternative medicine ID PLASMA BETA-ENDORPHIN; INTENSIVE BEHAVIORAL TREATMENT; PLACEBO-CONTROLLED CROSSOVER; DOUBLE-BLIND; INFANTILE-AUTISM; ALTERNATIVE MEDICINE; OPIATE ANTAGONISTS; REGRESSIVE AUTISM; CONTROLLED TRIAL; FOOD COLORINGS AB The use of complementary or alternative treatment approaches in children with autism spectrum disorders (ASDs) is increasing, and the most popular of such approaches are diets that eliminate either gluten or casein, or both. The popularity of these diets indicates a need for more rigorous research into their efficacy. Owing to significant methodological flaws, the currently available data are inadequate to guide treatment recommendations. The purpose of this review is to examine the available trials of gluten/casein diets in children with ASDs regarding the strength of their findings and also concerning points that may be useful in the design of future studies. Seven trials of these diets in ASD are critically reviewed; 6 of these were uncontrolled trials and 1 used a single-blind design. All reported efficacy in reducing some autism symptoms, and 2 groups of investigators also reported improvement in nonverbal cognition. Design flaws in all of the studies weaken the confidence that can be placed in their findings. Careful double-blind, placebo-controlled studies are needed to evaluate whether actual benefit undergirds the diets' popularity and to provide better guidance to clinicians and caregivers. The literature currently available suggests that diets eliminating both gluten and casein (rather than either alone) should be studied first and that outcome measures should include assessments of nonverbal cognition. C1 Loma Linda Univ, Sch Med, Dept Psychiat, Loma Linda, CA 92354 USA. Emory Univ, Sch Med, Dept Psychiat, Atlanta, GA USA. RP Christison, GW (reprint author), Loma Linda Univ, Sch Med, Dept Psychiat, 11374 Mt View Ave, Loma Linda, CA 92354 USA. 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H., 2000, Journal of Nutritional and Environmental Medicine (Abingdon), V10, P25, DOI 10.1080/13590840050000861 WEIZMAN R, 1984, PSYCHOPHARMACOLOGIA, V82, P363 WEIZMAN R, 1988, J AM ACAD CHILD PSY, V27, P430, DOI 10.1097/00004583-198807000-00009 Whiteley P, 1999, AUTISM, V3, P45, DOI 10.1177/1362361399003001005 Whiteley P, 2002, EXPERT OPINION THERA, V6, P175, DOI 10.1517/14728222.6.2.17512223079 WillemsenSwinkels SHN, 1996, BIOL PSYCHIAT, V39, P1023, DOI 10.1016/0006-3223(95)00297-9 WILLEMSENSWINKELS SHN, 1995, PSYCHIAT RES, V58, P203, DOI 10.1016/0165-1781(95)02749-M Williams PG, 2001, J AUTISM DEV DISORD, V31, P103, DOI 10.1023/A:1005674016014 WILSON N, 1989, CLIN EXP ALLERGY, V19, P267, DOI 10.1111/j.1365-2222.1989.tb02382.x NR 75 TC 25 Z9 26 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S162 EP S171 DI 10.1097/00004703-200604002-00015 PG 10 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300015 PM 16685183 ER PT J AU Cohen, H Amerine-Dickens, M Smith, T AF Cohen, H Amerine-Dickens, M Smith, T TI Early intensive behavioral treatment: Replication of the UCLA model in a community setting SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article; Proceedings Paper CT 4th International Meeting for Autism Research CY MAY 06, 2005 CL Boston, MA DE autism; early intervention; applied behavior analysis; behavioral treatment ID PERVASIVE DEVELOPMENTAL DISORDER; FOLLOW-UP; EARLY INTERVENTION; YOUNG-CHILDREN; AUTISM; PREDICTORS; TRIAL AB Although previous studies have shown favorable results with early intensive behavioral treatment (EIBT) for children with autism, it remains important to replicate these findings, particularly in community settings. The authors conducted a 3-year prospective outcome study that compared 2 groups: (1) 21 children who received 35 to 40 hours per week of EIBT from a community agency that replicated Lovaas' model of EIBT and (2) 21 age- and IQ-matched children in special education classes at local public schools. A quasi-experimental design was used, with assignment to groups based on parental preference. Assessments were conducted by independent examiners for IQ (Bayley Scales of Infant Development or Wechsler Preschool and Primary Scales of Intelligence), language (Reynell Developmental Language Scales), nonverbal skill (Merrill-Palmer Scale of Mental Tests), and adaptive behavior (Vineland Adaptive Behavior Scales). Analyses of covariance, with baseline scores as covariates and Year 1-3 assessments as repeated measures, revealed that, with treatment, the EIBT group obtained significantly higher IQ (F = 5.21, p =.03) and adaptive behavior scores (F = 7.84, p =.01) than did the comparison group. No difference between groups was found in either language comprehension (F = 3.82, p =.06) or nonverbal skill. Six of the 21 EIBT children were fully included into regular education without assistance at Year 3, and 11 others were included with support; in contrast, only 1 comparison child was placed primarily in regular education. Although the study was limited by the nonrandom assignment to groups, it does provide evidence that EIBT can be successfully implemented in a community setting. C1 Valley Mt Reg Ctr, Stockton, CA USA. Cent Valley Autism Project, Modesto, CA USA. Univ Rochester, Med Ctr, Dept Pediat, Rochester, NY 14642 USA. RP Amerine-Dickens, M (reprint author), Mila Amerine Dickens, 1317 Oakdale Rd,Suite 800, Modesto, CA 95355 USA. EM mamerine-dickens@cvap.org CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Anderson S. 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I., 2003, TEACHING INDIVIDUALS MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 MORTENSON S, 1996, ANN M ASS BEH AN MAY Nich C, 1997, J CONSULT CLIN PSYCH, V65, P252, DOI 10.1037/0022-006X.65.2.252 Reynell J., 1990, REYNELL DEV LANGUAGE Robinson BF, 1996, AM J MENT RETARD, V100, P666 Sallows GO, 2005, AM J MENT RETARD, V110, P417, DOI 10.1352/0895-8017(2005)110[417:IBTFCW]2.0.CO;2 SCHOPLER E, 1989, J CONSULT CLIN PSYCH, V57, P162 Smith ER, 2000, CAN J CARDIOL, V16, P86 Smith T, 2000, AM J MENT RETARD, V105, P269, DOI 10.1352/0895-8017(2000)105<0269:RTOIEI>2.0.CO;2 Smith T, 2000, RES DEV DISABIL, V21, P297, DOI 10.1016/S0891-4222(00)00043-3 Sparrow S, 1984, VINELAND ADAPTIVE BE Steerneman P, 2003, TOM TEST STUTSMAN R, 1948, GUIDE ADMINISTERING TAYLOR BA, 2001, MAKING DIFFERENCE BE, P97 Wechsler D., 1991, MANUAL WECHSLER INTE WEISS MJ, 2001, TEACHING SOCIAL SKIL Weiss MJ, 1999, BEHAV INTERVENT, V14, P3, DOI 10.1002/(SICI)1099-078X(199901/03)14:1<3::AID-BIN25>3.0.CO;2-F Zwaigenbaum L, 2005, INT J DEV NEUROSCI, V23, P143, DOI 10.1016/j.ijdevneu.2004.05.001 2004, REGION 6 AUTISM CONN NR 37 TC 68 Z9 72 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S145 EP S155 DI 10.1097/00004703-200604002-00013 PG 11 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300013 PM 16685181 ER PT J AU Dosreis, S Weiner, CL AF Dosreis, S Weiner, CL TI Autism spectrum disorder screening and management practices among general pediatric providers SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism spectrum disorder; screening; pediatric ASD screening; epidemiologic survey ID PERVASIVE DEVELOPMENTAL DISORDERS; PREVALENCE; DIAGNOSIS; CHILDREN; TRENDS; STATES AB It is unclear to what extent general developmental/behavioral assessments are screening for autism spectrum disorders (ASDs) is being conducted, and what the barriers to providing assessments are in routine pediatric practice. Therefore, this study examines (1) the factors influencing the of general developmental and autism-specific screening tools in primary care pediatric practice, (2) the to providing these assessments, and (3) pediatricians' beliefs regarding ASD prevalence. A survey was mailed in June 2004 to a 60% (n = 1119) random sample of Maryland and Delaware pediatricians. In August 2004, a second mailing was sent to nonrespondents. A total of 471 (42%) of the were returned, and of those, 255 (54%) who practiced in general primary care were eligible. The sample was male, 69% had more than 14 years' experience, 71 % were in private practices, and 56% had fewer than 10 patients. Most (82%) routinely screened for general developmental delays, but only 8% screened for ASID. main reasons reported for not screening for ASD were lack of familiarity with tools (62%), referred to a (47%), or not enough time (32%). Most specialist referrals (77%) were to a developmental pediatrician. pediatricians (71%) believed that ASD prevalence has increased, and nearly all attributed this to changes diagnostic criteria and treatment. Service system limitations must be overcome to increase awareness familiarity with screening tools, provide sufficient time and resources, improve screening, and enhance education. C1 Johns Hopkins Univ, Sch Med, Johns Hopkins Bloomberg Sch Publ Hlth, Div Child & Adolescent Psychiat, Baltimore, MD 21287 USA. Johns Hopkins Bloomberg Sch Publ Hlth, CADDRE, Baltimore, MD 21287 USA. RP Dosreis, S (reprint author), Johns Hopkins Univ, Sch Med, Johns Hopkins Bloomberg Sch Publ Hlth, Div Child & Adolescent Psychiat, 600 N Wolfe St,CMSC 346, Baltimore, MD 21287 USA. EM sdosreil@jhmi.edu CR [Anonymous], 2001, PEDIATRICS, V108, P192 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Blaxill MF, 2004, PUBLIC HEALTH REP, V119, P536, DOI 10.1016/j.phr.2004.09.003 Charman T, 2002, EUR CHILD ADOLES PSY, V11, P249, DOI 10.1007/s00787-002-0297-8 Charman T., 2003, EARLY CHILD DEV CARE, V173, P363, DOI 10.1080/0300443032000079050 Sandler AD, 2001, PEDIATRICS, V107, P1221 Filipek PA, 2000, NEUROLOGY, V55, P468 Fombonne E, 2004, BMC PUBLIC HEALTH, V4, DOI 10.1186/1471-2458-4-5 Glascoe FP, 2001, ARCH PEDIAT ADOL MED, V155, P54 Glascoe FP, 2005, MENT RETARD DEV D R, V11, P173, DOI 10.1002/mrdd.20068 Lauritsen MB, 2004, PSYCHOL MED, V34, P1339, DOI 10.1017/S0033291704002387 Mandell DS, 2005, ARCH PEDIAT ADOL MED, V159, P266, DOI 10.1001/archpedi.159.3.266 Newschaffer CJ, 2005, PEDIATRICS, V115, pE277, DOI 10.1542/peds.2004-1958 Newschaffer CJ, 2003, PUBLIC HEALTH REP, V118, P393, DOI 10.1016/S0033-3549(04)50270-4 Sand N, 2005, PEDIATRICS, V116, P174, DOI 10.1542/peds.2004-1809 SCHOR EL, 2004, COMMONWEALTH FUN OCT, P785 Sices L, 2003, J DEV BEHAV PEDIATR, V24, P409, DOI 10.1097/00004703-200312000-00002 Smeeth L, 2004, LANCET, V364, P963, DOI 10.1016/S0140-6736(04)17020-7 Spiker D, 2000, TOP EARLY CHILD SPEC, V20, P195, DOI 10.1177/027112140002000401 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 21 TC 50 Z9 52 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S88 EP S94 DI 10.1097/00004703-200604002-00006 PG 7 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300006 PM 16685190 ER PT J AU Eaves, LC Wingert, HD Ho, HH Mickelson, ECR AF Eaves, LC Wingert, HD Ho, HH Mickelson, ECR TI Screening for autism spectrum disorders with the social communication questionnaire SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE screening measures; autism spectrum disorders; preschool children; Social Communication Questionnaire ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; DISCREPANCIES; VALIDITY; CHILDREN; MOTHER; AGE AB The Social Communication Questionnaire (SCQ) is a parent report screening measure for autism spectrum disorders (ASDs) based on the Autism Diagnostic Interview-Revised (ADI-R). To examine its validity in a young sample, the SCQ was given to parents of 151 children at a mean age of 5 years, before assessment in tertiary autism or preschool clinics. Overall sensitivity was .71, the same for both clinics, but specificity was better for the preschool clinic (.62) than for the autism clinic (.53) reflecting fewer false-positives in the former. The "hit rate" was 65% with 28% of the children with autism missed by the SCQ at a cutoff score of 15 (falsenegatives) and 38% of the nonautistic misidentified as having an ASD (false-positives). Item validity analysis, contrary to what was previously published, indicated that only 15 or 46% of the items distinguished between children with and without ASD in this much younger sample. False-negatives were somewhat higher functioning. The SCQ would seem to be a useful tool for identifying young children in need of further assessment and assisting in routing them to the appropriate clinic, especially if used in conjunction with a screening by a community professional. There remain questions about the "best" cutoff score to use and whether a shorter version, based on the items that distinguished autistic from nonautistic, would be more reliable and valid with younger children. Furthermore, it may be that an adjusted score is required when parents omit items or with nonverbal children who cannot be scored on some of the items. C1 Sunny Hill Hlth Ctr Children, Dept Psychiat, Vancouver, BC V5M 3E8, Canada. Univ British Columbia, Fac Med, Dept Pediat, Div Dev Pediat,Sunny Hill Hlth Ctr Children, Vancouver, BC, Canada. RP Eaves, LC (reprint author), Sunny Hill Hlth Ctr Children, Dept Psychiat, 3644 Slocan St, Vancouver, BC V5M 3E8, Canada. EM leaves@cw.be.ca CR Achenbach T, 2000, CHILD BEHAV CHECKLIS American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2001, ARCH DIS CHILD, V84, P468, DOI 10.1136/adc.84.6.468 Bayley N, 1993, BAYLEY SCALES INFANT Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Bishop DVM, 2002, J CHILD PSYCHOL PSYC, V43, P917, DOI 10.1111/1469-7610.00114 BriggsGowan MJ, 1996, J ABNORM CHILD PSYCH, V24, P749, DOI 10.1007/BF01664738 Charman T, 2005, J CHILD PSYCHOL PSYC, V46, P500, DOI 10.1111/j.1469-7610.2004.00377.x CORSELLO C, 2005, INT M AUT RES MAY CORSELLO C, 2003, SOC RES CHILD DEV BI Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 Dumont-Mathieu T, 2005, MENT RETARD DEV D R, V11, P253, DOI 10.1002/mrdd.20072 EAVES LC, 2006, IN PRESS AUTISM, V10, P3 FOLEY D, 2004, J AM ACAD CHILD ADOL, V43, P432 Goodnow JJ, 1989, J APPL DEV PSYCHOL, V10, P209, DOI DOI 10.1016/0193-3973(89)90005-1 HANSON E, 2002, INT M AUT RES NOV LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LECOUTEUR A, 2003, AUTISM DIAGNOSTIC IN Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Mullen E, 1995, MULLEN SCALES EARLY PALANCIOS J, 1992, PARENTAL BELIEF SYST PERRY A, 2005, J AUTISM DEV DISORD, V20, P1 Reynolds C. R., 1998, BEHAV ASSESSMENT SYS Rutter M., 2003, SOCIAL COMMUNICATION SAESMUNDSEN E, 2003, J AUTISM DEV DISORD, V33, P319 Schopler E., 1988, CHILDHOOD AUTISM RAT Sparrow S, 1984, VINELAND ADAPTIVE BE Treutler CM, 2003, J ABNORM CHILD PSYCH, V31, P13, DOI 10.1023/A:1021765114434 Wechsler D., 1989, MANUAL WECHSLER PRES NR 30 TC 42 Z9 42 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S95 EP S103 DI 10.1097/00004703-200604002-00007 PG 9 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300007 PM 16685191 ER PT J AU Farzin, F Perry, H Hessl, D Loesch, D Cohen, J Bacalman, S Gane, L Tassone, F Hagerman, P Hagerman, R AF Farzin, F Perry, H Hessl, D Loesch, D Cohen, J Bacalman, S Gane, L Tassone, F Hagerman, P Hagerman, R TI Autism spectrum disorders and attention-deficit/hyperactivity disorder in boys with the fragile X premutation SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE FMR1; autism; FXTAS; RNA toxicity; ADHD; FMRP ID PERVASIVE DEVELOPMENTAL DISORDERS; TREMOR/ATAXIA SYNDROME FXTAS; FMR1 MESSENGER-RNA; PRE-MUTATION; DIAGNOSTIC INTERVIEW; STATUS CATEGORIES; INTENTION TREMOR; MALE CARRIERS; CHILDREN; ALLELES AB Fragile X syndrome (FXS) is caused by a full mutation expansion (> 200 CGG repeats) in the FMR1 gene that results in a deficiency of the fragile X mental retardation protein. Although most individuals with the premutation (55-200 CGG repeats) are considered unaffected by FXS, recent case studies have documented children with the premutation who have cognitive deficits, behavioral problems, and/or autism spectrum disorders. The objective of this study was to compare the prevalence of autism spectrum disorders (ASD) and attention-deficit hyperactivity disorder (ADHD) symptoms in boys with the premutation who presented as probands, in brothers with the premutation who did not present as probands, and in normal brothers of premutation and/or full mutation carriers. Participants included 43 male children: 14 probands who presented to clinic, 13 nonprobands who were identified through cascade testing (routine genetic testing of family members after identification of a proband) and confirmed to have the premutation, and a control group of 16 male siblings of individuals with the fragile X premutation or full mutation who were negative for the FMR1 mutation. Participants came from 1 of 2 collaborative sites: University of California, Davis and La Trobe University in Australia. Parents completed the Conners' Global Index-Parent Version for assessing symptoms of ADHD and the Social Communication Questionnaire (SCQ) for identifying symptoms of ASD. Children who were in the ASD range on the SCQ (n = 13) underwent further evaluation with either the Autism Diagnostic Observation Schedule-Generic (n = 10) or the Autism Diagnostic Interview-Revised (n = 3). A final diagnosis of ASD included clinical assessment utilizing DSMIV-TR criteria in addition to the standardized assessments. There was a higher rate of ASD in boys with the premutation presenting as probands (p < 0.001) or nonprobands (p <.04) compared with sibling controls without the premutation. In addition, probands had a significant increase in ADHD symptoms compared with controls (p <.0001). Of the probands, 93% had symptoms of ADHD and 79% had ASD. In the nonproband premutation group, 38% had symptoms of ADHD and 8% had ASD. Thirteen percent of sibling controls had symptoms of ADHD and none had ASD. IQ scores were similar in all 3 groups (p =.13), but the use of psychotropic medications was significantly higher in probands with the premutation compared with that in controls (p <.0001). Developmental problems have been observed in premutation carriers, particularly those who present clinically with behavioral difficulties. Although this study is based on a small sample size, it suggests that premutation carriers, even those who do not present clinically, may be at increased risk for an ASD and/or symptoms of ADHD. If the premutation is identified through cascade testing, then further assessment should be carried out for symptoms of ADHD, social deficits, or learning disabilities. C1 Univ Calif Davis, Med Ctr, MIND Inst, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Biochem & Mol Med, Sacramento, CA 95817 USA. Univ Calif Davis, Med Ctr, Dept Pediat, Sacramento, CA 95817 USA. La Trobe Univ, Sch Psychol Sci, Melbourne, Vic, Australia. Univ Calif Davis, Med Ctr, Dept Psychiat & Behav Sci, Sacramento, CA 95817 USA. RP Hagerman, R (reprint author), Univ Calif Davis, Med Ctr, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. 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Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S137 EP S144 DI 10.1097/00004703-200604002-00012 PG 8 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300012 PM 16685180 ER PT J AU Hansen, R AF Hansen, R TI Autism Spectrum Disorders - Preface SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Editorial Material C1 Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. RP Hansen, R (reprint author), Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S53 EP S53 DI 10.1097/00004703-200604002-00001 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300001 ER PT J AU Harrington, JW Rosen, L Garnecho, A AF Harrington, JW Rosen, L Garnecho, A TI Parental perceptions and use of complementary and alternative medicine practices for children with autistic spectrum disorders in private practice SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autistic disorder/diagnosis; autistic disorder/cause; autistic disorder/therapy; complementary and alternative medicine ID PERVASIVE DEVELOPMENTAL DISORDERS; GASTROINTESTINAL SYMPTOMS; YOUNG-CHILDREN; PEDIATRIC CARE; HEALTH-CARE; PREVALENCE; DIAGNOSIS; FAMILIES; IDENTIFICATION; DISABILITIES AB The prevalence of autistic spectrum disorder (ASD) in the United States is approximately 1 in 150 children. Many health care providers are unaware of parental beliefs and treatments, both medical and complementary, that parents use for their child with ASD. Understanding these beliefs and practices concerning diagnosis, cause, and utilization of medical and complementary care may help physicians provide better comprehensive care. Parents of children with ASD from 2 private practices-one in New York and one in New Jersey-were mailed a 6-page, self-administered survey. In addition to demographics and ASD type, the survey asked parents who diagnosed their child and if there was a perceived delay in that diagnosis; whether they believed there was any causal reason for their child's autism; what chronic symptoms, if any, their child experiences; and, if they had used any complementary and/or alternative therapies and at whose recommendation. Respondents included 77 of the 150 parents (51%) contacted. Most children were diagnosed by a neurologist and/or developmental pediatrician (54% and 47%, respectively). Average perceived delay in diagnosis was 18 months. Parents most frequently cited immunizations (54%), genetic predisposition (53%), and environmental exposure (38%) as a cause of their child's autism. Approximately half of children were reported as having at least one gastrointestinal, neurological, and/or allergic symptom; more than a third had immunological symptoms. Almost all parents (95%) indicated some use of complementary and alternative medicine (CAM) therapies, with most of the self-reported referrals generated from a physician or nurse (44%). Systemic complaints, parental beliefs, and use of CAM practices warrant open discussion by all health care professionals who provide care to this population. C1 New York Med Coll, Dept Pediat, Maria Fareri Childrens Hosp, Westchester Med Ctr, Valhalla, NY 10595 USA. New York Med Coll, Dept Med, Primary Care Res Unit, Valhalla, NY 10595 USA. RP Harrington, JW (reprint author), New York Med Coll, Dept Pediat, 312 Munger Pavilion, Valhalla, NY 10595 USA. 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PD APR PY 2006 VL 27 IS 2 SU S BP S156 EP S161 DI 10.1097/00004703-200604002-00014 PG 6 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300014 PM 16685182 ER PT J AU Mitchell, S Brian, J Zwaigenbaum, L Roberts, W Szatmari, P Smith, I Bryson, S AF Mitchell, Shelley Brian, Jessica Zwaigenbaum, Lonnie Roberts, Wendy Szatmari, Peter Smith, Isabel Bryson, Susan TI Early language and communication development of infants later diagnosed with autism spectrum disorder SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism; language; communication; gestures; infant behavior ID FAMILY-HISTORY; HOME VIDEOTAPES; YOUNG-CHILDREN; LATE TALKERS; FOLLOW-UP; RELATIVES; SYMPTOMS; INDIVIDUALS; RECOGNITION; REGRESSION AB It is well recognized that delayed "first words" is among the most common presenting symptoms of autistic spectrum disorders (ASD). However, data on earlier language and communication development in children with ASD are limited to retrospective reports from parents and from home videos. In this study, we prospectively collected parent report data on early communication and language development in 97 infant siblings of children with ASD and 49 low-risk controls. Parents completed the MacArthur Communicative Development Inventory-Infant Form at 12 and 18 months. Analysis compared 3 groups defined on the basis of diagnostic assessment at 24 months: (1) siblings with ASD (n = 15), (2) siblings not meeting diagnostic criteria for ASD (n = 82), and (3) low-risk controls, none of whom had ASD (n = 49). Children with ASD showed delays in early language and communication compared with non-ASD siblings and controls. At 12 months, the ASD group was reported to understand significantly fewer phrases and to produce fewer gestures. At 18 months, they showed delays in their understanding of phrases, comprehension and production of single words, and use of gestures. Siblings not diagnosed with ASD also used fewer play-related gestures at 18 months than low-risk controls, even when children with identified language delays were excluded. Overall, this prospective study confirms that delays in communication and language development are apparent early in life in children with ASD, and emphasizes that developmental surveillance should include monitoring for delays in gesture, which may be among the earliest signs of ASD. C1 Hosp Sick Children, Autism Res Unit, Toronto, ON M5G 1X8, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. Univ Toronto, Hosp Sick Children, Dept Pediat, Toronto, ON M5G 1X8, Canada. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. Dalhousie Univ, Dept Pediat & Psychol, Halifax, NS, Canada. RP Bryson, S (reprint author), IWK Hlth Ctr, Dept Pediat & Psychiat, POB 3070, Halifax, NS B3J 3G9, Canada. 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Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 BP S69 EP S78 DI 10.1097/00004703-200604002-00004 PG 10 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300004 PM 16685188 ER PT J AU Niehus, R Lord, C AF Niehus, R Lord, C TI Early medical history of children with autism spectrum disorders SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism; ASD history; ear infections ID NO EVIDENCE; MEASLES; MUMPS; VACCINATION; AGE AB Previous studies have suggested that children with autism spectrum disorders (ASD) may have different medical histories than nonspectrum children in several areas: their reactions to vaccinations, number of ear infections, chronic gastrointestinal problems, and use of antibiotics. Furthermore, some studies have found associations between regressive autism and gastrointestinal (GI) symptoms. The present study analyzes the medical records from birth to the age of 2 years of 99 children (24 typically developing; 75 with ASD, of whom 29 had parent-reported regression). Data were coded in the following areas: frequency and purpose of pediatrician visits, frequency and type of illnesses and medications, type and chronicity of GI complaints, date of vaccinations, growth data, and whether the pediatrician noted behaviors indicative of an ASD before the age of 2 years. Children with ASD were found to have significantly more ear infections than the typically developing children as well as to use significantly more antibiotics. Typically developing children had significantly more illness-related fevers. There was a nonsignificant trend toward the ASD group having more chronic gastrointestinal problems. There were no significant differences between the groups for the age of vaccination or for number of pediatrician visits. 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Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S120 EP S127 DI 10.1097/00004703-200604002-00010 PG 8 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300010 PM 16685178 ER PT J AU Palomo, R Belinchon Carmona, M Ozonoff, S AF Palomo, Ruben Belinchon Carmona, Mercedes Ozonoff, Sally TI Autism and family home movies: A comprehensive review SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism; family home movies; early diagnosis; methodology; review ID PERVASIVE DEVELOPMENTAL DISORDERS; RETROSPECTIVE VIDEO ANALYSIS; EARLY NATURAL-HISTORY; 1ST 2 YEARS; JOINT ATTENTION; CHILDHOOD PSYCHOSIS; SPECTRUM DISORDERS; INFANTILE-AUTISM; EARLY RECOGNITION; EARLY SIGNS AB In this article, we focus on the early development of autism studied through family home movies. We review all investigations published in English that met specific methodological standards, including the use of comparison samples, coding blind to group membership, and adequate levels of interrater reliability. After discussing in detail the pros and cons of the home-movie methodology, we review the results of all empirical studies conducted to date. We then present a summary of the features found consistently across studies that differentiate autism from typical development and mental retardation in the first 2 years of life. How family home movies can contribute to our understanding of the regression phenomenon is also addressed. Finally, the results are interpreted from both a theoretical and clinical point of view. C1 Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Univ Autonoma Madrid, Fac Psicol, E-28049 Madrid, Spain. RP Ozonoff, S (reprint author), Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. 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Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S59 EP S68 DI 10.1097/00004703-200604002-00003 PG 10 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300003 PM 16685187 ER PT J AU Robins, DL Dumont-Mathieu, TM AF Robins, DL Dumont-Mathieu, TM TI Early screening for autism spectrum disorders: Update on the modified checklist for autism in toddlers and other measures SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; 6-YEAR FOLLOW-UP; YOUNG-CHILDREN; EARLY IDENTIFICATION; EARLY INTERVENTION; EARLY RECOGNITION; HOME VIDEOTAPES; JOINT ATTENTION; 1ST YEAR; AGE AB Early intervention for autism spectrum disorders necessitates early detection. This need has led to widespread agreement across disciplines that screening is critical in very young children. Two screening issues are highlighted in this review. Level of screening refers to the type of sample: Level I is defined as an unselected sample, and Level II consists of selected children already identified as being at risk for a developmental disorder. Breadth or scope of screening refers to the range of difficulties the screening tool attempts to identify: broad screening instruments identify multiple range of developmental difficulties, whereas disorder-specific tools focus on a single disorder or class of disorders. Broad developmental instruments reviewed include the Parents' Evaluation of Developmental Status and the Ages and Stages Questionnaires; autism-specific tools reviewed include the Checklist for Autism in Toddlers, the Modified Checklist for Autism in Toddlers (M-CHAT), the Pervasive Developmental Disorders Screening Test, Second Edition, and the Screening Tool for Autism in Two-year-olds. The development of the M-CHAT, a Level I and Level II screening instrument, is described, and current research and clinical use of the M-CHAT are reviewed, including description of the structured follow-up interview which reduces the false-positive rate of the parent-report M-CHAT. C1 Georgia State Univ, Dept Psychol, Atlanta, GA 30302 USA. Univ Connecticut, Sch Med, Dept Pediat, Div Dev Behav Pediat, Farmington, CT 06032 USA. Univ Connecticut, Dept Psychol, Farmington, CT 06032 USA. RP Robins, DL (reprint author), Georgia State Univ, Dept Psychol, POB 5010, Atlanta, GA 30302 USA. 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Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S111 EP S119 DI 10.1097/00004703-200604002-00009 PG 9 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300009 PM 16685177 ER PT J AU Rutter, M AF Rutter, Michael TI Autism: Its recognition, early diagnosis, and service implications SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Editorial Material ID SPECTRUM DISORDERS; REGRESSION C1 Kings Coll London, MRC, SGDP Ctr, Inst Psychiat, London SE5 9AF, England. RP Rutter, M (reprint author), Kings Coll London, MRC, SGDP Ctr, Inst Psychiat, De Crespigny Pk,Denmark Hill, London SE5 9AF, England. 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Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S54 EP S58 DI 10.1097/00004703-200604002-00002 PG 5 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300002 PM 16685186 ER PT J AU Scambler, DJ Hepburn, SL Rogers, SJ AF Scambler, DJ Hepburn, SL Rogers, SJ TI A two-year follow-up on risk status identified by the checklist for autism in toddlers SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE screening; autism spectrum disorders; 2-year follow-up ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; YOUNG-CHILDREN; DIAGNOSIS; AGE AB We examined the characteristics of children at 4 to 5 years of age who were correctly and incorrectly classified as "at risk" for an autism spectrum diagnosis using the Checklist for Autism in Toddlers (CHAT) at age 2 to 3 years. Information is provided on the stability of risk/disorder status over a 2-year period of early development. Participants were 19 children with autism and 11 children with other developmental disabilities who had all been administered the CHAT between 2 and 3 years of age (Time 1) and received diagnostic and developmental reevaluations between 4 and 5 years of age (Time 2). The risk status of children was discussed based on the original CHAT authors' criteria for risk of autism and the Denver modification for risk. High levels of stability in risk/diagnostic status from Time 1 assessments to Time 2 assessments were noted. Specifically, the original CHAT criteria for medium to high risk of autism applied at Time 1 predicted Time 2 diagnostic classification for 83% of the sample, and the Denver modification of the CHAT risk criteria predicted Time 2 diagnostic classification for 93% of the sample. Implications of the findings are discussed as they relate to early screening and identification of autism spectrum disorders. C1 Oklahoma State Univ, Dept Psychol, Coll Arts & Sci, Stillwater, OK 74078 USA. Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80206 USA. Univ Calif Davis, Med Ctr, MIND Inst, Davis, CA 95616 USA. RP Scambler, DJ (reprint author), Oklahoma State Univ, Dept Psychol, Coll Arts & Sci, 215 N Murray, Stillwater, OK 74078 USA. EM scamble@okstate.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Lord C., 1997, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x Mullen E., 1989, MULLEN SCALES EARLY Robins DL, 2001, J AUTISM DEV DISORD, V31, P131, DOI 10.1023/A:1010738829569 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 Scambler D, 2001, J AM ACAD CHILD PSY, V40, P1457, DOI 10.1097/00004583-200112000-00017 SCAMBLER DJ, IN PRESS J INTELL DI Smith T, 1999, CLIN PSYCHOL-SCI PR, V6, P33, DOI 10.1093/clipsy/6.1.33 Sparrow S, 1984, VINELAND ADAPTIVE BE Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 STONE WLO, 2003, SCREENING TOOL AUTIS NR 20 TC 9 Z9 10 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S104 EP S110 DI 10.1097/00004703-200604002-00008 PG 7 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300008 PM 16685176 ER PT J AU Valicenti-McDermott, M McVicar, K Rapin, I Wershil, BK Cohen, H Shinnar, S AF Valicenti-McDermott, M McVicar, K Rapin, I Wershil, BK Cohen, H Shinnar, S TI Frequency of gastrointestinal symptoms in children with autistic spectrum disorders and association with family history of autoimmune disease SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article; Proceedings Paper CT Annual Meeting of the Pediatric-Academic-Societies CY MAY 14-17, 2005 CL Washington, DC SP Pediat Acad Soc DE autism; developmental disabilities; gastrointestinal; food selectivity; autoimmune; children ID GASTROESOPHAGEAL-REFLUX; DEVELOPMENTAL DISORDERS; REGRESSIVE AUTISM; CONSTIPATION; POPULATION; PREVALENCE; ACCURACY; MEASLES; GLUTEN; CANCER AB This is a cross-sectional study that compares lifetime prevalence of gastrointestinal (GI) symptoms in children with autistic spectrum disorders (ASDs) and children with typical development and with other developmental disabilities (DDs) and examines the association of GI symptoms with a family history of autoimmune disease. A structured interview was performed in 50 children with ASD and 2 control groups matched for age, sex, and ethnicity-50 with typical development and 50 with other DDs. Seventy-four percent were boys with a mean age of 7.6 years (SD, +/- 3.6). A history of GI symptoms was elicited in 70% of children with ASD compared with 28% of children with typical development (p <.001) and 42% of children with DD (p =.03). Abnormal stool pattern was more common in children with ASD (18%) than controls (typical development: 4%, p =.039; DD: 2%, p =.021). Food selectivity was also higher in children with ASD (60%) compared with those with typical development (22%, p =.001) and DD (36%, p =.023). Family history of autoimmune disease was reported in 38% of the ASD group and 34% of controls and was not associated with a differential rate of GI symptoms. In the multivariate analysis, autism (adjusted odds ratio (OR), 3.8; 95% confidence interval (CI), 1.7-11.2) and food selectivity (adjusted OR, 4.1; 95% CI, 1.8-9.1) were associated with GI symptoms. Children with ASD have a higher rate of GI symptoms than children with either typical development or other DDs. In this study, there was no association between a family history of autoimmune disease and GI symptoms in children with ASD. C1 RF Kennedy Ctr Excellence Dev Disabil, Dept Pediat, Childrens Evaluat & Rehabil Ctr, Bronx, NY 10461 USA. Albert Einstein Coll Med, Montefiore Med Ctr, Dept Pediat, Bronx, NY 10467 USA. Albert Einstein Coll Med, Montefiore Med Ctr, Saul R Korey Dept Neurol, Bronx, NY 10467 USA. Albert Einstein Coll Med, Montefiore Med Ctr, Dept Pediat, Bronx, NY 10467 USA. RP Valicenti-McDermott, M (reprint author), RF Kennedy Ctr Excellence Dev Disabil, Dept Pediat, Childrens Evaluat & Rehabil Ctr, Bronx, NY 10461 USA. 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Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S128 EP S136 DI 10.1097/00004703-200604002-00011 PG 9 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300011 PM 16685179 ER PT J AU Wiggins, LD Baio, J Rice, C AF Wiggins, LD Baio, J Rice, C TI Examination of the time between first evaluation and first autism spectrum diagnosis in a population-based sample SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE early identification; diagnosis; autism spectrum disorder; Centers for Disease Control and Prevention ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; BEHAVIORAL TREATMENT; PREVALENCE; INTERVENTION; FAMILIES AB Early identification of young children with an autism spectrum disorder (ASD) can lead to earlier entry into intervention programs that support improved developmental outcomes. The purpose of the present study was to examine identification and diagnostic patterns of children with ASD who live in a large metropolitan area. One hundred fifteen 8-year-old children diagnosed with ASD were identified from a population-based surveillance system at the Centers for Disease Control and Prevention. Primary variables of interest included earliest age of evaluation and earliest age of diagnosis identified from surveillance records, type of initial ASD diagnosis, evaluation sources that documented first ASD diagnosis, characteristics of professionals assigning first ASD diagnosis, and diagnostic tools used to aid the diagnostic process. We found that children with ASD identified by the surveillance system were initially evaluated at a mean of 48 months but were not diagnosed with ASD until a mean age of 61 months. There were no differences in timing of diagnosis based on sex or racial/ethnic classification, although degree of impairment associated with ASD predicted mean age at first evaluation and mean age at first ASD diagnosis. Most children were identified at nonschool sources, such as hospitals and clinics; 24% of the sample did not receive a documented ASD diagnosis until entering school. Most practitioners (70%) did not use a diagnostic instrument when assigning the first ASD diagnosis. Implications for early identification of ASD are discussed. C1 Ctr Dis Control & Prevent, Dev Disabilities Branch, Atlanta, GA 30333 USA. Battelle Mem Inst, Ctr Publ Hlth Res & Evaluat, Columbus, OH 43201 USA. RP Wiggins, LD (reprint author), Ctr Dis Control & Prevent, Dev Disabilities Branch, MS E-86,1600 Clifton Rd, Atlanta, GA 30333 USA. EM lwiggins@cdc.gov CR Blaxill MF, 2004, PUBLIC HEALTH REP, V119, P536, DOI 10.1016/j.phr.2004.09.003 Boyle C A, 1996, MMWR CDC Surveill Summ, V45, P1 *CDCP, 2005, LEARN SIGNS ACT EARL Chakrabarti S, 2005, AM J PSYCHIAT, V162, P1133, DOI 10.1176/appi.ajp.162.6.1133 CHARMAN T, 2002, EUR CHILD ADOLES PSY, V11, P219 Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Dawson G., 1997, EFFECTIVENESS EARLY, P307 Filipek PA, 2000, NEUROLOGY, V55, P468 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 GILBERG C, 1999, ACTA PSYCHIAT SCAND, V99, P399 Gray DE, 2002, J INTELLECT DEV DIS, V27, P215, DOI 10.1080/1366825021000008639 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 HOWLING P, 1998, CHILDREN AUTISM ASPE Kasari C, 2001, INT REV RES MENT RET, V23, P207 LANDA R, 2005, INT M AUT RES MAY LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Mandell DS, 2002, J AM ACAD CHILD PSY, V41, P1447, DOI 10.1097/01.CHI.0000024863.60748.53 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 Newschaffer C., 2005, PEDIATRICS, V115, P277 Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 Pisula E., 2003, ARCH PSYCHIAT PSYCHO, V5, P51 ROGERS SJ, 1989, J AM ACAD CHILD PSY, V28, P207, DOI 10.1097/00004583-198903000-00010 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 Sivberg Bengt, 2003, J Pediatr Nurs, V18, P433, DOI 10.1016/S0882-5963(03)00139-8 Soares I., 1993, COMMUNICATION, V27, P17 *SPSS INC, 2003, SPSS INC COMP PROGR Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 32 TC 87 Z9 90 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD APR PY 2006 VL 27 IS 2 SU S BP S79 EP S87 DI 10.1097/00004703-200604002-00005 PG 9 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 045KZ UT WOS:000237742300005 PM 16685189 ER PT J AU Jyonouchi, H Geng, L Ruby, A Reddy, C AF Jyonouchi, Harumi Geng, Lee Ruby, Agnes Reddy, Chitra TI Changes in cellular immune reactivity to cow's milk protein (CMP) following dietary intervention in young children with non-allergic food hypersensitivity (NFH) with or without autism spectrum disorders (ASD) SO JOURNAL OF IMMUNOLOGY LA English DT Meeting Abstract CT Annual Meeting of the American-Association-of-Immunologists CY MAY 12-16, 2006 CL Boston, MA SP Amer Assoc Immunologists C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07101 USA. NR 0 TC 0 Z9 0 PU AMER ASSOC IMMUNOLOGISTS PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814 USA SN 0022-1767 J9 J IMMUNOL JI J. Immunol. PD APR 1 PY 2006 VL 176 SU S BP S246 EP S246 PG 1 WC Immunology SC Immunology GA 060YD UT WOS:000238837102136 ER PT J AU Hemmings, CP Gravestock, S Pickard, M Bouras, N AF Hemmings, CP Gravestock, S Pickard, M Bouras, N TI Psychiatric symptoms and problem behaviours in people with intellectual disabilities SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE intellectual disabilities; problem behaviours; psychiatric symptoms ID PAS-ADD CHECKLIST; MENTAL-RETARDATION; CHALLENGING BEHAVIORS; LEARNING-DISABILITY; ASSESSMENT SCHEDULE; SELF-INJURY; 2 ADULTS; DEPRESSION; DISORDER; INDIVIDUALS AB Background Previous studies have suggested different patterns of associations between psychiatric symptoms and problem behaviours in people with intellectual disabilities (ID). The aim of this study was to investigate which problem behaviours are associated with specific psychiatric symptoms and the relative strength of these specific associations. Method A cross sectional survey using the Psychiatric Assessment Schedule for Adults with Developmental Disabilities Checklist and the Disability Assessment Schedule was carried out in a sample of 214 adults with ID. Results Self-injurious and, to a lesser extent, aggressive problem behaviours were most associated with affective type symptoms. Screaming and destructive behaviours tended to be more associated with autism-related social impairment rather than conventional psychiatric symptoms. Conclusions This study gives further evidence of associations between psychiatric symptoms and specific problem behaviours in people with ID. It may be particularly useful to consider the diagnosis of affective disorders if a person with ID shows self-injurious or aggressive behaviours. C1 Univ London Kings Coll, Inst Psychiat, Estia Ctr, London WC2R 2LS, England. Oxleas NHS Trust, London, England. RP Hemmings, CP (reprint author), Guys Hosp, York Clin, London SE1 9RT, England. 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L., 1995, DIAGNOSTIC ASSESSMEN McBrien JA, 2003, J INTELL DISABIL RES, V47, P1, DOI 10.1046/j.1365-2788.2003.00455.x McClintock K, 2003, J INTELL DISABIL RES, V47, P405, DOI 10.1046/j.1365-2788.2003.00517.x McDougle CJ, 1998, ARCH GEN PSYCHIAT, V55, P633, DOI 10.1001/archpsyc.55.7.633 MEINS W, 1995, J INTELL DISABIL RES, V39, P41 Moss S, 1998, J INTELL DISABIL RES, V42, P173, DOI 10.1046/j.1365-2788.1998.00116.x Moss S, 2000, BRIT J PSYCHIAT, V177, P452, DOI 10.1192/bjp.177.5.452 Perry DW, 2001, AUTISM, V5, P265, DOI 10.1177/1362361301005003004 REISS S, 1993, J INTELL DISABIL RES, V37, P287 Rojahn J, 2001, J AUTISM DEV DISORD, V31, P577, DOI 10.1023/A:1013299028321 Rojahn J, 2004, AM J MENT RETARD, V109, P21, DOI 10.1352/0895-8017(2004)109<21:RBPCAB>2.0.CO;2 Royal College of Psychiatrists DC-LD, 2001, DIAGN CRIT PSYCH DIS SOVNER R, 1993, J INTELL DISABIL RES, V37, P301 Sturmey P, 2005, BRIT J PSYCHIAT, V186, P319, DOI 10.1192/bjp.186.4.319 Tsiouris JA, 2003, J INTELL DISABIL RES, V47, P14, DOI 10.1046/j.1365-2788.2003.00456.x World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 25 TC 46 Z9 46 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 APR PY 2006 VL 50 BP 269 EP 276 DI 10.1111/j.1365-2788.2006.00827.x PN 4 PG 8 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 017LU UT WOS:000235695900004 PM 16507031 ER PT J AU Tyrer, F McGrother, CW Thorp, CF Donaldson, M Bhaumik, S Watson, JM Hollin, C AF Tyrer, F McGrother, CW Thorp, CF Donaldson, M Bhaumik, S Watson, JM Hollin, C TI Physical aggression towards others in adults with learning disabilities: prevalence and associated factors SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE aggression; behaviour; cross-sectional study; cohort; Leicestershire ID INTELLECTUAL DISABILITY; MENTAL-RETARDATION; CHALLENGING BEHAVIORS; MALADAPTIVE BEHAVIOR; PEOPLE; CHILDREN; POPULATION; DEPRESSION; DISORDERS; INDIVIDUALS AB Background Many people with learning disabilities (LD) show aggressive behaviour, but the extent of the problem and its associated factors and effects are unclear. Methods A cross-sectional analysis was carried out using interview data from 3065 adults with LD on the Leicestershire LD Register. Physical aggression towards others was defined as carers reporting frequent (more than three times per week) and/or severe episodes. Individuals with and without aggression were compared using multiple logistic regression models for potential physical and psychological factors. Results Carers reported that 443 (14%) of adults were physically aggressive towards others. Men (P = 0.001), younger individuals (P < 0.001), people with more severe LD (P < 0.001) and those in institutional settings (P < 0.001) had a significantly higher prevalence of physical aggression. People with Down syndrome had a lower prevalence of physical aggression (P < 0.001). After adjustment, we found no relationship between aggression and the presence of epilepsy or autism. Among psychological factors, symptoms of frustration (P < 0.001) and mood swings (P < 0.001) were associated with higher levels of aggression. Failure to cope among carers was reported by 14% overall: 42% of people caring for adults with aggression said they were unable to cope compared with 10% of those caring for adults without aggression. Conclusions Physical aggression towards other people presents a significant challenge to carers of adults with LD. Further research is needed to identify aetiological factors with a view to finding effective interventions to reduce, and improve management of, this behaviour. C1 Univ Leicester, Dept Hlth Sci, Leicester LE1 6TP, Leics, England. RP Tyrer, F (reprint author), Univ Leicester, Dept Hlth Sci, 22-28 Princess Rd W, Leicester LE1 6TP, Leics, England. 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Intell. Disabil. Res. PD APR PY 2006 VL 50 BP 295 EP 304 DI 10.1111/j.1365-2788.2005.00774.x PN 4 PG 10 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 017LU UT WOS:000235695900007 PM 16507034 ER PT J AU Ashwood, P Wakefield, AJ AF Ashwood, P Wakefield, AJ TI Immune activation of peripheral blood and mucosal CD3(+) lymphocyte cytokine profiles in children with autism and gastrointestinal symptoms SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE inflammation; mucosa; TNF alpha; IL-10; autism ID REGRESSIVE AUTISM; INTERFERON-GAMMA; DEVELOPMENTAL REGRESSION; BRAIN-BARRIER; DISORDERS; DOPAMINE; DISEASE; GUT; INTERLEUKIN-1-BETA; NOREPINEPHRINE AB Gastrointestinal pathology, characterized by lymphoid nodular hyperplasia and entero-colitis, has been demonstrated in a cohort of children with autistic spectrum disorder (ASD). Systemic and intestinal mucosal immune dysregulation was assessed in ASD children with gastrointestinal (GI) symptoms (n = 18), and typically developing controls (n = 27), including non-inflamed controls (NIC) and inflamed GI control children with Crohn's disease (CD), by analysis of intracellular cytokines in CD3(+) lymphocytes. In both peripheral blood and mucosa, CD3(+)TNF alpha(+) and CD3(+) IFN gamma(+) were increased in ASD children compared with NIC (p < 0.004) and reached levels similar to CD. In contrast, peripheral and mucosal CD3(+) IL-10(+) were markedly lower in ASID children with GI symptoms compared with both NIC and CD controls (p < 0.02). In addition, mucosal CD3(+) IL-4(+) cells were increased (p < 0.007) in ASD compared with NIC. There is a unique pattern of peripheral blood and mucosal CD3+ lymphocytes intracellular cytokines, which is consistent with significant immune dysregulation, in this ASID cohort. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Calif Davis, Dept Med Microbiol & Immunol, MIND Inst, Sacramento, CA 95817 USA. Thoughtful House Ctr Children, Austin, TX USA. RP Ashwood, P (reprint author), Univ Calif Davis, Dept Med Microbiol & Immunol, MIND Inst, Wet Lab Bldg,50th St, Sacramento, CA 95817 USA. 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Neuroimmunol. PD APR PY 2006 VL 173 IS 1-2 BP 126 EP 134 DI 10.1016/j.jneuroim.2005.12.007 PG 9 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 033CO UT WOS:000236824200014 PM 16494951 ER PT J AU Millar, DC Light, JC Schlosser, RW AF Millar, DC Light, JC Schlosser, RW TI The impact of augmentative and alternative communication intervention on the speech production of individuals with developmental disabilities: A research review SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article; Proceedings Paper CT 9th International Conference of the International-Society-for-Augmentative-and-Alternative-Communication CY AUG, 2000 CL WASHINGTON, D.C. SP Internat Soc Augmentat Alternat Comm DE augmentative and alternative communication; speech production; developmental disabilities; effectiveness; meta-analysis; systematic review ID MENTALLY-RETARDED CHILDREN; SIGN LANGUAGE; MANUAL SIGNS; EXPERIMENTAL-DESIGNS; AUTISTIC-CHILDREN; ACQUISITION; BEHAVIOR; SYSTEM; SKILLS AB Purpose: This article presents the results of a meta-analysis to determine the effect of augmentative and alternative communication (AAC) on the speech production of individuals with developmental disabilities. Method: A comprehensive search of the literature published between 1975 and 2003, which included data on speech production before, during, and after AAC intervention, was conducted using a combination of electronic and hand searches. Results: The review identified 23 studies, involving 67 individuals. Seventeen of these studies did not establish experimental control, thereby limiting the certainty of evidence bout speech outcomes. The remaining 6 studies, involving 27 cases, had sufficient a methodological rigor for the "best evidence analysis" (cf. R. E. Slavin, 1986). Most of the participants (aged 2-60 years) had mental retardation or autism; the AAC interventions involved instruction in manual signs or nonelectronic aided systems. None of the 27 cases demonstrated decreases in speech production as a result of AAC intervention, 11% showed no change, and the majority (89%) demonstrated gains in speech. For the most part, the gains observed were modest, but these data may underestimate the effect of AAC intervention on speech production because there were ceiling effects. Conclusions: Future research is needed to better delineate the relationship between AAC intervention and speech production across a wider range of participants and AAC interventions. C1 Penn State Univ, University Pk, PA 16802 USA. Univ N Texas, Denton, TX 76203 USA. Northeastern Univ, Boston, MA 02115 USA. 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PD APR PY 2006 VL 49 IS 2 BP 248 EP 264 DI 10.1044/1092-4388(2006/021) PG 17 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 038KD UT WOS:000237217500003 PM 16671842 ER PT J AU Williams, SK Scahill, L Vitiello, B Aman, MG Arnold, LE McDougle, CJ McCracken, JT Tierney, E Ritz, L Posey, DJ Swiezy, NB Hollway, J Cronin, P Ghuman, J Wheeler, C Cicchetti, D Sparrow, S AF Williams, SK Scahill, L Vitiello, B Aman, MG Arnold, LE McDougle, CJ McCracken, JT Tierney, E Ritz, L Posey, DJ Swiezy, NB Hollway, J Cronin, P Ghuman, J Wheeler, C Cicchetti, D Sparrow, S TI Risperidone and adaptive behavior in children with autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article; Proceedings Paper CT 38th Annual Meeting of the Association-for-the-Advancement-of-Behavior-Therapy CY NOV, 2004 CL New Orleans, LA SP Assoc Advancement Behav Therapy DE autism; risperidone; Vineland Adaptive Behavior Scales ID PERVASIVE DEVELOPMENTAL DISORDER; INTENSIVE EARLY INTERVENTION; MENTAL-RETARDATION; CLINICAL-TRIALS; YOUNG-CHILDREN; CHECKLIST; INDIVIDUALS; DOMAINS; SCORES; NORMS AB Objective: To evaluate the impact of risperidone on adaptive behavior in children with autistic disorder who have serious behavior problems and to examine different methods of scoring the Vineland Adaptive Behavior Scales to measure change. Method: Forty-eight children (5 years to 16 years, 5 months) who showed behavioral improvement during acute treatment with risperidone were followed for 6 months and assessed with the Vineland Scales. Results: Raw scores, age-equivalents, and special norm percentile scores all showed significant increases in adaptive behavior in the areas of communication, daily living skills, and socialization (p < .01). During a period of 6 to 8 months, children gained an average of 7.8 age-equivalent months in the area of socialization, a > 6% improvement beyond what would be expected based on baseline growth rates. Conclusions: Although limited by the absence of a control group, these results suggest that risperidone may improve adaptive skills in children with autistic disorder accompanied by serious behavioral problems. Vineland age-equivalent scores appear to be most useful in assessing change with treatment over time. C1 Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Ohio State Univ, Columbus, OH 43210 USA. Indiana Univ, Indianapolis, IN 46204 USA. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. Kennedy Krieger Inst, Baltimore, MD USA. NIMH, Bethesda, MD 20892 USA. RP Scahill, L (reprint author), Yale Univ, Ctr Child Study, POB 207900, New Haven, CT 06520 USA. 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Am. Acad. Child Adolesc. Psychiatr. PD APR PY 2006 VL 45 IS 4 BP 431 EP 439 DI 10.1097/01.chi.0000196423.80717.32 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 027NC UT WOS:000236421300010 PM 16601648 ER PT J AU Griffin, R Friedman, O Ween, J Winner, E Happe, F Brownell, H AF Griffin, Richard Friedman, Ori Ween, Jon Winner, Ellen Happe, Francesca Brownell, Hiram TI Theory of mind and the right cerebral hemisphere: Refining the scope of impairment SO LATERALITY LA English DT Article ID POSITRON-EMISSION-TOMOGRAPHY; FRONTAL-LOBE CONTRIBUTIONS; ASPERGER-SYNDROME; CENTRAL COHERENCE; AUTISTIC INDIVIDUALS; STORY COMPREHENSION; EXECUTIVE FUNCTIONS; PREFRONTAL CORTEX; CHILDHOOD AUTISM; PREMOTOR CORTEX AB The neuropsychological and functional characterisation of mental state attribution ("theory of mind'' (ToM)) has been the focus of several recent studies. The literature contains opposing views on the functional specificity of ToM and on the neuroanatomical structures most relevant to ToM. Studies with brain-lesioned patients have consistently found ToM deficits associated with unilateral right hemisphere damage (RHD). Also, functional imaging performed with non-brain-injured adults implicates several specific neural regions, many of which are located in the right hemisphere. The present study examined the separation of ToM impairment from other deficits associated with brain injury. We tested 11 patients with unilateral right hemisphere damage (RHD) and 20 normal controls (NC) on a humour rating task, an emotion rating task, a graded (first-order, second-order) ToM task with non-mentalistic control questions, and two ancillary measures: (1) Trails A and B, in order to assess overall level of impairment and set-shifting abilities associated with executive function, and (2) a homograph reading task to assess central coherence skills. Our findings indicate that RHD can result in a functionally specific deficit in attributing intentional states, particularly those involving second-order attributions. Performance on ToM questions was not reliably related to measures of cognitive impairment; however, performance on non-ToM control questions was reliably predicted by Trails A and B. We also discuss individual RHD patients' performance with attention to lesion locus. Our findings suggest that damage to the areas noted as specialised in neuroimaging studies may not affect ToM performance, and underscore the necessity of combining lesion and imaging studies in determining functional-anatomical relations. C1 Tufts Univ, Ctr Cognit Studies, Medford, MA 02155 USA. Univ Waterloo, Waterloo, ON N2L 3G1, Canada. Univ Toronto, Fac Med, Toronto, ON, Canada. Boston Univ, Boston, MA 02215 USA. Kings Coll London, London WC2R 2LS, England. RP Griffin, R (reprint author), Tufts Univ, Ctr Cognit Studies, 11 Miner Hall, Medford, MA 02155 USA. 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SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Michigan, Kresge Business Adm Lib, Ann Arbor, MI 48109 USA. RP Seeman, C (reprint author), Univ Michigan, Kresge Business Adm Lib, Ann Arbor, MI 48109 USA. CR Greenspan SI, 2006, ENGAGING AUTISM USIN NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD APR 1 PY 2006 VL 131 IS 6 BP 112 EP 112 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 028IY UT WOS:000236481800230 ER PT J AU Seeman, C AF Seeman, C TI Does my child have autism?: A parent's guide to early detection and intervention in autism spectrum disorders SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Michigan, Kresge Business Adm Lib, Ann Arbor, MI 48109 USA. RP Seeman, C (reprint author), Univ Michigan, Kresge Business Adm Lib, Ann Arbor, MI 48109 USA. CR STONE WL, 2006, DOES MY CHILD HAVE A NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD APR 1 PY 2006 VL 131 IS 6 BP 112 EP 112 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 028IY UT WOS:000236481800231 ER PT J AU Meadan, H Ostrosky, MM AF Meadan, H Ostrosky, MM TI "You're going to love this kid"! Teaching students with autism in the inclusive classroom SO MENTAL RETARDATION LA English DT Book Review C1 Univ Illinois, Urbana, IL 61801 USA. RP Meadan, H (reprint author), Univ Illinois, Urbana, IL 61801 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Kluth P., 2003, YOURE GOING LOVE THI NR 2 TC 0 Z9 0 PU AMER ASSOC MENTAL RETARDATION PI WASHINGTON PA 444 N CAPITOL ST, NW, STE 846, WASHINGTON, DC 20001-1512 USA SN 0047-6765 J9 MENT RETARD JI Ment. Retard. PD APR PY 2006 VL 44 IS 2 BP 156 EP 157 DI 10.1352/0047-6765(2006)44[156:BR]2.0.CO;2 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 030TF UT WOS:000236656800009 ER PT J AU Francke, U AF Francke, U TI Mechanisms of disease: neurogenetics of MeCP2 deficiency SO NATURE CLINICAL PRACTICE NEUROLOGY LA English DT Review DE autism; chromatin; congenital encephalopathy; methyl-CpG binding protein 2 ( MeCP2); Rett syndrome ID CPG-BINDING-PROTEIN; CHROMATIN-REMODELING COMPLEX; RETT-SYNDROME FAMILY; TRANSCRIPTIONAL REPRESSOR; MENTAL-RETARDATION; DNA METHYLATION; NEUROLOGICAL SYMPTOMS; NEURONAL MATURATION; GENE-EXPRESSION; MUTATION TYPE AB Rett syndrome (RTT) is unique among genetic, chromosomal and other developmental disorders because of its extreme female gender bias, early normal development, and subsequent developmental regression with loss of motor and language skills. RTT is caused by heterozygosity for mutations in the X-linked gene MECP2, which encodes methyl-CpG binding protein 2. MeCP2 is a multifunctional protein that can act as an architectural chromatin-binding protein, a function that is unrelated to its ability to bind methyl-CpG and to attract chromatin modification complexes. Inactivating mutations that cause RTT in females are not prenatally lethal in males, but lead to profound congenital encephalopathy. Molecular diagnoses of RTT, through demonstration of a MECP2 mutation, made at an early stage of the disorder, usually confirm the sporadic nature and very low recurrence risk of the condition. A positive DNA test result, however, also predicts the inevitable clinical course, given the lack of effective intervention. Initial hypotheses indicating that the MeCP2 protein acts as a genome-wide transcriptional repressor were not confirmed by global gene expression studies in various tissues of individuals with RTT and mouse models of MeCP2 deficiency. Rather, recent evidence points to low-magnitude effects of a small number of genes - including the brain-derived neurotrophic factor pathway and glucocorticoid response genes - that might affect formation and maturation of synapses or synaptic function in postmitotic neurons. C1 Stanford Univ, Sch Med, Dept Genet, Beckman Ctr Mol & Genet Med, Stanford, CA 94305 USA. RP Francke, U (reprint author), Stanford Univ, Sch Med, Dept Genet, Beckman Ctr Mol & Genet Med, B201,279 Campus Dr, Stanford, CA 94305 USA. 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Clin. Pract. Neurol. PD APR PY 2006 VL 2 IS 4 BP 212 EP 221 DI 10.1038/ncpneuro0148 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA 026RI UT WOS:000236359400009 PM 16932552 ER PT J AU Rezaie, P Mason, S Afzal, S Kibble, M Al-Sarraj, S Dean, AF Schmitz, C AF Rezaie, P Mason, S Afzal, S Kibble, M Al-Sarraj, S Dean, AF Schmitz, C TI Assessment of glial cell reactivity within the frontal lobe in autism SO NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY LA English DT Meeting Abstract CT 107th Meeting of the British-Neuropathological-Society CY JAN 11-13, 2006 CL London, ENGLAND SP British Neuropathol Soc C1 Open Univ, Dept Biol Sci, Neuropathol Res Lab, Fac Sci, Milton Keynes MK7 6AA, Bucks, England. Kings Coll London, Inst Psychiat, Dept Neurosci, London WC2R 2LS, England. Inst Psychiat, MRC, London Neurodegenerat Dis Brain Bank, London, England. Kings Coll Hosp London, Dept Clin Neuropathol, London, England. Addenbrookes Hosp NHS Trust, Dept Histopathol, Cambridge, England. Univ Maastricht, Dept Psychiat & Neruopsychol, Div Cellular Neurosci, Maastricht, Netherlands. EM p.rezaie@open.ac.uk NR 0 TC 1 Z9 1 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0305-1846 J9 NEUROPATH APPL NEURO JI Neuropathol. Appl. Neurobiol. PD APR PY 2006 VL 32 IS 2 BP 226 EP 227 PG 2 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 021MH UT WOS:000235986800027 ER PT J AU Biever, C AF Biever, C TI Please stop me if I'm boring you SO NEW SCIENTIST LA English DT Article AB One of the problems facing people with autism is an inability to pick up on social cues. Failure to notice that they are boring or confusing their listeners can be particularly damaging. An emotional social intelligence prosthetic device that can pick up on people's emotions such as happiness, sadness, anger, fear, surprise and disgust is being developed to help people with autism relate to those around them. It will alert its autistic user if the person they are talking to starts showing signs of getting bored or annoyed. EM celeste.biever@newscientist.com NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD APR 1 PY 2006 VL 190 IS 2545 BP 30 EP 30 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 029WH UT WOS:000236594600041 ER PT J AU Malow, BA McGrew, SG Harvey, M Henderson, LM Stone, WL AF Malow, BA McGrew, SG Harvey, M Henderson, LM Stone, WL TI Impact of treating sleep apnea in a child with autism spectrum disorder SO PEDIATRIC NEUROLOGY LA English DT Article ID BEHAVIORS; SYMPTOMS; DEFICITS AB Sleep disorders can affect daytime functioning in a variety of neurologic conditions, including autism spectrum disorder. This report describes improvements in sleep, social communication, attention, repetitive behaviors, and hypersensitivity after adenotonsillectomy for obstructive sleep apnea in a 5-year-old female with an autism spectrum disorder. Improvements were documented via pre- and postsurgical measures of parent report, polysomnography, validated sleep and behavior scales, and the Autism Diagnostic Observation Schedule. Identification and treatment of sleep disorders, including obstructive sleep apnea, may improve daytime behavior in children with autism spectrum disorders. (c) 2006 by Elsevier Inc. All rights reserved. C1 Vanderbilt Univ, Dept Neurol, Sch Med, Nashville, TN 37212 USA. Vanderbilt Univ, Kennedy Ctr, Sch Med, Nashville, TN 37212 USA. Vanderbilt Univ, Vanderbilt Childrens Hosp, Sch Med, Dept Pediat, Nashville, TN 37212 USA. Vanderbilt Univ, Dept Special Educ, Nashville, TN 37212 USA. Vanderbilt Univ, Dept Pediat, Sch Med, Nashville, TN 37212 USA. 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PD APR PY 2006 VL 34 IS 4 BP 325 EP 328 DI 10.1016/j.pediatrneurol.2005.08.021 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 039KS UT WOS:000237305100016 PM 16638513 ER PT J AU Sperner-Unterweger, B Winkler, C Fuchs, D AF Sperner-Unterweger, B Winkler, C Fuchs, D TI Immune activation in autism SO PEDIATRIC NEUROLOGY LA English DT Letter C1 Innsbruck Med Univ, Dept Psychiat, Bioctr, A-6020 Innsbruck, Austria. Innsbruck Med Univ, Div Biol Chem, Bioctr, A-6020 Innsbruck, Austria. RP Sperner-Unterweger, B (reprint author), Innsbruck Med Univ, Dept Psychiat, Bioctr, A-6020 Innsbruck, Austria. CR SPERNREUNTERWEG, IN PRESS DRUGS Wirleitner B, 2003, CURR MED CHEM, V10, P1581, DOI 10.2174/0929867033457179 Zimmerman AW, 2005, PEDIATR NEUROL, V33, P195, DOI 10.1016/j.pediatrneurol.2005.03.014 NR 3 TC 5 Z9 5 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0887-8994 J9 PEDIATR NEUROL JI Pediatr. Neurol. PD APR PY 2006 VL 34 IS 4 BP 333 EP 333 DI 10.1016/j.pediatrneurol.2005.12.013 PG 1 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 039KS UT WOS:000237305100018 PM 16638516 ER PT J AU Zimmerman, AW Connors, SL Jyonouchi, H Milstien, S Heyes, MP AF Zimmerman, AW Connors, SL Jyonouchi, H Milstien, S Heyes, MP TI Immune activation in autism - Response SO PEDIATRIC NEUROLOGY LA English DT Letter C1 Kennedy Krieger Inst, Baltimore, MD USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Newark, NJ 07103 USA. NIMH, Bethesda, MD 20892 USA. PsychoGenics Inc, Hawthorne, NY USA. RP Zimmerman, AW (reprint author), Kennedy Krieger Inst, Baltimore, MD USA. CR Ming X, 2005, PROSTAG LEUKOTR ESS, V73, P379, DOI 10.1016/j.plefa.2005.06.002 Vargas DL, 2005, ANN NEUROL, V57, P67, DOI 10.1002/ana.20315 NR 2 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0887-8994 J9 PEDIATR NEUROL JI Pediatr. Neurol. PD APR PY 2006 VL 34 IS 4 BP 333 EP 333 DI 10.1016/j.pediatrneurol.2006.03.001 PG 1 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 039KS UT WOS:000237305100019 ER PT J AU Shattuck, PT AF Shattuck, PT TI The contribution of diagnostic substitution to the growing administrative prevalence of autism in US special education SO PEDIATRICS LA English DT Article DE autism; prevalence ID ET-AL. 2002; CHANGING PREVALENCE; SPECTRUM DISORDERS; POPULATION; CALIFORNIA; CHILDREN; VACCINE; IDENTIFICATION; ASSOCIATION; MINNESOTA AB OBJECTIVE. Growing administrative prevalence of autism has stirred public controversy and concern. The extent to which increases in the administrative prevalence of autism have been associated with corresponding decreases in the use of other diagnostic categories is unknown. The main objective of this study was to examine the relationship between the rising administrative prevalence of autism in US special education and changes in the use of other classification categories. METHODS. The main outcome measure was the administrative prevalence of autism among children ages 6 to 11 in US special education. Analysis involved estimating multilevel regression models of time-series data on the prevalence of disabilities among children in US special education from 1984 to 2003. RESULTS. The average administrative prevalence of autism among children increased from 0.6 to 3.1 per 1000 from 1994 to 2003. By 2003, only 17 states had a special education prevalence of autism that was within the range of recent epidemiological estimates. During the same period, the prevalence of mental retardation and learning disabilities declined by 2.8 and 8.3 per 1000, respectively. Higher autism prevalence was significantly associated with corresponding declines in the prevalence of mental retardation and learning disabilities. The declining prevalence of mental retardation and learning disabilities from 1994 to 2003 represented a significant downward deflection in their preexisting trajectories of prevalence from 1984 to 1993. California was one of a handful of states that did not clearly follow this pattern. CONCLUSIONS. Prevalence findings from special education data do not support the claim of an autism epidemic because the administrative prevalence figures for most states are well below epidemiological estimates. The growing administrative prevalence of autism from 1994 to 2003 was associated with corresponding declines in the usage of other diagnostic categories. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. RP Shattuck, PT (reprint author), Univ Wisconsin, Waisman Ctr 533B, 1500 Highland Ave, Madison, WI 53705 USA. 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RP Newschaffer, CJ (reprint author), Johns Hopkins Bloomberg Sch Publ Hlth, Dept Epidemiol, Ctr Autism & Dev Disabilities Epidemiol, 615 N Wolfe St,Room E6030, Baltimore, MD 21205 USA. EM cnewscha@jhsph.edu CR NEWSCHAFFER CJ, 2005, PEDIATRICS, V115 Shattuck PT, 2006, PEDIATRICS, V117, P1028, DOI 10.1542/peds.2005-1516 NR 2 TC 11 Z9 11 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 APR PY 2006 VL 117 IS 4 BP 1436 EP 1437 DI 10.1542/peds.2005-2834 PG 2 WC Pediatrics SC Pediatrics GA 029EA UT WOS:000236540500081 PM 16585345 ER PT J AU Shattuck, PT AF Shattuck, PT TI Diagnostic substitution and changing autism prevalence SO PEDIATRICS LA English DT Editorial Material ID RELIABILITY; DISORDER C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. RP Shattuck, PT (reprint author), Univ Wisconsin, Waisman Ctr 533B, 1500 Highland Ave, Madison, WI 53705 USA. 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In particular, confirmatory factor analyses comparing a unifactorial structure and a three correlated factor structure suggest that the three factor structure proposed by Lawrence et al. (2004) is a better fit. Exploratory analysis using modification indices suggests that it might be possible to measure the three factors of empathy; cognitive empathy, emotional reactivity and social skills with three five item scales. The problems of self-report measures are discussed as are the problems posed by the pattern of sex differences on these three factors. Finally some links are suggested between the work on EQ and previous work on emotional intelligence. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Durham, Dept Psychol, Stockton On Tees TS17 6BH, England. Univ Keele, Sch Psychol, Keele ST5 5BG, Staffs, England. RP Muncer, SJ (reprint author), Univ Durham, Dept Psychol, Queens Campus, Stockton On Tees TS17 6BH, England. 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H., 1989, EZPATH CAUSAL MODELL NR 27 TC 64 Z9 65 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 APR PY 2006 VL 40 IS 6 BP 1111 EP 1119 DI 10.1016/j.paid.2005.09.020 PG 9 WC Psychology, Social SC Psychology GA 031KB UT WOS:000236702300003 ER PT J AU [Anonymous] AF [Anonymous] TI Risperidone - Behavioural disorders in children with autism or mental disabilities: no progress SO PRESCRIRE INTERNATIONAL LA English DT Article ID DOUBLE-BLIND; WEIGHT-GAIN; ADOLESCENTS; ANTIPSYCHOTICS AB Sedative drugs are one option when autistic or mentally disabled children have behavioural disorders that place them (or other people) in physical danger. Among the classic neuroleptics, haloperidol is the drug with the best-documented efficacy and safety. Placebo-controlled trials have also shown lithium to be effective for this use. Clinical evaluation of risperidone in children with mental disabilities includes 3 placebo-controlled double-blind trials, 2 of which involved 118 and 110 children aged from 5 to 12 years who were treated for 6 weeks. All 3 trials showed a partial behavioural improvement in about 75% of children receiving risperidone, versus about 30% of children in the placebo groups. Clinical evaluation of risperidone in autistic children includes 2 placebo-controlled double-blind trials involving 110 and 79 children who were treated for 8 weeks. One of these studies has been published in detail: 69% of children partially improved with risperidone, versus 12% of the children on placebo. Given the absence of clinical trials comparing risperidone with haloperidol or lithium, there is no evidence that risperidone is more effective than these other treatments. The principal adverse events observed in short-term trials of risperidone were drowsiness (affecting about 50% of children), weight gain (about 1.2 kg per month during the first months of treatment), and hyperprolactinaemia (affecting about 12% of children). Extrapyramidal disorders were infrequent during short-term trials, but their incidence reached about 25% after a year of risperidone treatment. The impact of long-term risperidone therapy on growth and mental development is not known. In France treatment is about 7 times more expensive with risperidone than with haloperidol. In practice, the risk-benefit balance of risperidone in the treatment of autistic or mentally disabled children with behavioural disorders is no better overall than that of older products such as haloperidol and lithium, which, in the absence of anything better, remain the standard drugs. 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PD APR PY 2006 VL 15 IS 82 BP 43 EP 45 PG 3 GA 025CW UT WOS:000236243900002 ER PT J AU Bu, B Ashwood, P Harvey, D King, IB Van de Water, J Jin, LW AF Bu, B Ashwood, P Harvey, D King, IB Van de Water, J Jin, LW TI Fatty acid compositions of red blood cell phospholipids in children with autism SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID SCHIZOPHRENIC-PATIENTS; SPECTRUM DISORDERS; LIPID-PEROXIDATION; OXIDATIVE STRESS; METABOLISM; OMEGA-3-FATTY-ACIDS; SUPPLEMENTATION; QUESTIONNAIRE; DEFICIENCY; MEMBRANES AB We compared the compositions of fatty acids including n-3, n-6 polyunsaturated fatty acids, trans- and cis-monounsaturated fatty acids, and saturated fatty acids in the red blood cell membranes of 40 children with autism (20 with early onset autism and 20 with developmental regression) and age-matched, 20 typically developing controls and 20' subjects with non-autistic developmental disabilities. The main findings include increased levels of eicosenoic acid (20:1n9) and erucic acid (22:1n9) in autistic subjects with developmental regression when compared with typically developing controls. In addition, an. increase in 20:2n6 and a decrease in 16:1 n7t were observed in children with clinical regression compared to those with early onset autism. Our results do not provide strong evidence for the hypothesis that abnormal fatty acid metabolism plays a role in the pathogenesis of autism spectrum disorder, although they suggest Borne metabolic or dietary abnormalities in the regressive form of autism., (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ Calif Davis, Dept Pathol, MIND Inst, Sacramento, CA 95817 USA. NIEHS, Dept Med Microbiol & Immunol, MIND Inst, Ctr Childrens Environm Hlth, Res Triangle Pk, NC 27709 USA. Univ Calif Davis, Div Biostat, Dept Publ Hlth Sci, Davis, CA 95616 USA. 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Essent. Fatty Acids PD APR PY 2006 VL 74 IS 4 BP 215 EP 221 DI 10.1016/j.plefa.2006.02.001 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA 035HT UT WOS:000236992300001 PM 16581239 ER PT J AU Tani, P Lindberg, N Appelberg, B Nieminen-Von Wendt, T Von Wendt, L Porkka-Heiskanen, T AF Tani, P Lindberg, N Appelberg, B Nieminen-Von Wendt, T Von Wendt, L Porkka-Heiskanen, T TI Clinical neurological abnormalities in young adults with Asperger syndrome SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE Asperger syndrome; neurological abnormalities; neurological soft signs ID SOFT-SIGNS; SCHIZOPHRENIC-PATIENTS AB Children with Asperger syndrome (AS), a neurodevelopmental disorder falling in the autism spectrum disorders, have an increased rate of neurological abnormalities, especially in motor coordination. While AS is a lifelong condition, little is known about the persistence of neurological abnormalities in adulthood. Twenty young adults with AS were compared with 10 healthy controls using a structured clinical neurological rating scale. The score for neurological abnormalities was higher in the AS group. In addition, a subscore for neurological soft signs indicating defective functioning of the central nervous system with a non-localizing value was significantly higher in the AS subjects. This preliminary study indicates that neurological abnormalities, soft signs in particular, represent a non-specific vulnerability factor for AS. Consistent with other features of AS, neurological abnormalities seem to persist into adulthood. C1 Univ Helsinki, Biomedicum Helsinki, Dept Physiol, Inst Biomed, FIN-00014 Helsinki, Finland. Univ Helsinki, Dept Psychiat, FIN-00014 Helsinki, Finland. Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Helsinki, Finland. RP Tani, P (reprint author), Univ Helsinki, Biomedicum Helsinki, Dept Physiol, Inst Biomed, POB 63, FIN-00014 Helsinki, Finland. 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Neurosci. PD APR PY 2006 VL 60 IS 2 BP 253 EP 255 DI 10.1111/j.1440-1819.2006.01494.x PG 3 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 020UV UT WOS:000235939000019 PM 16594952 ER PT J AU Senju, A Hasegawa, T AF Senju, Atsushi Hasegawa, Toshikazu TI Do the upright eyes have it? SO PSYCHONOMIC BULLETIN & REVIEW LA English DT Article ID UPSIDE-DOWN FACES; GAZE DIRECTION; PERCEPTION; CONTACT; RECOGNITION; LOOKING; AUTISM; EXPRESSION; EXPERTISE; CHILDREN AB Eye contact is crucial for social communication. A perceived direct gaze facilitates detection, whereas face inversion diminishes this facilitative effect (Senju, Hasegawa, & Tojo, 2005). In the present study, we adopted a visual search paradigm to investigate why a direct gaze facilitates detection in an upright face, but not in an upside-down face. Upright eyes were found to facilitate detection even when other parts of the face were inverted or absent, whereas inverted eyes had no effect on search performance. A critical role for the morphological information of upright eyes, which can be distorted by "eye inversion," in direct gaze processing is suggested. C1 Univ Tokyo, Tokyo, Japan. RP Senju, A (reprint author), Kyushu Univ, RISTEX, Japan Sci & Technol Agcy, Stn Collaborat Res 2,Higashi Ku, 705,3-1-1 Maidashi, Fukuoka 8128582, Japan. 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Bull. Rev. PD APR PY 2006 VL 13 IS 2 BP 223 EP 228 DI 10.3758/BF03193834 PG 6 WC Psychology, Mathematical; Psychology, Experimental SC Psychology GA 064OX UT WOS:000239100100004 PM 16892985 ER PT J AU Papp, S AF Papp, Szilvia TI A relevance-theoretic account of the development and deficits of theory of mind in normally developing children and individuals with autism SO THEORY & PSYCHOLOGY LA English DT Article DE Autism Spectrum Disorder (ASD); communication; development and deficits of pragmatic skills; relevance theory; mind-reading; Theory of Mind ID PRAGMATICS; MODULARITY AB This paper argues that positing a Theory of Mind and mind-reading abilities in particular is necessary in order to be able to account for the development and possible impairments of communication in normally developing children and individuals with autism. To account for the different impairments that people diagnosed with Autism Spectrum Disorder (ASD) exhibit, what is needed is a refinement of the levels or degrees of mind-reading abilities that are usually posited in the literature. Instead of the two-tiered system of first- and second-order mind-reading abilities, there is a need to propose several other layers of meta-representation to account for the comprehension of different communicative events, such as metaphors, under- and overstatements, direct and indirect speech acts, lies, deceits, humour, jokes, irony and sarcasm. This paper assumes a relevance theoretic perspective to explain deficits in communicative abilities in individuals with ASD. It suggests that the pragmatic impairments specific to autism can be accounted for by the role of context retrieval in the comprehension and production process, especially those related to knowledge about the speaker. C1 Univ Portsmouth, Sch Languages & Area Studies, Portsmouth PO1 2DZ, Hants, England. RP Papp, S (reprint author), Univ Portsmouth, Sch Languages & Area Studies, King Henry 1 St, Portsmouth PO1 2DZ, Hants, England. 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PD APR PY 2006 VL 16 IS 2 BP 141 EP 161 DI 10.1177/0959354306062532 PG 21 WC Psychology, Multidisciplinary SC Psychology GA 042MA UT WOS:000237530900002 ER PT J AU Colombino, T AF Colombino, T TI Problems with a relevance-theoretic account of autism SO THEORY & PSYCHOLOGY LA English DT Editorial Material DE autism; ethnomethodology; relevance theory; Theory of Mind AB This paper responds to Szilvia Papp's paper 'A Relevance Theoretic Account of the Development and Deficits of Theory of Mind in Normally Developing Children and Individuals with Autism'. This response argues that positing mind-reading abilities, in the form of a Theory of Mind, is necessary to account for autistic behavior only if one subscribes a priori to theoretical reductions of mental predicates (such as understanding) to cognitive and linguistic processes. This, in the author's opinion, is an unnecessary theoretical appropriation of concepts the meaning of which has not been logically distinguished from their common-sense use. Ordinary observable behavior (autistic or otherwise) is described in language that does not imply, and from which one can not unproblematically infer, theoretical propositions of a neurobehavioral kind. This response therefore argues that the refinement to Theory of Mind proposed by Szilvia Papp, into first- and second-order mind-reading abilities, does not, in fact, address this critique. C1 Xerox Res Ctr Europe, Work Practice Technol Grp, F-38240 Meylan, France. RP Colombino, T (reprint author), Xerox Res Ctr Europe, Work Practice Technol Grp, 6,Chemin Maupertuis, F-38240 Meylan, France. EM Tommaso.Colombino@xrce.xerox.com CR BENNETT MRP, 2003, PHILOSOPHICAL FDN NE Coulter J., 2005, CONVERSATION COGNITI, P79, DOI 10.1017/CBO9780511489990.004 Lynch M, 2005, CONVERSATION COGNITI, P226, DOI 10.1017/CBO9780511489990.011 Lynch Michael, 1993, SCI PRACTICE ORDINAR Papp S, 2006, THEOR PSYCHOL, V16, P141, DOI 10.1177/0959354306062532 Sacks H, 1995, LECT CONVERSATION Sharrock W, 2004, THEOR PSYCHOL, V14, P579, DOI 10.1177/0959354304046174 NR 7 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0959-3543 J9 THEOR PSYCHOL JI Theory Psychol. PD APR PY 2006 VL 16 IS 2 BP 169 EP 177 DI 10.1177/0959354306062534 PG 9 WC Psychology, Multidisciplinary SC Psychology GA 042MA UT WOS:000237530900004 ER PT J AU Del Viva, MM Igliozzi, R Tancredi, R Brizzolara, D AF Del Viva, MM Igliozzi, R Tancredi, R Brizzolara, D TI Spatial and motion integration in children with autism SO VISION RESEARCH LA English DT Article DE autism; spatial integration; motion perception ID CAT VISUAL-CORTEX; PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME; CONTOUR INTEGRATION; BIOLOGICAL MOTION; DEFICITS; CONNECTIONS; SENSITIVITY; INDIVIDUALS; SPECIFICITY AB Neuropsychological and psychophysical studies report controversial results regarding local-global visual processing and motion perception in autism. Here, we investigate contour integration and motion perception in an accurately diagnosed sample of autistic children, using low-level psychophysical tasks. We measured detection thresholds for a closed chain of Gabor patches, for different values of inter-element distance and we measured coherency thresholds of optic flow motion stimuli. Both experiments show comparable performances between autistics and normal subjects, demonstrating no evidence of early perceptual integration deficits. Some improvement in performance with age is detected in both groups. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Florence, Dept Psychol, I-50125 Florence, Italy. CNR, Area Ric Pisa, Ist Neurosci, I-56100 Pisa, Italy. IRCCS Stella Maris, Pisa, Italy. Univ Pisa, Dept Neuropsychiat, I-56100 Pisa, Italy. RP Del Viva, MM (reprint author), Univ Florence, Dept Psychol, Via S Niccolo,93, I-50125 Florence, Italy. 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PD APR PY 2006 VL 46 IS 8-9 BP 1242 EP 1252 DI 10.1016/j.visres.2005.10.018 PG 11 WC Neurosciences; Ophthalmology SC Neurosciences & Neurology; Ophthalmology GA 030VW UT WOS:000236664200010 PM 16384591 ER PT J AU Samochowiec, J Grzywacz, A Kucharska-Mazur, J Samochowiec, A Horodnicki, J Pelka-Wysiecka, J Syrek, S AF Samochowiec, J Grzywacz, A Kucharska-Mazur, J Samochowiec, A Horodnicki, J Pelka-Wysiecka, J Syrek, S TI Family-based and case-control association studies of glutamate receptor GRIK3 Ser310Ala polymorphism in Polish patients and families with alcohol dependence SO NEUROSCIENCE LETTERS LA English DT Article DE alcohol dependence; genetics; TDT; case-control study; kainate receptor ID KAINATE RECEPTOR; GLUTAMATE-RECEPTOR-6 GENE; DELIRIUM-TREMENS; INDIVIDUALS; TRANSMISSION; EXPRESSION; SUBUNITS; AUTISM AB The aim of this study was to evaluate the role of the GRIK3 functional polymorphism (Ser310Ala) in the pathogenesis of alcoholism. This polymorphism was investigated in two types of studies: (1) the association study in a whole group of alcoholics (116 patients fulfilling ICD-10 alcohol dependence (AD) criteria and 255 controls, Polish descent) and homogenous overlapping subgroups of patients with: a history of delirium tremens and/or alcohol seizures, early age of onset of alcoholism (AOO < 26 years), a co-occurrence of dissocial personality disorder, a history of familial alcoholism; (2) the family-based study (using Transmission Disequilibrium Test (TDT) in 100 Polish families with alcohol dependence). The history of alcoholism was obtained using SSAGA (Polish version). GRIK3 functional polymorphism was determined using PCR. TDT revealed an adequate transmission of both alleles to the affected offspring in the whole group of alcohol families (29 x Ser, 24 x Ala; chi(2) = 0.472; d.f. = 1; p=0.492) and in the homogenous subgroups of families. No significant associations between any of the above mentioned alcohol phenotypes and Ser310 allele were observed (the whole AD group: p = 0.66 AD with delirium and/or seizures: p = 0.521; early onset AD: p = 0.868; AD with familial history of alcoholism: p = 0.798 and AD with dissocial personality disorder: p = 0.618). These findings do not seem to support the hypothesis of the role of this polymorphism in the pathogenesis of alcoholism. (c) 2005 Elsevier Ireland Ltd. All rights reserved. C1 Pomeranian Med Univ, Dept Psychiat, PL-71460 Szczecin, Poland. Tech Univ Szczecin, MSKP, PL-71062 Szczecin, Poland. RP Samochowiec, J (reprint author), Pomeranian Med Univ, Dept Psychiat, Broniewskiego 26, PL-71460 Szczecin, Poland. 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PD MAR 24 PY 2006 VL 1079 BP 15 EP 24 DI 10.1016/j.brainres.2006.01.054 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 032NY UT WOS:000236782500003 PM 16680812 ER PT J AU Wheelwright, S Baron-Cohen, S Goldenfeld, N Delaney, J Fine, D Smith, R Weil, L Wakabayashi, A AF Wheelwright, S Baron-Cohen, S Goldenfeld, N Delaney, J Fine, D Smith, R Weil, L Wakabayashi, A TI Predicting autism spectrum quotient (AQ) from the systemizing quotient-revised (SQ-R) and empathy quotient (EQ) SO BRAIN RESEARCH LA English DT Article DE empathizing; systemizing; autism spectrum quotient ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME; ADULTS; BRAIN AB Background: Empathizing is a specific component of social cognition. Empathizing is also specifically impaired in autism spectrum condition (ASC). These are two dimensions, measurable using the Empathy Quotient (EQ) and the Autism Spectrum Quotient (AQ). ASC also involves strong systemizing, a dimension measured using the Systemizing Quotient (SQ). The present study examined the relationship between the EQ, AQ and SQ The EQ and SQ have been used previously to test for sex differences in 5 'brain types' (Types S, E, B and extremes of Type S or E). Finally, people with ASC have been conceptualized as an extreme of the male brain. Method: We revised the SQ to avoid a traditionalist bias, thus producing the SQ-Revised (SQR). AQ and EQ were not modified. All 3 were administered online. Sample: Students (723 males, 1038 females) were compared to a group of adults with ASC group (69 males, 56 females). Aims: (1) To report scores from the SQ-R. (2) To test for SQ-R differences among students in the sciences vs. humanities. (3) To test if AQ can be predicted from EQ and SQ-R scores. (4) To test for sex differences on each of these in a typical sample, and for the absence of a sex difference in a sample with ASC if both males and females with ASC are hyper-masculinized. (5) To report percentages of males, females and people with an ASC who show each brain type. Results: AQ score was successfully predicted from EQ and SQ-R scores. In the typical group, males scored significantly higher than females on the AQ and SQ-R, and lower on the EQ. The ASC group scored higher than sex-matched controls on the SQ-R, and showed no sex differences on any of the 3 measures. More than twice as many typical males as females were Type S, and more than twice as many typical females as males were Type E. The majority of adults with ASC were Extreme Type S, compared to 5% of typical males and 0.9% of typical females. The EQ had a weak negative correlation with the SQ-R. Discussion: Empathizing is largely but not completely independent of systemizing. The weak but significant negative correlation may indicate a trade-off between them. ASC involves impaired empathizing alongside intact or superior systemizing. Future work should investigate the biological basis of these dimensions, and the small trade-off between them. (c) 2006 Elsevier B.V. All rights reserved. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. Univ Illinois, Dept Phys, Urbana, IL 61801 USA. Chiba Univ, Dept Psychol, Chiba 2638522, Japan. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18b Trumpington Rd, Cambridge CB2 2AH, England. 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The deletion was transmitted from an asymptomatic mother to her two children with severe developmental delay, no speech development and autistic behavior. Assessment of the deletion boundaries by FISH and PCR analyses indicated that the deletions encompasses 27 genes. Several of these genes are associated with known disorders, like KAL1 (Kallmann syndrome), steroid sulfatase (STS) (X-linked ichtyosis), and arylsulfarase E (ARSE) (chondrodysplasia punctata). The deletion also includes all four VCX genes (VCX-A, VCX-B1, VCX-B, and VCX-C) and the neuroligin 4 (NLGN4) gene. VCX-A deficiency has been shown previously to be associated with mental retardation and NLGN4 Mutations lead to mental retardation in conjunction with autism. Functional deficiency of both MRX genes, VCX-A and NLGN4, are most likely associated with the impaired cognitive development of the patients described here. The phenotype associated with the Xp deletion was highly variable in female carriers and might be attributed to unfavorable X inactivation. However, all the 27 genes included in the deleted interval escape X inactivation and are expressed at variable levels from the normal X chromosome. Thus, the overall X inactivation pattern and inter-individual expression variability of the genes in distal Xp might be determinants of the phenotype associated with the deletion. (c) 2006 Wiley-Liss, Inc. C1 Univ Ulm, Dept Human Genet, Abt Human Genet, D-89081 Ulm, Germany. RP Kehrer-Sawatzki, H (reprint author), Univ Ulm, Dept Human Genet, Abt Human Genet, Albert Einstein Allee 11, D-89081 Ulm, Germany. 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J. Med. Genet. A PD MAR 15 PY 2006 VL 140A IS 6 BP 604 EP 610 DI 10.1002/ajmg.a.31145 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 019DT UT WOS:000235816500009 PM 16470742 ER PT J AU Mineur, YS Huynh, LX Crusio, WE AF Mineur, YS Huynh, LX Crusio, WE TI Social behavior deficits in the Fmr1 mutant mouse SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE Fragile X Syndrome; autism; social behavior; mouse model of autism; Fmr1 KO; C57BL/6J; DBA/2J; BALB/cJ ID FRAGILE-X-SYNDROME; KNOCKOUT MOUSE; AUTISM; MICE; MODEL; GENE AB Mice exhibiting deficits in social behavior may provide valuable models for autistic-like behavioral problems. We tested social interactions in male mice from three inbred strains: C57BL/6J (136), BALB/cJ (C) and DBA/2J (D2). All three strains showed gradual habituation of the number of social interactions with an ovariectomized female over four subsequent 2 min sessions, returning to initial levels when presented with another stimulus mouse. Next, we studied males with a knockout mutation in the Fmr1 gene on a B6 background. KO animals showed strongly reduced levels of social interaction, which were about similar as those of habituated controls. This social behavior deficit suggests that Fmr1 KO mice could possibly be used as models for autistic behaviors. (c) 2005 Elsevier B.V. All rights reserved. C1 Univ Massachusetts, Sch Med, Brudnick Neuropsychiat Res Inst, Worcester, MA USA. RP Crusio, WE (reprint author), CNRS, UMR 5106, Cognit Neurosci Lab, Ave Fac, F-33405 Talence, France. 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Brain Res. PD MAR 15 PY 2006 VL 168 IS 1 BP 172 EP 175 DI 10.1016/j.bbr.2005.11.004 PG 4 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 015VP UT WOS:000235579600020 PM 16343653 ER PT J AU Baron, CA Tepper, CG Liu, SY Davis, RR Wang, NJ Schanen, NC Gregg, JP AF Baron, CA Tepper, CG Liu, SY Davis, RR Wang, NJ Schanen, NC Gregg, JP TI Genomic and functional profiling of duplicated chromosome 15 cell lines reveal regulatory alterations in UBE3A-associated ubiquitin-proteasome pathway processes SO HUMAN MOLECULAR GENETICS LA English DT Article ID ANGELMAN-SYNDROME GENE; SUMO-1 MODIFICATION; IMPRINTED EXPRESSION; MECP2 DEFICIENCY; SNURF-SNRPN; SNP-ARRAY; AUTISM; UBE3A; PROTEIN; P53 AB Autism is a complex neurodevelopmental disorder having both genetic and epigenetic etiological elements. Isodicentric chromosome 15 (Idic15), characterized by duplications of the multi-disorder critical region of 15q11-q14, is a relatively common cytogenetic event. When the duplication involves maternally derived content, this abnormality is strongly correlated with autism disorder. However, the mechanistic links between Idic15 and autism are ill-defined. To gain insight into the potential role of these duplications, we performed a comprehensive, genomics-based characterization of an in vitro model system consisting of lymphoblast cell lines derived from individuals with both autism and Idic15. Array-based comparative genomic hybridization using commercial single nucleotide polymorphism arrays was conducted and found to be capable of sub-classifying Idic15 samples by virtue of the lengths of the duplicated chromosomal region. In further analysis, whole-genome expression profiling revealed that 112 transcripts were significantly dysregulated in samples harboring duplications. Paramount among changing genes was ubiquitin protein ligase E3A (UBE3A; 15q11-q13), which was found to be nearly 1.5-2.0-fold up-regulated in duplicated samples at both the RNA and protein levels. Other key findings from gene expression analysis included two down-regulated genes, APP and SUMO1, with well-characterized roles in the process of apoptosis. We further demonstrate in this lymphoblast model that the gene-dosage directed increases in UBE3A levels can lead to dysregulation of the process of ubiquitination in response to genotoxic insult. This study provides insight into the direct and indirect effects of copy number gains in chromosome 15 and provides a framework for the study of these effects in neuronal systems. C1 Univ Calif Davis, Sch Med, Dept Pathol, Sacramento, CA 95817 USA. Univ Calif Davis, Sch Med, Dept Biochem & Mol Med, Sacramento, CA 95817 USA. Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90024 USA. Alfred I Dupont Hosp Children, Ctr Pediat Res, Wilmington, DE USA. RP Gregg, JP (reprint author), MIND Inst Wet Lab, 2805 50th St,2420, Sacramento, CA 95817 USA. 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Mol. Genet. PD MAR 15 PY 2006 VL 15 IS 6 BP 853 EP 869 DI 10.1093/hmg/ddl004 PG 17 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 018NS UT WOS:000235771800005 PM 16446308 ER PT J AU Seeman, C AF Seeman, C TI Autism and the God connection: Redefining the autistic experience through extraordinary accounts of spiritual giftedness. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Michigan, Kresge Business Adm Lib, Ann Arbor, MI 48109 USA. RP Seeman, C (reprint author), Univ Michigan, Kresge Business Adm Lib, Ann Arbor, MI 48109 USA. CR Stillman W., 2006, AUTISM GOD CONNECTIO NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD MAR 15 PY 2006 VL 131 IS 5 BP 87 EP 87 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 023PJ UT WOS:000236138400159 ER PT J AU Mostofsky, SH Powell, SK Blankner, JG Goldberg, MC Denckla, MB Pekar, JJ AF Mostofsky, SH Powell, SK Blankner, JG Goldberg, MC Denckla, MB Pekar, JJ TI Differences in cerebellar-cerebral activation in autism during fMRI of simple sequential finger tapping SO NEUROLOGY LA English DT Meeting Abstract CT 58th Annual Meeting of the American-Academy-of-Neurology CY APR 01-08, 2006 CL San Diego, CA SP Amer Acad Neruol NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR 14 PY 2006 VL 66 IS 5 SU 2 BP 269 EP 269 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 022PM UT WOS:000236068103115 ER PT J AU Catani, M Daly, E Embrikos, N Jones, DK Deeley, Q Murphy, DG AF Catani, M Daly, E Embrikos, N Jones, DK Deeley, Q Murphy, DG TI Cerebellar connections in autism: Specific changes in intrinsic circuitry and cerebellar outputs SO NEUROLOGY LA English DT Meeting Abstract CT 58th Annual Meeting of the American-Academy-of-Neurology CY APR 01-08, 2006 CL San Diego, CA SP Amer Acad Neruol RI daly, eileen/B-6716-2011 NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD MAR 14 PY 2006 VL 66 IS 5 SU 2 BP A328 EP A328 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 022PM UT WOS:000236068104038 ER PT J AU De Jaco, A Comoletti, D Kovarik, Z Gaietta, G Radic, Z Lockridge, O Ellisman, MH Taylor, P AF De Jaco, A Comoletti, D Kovarik, Z Gaietta, G Radic, Z Lockridge, O Ellisman, MH Taylor, P TI Abnormal processing of an autism-linked Arg to Cys mutation in proteins of the alpha/beta hydrolase fold family SO FASEB JOURNAL LA English DT Meeting Abstract CT Experimental Biology 2006 Meeting CY APR 01-05, 2006 CL San Francisco, CA SP Amer Assoc Anatomists, Amer Physiol Soc, Amer Soc Biochem & Mol Biol, Amer Soc Investigat Pathol, Amer Soc Nutr, Amer Soc Pharmacol & Expt Therapeut C1 Univ Calif San Diego, Natl Ctr Microscopy & Imaging Res, La Jolla, CA 92093 USA. Inst Med Res & Occupat Hlth, HR-10001 Zagreb, Croatia. Univ Nebraska Med Ctr, Omaha, NE 68198 USA. NR 0 TC 0 Z9 0 PU FEDERATION AMER SOC EXP BIOL PI BETHESDA PA 9650 ROCKVILLE PIKE, BETHESDA, MD 20814-3998 USA SN 0892-6638 J9 FASEB J JI Faseb J. PD MAR 6 PY 2006 VL 20 IS 4 BP A502 EP A502 PN 1 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 024OW UT WOS:000236206504172 ER PT J AU Bishop, DVM Maybery, M Wong, D Maley, A Hallmayer, J AF Bishop, DVM Maybery, M Wong, D Maley, A Hallmayer, J TI Characteristics of the broader phenotype in autism: A study of siblings using the Children's Communication Checklist-2 SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE broad phenotype; communication; parent ratings ID SPECTRUM DISORDERS; IMPAIRMENT; FAMILY; IDENTIFY; QUOTIENT; PARENTS AB Non-autistic relatives of people with autistic disorder have an increased risk of social and communicative difficulties: this is known as the "broad phenotype." Better methods for characterizing the broad phenotype are needed to facilitate identification of risk genes for autism. 29 siblings of 20 children with autistic disorder, 13 siblings of 9 children with PDDNOS, and 46 typically developing control children from 26 families were assessed by parental report using the Children's Communication Checklist-2 (CCC-2). Groups were matched on age and IQ and siblings with autism were excluded. Group mean scores on the CCC-2 differed on only one subscale, syntax. However, siblings of children with autism or PDDNOS were over-represented in the tails of the distributions of several scales, and 10 (24%) scored more than 2 SD below the control mean on a total score based on all 10 subscales. Only two of these 10 children scored above threshold on one or more scales of the Autism Diagnostic Interview-Revised (ADI-R). Children with abnormal scores on the CCC-2 total were characterized by low-verbal IQ and their fathers tended to score high on the social and communication scales of the Autism Quotient, a measure of the broad phenotype in adults. The CCC-2 shows promise as a quick screening device for the broad phenotype in non-autistic siblings of children with autism. (C) 2006 Wiley-Liss, Inc. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. Univ Western Australia, Perth, WA 6009, Australia. Stanford Univ, Stanford, CA 94305 USA. RP Bishop, DVM (reprint author), Univ Oxford, Dept Expt Psychol, Tinbergen Bldg,S Parks Rd, Oxford OX1 3UD, England. EM dorothy.bishop@psy.ox.ac.uk RI Maybery, Murray/H-5390-2014 CR Auranen M, 2002, AM J HUM GENET, V71, P777, DOI 10.1086/342720 BADDELEY A, UNPUB NONWORD MEMORY Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Bishop D. V. 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J. Med. Genet. B PD MAR 5 PY 2006 VL 141B IS 2 BP 117 EP 122 DI 10.1002/ajmg.b.30267 PN B PG 6 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 009VT UT WOS:000235142200001 PM 16389586 ER PT J AU Timmann, D Richter, S Schoch, B Frings, M AF Timmann, D Richter, S Schoch, B Frings, M TI Cerebellum and cognition - A review of the literature SO AKTUELLE NEUROLOGIE LA German DT Review ID POSTERIOR-FOSSA TUMORS; POSITRON-EMISSION-TOMOGRAPHY; VERBAL WORKING-MEMORY; LONG-TERM SEQUELAE; SHIFTING ATTENTION; LANGUAGE FUNCTIONS; MENTAL SKILLS; MOTOR-SKILLS; CHILDREN; BRAIN AB Cerebellar involvement in a wide range of cognitive tasks, including language, visuo-spatial functions, attention, executive operations as well as affect and behaviour has been proposed almost 20 years ago. An increasing number of human lesion and functional brain imaging studies appear to support the hypothesis that the cerebellum contributes to non-motor functions. Likewise cognitive and behavioural changes in psychiatric disorders, such as autism and schizophrenia, have been linked to structural cerebellar abnormalities. The ,,cerebellum and cognition" hypothesis, however, is still a matter of ongoing controversial discussion. Frequently cited early findings, for example examining specific attention and language tasks, have not been replicated in later studies or have been explained by motor components of the tasks. In addition to impaired motor function, it is unclear to what extent deficits in neuropsychological tests are Caused by unspecific effects, such as hydrocephalus, depression or global effects on brain metabolism, in particular following focal cerebellar lesions. Effects of extracerebellar lesions have to be considered, too. On the other hand, the cerebellum may be involved in specific operations in certain cognitive tasks. One example, which has been studied in detail, is a likely role of the cerebellum in the computation of temporal aspects of verbal utterances in the domains of both speech production, including inner speech, and speech perception. Whether disorders of inner speech are related to significant clinical signs of cognitive dysfunction remains to be determined. Regardless of the question whether possible cognitive deficits are caused primarily by cerebellar dysfunction, it appears useful to carefully assess neuropsychological functions in patients with cerebellar disorders. C1 Univ Duisburg Essen, Neurol Klin, D-45138 Essen, Germany. Univ Duisburg Essen, Neurochirurg Klin, D-45138 Essen, Germany. RP Timmann, D (reprint author), Univ Duisburg Essen, Neurol Klin, Hufelandstr 55, D-45138 Essen, Germany. 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PD MAR PY 2006 VL 33 IS 2 BP 70 EP 80 DI 10.1055/s-2005-867016 PG 11 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 028CQ UT WOS:000236464300003 ER PT J AU Dennis, NR Veltman, MWM Thompson, R Craig, E Bolton, PF Thomas, NS AF Dennis, NR Veltman, MWM Thompson, R Craig, E Bolton, PF Thomas, NS TI Clinical findings in 33 subjects with large supernumerary marker(15) chromosomes and 3 subjects with triplication of 15q11-q13 SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE chromosome 15; Prader-Willi; Angelman; autism; learning disability; supernumerary marker chromosome ID INV DUP(15) CHROMOSOMES; MOLECULAR CHARACTERIZATION; INTRACHROMOSOMAL TRIPLICATION; INTERSTITIAL DUPLICATIONS; PARTIAL TRISOMY; P-GENE; DUP 15; BREAKPOINTS; PHENOTYPE; FEATURES AB We present clinical data on 33 subjects with additional copies of the Prader-Willi-Angelman critical region (PWACR) contained in a Supernumerary marker chromosome (SMC). Twenty-three subjects had a typical large non-mosaic SMC(15) containing two copies of the PWACR. They showed a variable but generally severe phenotype of learning disability and autism, With seizures in approximately two-thirds. The other 10 differed from this typical pattern in respect of mosaicism, variation in copy, number, or arrangement of the PWACR within the SMC Or number of SMC per cell. Clinical severity increased with the number of additional copies of the PWACR and decreased with mosaicism for a normal cell line. There was a trend for a larger number of seizures to be associated with more severe learning disability. Three subjects with interstitial triplications of 15q11-q13 showed a range of phenotypes similar to those of the typical large SMC(15). All additional copies of the PWACR in this series Were maternally-derived. FISH and molecular, data localizing the breakpoints of the rearrangements have been previously published or are included in this report. No correlations were found between specific clinical features and variations in breakpoints proximal and distal to the PWACR. (c) 2006 Wiley-Liss, Inc. C1 Univ Southampton, Div Human Genet, Southampton, Hants, England. Wessex Clin Genet Serv, Southampton, Hants, England. Univ Cambridge, Sect Dev Pscyhiat, Cambridge, England. Inst Psychiat, MRC, Ctr Social Genet & Dev Psychiat, London SE5 8AF, England. Wessex Reg Genet Lab, Salisbury, Wilts, England. RP Dennis, NR (reprint author), Princess Anne Hosp, Southampton SO16 5YA, Hants, England. 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This child has a severe communication disorder with evidence of oromotor dyspraxia, dysmorphic features, and mild developmental delay. She is unable to cough, sneeze. or laugh spontaneously. Her deletion is on the paternally inherited chromosome and includes the FOXP2 gene, which has recently been associated with speech and language impairment and a similar from of oromotor dyspraxia in at least three other published cases. We hypothesize that our patient's communication disorder and oromotor deficiency are due to haploinsufficiency for FOXP2 and that her dysmorphism and developmental delay are a consequence of the absence of the other genes involved in the microdeletion. We propose that this patient, together with others reported in the literature, may define a new contiguous gene deletion syndrome encompassing the 7q31-FOXP2 region. Cytogenetic and molecular analysis of this region should be considered for other individuals displayng similar characteristics. (c) 2006 Wiley-Liss, Inc. C1 Hosp Sick Children, Program Genet & Genom Biol, Dept Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Hosp Sick Children, Dept Pediat Lab Med, Toronto, ON M5G 1X8, Canada. Univ Toronto, Dept Pediat, Toronto, ON, Canada. Univ Toronto, Dept Med Imaging, Toronto, ON, Canada. Univ Toronto, Dept Med, Toronto, ON, Canada. Univ Toronto, Dept Mol & Med Genet, Toronto, ON, Canada. McMaster Univ, Dept Pathol & Mol Med, Hamilton, ON, Canada. Hamilton Reg Lab Med Program, Hamilton Hlth Sci, Hamilton, ON, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. RP Scherer, SW (reprint author), Hosp Sick Children, Program Genet & Genom Biol, Dept Genet & Genom Biol, Room 9107,555 Univ Ave, Toronto, ON M5G 1X8, Canada. 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PD MAR PY 2006 VL 163 IS 3 BP 551 EP 551 DI 10.1176/appi.ajp.163.3.551 PG 1 WC Psychiatry SC Psychiatry GA 017XG UT WOS:000235726000044 PM 16513891 ER PT J AU McDougle, CJ Scahill, L Aman, MG Arnold, LE McCracken, JT Tierney, E Vitiello, B AF McDougle, CJ Scahill, L Aman, MG Arnold, LE McCracken, JT Tierney, E Vitiello, B TI Risperidone for the core symptom domains of autism - Reply SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Letter CR Mccracken JT, 2005, AM J PSYCHIAT, V162, P1361 Scahill L, 2001, J CHILD ADOL PSYCHOP, V11, P377, DOI 10.1089/104454601317261555 NR 2 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD MAR PY 2006 VL 163 IS 3 BP 551 EP 552 DI 10.1176/appi.ajp.163.3.551-a PG 2 WC Psychiatry SC Psychiatry GA 017XG UT WOS:000235726000045 ER PT J AU Orsmond, GI Seltzer, MM Greenberg, JS Krauss, MW AF Orsmond, GI Seltzer, MM Greenberg, JS Krauss, MW TI Mother-child relationship quality among adolescents and adults with autism SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; EXPRESSED EMOTION; MENTAL-RETARDATION; YOUNG-CHILDREN; LATER-LIFE; PSYCHIATRIC-PATIENTS; DOWN-SYNDROME; FAMILIES; SCHIZOPHRENIA; DISABILITIES AB The mother-child relationship in families of 202 adolescents and adults with an autism spectrum disorder living at home and its association with maternal caregiving gains and strains were examined. Findings indicate a wide range of variability in the quality of the mother-child relationship, although most were characterized as positive across multiple measures. Characteristics of the son or daughter with autism (less severe maladaptive behaviors, better health, and less social impairments) and characteristics of the mother (lower levels of pessimism) were predictive of more positive mother-child relationships. In turn, specific aspects of the mother-child relationship (greater positive affect and warmth), along with other child and maternal characteristics, predicted fewer maternal caregiving strains and, to a lesser extent, greater caregiving gains. C1 Boston Univ, Sargent Coll Hlth & Rehabil Sci, Boston, MA 02215 USA. Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Brandeis Univ, Heller Sch Social Policy & Management, Waltham, MA 02254 USA. RP Orsmond, GI (reprint author), Boston Univ, Sargent Coll Hlth & Rehabil Sci, 635 Commonwealth Ave, Boston, MA 02215 USA. 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PD MAR PY 2006 VL 111 IS 2 BP 121 EP 137 DI 10.1352/0895-8017(2006)111[121:MRQAAA]2.0.CO;2 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 021YC UT WOS:000236020800005 PM 16466284 ER PT J AU Liss, M Saulnier, C Kinsbourne, DF Kinsbourne, M AF Liss, M Saulnier, C Kinsbourne, DF Kinsbourne, M TI Sensory and attention abnormalities in autistic spectrum disorders SO AUTISM LA English DT Article DE attention; autism; autistic spectrtun disorder; cluster analysis; sensory behavior ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDHOOD AUTISM; STEREOTYPED BEHAVIORS; D-AMPHETAMINE; CHILDREN; AROUSAL; BRAIN; DRUGS; MODEL; RAT AB Individuals with autistic spectrum disorders (ASDs) often experience, describe and exhibit unusual patterns of sensation and attention. These anomalies have been hypothesized to result from overarousal and consequent overfocused attention. Parents of individuals with ASD rated items in three domains, 'sensory overreactivity', 'sensory underreactivity' and 'sensory seeking behaviors', of an expanded version of the Sensory Profile, a 103-item rating scale developed for the present study. Parents also rated symptom severity, overselective attention and exceptional memory, and completed the Vineland Adaptive Behavior Scales. Of 222 rated subjects, 144 had complete data. Cluster analysis showed the predicted overfocused pattern of sensation and attention, comprising overreactivity, perseverative behavior and interests, overfocused attention and exceptional memory in 43 percent of this sample. This pattern was striking in 10 percent. The neurological basis of overreactivity and overfocusing is discussed in relation to the overarousal hypothesis. Attention is drawn to its considerable prevalence in the ASD population. C1 Univ Washington, Fredericksburg, VA USA. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. Univ Connecticut, Storrs, CT USA. New Sch Univ, New York, NY USA. RP Liss, M (reprint author), Univ Washington, Fredericksburg, VA USA. EM mliss@umw.edu CR ALVAREZ N, 1999, MOVEMENT DISORDERS N, P623 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERSON LT, 1989, J AUTISM DEV DISORD, V19, P227, DOI 10.1007/BF02211843 ANISMAN H, 1975, PSYCHOPHARMACOLOGIA, V45, P55, DOI 10.1007/BF00426210 BANNON MJ, 1983, PHARMACOL REV, V35, P53 Barrett NA, 2003, COGNITIVE BRAIN RES, V17, P1, DOI 10.1016/S0926-6410(02)00246-X BAUMAN ML, 1999, MOVEMENT DISORDERS N, P601 Belmonte MK, 2003, COGNITIVE BRAIN RES, V17, P651, DOI 10.1016/S0926-6410(03)00189-7 BERKSON G, 1964, PERCEPT MOTOR SKILL, V19, P635 Casanova MF, 2002, NEUROLOGY, V58, P428 Coleman M, 1985, BIOL AUTISTIC SYNDRO COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 COURCHESNE E, 1994, NEUROLOGY, V44, P214 CREESE I, 1974, PSYCHOPHARMACOLOGIA, V39, P345, DOI 10.1007/BF00422974 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Dawson G., 1989, AUTISM NATURE DIAGNO, P144 Dunn W, 1999, SENSORY PROFILE USER Dunn W, 2002, AM J OCCUP THER, V56, P97 EASTERBROOK JA, 1959, PSYCHOL REV, V66, P183, DOI 10.1037/h0047707 FREEMAN BJ, 1984, J AM ACAD CHILD PSY, V23, P588, DOI 10.1016/S0002-7138(09)60352-6 GAMBILL JD, 1976, PSYCHOPHARMACOLOGY, V50, P215, DOI 10.1007/BF00426835 GILLINGHAM G, 2000, AUSTIM NEW UNDERSTAN Godefroy O, 1996, BRAIN COGNITION, V30, P155, DOI 10.1006/brcg.1996.0010 Grandin T., 1996, THINKING PICTURES Harris NS, 1999, COGNITIVE BRAIN RES, V8, P61, DOI 10.1016/S0926-6410(99)00006-3 Hussman JP, 2001, J AUTISM DEV DISORD, V31, P247, DOI 10.1023/A:1010715619091 HUTT C, 1964, NATURE, V204, P908, DOI 10.1038/204908a0 KINSBOURNE M, 1979, CHILDRENS LEARNING A, pCH8 Kinsbourne M, 1980, J Dev Behav Pediatr, V1, P39 Kinsbourne M, 1991, PEDIAT NEUROLOGY BEH, P18 Kinsbourne M., 1987, NEUROBIOLOGICAL ISSU, P107, DOI DOI 10.1007/978-1-4899-1992-2_ LISS M, 1998, SENSORY SURVEY LOVAAS OI, 1971, BEHAV RES THER, V9, P305, DOI 10.1016/0005-7967(71)90042-8 LOVAAS OI, 1979, PSYCHOL BULL, V86, P1236, DOI 10.1037//0033-2909.86.6.1236 MAURER RG, 1982, J AUTISM DEV DISORD, V12, P195, DOI 10.1007/BF01531309 McDougle CJ, 1998, ARCH GEN PSYCHIAT, V55, P633, DOI 10.1001/archpsyc.55.7.633 MIKKELSEN EJ, 1982, SCHIZOPHRENIA BULL, V8, P320 Ornitz E., 1988, BRAIN DYSFUNCT, V1, P309 PUNJ G, 1983, J MARKETING RES, V20, P134, DOI 10.2307/3151680 ROBBINS TW, 1975, PSYCHOPHARMACOLOGIA, V45, P103, DOI 10.1007/BF00426218 SAULNIER C, 2002, 2 ANN INT M AUT RES SPARROWS S, 1984, VINELAND ADAPTIVE BE TROSTER H, 1994, J ABNORM CHILD PSYCH, V22, P79, DOI 10.1007/BF02169257 WARD JH, 1963, J AM STAT ASSOC, V58, P236, DOI 10.2307/2282967 Waterhouse L, 1996, PSYCHOL REV, V103, P457, DOI 10.1037/0033-295X.103.3.457 Watling RL, 2001, AM J OCCUP THER, V55, P416 NR 46 TC 94 Z9 94 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 MAR PY 2006 VL 10 IS 2 BP 155 EP 172 DI 10.1177/1362361306062021 PG 18 WC Psychology, Developmental SC Psychology GA 036GC UT WOS:000237058600004 PM 16613865 ER PT J AU Shaked, M Gamliel, I Yirmiya, N AF Shaked, M Gamliel, I Yirmiya, N TI Theory of mind abilities in young siblings of children with autism SO AUTISM LA English DT Article DE autism; broad phenotype; cognition; daily living skills; language; siblings; theory of mind ID PERVASIVE DEVELOPMENTAL DISORDERS; COGNITIVE DISABILITIES; INDIVIDUAL-DIFFERENCES; FAMILY HISTORY; RELATIVES; TWIN; PHENOTYPE; PARENTS; PAIRS AB Deficits in theory of mind (ToM), evident in most individuals with autism, have been suggested as a core deficit of autism. ToM difficulties in young siblings of children with autism (SIBS-A) compared to siblings of typically developing children (SIBS-TD) would place the former within the broad phenotype. We examined ToM's possible associations with measures of language, cognition, and daily living skills. Participants comprised 24 SIBS-A and 24 matched SIBS-TD aged 4.6 years. They completed the false belief and the strange stories tasks. We also collected measures of verbal and cognitive ability and daily living skills. Non-significant differences emerged between the groups on both ToM tasks. Differences did emerge in within-group associations between ToM ability and receptive language. The conclusion is that SIBS-A show resilience in ToM abilities. Possibly, these deficits are not genetically transferred to siblings, at least as measured in laboratory-based ToM tasks. C1 Hebrew Univ Jerusalem, IL-91905 Jerusalem, Israel. RP Yirmiya, N (reprint author), Hebrew Univ Jerusalem, IL-91905 Jerusalem, Israel. EM msnurit@mscc.huji.ac.ii CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th AUGUST GJ, 1981, BRIT J PSYCHIAT, V138, P416, DOI 10.1192/bjp.138.5.416 BAILEY A, 1995, PSYCHOL MED, V25, P63 BaronCohen S, 1997, J COGNITIVE NEUROSCI, V9, P548, DOI 10.1162/jocn.1997.9.4.548 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 Boutin P, 1997, J AUTISM DEV DISORD, V27, P165, DOI 10.1023/A:1025891824269 CHANDLER M, 1989, CHILD DEV, V60, P1263, DOI 10.1111/j.1467-8624.1989.tb04001.x Constantino JN, 2000, AM J PSYCHIAT, V157, P2043, DOI 10.1176/appi.ajp.157.12.2043 Cutting AL, 1999, CHILD DEV, V70, P853, DOI 10.1111/1467-8624.00061 Flavell JH, 2000, INT J BEHAV DEV, V24, P15 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x GILLBERG C, 1992, DEV MED CHILD NEUROL, V34, P389 GOPNIK A, 1990, CAN J PHILOS, V20, P89 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x Hughes C, 1999, PSYCHOL SCI, V10, P429, DOI 10.1111/1467-9280.00181 KAUFMAN AS, 1983, MANUAL KAUFMANN ASSE LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 OZONOFF S, 1993, J AUTISM DEV DISORD, V23, P429, DOI 10.1007/BF01046049 Peterson CC, 2000, MIND LANG, V15, P123, DOI 10.1111/1468-0017.00126 Piven J, 1997, AM J PSYCHIAT, V154, P185 Piven J, 1999, INT REV PSYCHIATR, V11, P299, DOI 10.1080/09540269974186 RITVO ER, 1985, AM J PSYCHIAT, V142, P74 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 Serra M, 2002, J CHILD PSYCHOL PSYC, V43, P885, DOI 10.1111/1469-7610.00104 Sicotte C, 1999, J AUTISM DEV DISORD, V29, P225, DOI 10.1023/A:1023032122489 SMALLEY SL, 1988, ARCH GEN PSYHCIAT, V4, P935 Sparrow S, 1984, VINELAND ADAPTIVE BE STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x SZATMARI P, 1993, J AM ACAD CHILD PSY, V32, P1264, DOI 10.1097/00004583-199311000-00022 Tager-Flusberg H, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P173 WELLLMAN H, 1990, CHILDS THEORY MIND Wiig E. H., 1992, CLIN EVALUATION LANG Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 Yirmiya N, 2001, RESEARCH BASIS FOR AUTISM INTERVENTION, P59 YIRMIYA N, IN PRESS J CHILD PSY YIRMIYA N, IN PRESS J AUSTIM DE NR 38 TC 10 Z9 10 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD MAR PY 2006 VL 10 IS 2 BP 173 EP 187 DI 10.1177/1362361306062023 PG 15 WC Psychology, Developmental SC Psychology GA 036GC UT WOS:000237058600005 PM 16613866 ER PT J AU Katleen, M Dissanayake, C AF Katleen, M Dissanayake, C TI A comparative study of the spontaneous social interactions of children with high-functioning autism and children with Asperger's disorder SO AUTISM LA English DT Article DE Asperger's disorder; highfunctioning autism; observations; peers; social interactions ID PEER INTERACTIONS; ADULTS; DELAYS AB A comparative observational study was undertaken of the spontaneous social interactions of children with high-functioning autism and Asperger's disorder. The sample comprised 20 children with high-functioning autism, 19 children with Asperger's disorder and 17 typically developing children matched on chronological age and overall mental age. A one-zero time sampling technique was used in live coding of the children's spontaneous social and play behaviours in the schoolyard. Few differences were found between children with high-functioning autism and Asperger's disorder on the dimensions of social interaction investigated. In contrast, the social behaviour of both clinical samples often deviated markedly from that of the typically developing children. The findings confirmed that although children with high-functioning autism or Asperger's disorder are often socially isolated relative to their typically developing peers, they are capable of spontaneously engaging socially with other children. The results were supportive of the hypothesis that Asperger's disorder is on a continuum with autistic disorder. C1 La Trobe Univ, Bundoora, Vic 3083, Australia. RP Dissanayake, C (reprint author), La Trobe Univ, Bundoora, Vic 3083, Australia. 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Mouse model systems are useful for identifying the many genes and environmental factors likely to affect complex behaviors, such as sociablilty(the tendency to seek social interaction). To progress toward developing such a model system, we tested the hypothesis that C57BL/6J inbred mice show higher levels of sociability than BALB/cJ inbred mice. Mice tested for sociability were 4 and 9-week old, male and female C57BL/6J and BALB/cJ mice. On 2 consecutive days, the sociability of each test mouse toward an unfamiliar 4-week-old DBA/2J stimulus mouse was assessed with a social choice paradigm conducted in a three-chambered apparatus. Measures of sociability included the time that the test mouse spent near versus far from the stimulus mouse, the time spent directly sniffing the stimulus mouse, and the time spent in contact between test and stimulus mice in a free interaction. C57BL/6J mice showed higher levels of sociability than BALB/cJ mice overall in each of these measures. We propose that C57BL/6J and BALB/cJ mice will be a useful mouse model system for future genetic and neurobiological studies of sociability. C1 Univ Penn, Sch Med, Ctr Neurobiol & Behav, Dept Psychiat, Philadelphia, PA 19104 USA. RP Brodkin, ES (reprint author), Univ Penn, Sch Med, Ctr Neurobiol & Behav, Dept Psychiat, 415 Curie Blvd,Room 111, Philadelphia, PA 19104 USA. 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In addition, we investigated the association between improvement in symptoms and changes in the cerebrospinal fluid (CSF) homovanillic acid (HVA),5-hydroxyindole-3-acetic acid (5-HIAA), and 6R-5,6,7,8-tetrahydro-L-bioptefin (BH4) levels after administration. After administration of secretin, the Autism Diagnostic Interview-Revised (ADI-R) score improved in 7 of the 12 children. However, the score deteriorated in 2 of the 12 children (in the item of 'restricted and repetitive, stereotyped interests and behaviors'). The HVA and BH4 levels in CSF were increased in all children with improvement in the ADI-R score. In contrast, no patient without the elevation of the BH4 level showed improvement in the score. These findings suggest that secretin activated metabolic turnover of dopamine in the central nervous system via BH4, improving symptoms. (c) 2005 Elsevier B.V. All rights reserved. C1 Univ Tokushima, Sch Med, Dept Pediat, Tokushima, Tokushima 7708503, Japan. 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PD MAR PY 2006 VL 28 IS 2 BP 99 EP 103 DI 10.1016/j.braindev.2005.05.005 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 017WA UT WOS:000235722800006 PM 16168596 ER PT J AU Peterson, CC Slaughter, VP AF Peterson, CC Slaughter, VP TI Telling the story of theory of mind: Deaf and hearing children's narratives and mental state understanding SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID FALSE BELIEF; AUTISM; SIBLINGS; MOTHERS; LANGUAGE; TASKS; TALK AB Theory of mind (ToM) was examined in late-signing deaf children in two studies by using standard tests and measures of spontaneous talk about inner states of perception, affect and cognition during storytelling. In Study 1, there were 21 deaf children aged 6 to 11 years and 13 typical-hearing children matched with the deaf by chronological age. In Study 2, there were 17 deaf children aged 6 to 12 years and 17 typical-hearing preschoolers aged 4 to 5 years who were matched with the deaf by ToM test performance. In addition to replicating the consistently reported finding of poor performance on standard false belief tests by late-signing deaf children, significant correlations emerged in both studies between deaf children's ToM test scores and their spontaneous narrative talk about imaginative cognition (e.g. 'pretend'). In Study 2, with a new set of purpose-built pictures that evoked richer and more complex mentalistic narration than the published picture book of Study 1, results of multiple regression analyses showed that children's narrative talk about imaginative cognition was uniquely important, over and above hearing status and talking of other kinds of mental states, in predicting ToM scores. The same was true of children's elaborated narrative talk using utterances that either spelt out thoughts, explained inner states or introduced contrastives. In addition, results of a Guttman scalograrn analysis in Study 2 suggested a consistent sequence in narrative and standard test performance by deaf and hearing children that went from (1) narrative mention of visible (affective or perceptual) mental states only, along with FB failure, to (2) narrative mention of cognitive states along with (1), to (3) elaborated narrative talk about inner states along with (2), and finally to (4) simple and elaborated narrative talk about affective/perceptual and cognitive states along with FIB test success. Possible explanations for this performance ordering, as well as for the observed correlations in both studies between ToM test scores and narrative variables, were considered. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. 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Recent evidence suggests that this peptide is widely expressed in the brain but some areas, notably the cerebellum, show a prominent expression of the peptide and its specific receptor. In this article we summarize our current understanding of the expression pattern and action of secretin in the cerebellum. We discuss the findings supporting the endogenous release of this peptide from Purkinje neurons and its role as a retrograde messenger modulating GABAergic synaptic transmission via multiple mechanisms. In addition, we would like to propose other possible, but still to be confirmed, functions of secretin in the cerebellum.. C1 Chinese Univ Hong Kong, Fac Med, Dept Physiol, Shatin, Hong Kong, Peoples R China. Univ Hong Kong, Dept Physiol, Pokfulam, Hong Kong, Peoples R China. Univ Hong Kong, Dept Zool, Pokfulam, Hong Kong, Peoples R China. Nanjing Univ, Dept Biol Sci & Technol, Nanjing 210008, Peoples R China. 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Philosophically they were regarded as the alternative leading to the dualism of mind and body, while it is an adequate problem for the endo-physics. Qualia are conjectured as the hard problem under those situations. To overcome such an impasse, we propose an abstract brain model featuring the dynamical duality of two parts of computations in a brain, in a term of endo-physics and internal measurement. Two parts of computations are expressed as binary relations, and the relationship between them is expressed as a pair of maps, called an infomorphism [Barwise J, Seligman J. Information flow, the logic of distributed systems. Cambridge University Press 1997]. Dynamical duality is implemented by the interaction between a binary relation and an infomorphism, and that leads to a dynamical change of a pair of binary relations. When a binary relation is expressed as a partial ordered set, one can check whether a part of computation is closed with respect to logical operations (i.e., a lattice) or not. By estimating a binary relation in terms of properties of lattice, we show that dynamical infomorphism robustly develops to a pair of logical computations corresponding to type cognition and non-logical one corresponding to qualia perception. It implies origin of differentiation and robust co-existence of type-cognition and qualia-perception. It is easy to see that dynamical infomorphism can also develop to a pair of singleton sets corresponding to savants' special cognitive style. (c) 2005 Elsevier Ltd. All rights reserved. C1 Kobe Univ, Fac Sci, Dept Earth & Planetary Sci, Kobe, Hyogo, Japan. Kobe Univ, Grad Sch Sci & Technol, Kobe, Hyogo, Japan. Kyoto Sangyo Univ, Fac Sci, Dept Comp Sci, Kyoto, Japan. RP Gunji, YP (reprint author), Kobe Univ, Fac Sci, Dept Earth & Planetary Sci, Kobe, Hyogo, Japan. 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Vaccine prices skyrocketed, and research on new products was threatened. In response, Congress created the National Vaccine Injury Compensation Program, which is tort reform legislation designed to compensate individuals quickly, easily, and generously. Since 1988, the Vaccine Injury Compensation Program has stabilized the marketplace, as evidenced by high immunization rates, stable pricing, and an increasing number of vaccine candidates in development. Although current vaccine shortages do not appear to be related to issues of liability, a new wave of tort litigation alleging that some vaccines cause autism has led to speculation that history could repeat itself. C1 Hlth Resources & Serv Adm, Dept Hlth & Human Serv, Natl Vaccine Injury Compensation Program, Rockville, MD 20857 USA. RP Evans, G (reprint author), Hlth Resources & Serv Adm, Dept Hlth & Human Serv, Natl Vaccine Injury Compensation Program, 5600 Fishers Ln,Rm 11C-26, Rockville, MD 20857 USA. 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Infect. Dis. PD MAR 1 PY 2006 VL 42 SU 3 BP S130 EP S137 DI 10.1086/499592 PG 8 WC Immunology; Infectious Diseases; Microbiology SC Immunology; Infectious Diseases; Microbiology GA 008TJ UT WOS:000235063300008 PM 16447135 ER PT J AU Shaked, M Bilu, Y AF Shaked, Michal Bilu, Yoram TI Grappling with affliction: Autism in the Jewish ultraorthodox community in Israel SO CULTURE MEDICINE AND PSYCHIATRY LA English DT Article DE autism; Israel; ultraorthodox; explanatory models ID INFANTILE-AUTISM; CULTURAL MODELS; CARE; ILLNESS; NARRATIVES; PATTERNS; MEDICINE; CHILDREN; STORIES; CANCER AB In this essay we seek to examine the cultural tool kit employed in the Jewish ultraorthodox community to cope with autism, a predicament deemed resistant to massive cultural molding. Through 30 open-ended interviews with ultraorthodox mothers of children with autism we portray the mothers' emerging recognition of the disorder, their care seeking activities, and their construction of explanatory models. The health care system on which the ultraorthodox mothers rely is extremely diverse, including mainstream medical and educational services, various alternative therapies, therapies specific to autism, and spiritual and mystical interventions. The outcome of these endeavors is a dual system of illness perception in which bio-medical and spiritual-religious frames of references coexist. This duality cuts across all the facets of the explanatory system: etiology, pathophysiology, treatment, and prognosis. Metaphysical accounts, and especially the notion of the transmigration of souls, serve as meta-accounts, bridging the epistemological gap between God's mysterious intention and the specific bodily mechanisms underlying the disorder. The religious and moral theme of suffering is highlighted in the narratives as a salient constituent of the ultraorthodox mothers' attempts to understand and come to terms with their plight. C1 Hebrew Univ Jerusalem, Dept Psychol, IL-91905 Jerusalem, Israel. 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Med. Psychiatr. PD MAR PY 2006 VL 30 IS 1 BP 1 EP 27 DI 10.1007/s11013-006-9006-2 PG 27 WC Anthropology; Psychiatry; Social Sciences, Biomedical SC Anthropology; Psychiatry; Biomedical Social Sciences GA 074DL UT WOS:000239792800001 PM 16783528 ER PT J AU Dissanayake, C Bui, QM Huggins, R Loesch, DZ AF Dissanayake, C Bui, QM Huggins, R Loesch, DZ TI Growth in stature and head circumference in high-functioning autism and Asperger disorder during the first 3 years of life SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; FRAGILE-X-SYNDROME; LONGITUDINAL DATA; CHILDREN; ADULTS; DIFFERENTIATION; ABNORMALITIES; NEUROTROPHINS; MELATONIN; HORMONE AB Little effort has been made to characterize the developmental anatomic phenotype of autism; although there is evidence of an increased head circumference and brain size, few other physical characteristics have been studied. The head circumference, body length/height, and weight measurements of infants, who were later diagnosed with high-functioning autism (HFA, n = 16) and Asperger disorder (AsD, n = 12), were extracted from health records over the first 3 years of life and compared to the measurements of I matched normal control group (11 = 19). Using linear mixed-effects models, no differences were found in the average growth rate for head circumference, stature, or weight between the children with HFA and AsD. However, a significantly higher growth rate in body length/height and weight was found for the combined group of children with HFA and AsD compared to the normal control group. A trend toward higher growth rate in head circumference was also found among the former group. The results indicate that growth dysregulation in autism is not specific to the brain but also involves growth in stature. C1 La Trobe Univ, Sch Psychol Sci, Bundoora, Vic 3086, Australia. 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Psychopathol. PD SPR PY 2006 VL 18 IS 2 BP 381 EP 393 DI 10.1017/S0954579406060202 PG 13 WC Psychology, Developmental SC Psychology GA 033IJ UT WOS:000236840200004 PM 16600060 ER PT J AU Golan, O Baron-Cohen, S AF Golan, O Baron-Cohen, S TI Systemizing empathy: Teaching adults with Asperger syndrome or high-functioning autism to recognize complex emotions using interactive multimedia SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article; Proceedings Paper CT 3rd International Meeting for Autism Research CY MAY 07-08, 2004 CL Sacramento, CA ID PERVASIVE DEVELOPMENTAL DISORDERS; CEREBRAL-BLOOD-FLOW; FUSIFORM FACE AREA; SPECTRUM DISORDERS; FACIAL EXPRESSIONS; CHILDS APPRAISAL; SOCIAL COGNITION; MIND; PEOPLE; BRAIN AB This study evaluated Mind Reading, an interactive systematic guide to emotions. for its effectiveness in reaching adults with Asperger syndrome (AS) and high-functioning autism (HFA) to recognize complex emotions in faces and voices. Experiment I tested a group of adults diagnosed with AS/HFA (n = 19) who used the software at home for 10-15 weeks. Participants were tested on recognition of faces and voices at three different levels of generalization. A matched control group of adults with AS/HFA (it = 22) were assessed without any intervention. In addition, a third group of general Population controls (it = 24) was tested. Experiment 2 repeated the design of Experiment I with a group of adults with AS/HFA who used the software at home and met in a group with a tutor on a weekly basis. They were matched to a control group of adults with AS/HFA attending social skills training and to a general population control group (it = 13 for all three groups). In both experiments the intervention group improved significantly more than the control group on close, but not distant, generalization tasks. Verbal IQ had significant effects in Experiment 2. Using Mind Reading for a relatively short period of time allows users to learn to recognize a variety of complex emotions and mental states. However, additional methods are required to enhance generalization. C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. RP Golan, O (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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SO DEVELOPMENTAL SCIENCE LA English DT Review ID JOINT VISUAL-ATTENTION; WILLIAMS-SYNDROME; EYE-MOVEMENTS; EARLY INFANCY; AUTISM; CHILDREN; DIRECTION; FACE; LANGUAGE; RECOGNITION AB We propose a computational model of the emergence of gaze following skills in infant-caregiver interactions. The model is based oil the idea that infants learn that monitoring their caregivers direction of gaze allows their to predict the locations of interesting objects or events in their environment (Moore & Corkinn, 1994). Elaborating on this theory, we demonstrate that a specific Basic Set of structures and mechanisms is sufficient for gaze following to emerge. This Basic Set includes the infant's perceptual skills and preferences, habituation and reward-driven learning, and a structured social environment featuring a caregiver who tends to look at things the infant will find interesting. 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Sci. PD MAR PY 2006 VL 9 IS 2 BP 125 EP 147 DI 10.1111/j.1467-7687.2006.00470.x PG 23 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 021WK UT WOS:000236016400003 PM 16472311 ER PT J AU Petersen, DJ Bilenberg, N Hoerder, K Gillberg, C AF Petersen, DJ Bilenberg, N Hoerder, K Gillberg, C TI The population prevalence of child psychiatric disorders in Danish 8-to 9-year-old children SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE prevalence; psychopathology; epidemiology; K-SADS-PL; non-respondent analysis ID 7-YEAR-OLD CHILDREN; PSYCHOPATHOLOGY AB The overall prevalence rates of general and specific child psychiatric disorders in Danish children are unknown. In this study, which aimed to estimate prevalence rates, a multi-method strategy using a two-step design was employed. The first step involved assessment with the Child Behaviour Checklist (CBCL). The second step consisted of assessment using the Schedule for Affective Disorders and Schizophrenia for School-Aged Children; Present and Lifetime version (K-SADS-PL), The Children's Global Assessment Scale (C-GAS), The Wechsler Intelligence Scale for Children (WISC-III), The Autism Spectrum Disorder Screening Questionnaire (ASSQ), and a checklist containing the diagnostic criteria for Pervasive Developmental Disorders (PDD). Non-respondents were assessed through teachers using a modified brief version of the K-SADS-PL. A total of 751 children were targeted. The overall estimated prevalence rate of child psychopathology was 11.8 % [95% confidence interval (CI): 8.8, 14.8]. Attention Deficit/Hyperactivity Disorder (ADHD) was found to be the most common specific child psychiatric disorder. There was no difference in prevalence rates between respondents and non-respondents. The estimated prevalence rates were broadly comparable to prevalence rates found in other epidemiological studies. 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Child Adolesc. Psych. PD MAR PY 2006 VL 15 IS 2 BP 71 EP 78 DI 10.1007/s00787-006-0488-9 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 020CX UT WOS:000235886700002 PM 16477477 ER PT J AU Melfsen, S Walitza, S Warnke, A AF Melfsen, S Walitza, S Warnke, A TI The extent of social anxiety in combination with mental disorders SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE social phobia; social anxiety; selective mutism; Asperger's Syndrome; children and adolescents ID QUALITY-OF-LIFE; ELECTIVE MUTISM; CO-MORBIDITY; CHILDREN; PHOBIA; ADOLESCENTS; PREVALENCE; COMMUNITY; AUTISM; DISABILITY AB The aim of the study was to investigate the extent of social anxiety in different mental disorders. A total of 341 patients aged 7-18 years participated in the study. To measure social anxiety, the German version (SPAIK) of the Social Phobia and Anxiety Inventory for Children (SPAI-C) was used. Subgroups were built dependent on mental disorders. A total score above 20, which was assumed to indicate social anxiety, was observed in children with selective mutism (n=9; M=22.68; SD=11.29) and in children with Asperger's Syndrome (n=7; M=20.77; SD=13.77). Patients who had the following mental disorders also showed a higher total score of social anxiety: obsessive-compulsive disorder, anorexia nervosa, schizophrenia, depression and conduct disorder. In none of these disorders, however, did the mean total score exceed the cut-off of 20. C1 Univ Wurzburg, Dept Psychiat Children & Adolescents, D-97080 Wurzburg, Germany. RP Melfsen, S (reprint author), Univ Wurzburg, Dept Psychiat Children & Adolescents, Fuechsleinstr 15, D-97080 Wurzburg, Germany. 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SO EUROPEAN NEUROPSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Workshop on Neuropsychopharmacology for Young Scienctists in Europe CY MAR 09-12, 2006 CL Nice, FRANCE SP ECNP C1 Aristotle Univ Thessaloniki, GR-54006 Thessaloniki, Greece. CR STAAL WG, 2005, MOL PSYCHIAT NR 1 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD MAR PY 2006 VL 16 SU 1 BP S6 EP S6 DI 10.1016/S0924-977X(06)80008-8 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 040TL UT WOS:000237403200009 ER PT J AU Walker, MA AF Walker, MA TI Evaluation of recent patent applications for the diagnosis and treatment of autism and pervasive developmental disorders SO EXPERT OPINION ON THERAPEUTIC PATENTS LA English DT Review DE glutein; oxytocin; pervasive development disorder; secretin; serotonin ID MENTALLY-RETARDED CHILDREN; AMINO-ACID DECARBOXYLASE; PLASMA CYCLIC-AMP; SPECTRUM DISORDERS; DOUBLE-BLIND; REPETITIVE BEHAVIORS; CYTOKINE PRODUCTION; ENGRAILED CONTROLS; OPEN-LABEL; CELL FATE AB This review covers patent literature for new targets, biomarkers and potential drugs for the treatment of autism and related pervasive developmental disorders, for patent applications published between 2000 and mid-year 2005. 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Ther. Patents PD MAR PY 2006 VL 16 IS 3 BP 249 EP 264 DI 10.1517/13543776.16.3.249 PG 16 WC Chemistry, Medicinal; Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 021EN UT WOS:000235966600003 ER PT J AU Knickmeyer, R Baron-Cohen, S Raggatt, P Taylor, K Hackett, G AF Knickmeyer, R Baron-Cohen, S Raggatt, P Taylor, K Hackett, G TI Fetal testosterone and empathy SO HORMONES AND BEHAVIOR LA English DT Article DE fetal testosterone; social development; empathy; theory of mind; autism ID CENTRAL NERVOUS-SYSTEM; SEXUAL-DIFFERENTIATION; ASPERGER-SYNDROME; AMNIOTIC-FLUID; FUNCTIONING AUTISM; CHILDREN; BRAIN; MIND; CONVERSATIONS; ATTRIBUTION AB Background: In animals, fetal testosterone (fT) plays a central role in organizing the brain and in later social behavior. In humans, exposure to atypical levels of prenatal androgens may result in masculine behavior and ability patterns. Normal inter-individual variation in fT levels has also been correlated with later sex-typed behavior. 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Behav. PD MAR PY 2006 VL 49 IS 3 BP 282 EP 292 DI 10.1016/j.yhbeh.2005.08.010 PG 11 WC Behavioral Sciences; Endocrinology & Metabolism SC Behavioral Sciences; Endocrinology & Metabolism GA 020LW UT WOS:000235911900004 PM 16226265 ER PT J AU Gupta, G AF Gupta, G TI Autism and head size SO INDIAN PEDIATRICS LA English DT News Item C1 Charak Clin, Chandigarh, India. RP Gupta, G (reprint author), Charak Clin, Chandigarh, India. 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PD MAR PY 2006 VL 30 IS 2 BP 178 EP 190 DI 10.1177/0165025406063637 PG 13 WC Psychology, Developmental SC Psychology GA 051FT UT WOS:000238147700009 ER PT J AU O'Toole, C Chiat, S AF O'Toole, C Chiat, S TI Symbolic functioning and language development in children with Down syndrome SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE Down syndrome; symbolic play; understanding of symbols; language development; assessment; intervention ID YOUNG-CHILDREN; PLAY; COMMUNICATION; INFANTS; ABILITY; AUTISM; SKILLS; DELAYS AB Background: Understanding the relationship between preverbal skills and language development has important implications for identifying communication delay/ disorders and for early childhood intervention. In the case of children with Down syndrome, it is well established that symbolic play is associated with the emergence of language. However, the exact nature of this relationship remains unclear, as many previous studies have addressed functional play and not actual symbolic play, which is felt to have stronger links to language development. The design of studies has also meant that adults may have inadvertently modelled the targeted behaviours, in which case it is unclear whether the children truly comprehend the symbolic acts that they produce. Aims: This study set out to investigate further symbolic functioning and language in children with Down syndrome by exploring truly symbolic play as opposed to functional play, as well as the understanding of a graded set of novel symbols. The aim was to find out whether the symbolic behaviours would be associated with each other and with language development or non-verbal cognition. It was hypothesized that symbolic functioning on a test of symbolic play and symbolic comprehension would be significantly correlated with each other and with language abilities as they all measure underlying skills in symbolic representation. It was hypothesized that symbolic skills and language would be less closely correlated with non-verbal abilities. Another goal was to study understanding of three types of symbols: gestures, miniatures and abstract symbols. It was hypothesized that gestures would be significantly easier to understand than miniatures or abstract symbols. Methods & Procedures: Twenty-one children with Down syndrome aged between 32 and 95 months were assessed on the Test of Pretend Play and a novel symbolic comprehension task as well as on standardized language and nonverbal tests. Correlational analysis was carried out to determine the relationship between the various tests, and the children were divided into three age categories to examine how the relationship changed with development. Analysis was also carried out on the children's performance across the gesture, miniature and symbolic subtests of the symbolic comprehension task. Outcomes & Results: When effects of chronological age were partialled out, symbolic play and symbolic comprehension were significantly correlated with each other and with expressive and receptive language, but not with non- verbal ability. The association between language and symbolic functioning was significantly stronger in the younger children, but these measures started to dissociate with increasing age and language development. The data support the proposition that language becomes more domain specific as a result of experience and development. The results from the symbolic comprehension experiment revealed that the children found gestures significantly easier to understand than miniatures or substitute objects used as abstract symbols to represent other objects. Conclusions: The findings indicate that tests of symbolic functioning offer valuable contributions to assessment with implications for intervention in children with Down syndrome and to the understanding of disorders of language and communication. C1 Natl Univ Ireland Univ Coll Cork, Dept Speech & Hearing Sci, Cork, Ireland. City Univ London, Dept Language & Commun Sci, London EC1V 0HB, England. RP O'Toole, C (reprint author), Natl Univ Ireland Univ Coll Cork, Dept Speech & Hearing Sci, Brookfield Hlth Sci Complex,Coll Rd, Cork, Ireland. EM c.otoole@ucc.ie CR BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 Bates E., 1984, CONTINUITIES DISCONT, P229, DOI 10.1007/978-1-4613-2725-7_8 Beeghly M., 1990, CHILDREN DOWN SYNDRO, P329, DOI 10.1017/CBO9780511581786.011 Buckley S., 2003, SPEECH LANGUAGE INTE, P132 Capone NC, 2004, J SPEECH LANG HEAR R, V47, P173, DOI [10.1044/1092-4388(2004/015), 10.1044/1092-4388(2004/15)] Chapman R S, 2001, Downs Syndr Res Pract, V7, P1, DOI 10.3104/reviews.108 Cicchetti D, 1994, CHILDREN PLAY CLIN D, P206 Clift S., 1998, CHILD LANG TEACH THE, V14, P199, DOI 10.1191/026565998675895190 CUNNINGHAM CC, 1985, J CHILD PSYCHOL PSYC, V26, P255, DOI 10.1111/j.1469-7610.1985.tb02264.x DeLoache JS, 1999, COGNITIVE DEV, V14, P299, DOI 10.1016/S0885-2014(99)00006-4 DOSWELL G, 1994, EUROPEAN J DISORDERS, V29, P291 Elliott C. D., 1996, BRIT ABILITY SCALES Fewell RR, 1997, TOP EARLY CHILD SPEC, V17, P103 HARRIS PL, 1994, CHILD DEV, V65, P16, DOI 10.1111/j.1467-8624.1994.tb00731.x Karmiloff-Smith A., 1992, MODULARITY DEV PERSP Karmiloff-Smith A, 1998, TRENDS COGN SCI, V2, P389, DOI 10.1016/S1364-6613(98)01230-3 KENNEDY MD, 1991, J SPEECH HEAR RES, V34, P112 Lewis V, 2000, INT J LANG COMM DIS, V35, P117 LEWIS V, 1992, EUR J DISORDER COMM, V27, P231 Lewis V., 1997, TEST PRETEND PLAY Lowe M., 1988, SYMBOLIC PLAY TEST LYYTINEN P, 1999, SCAND J PSYCHOL, V40, P117 McCathren R., 1996, ASSESSMENT COMMUNICA, P57 MCCUNE L, 1995, DEV PSYCHOL, V31, P198, DOI 10.1037//0012-1649.31.2.198 MCCUNENICOLICH L, 1981, CHILD DEV, V52, P785, DOI 10.2307/1129078 MOGFORDBEVAN K, 1994, PLAY INTERVENTION, P157 MUNDY P, 1995, J SPEECH HEAR RES, V38, P157 Namy LL, 1998, CHILD DEV, V69, P295, DOI 10.1111/j.1467-8624.1998.tb06189.x OGURA T, 1991, J CHILD LANG, V18, P273 Pellegrini AD, 2001, J CHILD PSYCHOL PSYC, V42, P861, DOI 10.1111/1469-7610.00783 RONDAL J, 1998, LANGUAGE MENTAL RETA ROY P, 2005, SYMBOLIC COMPREHENSI SHIMADA S, 1990, RIEEC REPORT, V26, P55 Shore C., 1987, HDB INFANT DEV, P149 Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 SMITH L, 1986, AM J MENT RETARD, V91, P57 TAMISLEMONDA CS, 1993, NEW DIR CHILD ADOLES, V59, P17 Tomasello M, 1999, BRIT J DEV PSYCHOL, V17, P563, DOI 10.1348/026151099165483 WISHART JG, 1990, BRIT J EDUC PSYCHOL, V60, P10 ZIMMERMAN I, 1997, PRESCHOOL LANGUAGE S, V3 NR 40 TC 5 Z9 6 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1368-2822 J9 INT J LANG COMM DIS JI Int. J. Lang. Commun. Disord. PD MAR-APR PY 2006 VL 41 IS 2 BP 155 EP 171 DI 10.1080/13682820500221600 PG 17 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 022SD UT WOS:000236075100003 PM 16546893 ER PT J AU Wiley, S Choo, D Meinzen-Derr, J Hilbert, L Greinwald, J AF Wiley, S Choo, D Meinzen-Derr, J Hilbert, L Greinwald, J TI GJB2 mutations and additional disabilities in a pediatric cochlear implant population SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY LA English DT Article DE GJB2; connexin 26; sensorineural hearing loss; pediatric cochlear implantation; multi-handicap ID SENSORINEURAL HEARING-LOSS; GENE-RELATED DEAFNESS; GJB2-RELATED DEAFNESS; CONNEXIN-26 MUTATIONS; HANDICAPPED-CHILDREN; SPEECH-PERCEPTION; PERFORMANCE; RECIPIENTS; PHENOTYPE AB Background: Children with severe to profound sensorineural hearing loss due to GJB2 mutations have often been deemed good cochlear implant candidates. Studies on children with GJB2 mutations and cochlear implants have typically excluded children with additional disabilities. Objective: To investigate the presence of additional disabilities among children with and without GJB2 mutations in a cochlear implant population. Methods: A retrospective chart review was performed of children with non-syndromic sensorineural hearing Loss (SNHL) who received a cochlear implant between 1993 and 2004. Results: Among 108 children within the cochlear implant database; 46 patients met the inclusion criteria of idiopathic non-syndromic hearing loss. Sixteen children had GJB2 mutations, 12 were GJB2 negative, and 17 did not receive GJB2 testing but had no other identifiable etiology or risk factor contributing to hearing Loss. The proportion of children with additional disabilities that would affect either preoperative assessments or post-operative results in the GJB2 positive group was 44% compared to 33% of children in the GJB2 negative. Additional disabilities were present in 41% of the children who did not receive GJB2 testing. The disabilities in the GJB2 positive group included specific learning disability, apraxia, epileptiform aphasia, attention deficit disorder, global developmental delay, and gross motor delay. The GJB2 negative and those children not receiving GJB2 testing had motor delays, language delay, autism, specific learning disability, and attention deficit disorder. The proportion of children with at least 6 months Cl use who relied on oral communication was 62% in the GJB2 positive group, 66% in the GJB2 negative group, and 38% in the untested group. A majority of the genetic alleles were 35delG (81%)and 10 of 16 (63%) patients with GJB2 mutations were homozygous 35delG. The rate of developmental diagnoses was similar in patients with homozygous GJB2 compared to compound heterozygous genotypes. Conclusions: The presence of biallelic GJB2 mutations does not rule out non-hearing related disorders that can have an effect on speech, language and learning. Forty-four percent of children with GJB2 mutations had other conditions that could directly affect pre-implant evaluation and post-implant performance. This rate is similar to the reported prevalence among the overall population of children with hearing toss. All children should have a comprehensive evaluation of development and behavior regardless of the etiology of hearing loss. (c) 2005 Elsevier Ireland Ltd. All rights reserved. C1 Univ Cincinnati, Cincinnati Childrens Hosp, Med Ctr, Dept Pediat,Div Dev Disabilities, Cincinnati, OH 45229 USA. Univ Cincinnati, Coll Med, Cincinnati Childrens Med Ctr, Dept Otolaryngol Head & Neck Surg, Cincinnati, OH 45229 USA. Cincinnati Childrens Hosp, Med Ctr, Ctr Epidemiol & Biostat, Cincinnati, OH 45229 USA. Cincinnati Childrens Hosp, Med Ctr, Div Audiol, Cincinnati, OH 45229 USA. RP Wiley, S (reprint author), Univ Cincinnati, Cincinnati Childrens Hosp, Med Ctr, Dept Pediat,Div Dev Disabilities, 3333 Burnet Ave ML 4002, Cincinnati, OH 45229 USA. 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PD MAR PY 2006 VL 18 IS 1 BP 171 EP 173 DI 10.1017/S1041610205213474 PG 3 WC Psychology, Clinical; Geriatrics & Gerontology; Gerontology; Psychiatry; Psychology SC Psychology; Geriatrics & Gerontology; Psychiatry GA 043VW UT WOS:000237632000014 PM 16734928 ER PT J AU Lattimore, LP Parsons, MB Reid, DH AF Lattimore, LP Parsons, MB Reid, DH TI Enhancing job-site training of supported workers with autism a reemphasis on simulation SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE supported work; simulation training; autism ID MENTAL-RETARDATION; EMPLOYMENT; MAINTENANCE; SKILLS; DISABILITIES; ACQUISITION; INSTRUCTION; CLASSROOM AB Currently recommended practice in supported work emphasizes training job skills to workers with severe disabilities while on the job. Early behavioral research indicated that skills needed in natural environments could also be trained in simulated settings. 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Appl. Behav. Anal. PD SPR PY 2006 VL 39 IS 1 BP 91 EP 102 DI 10.1901/jaba.2006.154-04 PG 12 WC Psychology, Clinical SC Psychology GA 018QT UT WOS:000235780600008 PM 16602388 ER PT J AU Marckel, JM Neff, NA Ferreri, SJ AF Marckel, JM Neff, NA Ferreri, SJ TI A preliminary analysis of teaching improvisation with the picture exchange communication system to children with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE improvisation; problem solving; picture exchange communication system; augmentative and alternative communication; autism ID CREATIVITY AB Two young boys with autism who used the picture exchange communication system were taught to solve problems (improvise) by using descriptors (functions, colors, and shapes) to request desired items for which specific pictures were unavailable. 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PD SPR PY 2006 VL 39 IS 1 BP 109 EP 115 DI 10.1901/jaba.2006.131-04 PG 7 WC Psychology, Clinical SC Psychology GA 018QT UT WOS:000235780600010 PM 16602390 ER PT J AU Sturmey, P AF Sturmey, P TI On some recent claims for the efficacy of cognitive therapy for people with intellectual disabilities SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE applied behaviour analysis; cognitive therapy; evidence based practice ID MENTALLY-RETARDED ADULTS; FUNCTIONAL-ANALYSIS; PROBLEM BEHAVIOR; SELF-REGULATION; RETARDATION; PSYCHOTHERAPY; AUTISM; INTERVENTION; INDIVIDUALS; RELAXATION AB Backgrounf Many authors have expressed concern regarding the efficacy of psychotherapy, including psychotherapy for people with intellectual disabilities. Materials and Methods Recently, many authors have made claims for the effectiveness of cognitive therapy for treating people with intellectual disabilities. During this debate, applied behaviour analysis has been misrepresented by incorrectly labelling behavioural as cognitive techniques, repeated misrepresentations of behaviourism and attributing the efficacy of treatment packages to cognitive components of undemonstrated efficacy when it is more parsimonious to attribute efficacy to behavioural elements of known efficacy. Conclusions This article documents and corrects these errors. C1 CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA. CUNY Queens Coll, Grad Ctr, Flushing, NY 11367 USA. RP Sturmey, P (reprint author), CUNY Queens Coll, Dept Psychol, 65-30 Kissean Blvd, Flushing, NY 11367 USA. 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A growing body of evidence links autism spectrum disorders to abnormalities in serotonin function, and the selective serotonin reuptake inhibitors (SSRIs) have been utilized to target various symptoms of the disorders. This article reviews the available data on the efficacy and tolerability of SSRIs in individuals with autism spectrum disorders. Objectives for future research in this area will also be suggested. Data Sources and Study Selection: The entire PubMed database including MEDLINE (1966-July 2005) was searched for English-language biomedical articles. Search terms included autism, autism spectrum disorder, citalopram, escitalopram,fluoxetine, fluvoxamine, paroxetine, pervasive developmental disorder, selective serotonin reuptake inhibitors, and sertraline. All clinical trials evaluating treatment outcomes associated with the use of SSRIs in managing symptoms of autism that were identified in the search were reviewed. All randomized controlled trials and open-label trials were included in this review. Case reports and case series were excluded. Data Synthesis: We identified 3 randomized controlled trials and 10 open-label trials or retrospective chart reviews on the use of SSRIs in autism and autism spectrum disorders. The SSRIs that have been studied in autism spectrum disorders are citalopram, escitalopram, fluoxetine, fluvoxamine, and sertraline. Most studies demonstrate significant improvement in global functioning and in symptoms associated with anxiety and repetitive behaviors. While side effects were generally considered to be mild, increased activation and agitation occurred in some subjects. Conclusions: Although SSRIs may demonstrate therapeutic benefit in autism spectrum disorders, methodological weaknesses of many of the clinical trials suggest the need for additional randomized controlled trials. 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Clin. Psychiatry PD MAR PY 2006 VL 67 IS 3 BP 407 EP 414 PG 8 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 031RL UT WOS:000236721600010 PM 16649827 ER PT J AU Williams, G Sears, L Allard, A AF Williams, Gail Sears, Lonnie Allard, AnnaMary TI Parent perceptions of efficacy for strategies used to facilitate sleep in children with autism SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; sleep ID PATTERNS; DISORDERS AB Autism is a relatively common developmental disability that has neurobiological origins and is characterized by pervasive deficits in social interaction, communication and range of interests. In a previously published article, the authors described commonly occurring sleep problems in children with autism [Williams, P. G., Sears, L. L., and Allard, A. (2004). J. Sleep Res. 13: 265-268.] Current estimates of sleep disorders in this population range from 44 to 83% [Richdale, A. (1999). Develop. Med. Child Neurol. 41: 60-66]. Parents often have to devise their own strategies for dealing with sleep problems. This study surveyed interventions being used by families of children with autism. Likert-based surveys were sent out to 500 families of autistic children with 210 returned. Based on records of psychological testing, survey responses for these children were categorized into mental retardation (MR) or not mental retardation (not MR) groups. Among the most frequently used behavior interventions for both groups were establishing a regular bedtime and waking time, providing a darkened room, reading to the child, and providing toys to play with in bed. Behavioral strategies considered most effective included establishing a regular bedtime, bringing the child into the parents' bed, wrapping the child, using a noise masker, and allowing the child to have toys in his bed. When surveys were divided into MR/not MR groups, some differences in perceived effectiveness of behavioral interventions for sleep were noted. Reading a story and using a nightlight were perceived as much less effective for the MR group as compared to those in the not MR group. In general, medications were used much less frequently than behavioral interventions to help with sleep. When comparisons between the MR/not MR groups were made, no statistically significant differences were seen for perceived effectiveness of medications. This study points to the need for more systematic study of sleep problems and interventions for children with autism. C1 Univ Louisville, Weisskopf Ctr Evaluat Children, Louisville, KY 40202 USA. RP Williams, G (reprint author), Univ Louisville, Weisskopf Ctr Evaluat Children, 571 S Floyd St,Ste 100, Louisville, KY 40202 USA. 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Dev. Phys. Disabil. PD MAR PY 2006 VL 18 IS 1 BP 25 EP 33 DI 10.1007/s10882-006-9003-y PG 9 WC Rehabilitation SC Rehabilitation GA 064KM UT WOS:000239088200003 ER PT J AU Woodbury-Smith, MR Clare, ICH Holland, AJ Kearns, A AF Woodbury-Smith, MR Clare, ICH Holland, AJ Kearns, A TI High functioning autistic spectrum disorders, offending and other law-breaking: findings from a community sample SO JOURNAL OF FORENSIC PSYCHIATRY & PSYCHOLOGY LA English DT Article DE autistic spectrum disorders; Asperger Syndrome; offending; law-breaking; mental disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGERS-SYNDROME; PREVALENCE; VIOLENCE; BEHAVIOR AB The prevalence and pattern of offending and other law-breaking among groups of men and women with High Functioning Autism/Asperger Syndrome (ASDs) living in the community has not, so far, been examined empirically. In this study, the illegal behaviours of a small sample (N = 25) of people with ASDs were investigated. Unexpectedly, both self-report and 'official' data indicated that the rate of lawbreaking, including offending, was very low. Indeed, it was significantly (p < 0.05) lower than that of a stringent non-ASD comparison group (N = 20). Despite similarities, however, there were some striking differences between the patterns of illegal behaviours in the two groups. The participants with a diagnosis of an ASD were significantly (p < 0.01) less likely to report that they had engaged in illicit drugtaking; in contrast, they were significantly more likely (p < 0.05) to report activities which could be categorised as 'criminal damage'. Moreover, they tended to have a greater history of violent behaviours. The methodological limitations of this study, particularly the difficulties of recruiting an adequate community sample of people with ASDs, are discussed, together with the implications for the development of services for the small minority of men and women with this diagnosis who are involved in criminal offending and other law-breaking. C1 Univ Cambridge, Dept Psychiat, Sect Dev Psychiat, Cambridge CB2 2AH, England. Barnet & Chase Farm Hosp NHS Trust, Enfield, Middx, England. RP Clare, ICH (reprint author), Univ Cambridge, Dept Psychiat, Sect Dev Psychiat, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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C., 2002, INT J FORENSIC MENTA, V1, P59, DOI DOI 10.1080/14999013.2002.10471161 Palermo MT, 2004, INT J OFFENDER THER, V48, P40, DOI 10.1177/0306624X03257713 Powell A., 2002, TAKING RESPONSIBILIT Scott FJ, 2002, AUTISM, V6, P231, DOI 10.1177/1362361302006003002 SCRAGG P, 1994, BRIT J PSYCHIAT, V165, P679, DOI 10.1192/bjp.165.5.679 Silva JA, 2004, BEHAV SCI LAW, V22, P787, DOI 10.1002/bsl.620 Silvas JA, 2002, J FORENSIC SCI, V47, P1 *STAT CORP, 2003, STAT VERS 8 TANTAM D, 1999, AUSTISM99 INT ONL C The Psychological Corporation, 1999, WECHSL ABBR SCAL INT Volkmar FR, 1998, J AUTISM DEV DISORD, V28, P457, DOI 10.1023/A:1026012707581 Williams JG, 2006, ARCH DIS CHILD, V91, P8, DOI 10.1136/adc.2004.062083 Wing L, 1997, J FORENSIC PSYCHIATR, V8, P253, DOI 10.1080/09585189708412008 World Health Organisation, 1992, ICD 10 INT STAT CLAS NR 42 TC 21 Z9 21 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1478-9949 J9 J FORENSIC PSYCHI PS JI J. Forensic Psychiatry Psychol. PD MAR PY 2006 VL 17 IS 1 BP 108 EP 120 DI 10.1080/14789940600589464 PG 13 WC Criminology & Penology; Psychiatry SC Criminology & Penology; Psychiatry GA 035SC UT WOS:000237021000007 ER PT J AU Eaves, RC Williams, TO AF Eaves, RC Williams, TO TI Exploratory and confirmatory factor analyses of the Pervasive Developmental Disorders Rating Scale for young children with autistic disorder SO JOURNAL OF GENETIC PSYCHOLOGY LA English DT Article DE affect; arousal; autism; cognition; PDDRS ID DIAGNOSTIC INTERVIEW; BEHAVIOR CHECKLIST; COVARIANCE-STRUCTURES; CONSTRUCT-VALIDITY; RELIABILITY AB In this study, the authors examined the construct validity of the Pervasive Developmental Disorder Rating Scale (PDDRS; R. C. Eaves, 1993), which is a screening instrument used to identify individuals with autistic disorder and other pervasive developmental disorders. The PDDRS is purported to measure 3 factors-arousal, affect, and cognition-that collectively make up the construct of autism. Using scores from 199 children (aged 1-6 years) diagnosed with autistic disorder, the authors submitted data to exploratory and confirmatory factor analyses. In the 1st series of analyses, the authors analyzed a user-specified 3-factor solution using principal axis factor analysis with a pro-max rotation to evaluate the assertion of a correlated 3-factor structure. Next, the authors analyzed 1-factor and 2-factor solutions to determine if they provided a better factor structure for the data. In the 2nd series, the authors conducted confirmatory factor analyses, which compared the theorized hierarchical 2nd-order factor model with 5 plausible competing models. The results of the exploratory analyses supported the 3-factor solution. With the confirmatory analyses, the 2nd-order factor model provided the best fit for the data. The exploratory and confirmatory analyses supported the theoretical assumptions undergirding the development of the PDDRS. The authors discuss theoretical implications, practical implications, and areas for further research. C1 Auburn Univ, Dept Rehabil & Special Educ, Auburn, AL 36849 USA. Virginia Polytech Inst & State Univ, Dept Teaching & Learning, Blacksburg, VA 24061 USA. RP Eaves, RC (reprint author), Auburn Univ, Dept Rehabil & Special Educ, Auburn, AL 36849 USA. EM eaves11@charter.net CR AKAIKE H, 1987, PSYCHOMETRIKA, V52, P317, DOI 10.1007/BF02294359 Arbuckle J.L., 1995, AMOS 4 0 USERS GUIDE Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bentler P. M., 1993, EQS STRUCTURAL EQUAT BENTLER PM, 1980, PSYCHOL BULL, V88, P588, DOI 10.1037//0033-2909.88.3.588 BROWNE MW, 1989, MULTIVAR BEHAV RES, V24, P445, DOI 10.1207/s15327906mbr2404_4 Browne MW, 1993, TESTING STRUCTURAL E, P136, DOI DOI 10.1177/0049124192021002001 Byrne B. 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Genet. Psychol. PD MAR PY 2006 VL 167 IS 1 BP 65 EP 92 DI 10.3200/GNTP.167.1.65-92 PG 28 WC Psychology, Developmental; Psychology; Psychology, Multidisciplinary SC Psychology GA 030GA UT WOS:000236621200005 PM 16629404 ER PT J AU Lecavalier, L Leone, S Wiltz, J AF Lecavalier, L Leone, S Wiltz, J TI The impact of behaviour problems on caregiver stress in young people with autism spectrum disorders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; behaviour problems; parent stress; pervasive developmental disorder; teacher stress; transactional model ID RATING FORM; PRESCHOOL-CHILDREN; PARENTING STRESS; TEACHER STRESS; FAMILY STRESS; DISABILITIES; ADOLESCENTS; PERCEPTIONS; STRATEGIES; SYMPTOMS AB Background The purpose of this study was to examine the correlates of caregiver stress in a large sample of young people with autism spectrum disorders (ASDs). Two main objectives were to: (1) disentangle the effects of behaviour problems and level of functioning on caregiver stress; and (2) measure the stability of behaviour problems and caregiver stress. Methods Parents or teachers of 293 young people with ASDs completed measures of stress, behaviour problems and social competence. Parents also completed an adaptive behaviour scale. Eighty-one young people were rated twice at a 1-year interval. Results Parents and teachers did not perfectly agree on the nature and severity of behaviour problems. However, both sets of ratings indicated that behaviour problems were strongly associated with stress. Conduct problems in particular were significant predictors of stress. Adaptive skills were not significantly associated with caregiver stress. Parental reports of behaviour problems and stress were quite stable over the 1-year interval, much more so than teacher reports. Parent ratings suggested that behaviour problems and stress exacerbated each other over time. This transactional model did not fit the teacher data. Conclusion Results of this study suggested that it is a specific group of externalized behaviours that are the most strongly associated with both parent and teacher stress. Results were discussed from methodological and conceptual perspectives. C1 Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. Ohio State Univ, Dept Psychol, Columbus, OH 43210 USA. RP Lecavalier, L (reprint author), Ohio State Univ, Nisonger Ctr, 305 McCampbell Hall,1581 Dodd Dr, Columbus, OH 43210 USA. EM lecavalier.I@osu.edu CR Abidin RR, 1995, PARENTING STRESS IND ACHENBACH TM, 1987, PSYCHOL BULL, V101, P213, DOI 10.1037/0033-2909.101.2.213 Aman MG, 1996, RES DEV DISABIL, V17, P41, DOI 10.1016/0891-4222(95)00039-9 Baker B. L., 1997, INT REV RES MENT RET, V20, P1, DOI 10.1016/S0074-7750(08)60174-3 Baker BL, 2002, AM J MENT RETARD, V107, P433, DOI 10.1352/0895-8017(2002)107<0433:BPAPSI>2.0.CO;2 Baker BL, 2003, J INTELL DISABIL RES, V47, P217, DOI 10.1046/j.1365-2788.2003.00484.x BEBKO JM, 1987, J AUTISM DEV DISORD, V17, P565, DOI 10.1007/BF01486971 Bruininks R., 1996, SCALES INDEPENDENT B Cichetti D. V., 1994, PSYCHOL ASSESSMENT, V6, P284 Cockburn AD, 1996, BRIT J EDUC PSYCHOL, V66, P399 Cohen J., 1988, STAT POWER ANAL BEHA, V2nd DONOVAN AM, 1988, AM J MENT RETARD, V92, P502 Dumas J. E., 1991, EXCEPTIONALITY, V2, P97, DOI [10.1080/09362839109524770, DOI 10.1080/09362839109524770] Einfeld S. L., 2002, MANUAL DEV BEHAV CHE FONG PL, 1991, J CONSULT CLIN PSYCH, V59, P471, DOI 10.1037/0022-006X.59.3.471 FREEMAN NL, 1991, J CHILD PSYCHOL PSYC, V32, P1025, DOI 10.1111/j.1469-7610.1991.tb01927.x GADOW KD, 2005, IN PRESS AUTISM Gadow KD, 2004, J AUTISM DEV DISORD, V34, P379, DOI 10.1023/B:JADD.0000037415.21458.93 Greene RW, 1997, J SCHOOL PSYCHOL, V35, P239, DOI 10.1016/S0022-4405(97)00006-X HAMMER D, 2003, SUCCESSFUL MODELS DE Hastings RP, 2003, J INTELL DISABIL RES, V47, P231, DOI 10.1046/j.1365-2788.2003.00485.x Hastings RP, 2001, J AUTISM DEV DISORD, V31, P327, DOI 10.1023/A:1010799320795 Hastings RP, 2002, MENT RETARD, V40, P148, DOI 10.1352/0047-6765(2002)040<0148:CSATIO>2.0.CO;2 Hauser-Cram P, 2001, MONOGR SOC RES CHILD, V66, P1, DOI 10.1111/1540-5834.00151 Jennett HK, 2003, J AUTISM DEV DISORD, V33, P583, DOI 10.1023/B:JADD.0000005996.19417.57 Kasari C, 1997, J AUTISM DEV DISORD, V27, P39, DOI 10.1023/A:1025869105208 KONSTANTAREAS MM, 1989, J CHILD PSYCHOL PSYC, V30, P459, DOI 10.1111/j.1469-7610.1989.tb00259.x KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x KYRIACOU C, 1978, BRIT J EDUC PSYCHOL, V48, P159 Lecavalier L, 2004, J AUTISM DEV DISORD, V34, P709, DOI 10.1007/s10803-004-5291-1 LECAVALIER L, 2005, IN PRESS J AUTISM DE Orsmond GI, 2003, AM J MENT RETARD, V108, P257, DOI 10.1352/0895-8017(2003)108<257:BPIAWM>2.0.CO;2 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SZATMARI P, 1994, J AUTISM DEV DISORD, V24, P703, DOI 10.1007/BF02172281 Tasse MJ, 1996, RES DEV DISABIL, V17, P59, DOI 10.1016/0891-4222(95)00037-2 Tasse MJ, 2000, AM J MENT RETARD, V105, P252, DOI 10.1352/0895-8017(2000)105<0252:CPATRO>2.0.CO;2 TELLENBACK S, 1983, J OCCUP PSYCHOL, V56, P19 TONGE BJ, 2003, INT REV RES MENT RET, P26 ZIGLER E, 1999, PERSONALITY DEV INDI NR 39 TC 237 Z9 242 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 MAR PY 2006 VL 50 BP 172 EP 183 DI 10.1111/j.1365-2788.2005.00732.x PN 3 PG 12 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 005WG UT WOS:000234855100002 PM 16430729 ER PT J AU Blacher, J McIntyre, LL AF Blacher, J McIntyre, LL TI Syndrome specificity and behavioural disorders in young adults with intellectual disability: cultural differences in family impact SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article ID MENTALLY-RETARDED CHILDREN; DEVELOPMENTAL-DISABILITIES; LATINA MOTHERS; DOWN-SYNDROME; AUTISTIC-CHILDREN; PARENTING STRESS; RETARDATION; ADOLESCENTS; DEPRESSION; ACCULTURATION AB Backgound This study examined whether behaviour problems and adaptive behaviour of low functioning young adults, and well-being of their families, varied by diagnostic syndrome [intellectual disability (ID) only, cerebral palsy, Down syndrome, autism], as well as by cultural group. Methods Behaviour disorders in young adults with moderate to severe ID were assessed from information provided by 282 caregivers during in-home interviews. The sample consisted of 150 Anglo participants, and 132 Latino, primarily Spanish-speaking, participants drawn from Southern California. Results Behaviour disorders and maternal well-being showed the same pattern across disability syndromes. Autism was associated with the highest scores in multiple behaviour problem areas as well as maternal reports of lower well-being. Down syndrome was associated with the lowest behaviour problem scores and the highest maternal well-being. When behaviour problems were controlled for, diagnostic groups accounted for no additional variance in maternal stress or depression. The pattern of behaviour problems and well-being did not differ by sample (Anglo vs. Latino), although level on well-being measures did. Latina mothers reported significantly higher depression symptoms and lower morale, but also higher positive impact from their child than did Anglo mothers. Conclusion Caregivers of young adults with autism report more maladaptive behaviour problems and lower personal well-being, or stress, relative to other diagnostic groups, regardless of cultural group. However, cultural differences exist in caregiver reports of depression, morale, and positive perceptions. Implications for service provision aimed at families of children with challenging behaviour problems are discussed in the context of culture. C1 Univ Calif Riverside, Grad Sch Educ, Riverside, CA 92521 USA. Syracuse Univ, Syracuse, NY 13244 USA. RP Blacher, J (reprint author), Univ Calif Riverside, Grad Sch Educ, Riverside, CA 92521 USA. 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Intell. Disabil. Res. PD MAR PY 2006 VL 50 BP 184 EP 198 DI 10.1111/j.1365-2788.2005.00768.x PN 3 PG 15 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 005WG UT WOS:000234855100003 PM 16430730 ER PT J AU Seung, H Siddiqi, S Elder, JH AF Seung, H Siddiqi, S Elder, JH TI Intervention outcomes of a bilingual child with autism SO JOURNAL OF MEDICAL SPEECH-LANGUAGE PATHOLOGY LA English DT Article ID JOINT ATTENTION; LANGUAGE-DEVELOPMENT; PRESCHOOL-CHILDREN; DISORDERS; SPECTRUM; COMMUNICATION; UPDATE AB This longitudinal case study examined a child who was initially diagnosed with language delay at age 3 and subsequently diagnosed with autism at age 3 years 6 months. This case study is particularly interesting because it followed the child for 24 months and evaluated the efficacy of a unique Korean-English bilingual speech-language intervention. Speech-language intervention was provided twice weekly in his primary language, Korean, for the first 12 months by a Korean-English bilingual speech-language clinician. During the next 6 months, the intervention was gradually introduced in English; and by the final 6 months, the intervention was provided almost entirely in English. This study also incorporated information regarding parent interventions that was implemented by the parents at home. The child in this report made notable gains in expressive and receptive language development in both languages over the study period as well as decreases in aberrant behaviors. At the 24-month follow-up, he was able to respond to testing that was done completely in English. The results of this study support the practice of providing services in the primary language when English is not the language used at home to establish linguistic foundation of the primary language. As the child makes gains in the primary language, a gradual transition can be made to intervention in English. Results of this study have important implications for future research and clinical decision making for assisting families of children from a variety of cultural and ethnic backgrounds. C1 Univ Florida, Hlth Sci Ctr, Gainesville, FL 32610 USA. RP Seung, H (reprint author), Univ Florida, Hlth Sci Ctr, 101 S Newell Rd 2150,POB 100174, Gainesville, FL 32610 USA. EM hkseung@phhp.ufl.edu CR Abidin RR, 1995, PARENTING STRESS IND Alexander D, 1996, J AUTISM DEV DISORD, V26, P117, DOI 10.1007/BF02172001 American Psychiatric Association, 2002, DIAGN STAT MAN MENT BANGO TE, 1986, BIRTH 3 CHECKLIST LE BLOM L, 1973, ONE WORD TIME USE SI Bruner J. 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T., 1997, EXPRESSIVE VOCABULAR NR 36 TC 7 Z9 8 PU DELMAR LEARNING PI CLIFTON PARK PA EXECUTIVE WOODS, 5 MAXWELL DR, CLIFTON PARK, NY 12065 USA SN 1065-1438 J9 J MED SPEECH-LANG PA JI J. Med. Speech-Lang. Pathol. PD MAR PY 2006 VL 14 IS 1 BP 53 EP 63 PG 11 WC Audiology & Speech-Language Pathology; Clinical Neurology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology GA 029LV UT WOS:000236565100009 ER PT J AU Canitano, R AF Canitano, R TI Self injurious behavior in autism: clinical aspects and treatment with risperidone SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE self-injury behavior; autism; childhood; risperidone ID PERVASIVE DEVELOPMENTAL DISORDERS; REPETITIVE BEHAVIOR; YOUNG-CHILDREN; OPEN TRIAL; ADOLESCENTS; SEROTONIN; TERM AB Self injurious behavior (SIB) is frequent in autistic spectrum disorders. The aim of this study was to investigate the phenomenology of SIB in a group of children with autistic disorder, and to test whether treatment with risperidone might reduce it. A group of eleven children diagnosed with autistic disorder according to the DSM-IV criteria (mean age 8.7 +/- 2.2ys) and with severe SIB were recruited for an open study of six months of treatment with risperidone. The Yale-Paris Self-Injurious Behavior Scale was used to delineate the clinical characteristics and as an outcome measure. Head-hitting and hand biting were the most frequent forms of self aggression observed. Nine children presented a mild improvement in SIB and 2 did not show any variation. A decrease in Yale-Paris Self Injurious Behavior Scale score (from M 15.1 +/- 1.4 to 13.3 +/- 1.4) was noted mainly due to the reduction of frequency. Side effects of risperidone were not severe. C1 Univ Siena, Gen Hosp, Div Child Neuropsychiat, I-53100 Siena, Italy. RP Canitano, R (reprint author), Univ Siena, Gen Hosp, Div Child Neuropsychiat, Viale Bracci 1, I-53100 Siena, Italy. EM r.canitano@ao-siena.toscana.it CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 Buitelaar J K, 1993, Acta Paedopsychiatr, V56, P105 Buitelaar JK, 2000, EUR CHILD ADOLES PSY, V9, P85 Campbell M, 1999, J AM ACAD CHILD PSY, V38, P537, DOI 10.1097/00004583-199905000-00015 Chugani DC, 1999, ANN NEUROL, V45, P287, DOI 10.1002/1531-8249(199903)45:3<287::AID-ANA3>3.0.CO;2-9 Cook Edwin H. 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Neural Transm. PD MAR PY 2006 VL 113 IS 3 BP 425 EP 431 DI 10.1007/s00702-005-0337-x PG 7 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 009LZ UT WOS:000235114800015 PM 16075185 ER PT J AU Rossman, I Kamdar, S Millonig, J Dicicco-Bloom, E AF Rossman, I Kamdar, S Millonig, J Dicicco-Bloom, E TI Extracellular growth factors interact with Engrailed2 (EN2), an autism-associated gene, to control cerebellar development SO JOURNAL OF NEUROCHEMISTRY LA English DT Meeting Abstract CT Annual Meeting of the American-Society-for-Neurochemistry CY MAR 11-15, 2006 CL Portland, OR SP Amer Soc Neurochem C1 Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Piscataway, NJ 08854 USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0022-3042 J9 J NEUROCHEM JI J. Neurochem. PD MAR PY 2006 VL 96 SU 1 BP 24 EP 24 PG 1 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 021KU UT WOS:000235982900055 ER PT J AU Molloy, CA Morrow, AL Meinzen-Derr, J Schleifer, K Dienger, K Manning-Courtney, P Altaye, M Wills-Karp, M AF Molloy, CA Morrow, AL Meinzen-Derr, J Schleifer, K Dienger, K Manning-Courtney, P Altaye, M Wills-Karp, M TI Elevated cytokine levels in children with autism spectrum disorder SO JOURNAL OF NEUROIMMUNOLOGY LA English DT Article DE autism; cytokines; adaptive immune responses ID RHEUMATOID-ARTHRITIS; AUTOIMMUNE-DISEASES; CANADIAN POPULATION; TH2 SUBSETS; T-CELLS; PREVALENCE; AUTOANTIBODIES; INTERLEUKIN-12; ASSOCIATION; ACTIVATION AB This study compared production of IL-2, IFN-gamma, IL-4, IL-13, IL-5 and IL-10 in peripheral blood mononuclear cells from 20 children with autism spectrum disorder to those from matched controls. Levels of all Th2 cytokines were significantly higher in cases after incubation in media alone, but the IFN-gamma/IL-13 ratio was not significantly different between cases and controls. Cases had significantly higher IL-13/IL-10 and IFN-gamma/IL-10 than controls. Conclusion: Children with ASD had increased activation of both Th2 and Th1 arms of the adaptive immune response, with a Th2 predominance, and without the compensatory increase in the regulatory cytokine IL-10. (C) 2005 Elsevier B.V. All rights reserved. C1 Cincinnati Childrens Hosp, Med Ctr, Ctr Biostat & Epidemiol, Cincinnati, OH 45229 USA. Cincinnati Childrens Hosp, Med Ctr, Div Dev & Behav Pediat, Cincinnati, OH 45229 USA. Cincinnati Childrens Hosp, Med Ctr, Div Immunobiol, Cincinnati, OH 45229 USA. Univ Cincinnati, Coll Med, Dept Pediat, Cincinnati, OH 45221 USA. RP Molloy, CA (reprint author), Cincinnati Childrens Hosp, Med Ctr, Ctr Biostat & Epidemiol, 3333 Burnet Ave,MLC 5041, Cincinnati, OH 45229 USA. 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Neuroimmunol. PD MAR PY 2006 VL 172 IS 1-2 BP 198 EP 205 DI 10.1016/j.jneuroim.2005.11.007 PG 8 WC Immunology; Neurosciences SC Immunology; Neurosciences & Neurology GA 025LF UT WOS:000236266900022 PM 16360218 ER PT J AU Ingersoll, B Dvortcsak, A AF Ingersoll, B Dvortcsak, A TI Including parent training in the early childhood special education curriculum for children with autism spectrum disorders SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID PRESCHOOL-CHILDREN; EARLY INTERVENTION; TEACHERS AB Parent training has been shown to be a very effective method for promoting generalization and maintenance of skills in children with autism. However, despite its well-established benefits, few public school programs include parent training as part of the early childhood special education (ECSE) curriculum. 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Posit. Behav. Interv. PD SPR PY 2006 VL 8 IS 2 BP 79 EP 87 DI 10.1177/10983007060080020601 PG 9 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 028HS UT WOS:000236478400003 ER PT J AU Maione, L Mirenda, P AF Maione, L Mirenda, P TI Effects of video modeling and video feedback on peer-directed social language skills of a child with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID INITIATIONS; TECHNOLOGY; PACKAGE; SELF AB Identifying practical strategies for teaching children with autism to use social language with their peers is a challenge for professionals designing treatment programs. The purpose of this multiple baseline study was to assess the effectiveness of video modeling and video feedback for teaching a child with autisin to use social language with typical peers during play. Video modeling was effective in increasing social language in two of the three activities. 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RP Openden, D (reprint author), Univ Calif Santa Barbara, Gevirtz Grad Sch Educ, UCSB Koegel Autism Ctr, Santa Barbara, CA 93106 USA. EM dopenden@education.ucsb.edu CR Carr EG, 2002, J POSIT BEHAV INTERV, V4, P4, DOI 10.1177/109830070200400102 Clark H. B., 1999, Journal of Positive Behavior Interventions, V1, P183, DOI 10.1177/109830079900100307 DIGGLE T, 2002, COCHRANE DATABASE SY, V2 Koegel L. K., 1996, POSITIVE BEHAV SUPPO KOEGEL LK, 2002, MODEL INCREASING IN MARQUIS JG, 2000, CONT SPECIAL ED RES, P137 Moes D., 1995, TEACHING CHILDREN AU, P79 MOES D, 1992, PSYCHOL REP, V71, P1272, DOI 10.2466/PR0.71.8.1272-1274 Singer G. H., 2002, FAMILIES POSITIVE BE, P155 NR 9 TC 4 Z9 4 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 SPR PY 2006 VL 8 IS 2 BP 119 EP 123 DI 10.1177/10983007060080020301 PG 5 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 028HS UT WOS:000236478400007 ER PT J AU [Anonymous] AF [Anonymous] TI New resource for autism SO JOURNAL OF PSYCHOSOCIAL NURSING AND MENTAL HEALTH SERVICES LA English DT News Item NR 0 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 MAR PY 2006 VL 44 IS 3 BP 11 EP 11 PG 1 WC Nursing SC Nursing GA V59LF UT WOS:000204017500006 ER PT J AU Jurecic, A AF Jurecic, Ann TI Mindblindness: Autism, writing, and the problem of empathy SO LITERATURE AND MEDICINE LA English DT Article C1 Rutgers State Univ, Dept English, Piscataway, NJ 08855 USA. RP Jurecic, A (reprint author), Rutgers State Univ, Dept English, Piscataway, NJ 08855 USA. CR [Anonymous], 1994, DIAGNOSTIC STAT MANU Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bauman M.L, 1994, NEUROBIOLOGY AUTISM BETTELHEIM B, 1959, SCI AM, V200, P116 Bettelheim B., 1967, EMPTY FORTRESS INFAN BLAKESLEE S, 2003, NY TIMES 0514 Folstein SE, 2001, NAT REV GENET, V2, P943, DOI 10.1038/35103559 FRITH U, 1994, PHILOS T BIOL SCI, V346, P1315 FROMBONNE E, 2002, MOL PSYCHIATR, V7, pS4 Frombonne E., 1999, PSYCHOL MED, V29, P769 Grandin T., 1995, THINKING PICTURES OT Grandin T., 1986, EMERGENCE LABELED AU Halpern J., 1993, EMPATHY PRACTICE MED, P160 Halpern J, 2001, DETACHED EMPATHY HUM Klein M, 1986, SELECTED M KLEIN, P95 Lynch Dennis A., 1998, RHETOR SOC Q, V28.1, P5 More Ellen Singer, 1994, EMPATHIC PRACTITIONE Nussbaum M., 2001, UPHEAVALS THOUGHT Rodier PM, 2000, SCI AM, V282, P56 Sacks O, 1995, ANTHR MARS 7 PARADOX, P244 SEIDEL K, AUTISTIC AUTOBIOGRAP Silberman Steve, 2001, WIRED, V9 Sontag S., 1988, ILLNESS METAPHOR AID Spiro H, 1993, EMPATHY PRACTICE MED Tager-Flusberg H., 1993, UNDERSTANDING OTHER, P3 Turner M, 2000, MOL MED TODAY, V6, P238, DOI 10.1016/S1357-4310(00)01712-3 Williams D., 1994, SOMEBODY SOMEWHERE B Williams D., 1992, NOBODY NOWHERE EXTRA NR 29 TC 10 Z9 10 PU JOHNS HOPKINS UNIV PRESS PI BALTIMORE PA JOURNALS PUBLISHING DIVISION, 2715 NORTH CHARLES ST, BALTIMORE, MD 21218-4363 USA SN 0278-9671 J9 LIT MED JI Lit. 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PD SPR PY 2006 VL 25 IS 1 BP 24 EP 45 DI 10.1353/lm.2006.0025 PG 22 WC Literature SC Literature GA 087TN UT WOS:000240765400003 PM 17040083 ER PT J AU Mousain-Bosc, M Roche, M Polge, A Pradal-Prat, D Rapin, J Bali, JP AF Mousain-Bosc, M Roche, M Polge, A Pradal-Prat, D Rapin, J Bali, JP TI Improvement of neurobehavioral disorders in children supplemented with magnesium-vitamin B6I. Attention deficit hyperactivity disorders SO MAGNESIUM RESEARCH LA English DT Article DE hyperactive children; attention deficit hyperactivity disorders; magnesium-vitamin B6 diet; intraerythrocyte magnesium; ionized Ca2+ ID MAGNESIUM CONCENTRATION; CALCIUM; AUTISM; ADHD; RATS; MG2+ AB Some previous studies have reported the involvement of magnesium (Mg) deficiency in children with ADHD syndrome. In this work, 40 children with clinical symptoms of ADHD were followed clinically and biologically during a magnesium-vitamin 136 (Mg-B6) regimen (6 mg/kg/d Mg, 0.6 mg/kg/d vit-136) which was set up for at least 8 weeks. Symptoms of ADHD (hyperactivity, hyperemotivity/aggressiveness, lack of attention at school) were scored (0-4) at different times; in parallel, intraerythrocyte Mg2+ (Erc-Mg) and blood ionized Ca2+ (i-Ca) were measured. Children from the ADHD group showed significantly lower Erc-Mg values than control children (n = 36). In almost all cases of ADHD, Mg-136 regimen for at least two months significantly modified the clinical symptoms of the disease: namely, hyperactivity and hyperemotivity/aggressiveness were reduced, school attention was improved. In parallel, the Mg-136 regimen led to a significant increase in Erc-Mg values. When the Mg-136 treatment was stopped, clinical symptoms of the disease reappeared in few weeks together with a decrease in Erc-Mg values. This study brings additional information about the therapeutic role of a Mg-136 regimen in children with ADHD symptoms . C1 Fac Pharm Montpellier, Biochim Lab, F-34093 Montpellier 5, France. Ctr Hosp Univ Caremeau, Explorat Fonctionnelles Syst Nerveux, Nimes, France. Ctr Hosp Univ Caremeau, Biochim Lab, Nimes, France. Univ Bourgogne, Dept Pharmacol, Dijon, France. RP Bali, JP (reprint author), Fac Pharm Montpellier, Biochim Lab, 15,Ave Charles Flahault,BP 14491, F-34093 Montpellier 5, France. EM jp.bali@wanadoo.fr CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Basso LE, 2000, CLIN CHIM ACTA, V291, P1, DOI 10.1016/S0009-8981(99)00168-0 Borella Paola, 1993, Magnesium Research, V6, P149 De Franceschi L, 2000, BRIT J HAEMATOL, V108, P284 Demougeot C, 2004, NEUROSCI LETT, V362, P17, DOI 10.1016/j.neulet.2004.01.034 Ebel H, 2005, MAGNESIUM RES, V18, P175 Feillet-Coudray C, 2004, METABOLISM, V53, P660, DOI 10.1016/j.metabol.2003.12.014 FERGUSON JW, 1964, ANAL CHEM, V36, P796, DOI 10.1021/ac60210a028 Gervais H, 2004, NAT NEUROSCI, V7, P801, DOI 10.1038/nn1291 HELPERN JA, 1993, NEUROLOGY, V43, P1577 Kozielec T, 1997, MAGNESIUM RES, V10, P143 LIEBSCHER DH, 2003, 10 INT MAGN S CAIRNS Macdonald RL, 2004, J NEUROSURG, V100, P106, DOI 10.3171/jns.2004.100.1.0106 Mousain-Bosc M, 2004, J AM COLL NUTR, V23, p545S SCHMIDT CJ, 1988, EUR J PHARMACOL, V156, P111, DOI 10.1016/0014-2999(88)90153-7 SCHMIDT ME, 1994, PSYCHIAT RES, V54, P199, DOI 10.1016/0165-1781(94)90007-8 Shalev H, 1998, ARCH DIS CHILD, V78, P127 Spencer TJ, 2002, J CLIN PSYCHIAT, V63, P3 StarobratHermelin B, 1997, MAGNESIUM RES, V10, P149 Vink R., 2001, Advances in magnesium research: nutrition and health, P405 Zilbovicius M, 2000, AM J PSYCHIAT, V157, P1988, DOI 10.1176/appi.ajp.157.12.1988 NR 21 TC 29 Z9 31 PU JOHN LIBBEY & CO LTD PI LONDON PA 13 SMITHS YARD, SUMMERLEY ST, LONDON SW18 4HR, ENGLAND SN 0953-1424 J9 MAGNESIUM RES JI Magnes. Res. PD MAR PY 2006 VL 19 IS 1 BP 46 EP 52 PG 7 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 054TE UT WOS:000238400700007 PM 16846100 ER PT J AU Mousain-Bosc, M Roche, M Polge, A Pradal-Prat, D Rapin, J Bali, JP AF Mousain-Bosc, M Roche, M Polge, A Pradal-Prat, D Rapin, J Bali, JP TI Improvement of neurobehavioral disorders in children supplemented with magnesium-vitamin B6II. Pervasive developmental disorder-autism SO MAGNESIUM RESEARCH LA English DT Article DE pervasive developmental disorders; autism; magnesium-vitamin B6 diet; intraerythrocyte magnesium; ionized Ca2+ ID NA+/MG2+ ANTIPORT; MAGNESIUM LEVELS; DOUBLE-BLIND; PYRIDOXINE; HYPERACTIVITY; ERYTHROCYTES; SUBGROUP; ADHD; RATS; MG2+ AB Previous studies reported positive results with the use of Mg-vitamin B6 in autism. Despite these reports, this intervention remains controversial. In order to study relationships between changes in clinical symtoms and biological parameters, 33 children (mean age: 4 [1-10] years old) with clinical symptoms of pervasive developmental disorder or autism (PDD, as defined in DSM-IV) were followed for at least 6 months; another group of 36 children (same age) devoided of any known pathology was used is control. All PDD children received a magnesium-vit 136 (Mg-B6) regimen (6 mg/kg/d Mg and 0.6 mg/kg/d vit 136). Intraerythrocyte Mg2+, (Erc-Mg), serum Mg2+ (s-Mg) and blood ionized Ca2+ (i-Ca) were measured before and after treatment. Clinical symptoms of PDD were scored (0 to 4). In contrast to s-Mg or i-Ca, PDD children exhibited significantly lower Erc-Mg values than controls (2.17 +/- 0.4 versus 2.73 +/- 0.23 mmol/L; 16/33). The Mg-B6 regimen led to an increase in Erc-Mg values (2.42 +/- 0.41 (after) versus 2.17 +/- 0.4 mmol/l (before), 11/17) and this supplementation improved PDD symptoms in 23/33 children (p < 0.0001) with no adverse effects: social interactions (23/33), communication (24/33), stereotyped restricted behavior (18/33), and abnormal/delayed functioning (17/33); 15/33 children were improved in the first three groups of symptoms. When the Mg-B6 treatment was stopped, PDD symptoms reappeared in few weeks. A statistically significant relationship was found in Erc-Mg values from children before treatment and their mothers. In conclusion, this study suggests that the behavioral improvement observed with the combination vitamin B6-magnesium in PDD/autism is associated with concomitant modifications of Erc-Mg values. C1 Fac Pharm Montpellier, Biochim Lab, F-34093 Montpellier 5, France. Ctr Hosp Univ Caremeau, Explorat Fonctionnelles Syst Nerveux, Nimes, France. Ctr Hosp Univ Caremeau, Biochim Lab, Nimes, France. Univ Bourgogne, Dept Pharmacol, Dijon, France. RP Bali, JP (reprint author), Fac Pharm Montpellier, Biochim Lab, 15,Ave Charles Flahault, F-34093 Montpellier 5, France. 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Res. PD MAR PY 2006 VL 19 IS 1 BP 53 EP 62 PG 10 WC Biochemistry & Molecular Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Endocrinology & Metabolism GA 054TE UT WOS:000238400700008 PM 16846101 ER PT J AU Dam, J AF Dam, J TI Insight in schizophrenia: A review SO NORDIC JOURNAL OF PSYCHIATRY LA English DT Review DE awareness; compliance; insight; schizophrenia ID ILLNESS; PSYCHOSIS; PSYCHOPATHOLOGY; PERFORMANCE; AWARENESS; SCALE; NEUROCOGNITION; UNAWARENESS; MANAGEMENT; MEDICATION AB The issue of insight in schizophrenia must be assumed to be one of the most important aspects of the clinical examination. Comprehensive studies have shown that between 50% and 80% of all patients suffering from schizophrenia do not believe that they have a disorder. In recent years, poor insight in schizophrenia has been the subject of increasing interest, as manifested in a number of studies discussed in the present review. Some of these studies focus on insight correlated to various parameters such as psychopathology, neuropsychology, clinical relevance and compliance. Other studies refer to more theoretical implications, among these the issue of defining the concept of insight: whether insight can be seen as a "primary'' phenomenon in schizophrenia, and whether insight may be graduated, dimensioned or increased. Several authors have developed rating scales in an attempt to obtain a measure for the degree or dimension of insight. Here, the range of parameters employed gives an excellent impression of the complexity of the concept of insight. In the concluding discussion, a phenomenological aspect is brought in, in an attempt to place the concept of insight in relation to disturbances of the self in schizophrenia and to primary symptoms in schizophrenia, amongst these autism. C1 Frederiksborg Cent Cty Hosp, Psychiat Dept 5, DK-2970 Horsholm, Denmark. 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PD MAR PY 2006 VL 60 IS 2 BP 114 EP 120 DI 10.1080/08039480600600185 PG 7 WC Psychiatry SC Psychiatry GA 050MN UT WOS:000238092200006 PM 16635929 ER PT J AU Larson, E AF Larson, E TI Caregiving and autism: How does children's propensity for routinization influence participation in family activities? SO OTJR-OCCUPATION PARTICIPATION AND HEALTH LA English DT Article DE human activity and occupation; occupational science; parenting ID PARENTING STRESS; SOCIAL SUPPORT; MOTHERS; DISORDER; OUTCOMES; LIFE AB Children With autism characteristically prefer routinization, yet their mothers seem to experience greater parenting stress orchestrating family life than mothers parenting children with other disabilities. This qualitative study examined the development and use of routines for nine mothers parenting children with autism spectrum diagnoses. Interview transcripts were coded by sorting data into categories and searching for variations within the category and the relationships between categories. Findings describe: (1) development of routines, (2) child's comfort or discontent in routines, (3) child's fluctuations in participation in routines, (4) effects of irregular routines on participation, (5) maternal strategies to manage irregular routines, (6) mothers' selective modification of routines, and (7) alterations in family activities and rituals. The implications of these findings for practice are discussed. C1 Univ Wisconsin, Dept Kinesiol, Occupat Therapy Program, Madison, WI 53706 USA. RP Larson, E (reprint author), Univ Wisconsin, Dept Kinesiol, Occupat Therapy Program, Madison, WI 53706 USA. 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PD MAR PY 2006 VL 2 IS 3 BP 146 EP 159 AR e22 DI 10.1371/journal.pcbi.0020022 PG 14 WC Biochemical Research Methods; Mathematical & Computational Biology SC Biochemistry & Molecular Biology; Mathematical & Computational Biology GA 070AV UT WOS:000239493600004 PM 16557292 ER PT J AU Carminati, GG Deriaz, N Bertschy, G AF Carminati, GG Deriaz, N Bertschy, G TI Low-dose venlafaxine in three adolescents and young adults with autistic disorder improves self-injurious behavior and attention deficit/hyperactivity disorders (ADHD)-like symptoms SO PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY LA English DT Review DE autism; pervasive developmental disorder; self-injurious behavior; venlafaxine ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; ANTIDEPRESSANT; CHILDREN; NORADRENALINE; FLUVOXAMINE; AGGRESSION; MECHANISMS; PAROXETINE AB In our clinical practice, we have had good experiences with venlafaxine in the treatment of self-injurious behavior (SIB) and attention deficit/hyperactivity disorders (ADHD)-like symptoms in patients with pervasive developmental disorders (PDD), and we report here three cases of possible therapeutic response: (A) a 17-year-old boy with autism and severe behavioral symptoms, including aggression toward self or property, SIB and hyperactivity, who appeared to respond to low-dose venlafaxine (18.75 mg/day); (B) a 23-year-old woman with autism hyperactivity who appeared to respond to low-dose venlafaxine (18.75 mg/day); (C) a 17-year-old girl with autism hyperactivity who appeared to respond to low-dose venlafaxine (18.75 mg/day). 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PD SPR PY 2006 VL 56 IS 2 BP 233 EP 244 PG 12 WC Psychology, Multidisciplinary SC Psychology GA 043KB UT WOS:000237598800006 ER PT J AU Mohler, E AF Mohler, E TI Rare, but existent: the "female version" of Asperger syndrome SO PSYCHOTHERAPEUT LA German DT Article ID AUTISM; DISORDERS C1 Abt Kinder & Jugendpsychiat, D-69115 Heidelberg, Germany. RP Mohler, E (reprint author), Abt Kinder & Jugendpsychiat, Blumenstr 8, D-69115 Heidelberg, Germany. EM eva.moehler@med.uni-heidelberg.de CR BUDDENSIEK N, 2005, PSYCHOPRAXIS, V5, P12 Cederlund M, 2004, DEV MED CHILD NEUROL, V46, P652 Fombonne E, 2003, CHILD ADOL PSYCH CL, V12, P15, DOI 10.1016/S1056-4993(02)00050-0 Ghaziuddin M, 2004, J AUTISM DEV DISORD, V34, P279, DOI 10.1023/B:JADD.0000029550.19098.77 Lauritsen MB, 2004, PSYCHOL MED, V34, P1339, DOI 10.1017/S0033291704002387 Schlange H, 1977, GOTTINGER FORMREPROD SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Sturm H, 2004, DEV MED CHILD NEUROL, V46, P444, DOI 10.1017/S0012162204000738 Tewes U., 2000, HAMBURG WECHSLER INT Perera H., 2003, Ceylon Medical Journal, V48, P57 NR 10 TC 1 Z9 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0935-6185 J9 PSYCHOTHERAPEUT JI Psychotherapeut PD MAR PY 2006 VL 51 IS 2 BP 154 EP 156 DI 10.1007/s00278-006-0473-2 PG 3 WC Psychology, Clinical; Psychology, Psychoanalysis SC Psychology GA 022CU UT WOS:000236033100009 ER PT J AU MacDonald, R Anderson, J Dube, WV Geckeler, A Green, G Holcomb, W Mansfield, R Sanchez, J AF MacDonald, R Anderson, J Dube, WV Geckeler, A Green, G Holcomb, W Mansfield, R Sanchez, J TI Behavioral assessment of joint attention: A methodological report SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE behavioral assessment; joint attention; shifting gaze; autism ID LANGUAGE-DEVELOPMENT; AUTISTIC-CHILDREN; INTERVENTION; PLAY AB This paper describes a highly structured assessment protocol with objective behavioral measures for joint attention responding and initiation. The assessment was given to 26 children diagnosed with autism spectrum disorders and 21 typically developing children, aged two to four years. Interobserver agreement was high for all behavioral measures. Children with autism had relatively minor deficits in joint attention responding and more severe deficits in joint attention initiation, relative to typically developing children. These results replicate those reported in previous research. The protocol can be used reliably to assess behavior indicative of joint attention responding and initiation in typically developing children and children with autism. (c) 2005 Elsevier Ltd. All rights reserved. C1 New England Ctr Children, Southborough, MA 01772 USA. Univ Massachusetts, Sch Med, Shriver Ctr, Amherst, MA USA. RP MacDonald, R (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. 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Dev. Disabil. PD MAR-APR PY 2006 VL 27 IS 2 BP 138 EP 150 DI 10.1016/j.ridd.2004.09.006 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 015SP UT WOS:000235571500003 PM 15979843 ER PT J AU Cotton, S Richdale, A AF Cotton, S Richdale, A TI Brief report: Parental descriptions of sleep problems in children with autism, Down syndrome, and Prader-Willi syndrome SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE sleep problems; autism; Down syndrome; Prader-Willi syndrome ID EXCESSIVE DAYTIME SLEEPINESS; HANDICAPPED-CHILDREN; MENTAL HANDICAP; PATTERNS; BEHAVIOR; ABNORMALITIES; ADULTS; QUESTIONNAIRE; DISTURBANCE; DISORDERS AB Children with an intellectual disability (ID) are at high risk of developing sleep problems. The extent to which the prevalence and nature of sleep problems in these children is dependent on the disorder underlying their intellectual impairments remains unclear. This study examined and compared parental descriptions of sleep problems in children with autism (n = 37), Down syndrome (DS; n = 15), Prader-Willi syndrome (PWS; n = 29), presumed familial intellectual disability (FID; n = 29), and typically developing children (TD; n = 55) in order to determine any influences of disorder on sleep patterns. The prevalence of sleep problems in the disability groups was at least four times higher than for TD children. Sleep problems were more prevalent in autism than the other disorders. Settling difficulties and co-sleeping were more common in the children with autism, whereas sleep maintenance problems were common in autism, DS, and FID, and daytime napping and excessive daytime sleepiness differentiated the children with PWS. These findings are discussed in light of the specific disorders, and with respect to the impact that sleep problems can have on the child and his/her family. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Melbourne, Dept Psychiat, ORYGEN Youth Hlth, Parkville, Vic 3052, Australia. RMIT Univ, Sch Hlth Sci, Bundoora, Vic, Australia. RP Cotton, S (reprint author), Univ Melbourne, Dept Psychiat, ORYGEN Youth Hlth, Locked Bag 10,35 Poplar Rd, Parkville, Vic 3052, Australia. 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Dev. Disabil. PD MAR-APR PY 2006 VL 27 IS 2 BP 151 EP 161 DI 10.1016/j.ridd.2004.12.003 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 015SP UT WOS:000235571500004 PM 15975763 ER PT J AU van Lang, NDJ Bouma, A Sytema, S Kraijer, DW Minderaa, RB AF van Lang, NDJ Bouma, A Sytema, S Kraijer, DW Minderaa, RB TI A comparison of central coherence skills between adolescents with an intellectual disability with and without comorbid autism spectrum disorder SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE central coherence theory; cognitive style; detail-focused processing; intellectual disability; autism spectrum disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; INDIVIDUALS; PERFORMANCE; DEFICIT; MEMORY; TASKS AB Central coherence theory hypothesizes individuals with autism process information in a detail-focused fashion. The present study examined whether adolescents with an intellectual disability and comorbid autism spectrum disorder showed a weaker central coherence than age- and IQ-matched controls. The central coherence skills of 43 adolescents from schools for students with severe learning problems were examined with two cognitive tasks. In these two tasks, detail-focused processing is beneficial to global processing to perform the tasks accurately and quickly. The group with autism spectrum disorder performed better than the control group. Adolescents with an intellectual disability and with comorbid autism spectrum disorder have a weaker central coherence than age- and IQ-matched controls. Partial support was also given for variability in weak central coherence within the autism spectrum. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Groningen, Dept Clin & Dev Psychol, NL-9712 TS Groningen, Netherlands. RP Bouma, A (reprint author), Univ Groningen, Dept Clin & Dev Psychol, Grote Kruisstr 2-1, NL-9712 TS Groningen, Netherlands. EM j.m.bouma@ppsw.rug.nl RI Sytema, Sjoerd/B-2058-2010 CR Booth R, 2003, PHILOS T ROY SOC B, V358, P387, DOI 10.1098/rstb.2002.1204 Bos A, 1997, WECHSLER PRESCHOOL P Brian JA, 1996, J CHILD PSYCHOL PSYC, V37, P865, DOI 10.1111/j.1469-7610.1996.tb01482.x Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 Frith U., 1989, AUTISM EXPLAINING EN Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Jarrold C, 1997, J AUTISM DEV DISORD, V27, P25, DOI 10.1023/A:1025817121137 Jolliffe T, 1999, COGNITION, V71, P149, DOI 10.1016/S0010-0277(99)00022-0 Kraijer D. 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Dev. Disabil. PD MAR-APR PY 2006 VL 27 IS 2 BP 217 EP 226 DI 10.1016/j.ridd.2004.12.005 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 015SP UT WOS:000235571500009 PM 16005604 ER PT J AU Rabeharisoa, V AF Rabeharisoa, V TI Towards a new form of medical work in psychiatry genetics: the case of autism SO SCIENCES SOCIALES ET SANTE LA French DT Article ID RATIONALIZATION; DIAGNOSIS; ONCOLOGY; GENOME AB This articles draws on ethnographic observations of a series of medical consultations and staffs which gather child psychiatrists and paediatric-geneticists. Its objective is to take over the diagnostic work for adolescents and young adults who had been diagnosed with << autism >> in their childhood. The author shows that an original medical work is taking shape. It consists of inquiring about the patient's body troubles, whose psychiatric versus organic origins are not easy to pin down. Child psychiatrists and paediatric-geneticists are thus forced to question the articulation between biological and psychiatric facts, and the very nature of investigations that should be planned to highligth each patient's situation. The author's contention is that this form of medical investigation stands as far from genetic reductionism, as from << bio-psycho-social >> relativism. C1 Ecole Mines, Ctr Sociol Innovat, F-75272 Paris 06, France. RP Rabeharisoa, V (reprint author), Ecole Mines, Ctr Sociol Innovat, 60,Blvd St Michel, F-75272 Paris 06, France. 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Sociales Sante PD MAR PY 2006 VL 24 IS 1 BP 83 EP 116 PG 34 WC Health Policy & Services; Social Sciences, Interdisciplinary SC Health Care Sciences & Services; Social Sciences - Other Topics GA 035OP UT WOS:000237011400005 ER PT J AU Young, A AF Young, A TI Psychiatry's search for a post-genomic mind SO SCIENCES SOCIALES ET SANTE LA English DT Article ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; MIRROR NEURONS; ASPERGER-SYNDROME; PREMOTOR CORTEX; NEURAL BASIS; REPRESENTATION; EVOLUTION; DELUSIONS; LANGUAGE AB The publication of DSM-III (Diagnostic Manual of the American Psychiatric Association, third edition, 1980) promoted a revolution in American psychiatry. Its most visible target was psychodynamic psychiatry and the concept of psychoneurosis. The revolution shifted the clinical gaze away from mental etiology, mechanism and process onto manifest symptoms, and redefined these symptoms as signifiers of classification rather than polymorphous adaptations. The revolution was fed by the successes of biological psychiatry, the increasing popularity of explanatory reductionism, and access to technologies that could track behavioural symptoms and self-reported mental states to their biological sources. This paper focuses on a second revolution, initiated by developments in molecular genetics and the accessibility of functional neuroimaging technology. At first glance, these developments seem to complete the earlier trend by moving explanatory reductionism to the most basic biological level, the molecular << blueprints of life >>, further undermining the usefulness of << mind >> as a construct for understanding and explaining psychiatric disorders. In reality, the second revolution is an occasion for re-inventing the mind along evolutionary lines. C1 McGill Univ, Dept Social Studies Med, Montreal, PQ H3A 1X1, Canada. RP Young, A (reprint author), McGill Univ, Dept Social Studies Med, 3647 Peel, Montreal, PQ H3A 1X1, Canada. 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Sociales Sante PD MAR PY 2006 VL 24 IS 1 BP 117 EP 146 PG 30 WC Health Policy & Services; Social Sciences, Interdisciplinary SC Health Care Sciences & Services; Social Sciences - Other Topics GA 035OP UT WOS:000237011400006 ER PT J AU Chouchourelou, A Matsuka, T Harber, K Shiffrar, M AF Chouchourelou, Arieta Matsuka, Toshihiko Harber, Kent Shiffrar, Maggie TI The visual analysis of emotional actions SO SOCIAL NEUROSCIENCE LA English DT Article ID POINT-LIGHT DISPLAYS; BIOLOGICAL MOTION; HUMAN AMYGDALA; FACIAL EXPRESSIONS; NEURAL RESPONSES; MACAQUE MONKEY; HUMAN BRAIN; PERCEPTION; AUTISM; BODY AB Is the visual analysis of human actions modulated by the emotional content of those actions? This question is motivated by a consideration of the neuroanatomical connections between visual and emotional areas. Specifically, the superior temporal sulcus (STS), known to play a critical role in the visual detection of action, is extensively interconnected with the amygdala, a center for emotion processing. To the extent that amygdala activity influences STS activity, one would expect to find systematic differences in the visual detection of emotional actions. A series of psychophysical studies tested this prediction. Experiment 1 identified point-light walker movies that convincingly depicted five different emotional states: happiness, sadness, neutral, anger, and fear. In Experiment 2, participants performed a walker detection task with these movies. Detection performance was systematically modulated by the emotional content of the gaits. Participants demonstrated the greatest visual sensitivity to angry walkers. The results of Experiment 3 suggest that local velocity cues to anger may account for high false alarm rates to the presence of angry gaits. 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Neurosci. PD MAR PY 2006 VL 1 IS 1 BP 63 EP 74 DI 10.1080/17470910600630599 PG 12 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 242ZL UT WOS:000251764600007 PM 18633776 ER PT J AU Sand, P Langguth, B Hajak, G Kick, C Stoertebecker, P Eichhammer, P Perna, M Prikryl, R Kucerova, H Ceskova, E AF Sand, P Langguth, B Hajak, G Kick, C Stoertebecker, P Eichhammer, P Perna, M Prikryl, R Kucerova, H Ceskova, E TI Screening for Neuroligin 4 (NLGN4) truncating and transmembrane domain mutations in schizophrenia SO SCHIZOPHRENIA RESEARCH LA English DT Letter ID AUTISM; GENES C1 Univ Regensburg, Dept Psychiat, D-93053 Regensburg, Germany. Univ Brno, Dept Psychiat, Brno, Czech Republic. RP Sand, P (reprint author), Univ Regensburg, Dept Psychiat, Univ Str 84, D-93053 Regensburg, Germany. 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PD FEB 28 PY 2006 VL 82 IS 2-3 BP 277 EP 278 DI 10.1016/j.schres.2005.11.003 PG 2 WC Psychiatry SC Psychiatry GA 028MT UT WOS:000236492500021 PM 16377159 ER PT J AU Stein, JM Bergman, W Fang, YS Davison, L Brensinger, C Robinson, MB Hecht, NB Abel, T AF Stein, JM Bergman, W Fang, YS Davison, L Brensinger, C Robinson, MB Hecht, NB Abel, T TI Behavioral and neurochemical alterations in mice lacking the RNA-binding protein translin SO JOURNAL OF NEUROSCIENCE LA English DT Article DE anxiety; attention; RNA trafficking; local translation; fragile X syndrome; norepinephrine ID X MENTAL-RETARDATION; FMR1 KNOCKOUT MICE; ELEVATED PLUS-MAZE; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; INBRED MOUSE STRAINS; BRAIN MESSENGER-RNAS; BC1 RNA; WATER MAZE; HIPPOCAMPAL-NEURONS; TRANSGENIC MICE AB Synapse-specific local protein synthesis is thought to be important for neurodevelopment and plasticity and involves neuronal RNA-binding proteins that regulate the transport and translation of dendritically localized transcripts. The best characterized of these RNA-binding proteins is the fragile X mental retardation protein ( FMRP). Mutations affecting the expression or function of FMRP cause fragile X syndrome in humans, and targeted deletion of the gene encoding FMRP results in developmental and behavioral alterations in mice. Translin is an RNA-binding protein that regulates mRNA transport and translation in mouse male germ cells and is proposed to play a similar role in neurons. Like FMRP, translin is present in neuronal dendrites, binds dendritically localized RNA, and associates with microtubules and motor proteins. We reported previously the production of viable homozygous translin knock-out mice, which demonstrate altered expression of multiple mRNA transcripts in the brain and mild motor impairments. Here, we report that translin knock-out mice also exhibit sex-specific differences in tests of learning and memory, locomotor activity, anxiety-related behavior, and sensorimotor gating, as well as handling-induced seizures and alterations in monoamine neurotransmitter levels in several forebrain regions. Similar behavioral and neurochemical alterations have been observed in mice lacking FMRP, suggesting that both proteins may act within the same neuronal systems and signaling pathways. Our results in mice indicate that mutations in translin may contribute to fragile X-like syndromes, mental retardation, attention deficit hyperactivity disorder, epilepsy, and autism spectrum disorders in humans. C1 Univ Penn, Dept Biol, Leidy Labs 319, Philadelphia, PA 19104 USA. Univ Penn, Childrens Hosp Philadelphia, Dept Pediat, Philadelphia, PA 19104 USA. Univ Penn, Childrens Hosp Philadelphia, Dept Pharmacol, Philadelphia, PA 19104 USA. 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Biol. PD FEB 21 PY 2006 VL 16 IS 4 BP R131 EP R133 DI 10.1016/j.cub.2006.02.008 PG 3 WC Biochemistry & Molecular Biology; Cell Biology SC Biochemistry & Molecular Biology; Cell Biology GA 018UD UT WOS:000235789400014 PM 16488864 ER PT J AU Baron-Cohen, S Knickmeyer, RC Belmonte, MK AF Baron-Cohen, S Knickmeyer, RC Belmonte, MK TI Genetic research into autism - Response SO SCIENCE LA English DT Letter C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, 18B Trumpington Rd, Cambridge CB2 2AH, England. RI Knickmeyer, Rebecca/G-8128-2014 OI Knickmeyer, Rebecca/0000-0001-7708-1388 CR Medland SE, 2005, BEHAV GENET, V35, P735, DOI 10.1007/s10519-005-6187-3 Rinn JL, 2005, TRENDS GENET, V21, P298, DOI 10.1016/j.tig.2005.03.005 Ronald A, 2005, DEVELOPMENTAL SCI, V8, P444, DOI 10.1111/j.1467-7687.2005.00433.x WHEELWRIGHT S, IN PRESS BRAIN RES NR 4 TC 2 Z9 2 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD FEB 17 PY 2006 VL 311 IS 5763 BP 952 EP 952 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 014CS UT WOS:000235456900021 ER PT J AU Ronald, A Happe, F Plomin, R AF Ronald, A Happe, F Plomin, R TI Genetic research into autism SO SCIENCE LA English DT Letter C1 Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, London SE5 8AF, England. RP Ronald, A (reprint author), Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, De Crespigny Pk, London SE5 8AF, England. RI Happe, Francesca/D-5544-2012; Ronald, Angelica/C-7812-2009; Plomin, Robert/B-8911-2008 OI Ronald, Angelica/0000-0002-9576-2176; CR Baron-Cohen S, 2005, SCIENCE, V310, P819, DOI 10.1126/science.1115455 Ronald A, 2005, DEVELOPMENTAL SCI, V8, P444, DOI 10.1111/j.1467-7687.2005.00433.x RONALD A, 2006, THESIS U LONDON RONALD A, IN PRESS J AM ACAD C NR 4 TC 11 Z9 11 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD FEB 17 PY 2006 VL 311 IS 5763 BP 952 EP 952 DI 10.1126/science.311.5763.952a PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 014CS UT WOS:000235456900020 PM 16484478 ER PT J AU Battaglia, A Carey, JC AF Battaglia, A Carey, JC TI Etiologic yield of autistic spectrum disorders: A prospective study SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE autism; autism spectrum disorders; pervasive developmental disorders; comprehensive assessment; diagnostic yield; rational evaluation ID PERVASIVE DEVELOPMENTAL DISORDERS; FRAGILE-X SYNDROME; MENTAL-RETARDATION; GENOMEWIDE SCREEN; DIAGNOSTIC YIELD; CHILDREN; INDIVIDUALS; CHROMOSOME-15; DUPLICATION; PHENOTYPE AB Studies addressing etiologic yield in childhood developmental disabilities have mainly looked at individuals with developmental delay/mental retardation. The few studies addressing the question of etiologic yield in patients with pervasive developmental disorders (PDDs) had a major drawback, in that the enrolled subjects were diagnosed as having the autistic spectrum disorders based only on history and clinical examination, and/or on unspecified instruments. In addition, only some of these patients underwent a complete laboratory evaluation. To investigate the etiologic yield of PDDs, we undertook a large prospective study on subjects selected according to very strict criteria and diagnosed as having PDD based on the present "gold standard" (ADI-R and ADOS-G), and a clinical diagnosis made by a child psychiatrist. Eighty-five (85) patients with PDD and their first degree relatives participated in this study. These patients were selected from a sample of 236 subjects who had received a clinical diagnosis of PDD at the Stella Maris Institute between March 2002 and 2005. Selection criteria for entering the study were: (1) a diagnosis of PDD (with exclusion of the Rett syndrome) confirmed after the administration of the ADI-R (autism diagnostic interview-revised) and the ADOS-G (autism diagnostic observation schedule-generic). In addition, a clinical diagnosis was made by the child psychiatrist, on the basis of presence or absence of DSM-IV symptoms of autism, (2) chronological age between 4 and 18 years, (3) IQ>30; (4) availability of both biologic parents. Patients, 65/85 (76.5%), had autism, 18/85 (21.2%) had PDD-NOS, and the remaining 2/85 (2.3%) had Asperger syndrome. Ages varied between 4 years 2 months and 12 years 5 months (mean 7.6 years), and there was a marked male preponderance (68/85). All subjects underwent various laboratory studies and neuroimaging. With respect to possible etiologic determination, a detailed history and physical examination in this group of patients with PDD was informative in 10.5% (9/85). HRB karyotype was diagnostic in one, and molecular fragile X studies in one child. Brain MRI was informative in two children (2.3%) with relative macrocrania but no neurological features and EEG was helpful in one child, identifying a Landau-Kleffner disorder. Audiometry and brainstem auditory evoked potentials (BAEPs) showed a bilateral sensorineural loss in another child. Metabolic evaluation gave normal results in all subjects. The results suggest an evaluation paradigm with reference to etiologic determination for individuals with PDDs that does not presently justify metabolic or neuroimaging on a screening basis. Recurrence risk, treatment implications, and significant and long-lasting emotional relief for the parents suggest that serious consideration be given to clinical genetic examination, genetic testing, EEG study (during wakefulness and sleep), and audiometry, despite a relatively low yield. (C) 2006 Wiley-Liss, Inc. C1 Stella Maris Clin Res Inst Child Adolescent Neuro, Ctr Study Congenital Malformat Syndromes, Clin Neurophysiol Serv, I-56018 Pisa, Italy. Univ Pisa, I-56100 Pisa, Italy. Univ Utah, Hlth Sci Ctr, Div Med Genet, Dept Pediat, Salt Lake City, UT USA. RP Battaglia, A (reprint author), Stella Maris Clin Res Inst Child Adolescent Neuro, Ctr Study Congenital Malformat Syndromes, Clin Neurophysiol Serv, Via Giacinti 2, I-56018 Pisa, Italy. 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J. Med. Genet. C PD FEB 15 PY 2006 VL 142C IS 1 BP 3 EP 7 DI 10.1002/ajmg.c.30076 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 011XM UT WOS:000235302100002 PM 16419094 ER PT J AU Battaglia, A Bonaglia, MC AF Battaglia, A Bonaglia, MC TI The yield of subtelomeric FISH analysis in the evaluation of autistic spectrum disorders SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE autism; autism spectrum disorders; pervasive developmental disorders; telomere; subtelomeric regions, subtelomeric FISH analysis ID IDIOPATHIC MENTAL-RETARDATION; PERVASIVE DEVELOPMENTAL DISORDERS; GENOMEWIDE SCREEN; CHROMOSOMAL REARRANGEMENTS; CLINICAL-APPLICATION; MOLECULAR ANALYSIS; GENOMIC SCREEN; INV DUP(15); CHILDREN; DELETION AB To assess the frequency of cryptic subtelomeric rearrangements in children and adolescents with autism spectrum disorders, blood samples were studied using a complete set of subtelomeric FISH probes in 72 children with autism spectrum disorders. All children had normal high resolution karyotype, DNA fra-X analysis, brain MRI, metabolic work-up, and physical/neirological examination. Subtelomeric analysis did not detect abnormalities in any of the subjects, suggesting the uselessness of such investigations in individuals with primary autism spectrum disorders. (C) 2006 Wiley-Liss, Inc. C1 Stella Maris Clin Res Inst Child & Adolescent Neu, Ctr Study Congenital Malformat Syndromes, Clin Neurophysiol Serv, I-56018 Pisa, Italy. Univ Pisa, I-56100 Pisa, Italy. Univ Utah, Hlth Sci Ctr, Div Med Genet, Dept Pediat, Salt Lake City, UT USA. Sci Inst E Medea, Bosisio Parini, Lecco, Italy. RP Battaglia, A (reprint author), Stella Maris Clin Res Inst Child & Adolescent Neu, Ctr Study Congenital Malformat Syndromes, Clin Neurophysiol Serv, Via Giacinti 2, I-56018 Pisa, Italy. 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J. Med. Genet. C PD FEB 15 PY 2006 VL 142C IS 1 BP 8 EP 12 DI 10.1002/ajmg.c.30077 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 011XM UT WOS:000235302100003 PM 16419095 ER PT J AU Bacchelli, E Maestrini, E AF Bacchelli, E Maestrini, E TI Autism spectrum disorders: Molecular genetic advances SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE autism spectrum disorders; pervasive developmental disorders; genetics; linkage studies; linkage disequilibrium; candidate genes ID SEROTONIN TRANSPORTER GENE; PERVASIVE DEVELOPMENTAL DISORDERS; RIGID-COMPULSIVE BEHAVIORS; COPY NUMBER VARIATION; SUSCEPTIBILITY GENES; GENOMEWIDE SCREEN; GENOMIC SCREEN; CHROMOSOME 7Q; REELIN GENE; LANGUAGE DISORDER AB Despite the strong genetic basis of autism spectrum disorders (ASD), research efforts in the last decade have not been successful in the identification of confirmed susceptibility genes. We review the present status of genetic linkage, candidate gene, and association studies, pointing out the limitations of these approaches and the challenge of dealing with the clinical and genetic complexity of autism. Finally, we outline how recent technological and bioinformatic advances, together with an increasing understanding of the structure of the human genome, have set the stage to perform more comprehensive and well powered studies, possibly leading to a turning point in the understanding of the genetic basis of this devastating disorder. (C) 2006 Wiley-Liss, Inc. C1 Univ Bologna, Dipartimento Biol Evoluz Sperimentale, I-40126 Bologna, Italy. Univ Bologna, Int Mol Genet Study Autism Project, I-40126 Bologna, Italy. RP Maestrini, E (reprint author), Univ Bologna, Dipartimento Biol Evoluz Sperimentale, Via Selmi 3, I-40126 Bologna, Italy. 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J. Med. Genet. C PD FEB 15 PY 2006 VL 142C IS 1 BP 13 EP 23 DI 10.1002/ajmg.c.30078 PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 011XM UT WOS:000235302100004 PM 16419096 ER PT J AU Coon, H AF Coon, H TI Current perspectives on the genetic analysis of autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Review DE autism; intermediate phenotype; genetic linkage; genetic association ID PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN TRANSPORTER GENE; MAJOR SUSCEPTIBILITY LOCUS; QUANTITATIVE TRAIT LOCI; WHOLE-BLOOD SEROTONIN; GENOME-WIDE SCAN; LINKAGE ANALYSIS; FAMILY HISTORY; TRANSMISSION/DISEQUILIBRIUM TEST; ALLELIC ASSOCIATIONS AB Although no definitive genetic mutations leading to autism susceptibility have been established, the field has many new resources to tackle this difficult problem. Numbers of families at many research sites are now large, and new collaborations among these groups will allow for collections of subjects with enough statistical power to detect relatively small gene effects. New technological advances in genotyping will allow for more fine-grained genetic analysis, and more sophisticated techniques have been developed to address the vast amounts of data acquired. Researchers have also begun to focus on intermediate phenotypes associated with autism, such as elevated serotonin, increased head circumference, social difficulties, or language impairment or delay. These phenotypes may help to stratify affected cases into more genetically homogeneous subgroups, and may also occur in their clinically unaffected relatives. The study of intermediate phenotypes may allow investigators to find common gene variants that lead to autism susceptibility. Here we discuss the major intermediate phenotypes, and give an overview of current genetic analysis techniques. 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J. Med. Genet. C PD FEB 15 PY 2006 VL 142C IS 1 BP 24 EP 32 DI 10.1002/ajmg.c.30079 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 011XM UT WOS:000235302100005 PM 16419097 ER PT J AU Lainhart, JE AF Lainhart, JE TI Advances in autism neuroimaging research for the clinician and geneticist SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE autism; neuroimaging; brain volume; brain connectivity ID HIGH-FUNCTIONING INDIVIDUALS; SPECTRUM DISORDER; HEAD CIRCUMFERENCE; ASPERGER-SYNDROME; YOUNG-CHILDREN; CHILDHOOD AUTISM; MATTER VOLUME; BRAIN GROWTH; MRI; ABNORMALITIES AB This review focuses on recent advances in the in vivo study of the whole brain in idiopathic autism. The brain is abnormally large in some but not all children with autism during post-natal development, Age-related changes in brain volume in autism are complex and appear to be abnormal from infancy into adulthood. Diffuse differences in total and regional gray and white matter volumes are found. The volumetric abnormalities appear to follow anomalous, complex, and non-uniform developmental curves. Diffuse abnormalities of brain chemical concentrations, neural network anatomy, brain lateralization, intra- and inter-hemispheric morphologic and functional connectivity, and serotonin synthesis capacity are also found. Abnormalities of head growth are first apparent during infancy. Abnormalities of total brain volume, gray and white matter volumes, brain chemistry, serotonin synthesis, and brain electrophysiology are evident by early childhood. Currently, no method of brain imaging helps with diagnosis or treatment of idiopathic autism, but ongoing research aims to unravel the heterogeneity of autism and may provide future diagnostic tools that inform treatment. (C) 2006 Wiley-Liss, Inc. C1 Univ Utah, Utah Autism Res Program, Salt Lake City, UT 84108 USA. Univ Utah, NICHD NICDC Collaborat Program Excellence Autism, Salt Lake City, UT 84108 USA. RP Lainhart, JE (reprint author), Univ Utah, Utah Autism Res Program, 421 Wakara Way,Suite 143, Salt Lake City, UT 84108 USA. 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J. Med. Genet. C PD FEB 15 PY 2006 VL 142C IS 1 BP 33 EP 39 DI 10.1002/ajmg.c.30080 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 011XM UT WOS:000235302100006 PM 16419098 ER PT J AU Moy, SS Nadler, JJ Magnuson, TR Crawley, JN AF Moy, SS Nadler, JJ Magnuson, TR Crawley, JN TI Mouse models of autism spectrum disorders: The challenge for behavioral genetics SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Review DE autism; fragile X; mice; repetitive behavior; Rett syndrome; social interaction ID FRAGILE-X-SYNDROME; FMR1 KNOCKOUT MOUSE; SENSORIMOTOR GATING ABNORMALITIES; GABA(A) RECEPTOR-BETA-3 SUBUNIT; TRANSPORTER-DEFICIENT MICE; HETEROZYGOUS REELER MOUSE; CPG-BINDING PROTEIN-2; LEMLI-OPITZ-SYNDROME; SEROTONIN TRANSPORTER; DOWN-SYNDROME AB Autism is a severe neurodevelopmental disorder, which typically emerges early in childhood. The core symptoms of autism include deficits in social interaction, impaired communication, and aberrant repetitive behavior, including self-injury. Despite the strong genetic component for the disease, most cases of autism have not been linked to mutations in a specific gene, and the etiology of the disorder has yet to be established. At the present time, there is no generally accepted therapeutic strategy to treat the core symptoms of autism, and there remains a critical need for appropriate animal models and relevant behavioral assays to promote the understanding and treatment of the clinical syndrome. Challenges for the development of valid mouse models include complex genetic interactions underlying the high heritability of the disease in humans, diagnosis based on deficits in social interaction and communication, and the lack of confirmatory neuropathological markers to provide validation for genetic models of the disorder. Research focusing on genes that mediate social behavior in mice may help identify neural circuitry essential for normal social interaction, and lead to novel genetic animal models of the autism behavioral phenotype. (C) 2006 Wiley-Liss, Inc. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Mouse Behav Phenotyping Lab, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Genet, Chapel Hill, NC 27599 USA. Univ N Carolina, Caroline Ctr Genome Sci, Chapel Hill, NC 27599 USA. Univ N Carolina, NIMH, Chapel Hill, NC 27599 USA. RP Moy, SS (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, Mouse Behav Phenotyping Lab, CB 7146, Chapel Hill, NC 27599 USA. 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J. Med. Genet. C PD FEB 15 PY 2006 VL 142C IS 1 BP 40 EP 51 DI 10.1002/ajmg.c.30081 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA 011XM UT WOS:000235302100007 PM 16419099 ER PT J AU McMahon, WM Baty, BJ Botkin, J AF McMahon, WM Baty, BJ Botkin, J TI Genetic counseling and ethical issues for autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART C-SEMINARS IN MEDICAL GENETICS LA English DT Article DE autism; autism spectrum disorders; genetic counseling; genetic testing; ethics ID BROADER PHENOTYPE; ALZHEIMER-DISEASE; FAMILY HISTORY; INFORMATION; DISORDERS; CHILDREN; PARENTS; IMPACT; TESTS; TWIN AB Exciting progress is being made in the journey toward discovery of genes conferring risk for autism and autism spectrum disorders. Currently, genetic counseling for idiopathic autism rests on clinical diagnosis and empiric risk estimates. While no genetic test for risk of autism currently exists, it is possible that such a test may emerge in the near future, and that commercial availability may precede adequate understanding of test characteristics. The complexity of multifactorial conditions like autism raises a host of ethical and counseling challenges. For families to benefit from new genetic knowledge about autism, it will be important for their practitioners to be knowledgeable about the issues, utilize appropriate educational interventions and emerging management options, and help families across the cultural spectrum cope with these challenges. (C) 2006 Wiley-Liss, Inc. C1 Univ Utah, Utah Autism Res Program, Dept Psychiat, Salt Lake City, UT 84108 USA. Univ Utah, Dept Pediat, Div Med Genet, Salt Lake City, UT 84108 USA. Univ Utah, Grad Program Genet Counseling, Salt Lake City, UT 84108 USA. RP McMahon, WM (reprint author), Univ Utah, Utah Autism Res Program, Dept Psychiat, 421 Wakara Way,Suite 143, Salt Lake City, UT 84108 USA. 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C PD FEB 15 PY 2006 VL 142C IS 1 BP 52 EP 57 DI 10.1002/ajmg.c.30082 PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 011XM UT WOS:000235302100008 PM 16419100 ER PT J AU Connolly, AM Chez, M Streif, EM Keeling, RM Golumbek, PT Kwon, JM Riviello, JJ Robinson, RG Neuman, RJ Deuel, RMK AF Connolly, AM Chez, M Streif, EM Keeling, RM Golumbek, PT Kwon, JM Riviello, JJ Robinson, RG Neuman, RJ Deuel, RMK TI Brain-derived neurotrophic factor and autoantibodies to neural antigens in sera of children with autistic spectrum disorders, Landau-Kleffner syndrome, and epilepsy SO BIOLOGICAL PSYCHIATRY LA English DT Article DE antiendothelial antibodies; autoantibodies; antinuclear antibodies; Landau-Kleffner syndrome; autistic spectrum disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; ACQUIRED APHASIA; CONVULSIVE DISORDER; NEUROFILAMENT PROTEIN; FOLLOW-UP; T-CELLS; OPSOCLONUS-MYOCLONUS; INFANTILE-AUTISM; B-CELLS; ANTIBODIES AB Background: Brain derived neurotrophic factor (BDNF) elevation in newborn sera predicts intellectual/social developmental abnormalities, Other autoantibodies (AAs) to endothelial cells (ECs) and myelin basic protein (MBP) are also elevated in some children. We tested relationships between BDNF, BDNF AAs, and other AAs in children with these disorders. Methods: BDNF levels and IgG/IgM autoantibodies to BDNF, ECs, MBP, and histones were measured in children with autism, childhood disintegrative disorder (CDD), pervasive developmental delay-not otherwise specified (PDD-nos), acquired epilepsy, Landau-Kleffner syndrome (LKS); healthy children (HC), and children with non-neurological illnesses (NNI). Results: Mean BDNF levels were elevated in children with autism and CDD, (p <= 0.0002) compared to HC or NNI. Mean IgG and IgM BDNF AAs were elevated in children with autism, CDD and epilepsy (p <= 0.0005) compared to HC but not to NNI. Mean IgM AA EC titers detected by immunocytochemistry were higher in autism, PDD-NOS, epilepsy, and LKS (p <= 0.005) compared to HC and NNI. While mean ELISA IgG EC AAs were higher in autism and PPD-NOS (p < 0.005) compared to HC but not NNI, ELISA IgM ECAAs were higher in children with autism, CDD, PDD-NOS, and epilepsy compared to both HC and NNI (p < 0.0005). Mean anti-MBP IgG and IgM titers were higher in all study groups (p < 0.005) except for LKS compared to both HC and NNI. Conclusion: Children with developmental disorders and epilepsy have higher AAs to several neural antigens compared to controls. The presence of both BDNF AAs and elevated BDNF levels in some children with autism and CDD suggests a previously unrecognized interaction between the immune system and BDNF. C1 Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Psychiat & Genet, St Louis, MO 63110 USA. Rosalind Franklin Univ, Chicago Med Sch, Dept Neurol, Chicago, IL USA. Univ Rochester, Rochester, NY USA. Harvard Univ, Sch Med, Boston, MA USA. USC, Keck Sch Med, Los Angeles, CA USA. St Louis Univ, St Louis, MO 63103 USA. RP Connolly, AM (reprint author), Washington Univ, Sch Med, Dept Neurol, Box 8111,660 S Euclid Ave, St Louis, MO 63110 USA. 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Psychiatry PD FEB 15 PY 2006 VL 59 IS 4 BP 354 EP 363 DI 10.1016/j.biopsych.2005.07.004 PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 017CD UT WOS:000235670800009 PM 16181614 ER PT J AU Verte, S Geurts, HM Roeyers, H Oosterlaan, J Sergeant, JA AF Verte, S Geurts, HM Roeyers, H Oosterlaan, J Sergeant, JA TI The relationship of working memory, inhibition, and response variability in child psychopathology SO JOURNAL OF NEUROSCIENCE METHODS LA English DT Review DE working memory; inhibition; response variability; child psychopathology; ADHD; HFA; TS ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT-HYPERACTIVITY-DISORDER; PREFRONTAL COGNITIVE-PROCESSES; EXECUTIVE FUNCTIONS; MOTOR CONTROL; COMMUNICATION-CHECKLIST; FRONTAL LOBES; BEHAVIORAL-INHIBITION; DIAGNOSTIC INTERVIEW; SUSTAINED ATTENTION AB Introduction: The aim of this study was to investigate the relationship between working memory and inhibition in children with attention deficit hyperactivity disorder (ADHD), high-functioning autism (HFA), and Tourette syndrome (TS), compared to normally developing children. Furthermore, the contribution of variation in processing speed on working memory and inhibition was investigated in these childhood psychopathologies. Method: Four groups of children are reported in this study: 65 children with ADHD, 66 children with HFA, 24 children with TS, and 82 normal control children. All children were in the age range of 6-13 years. Results: The relationship between working memory and inhibition was similar in children with ADHD, HFA, TS, and normally developing children. The relationship between both domains did not alter significantly for any of the groups, when variation in processing speed was taken into account. More symptoms of hyperactivity/impulsivity are related to a poorer inhibitory process and greater response variability. More symptoms of autism are related to a poorer working memory process. 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Neurosci. Methods PD FEB 15 PY 2006 VL 151 IS 1 BP 5 EP 14 DI 10.1016/j.jneumeth.2005.08.023 PG 10 WC Biochemical Research Methods; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 023AU UT WOS:000236098300002 PM 16427129 ER PT J AU Seeman, C AF Seeman, C TI When babies read: A practical guide to helping young children with hyperlexia, Asperger syndrome and high-functioning autism. SO LIBRARY JOURNAL LA English DT Book Review CR JENSEN A, 2005, BABIES READ PRACTICA NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD FEB 15 PY 2006 VL 131 IS 3 BP 128 EP 128 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 015BJ UT WOS:000235526600141 ER PT J AU Hendry, J DeVito, T Gelman, N Densmore, M Rajakumar, N Pavlosky, W Williamson, PC Thompson, PM Drost, DJ Nicolson, R AF Hendry, J DeVito, T Gelman, N Densmore, M Rajakumar, N Pavlosky, W Williamson, PC Thompson, PM Drost, DJ Nicolson, R TI White matter abnormalities in autism detected through transverse relaxation time imaging SO NEUROIMAGE LA English DT Article; Proceedings Paper CT 13th Annual Meeting of the International-Society-for-Magnetic-Resonance-in-Medicine CY MAY 07-13, 2005 CL Miami, FL SP Int Soc Magnet Resonance Med ID PERVASIVE DEVELOPMENTAL DISORDERS; MAGNETIC-RESONANCE; HUMAN BRAIN; SPATIAL NORMALIZATION; SPECTRUM DISORDER; T2-WEIGHTED MRI; T2 RELAXOMETRY; T-2 RELAXATION; YOUNG-CHILDREN; IRON AB While neuroimaging studies have reported neurobiological abnormalities in autism, the underlying tissue abnormalities remain unclear. Quantitative transverse relaxation time (T2) imaging permits the examination of tissue abnormalities in vivo, with increased T2 largely reflecting increased tissue water. Blood flow and the presence of tissue iron may also affect T2. In this study, we used voxel-based relaxometry of the cerebrum and global averages to examine T2 abnormalities in autism. Nineteen males with autism (age: 9.2 +/- 3.0 years) and 20 male controls (age: 10.7 +/- 2.9 years) underwent magnetic resonance imaging at 3.0 T. Quantitative T2 maps, generated through gradient echo sampling of the free induction decay and echo, were segmented into gray matter, white matter, and cerebrospinal fluid. Average cerebral gray and white matter T2 were determined and compared between groups. To assess localized T2 differences, the quantitative T2 maps were warped to a template created for this study, smoothed, and compared using statistical parametric mapping. Patients with autism had an increase in average cerebral white matter T2, although no group differences were seen in average cerebral gray matter T2. Patients with autism also had bilateral regional T2 increases in the gray matter and associated white matter of the parietal lobes (primary sensory association areas) and occipital lobes (visual association areas) and in the white matter within the supplementary motor areas in the frontal lobes. The regional and global elevations in white matter T2 suggest abnormalities of white matter tissue water content in autism, which may represent a neurobiological basis for the aberrant cortical connectivity hypothesized to underlie the disorder. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ Western Ontario, Dept Med Biophys, London, ON, Canada. Univ Western Ontario, Dept Psychiat, London, ON N6A 3K7, Canada. Univ Western Ontario, Dept Diagnost Radiol & Nucl Med, London, ON N6A 3K7, Canada. Univ Calif Los Angeles, Sch Med, Dept Neurol, Lab Neuroimaging, Los Angeles, CA 90095 USA. RP Nicolson, R (reprint author), London Hlth Sci Ctr, Victoria Campus,800 Commissioners Rd E,E-2-601, London, ON N6C 2V5, Canada. 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Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 015EJ UT WOS:000235534400003 PM 16214373 ER PT J AU Lawrence, EJ Shaw, P Giampietro, V Surguladze, S Brammer, MJ David, AS AF Lawrence, EJ Shaw, P Giampietro, V Surguladze, S Brammer, MJ David, AS TI The role of 'shared representations' in social perception and empathy: An fMRI study SO NEUROIMAGE LA English DT Article ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; GENERIC BRAIN ACTIVATION; ASPERGER-SYNDROME; FACIAL EXPRESSIONS; PERSPECTIVE-TAKING; NEURAL SYSTEMS; SELF-AWARENESS; MOTOR THEORY; OTHERS AB Evidence suggests that we use the same mechanisms for both producing and perceiving actions. Such 'shared representations' may also underlie social perception and empathy. However, this idea raises some important and as yet unresolved questions: (i) how do we distinguish other-orientated empathic responses from a self-orientated reactions such as personal distress and (ii) what are the neural substrates underpinning these processes? We employed event-related functional magnetic resonance imaging (fMRI) to explore whether I shared representations' were recruited to decode dynamic social stimuli in 12 healthy volunteers. We used an adapted version of the Profile of Non-Verbal Sensitivity (Rosenthal, H., Hall, J.A., DiMatteo, M.R., Rogers, P.L., Archer, D., (1979). Sensitivity to nonverbal communication: the PONS test. The Johns Hopkins University Press, Baltimore) which taps social perception using brief silent video clips. Participants chose one of two words that best described the state conveyed by the actor, or in the control condition using the same clips, the word describing which parts of the body were visible (nonsocial labelling). Off-line self-report measures of empathy and personal distress engendered by thoughts about others, were also given along with an experimentally-derived index of the degree of self-other overlap during social perception. Brain activation specific to the main experimental condition was found in the inferior frontal gyros (BA44.) and premotor areas (BA6) consistent with the use of 'shared representations'. Somatosensory areas such as the insula and supramarginal gyros (BA40) were also activated suggesting that participants constructed a qualitative representation of the target state. Activity in the rostral anterior cingulate was associated with self-reports of personal distress and increased blood flow to the anterior cingulate (BA24) and inferior parietal cortex (BA40) was related to self-other overlap. (c) 2005 Elsevier Inc. All rights reserved. C1 Inst Psychiat, Sect Cognit Neuropsychiat, London SE5 8AF, England. GKT Sch Med, London SE5 8AF, England. Warren G Magnuson Clin Ctr, Child Psychiat Branch, Inst Psychiat, Bethesda, MD 20814 USA. Inst Psychiat, Brain Image Anal Unit, Dept Biostat & Comp, London SE5 8AF, England. RP Lawrence, EJ (reprint author), Inst Psychiat, Sect Cognit Neuropsychiat, POB 68, London SE5 8AF, England. 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Association of such a locus with a disease is therefore generally tested with a case-control design. When subjects have already been ascertained in a case-parent design however, the question arises as to whether the data can still be used to test disease association at such a locus. Results: A likelihood ratio test was constructed that can be used with a case-parents design but has somewhat less power than a Pearson's chi-squared test that uses a case-control design. The test is illustrated on a novel dataset showing a genotype relative risk near 2 for the homozygous GSTM1 deletion genotype and autism. Conclusion: Although the case-control design will remain the mainstay for a locus with a deletion, the likelihood ratio test will be useful for such a locus analyzed as part of a larger case-parent study design. The likelihood ratio test has the advantage that it can incorporate complete and incomplete case-parent trios as well as independent cases and controls. Both analyses support ( p = 0.046 for the proposed test, p = 0.028 for the case-control analysis) an association of the homozygous GSTM1 deletion genotype with autism. C1 Rutgers State Univ, Dept Stat & Genet, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Neurol, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Pediat, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Ctr Childhood Neurotoxicol & Exposure Assessment, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Pediat, Newark, NJ 07103 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Neurosci, Newark, NJ 07103 USA. RP Buyske, S (reprint author), Rutgers State Univ, Dept Stat & Genet, 110 Frelinghuysen Rd, Piscataway, NJ 08854 USA. EM buyske@stat.rutgers.edu; williata@umdnj.edu; marsau@umdnj.edu; stenroos@umdnj.edu; mingxu@umdnj.edu; wangro@umdnj.edu; msreenat@eden.rutgers.edu; mfactura@hotmail.com; reddych@umdnj.edu; glambert@umdnj.edu; wjohnson@umdnj.edu RI Buyske, Steven/B-8130-2009 CR Alexandrie AK, 2004, CANCER EPIDEM BIOMAR, V13, P908 Auranen M, 2000, MOL PSYCHIATR, V5, P320, DOI 10.1038/sj.mp.4000708 CHACKO P, 2005, MUTAT RES, V581, P2153, DOI DOI 10.1016/J.MRGENTOX.2004.11.018 Chen CL, 1996, PHARMACOGENETICS, V6, P187, DOI 10.1097/00008571-199604000-00005 CHEN GK, 2005, MOL PSYCHIAT Coles BF, 2003, BIOFACTORS, V17, P115 Garte S, 2001, CANCER EPIDEM BIOMAR, V10, P1239 Hung RG, 2004, INT J CANCER, V110, P4598, DOI DOI 10.1002/IJC.20157 James SJ, 2004, AM J CLIN NUTR, V80, P1611 Kirk GD, 2005, CANCER EPIDEM BIOMAR, V14, P373, DOI 10.1158/1055-9965.EPI-04-0161 Knapp M, 1999, AM J HUM GENET, V64, P1177, DOI 10.1086/302334 LI Y, 2004, APPL MICROBIOL BIOT, V66, P3233, DOI DOI 10.1007/S00253-004-1751-Y 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 Parkinson A, 2001, CASARETT DOULLS TOXI, P133 R Development Core Team, 2005, R LANG ENV STAT COMP Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 SCHAID DJ, 1993, AM J HUM GENET, V53, P1114 Schaid DJ, 1999, GENET EPIDEMIOL, V16, P250, DOI 10.1002/(SICI)1098-2272(1999)16:3<250::AID-GEPI2>3.0.CO;2-T Sogut S, 2003, CLIN CHIM ACTA, V331, P111, DOI 10.1016/S0009-8981(03)00119-0 TAMER L, 2004, RESPIROLOGY, V9, P4493, DOI DOI 10.1111/J.1440-1843.2004.00657.X Vargas DL, 2005, ANN NEUROL, V57, P67, DOI 10.1002/ana.20315 Veenstra-VanderWeele J, 2004, ANNU REV GENOM HUM G, V5, P379, DOI 10.1146/annurev.genom5.061903.180050 WASSINK TH, 2004, MENT RETARD DEV D R, V10, P4272, DOI DOI 10.1002/MRDD.20041 Weinberg CR, 1998, AM J HUM GENET, V62, P969, DOI 10.1086/301802 Yang P, 2002, LUNG CANCER-J IASLC, V35, P221, DOI 10.1016/S0169-5002(01)00426-3 Yeh CC, 2005, WORLD J GASTROENTERO, V11, P1473 Ylisaukko-oja T, 2006, ANN NEUROL, V59, P145, DOI 10.1002/ana.20722 NR 28 TC 36 Z9 36 PU BIOMED CENTRAL LTD PI LONDON PA MIDDLESEX HOUSE, 34-42 CLEVELAND ST, LONDON W1T 4LB, ENGLAND SN 1471-2156 J9 BMC GENET JI BMC Genet. PD FEB 10 PY 2006 VL 7 AR 8 DI 10.1186/1471-2156-7-8 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 015KE UT WOS:000235549500001 PM 16472391 ER PT J AU Taylor, I AF Taylor, I TI 'Animals in translation': Using the mysteries of autism to decode animal behavior SO NEW YORK TIMES BOOK REVIEW LA English DT Book Review CR GRANDIN T, ANIMALS IN TRANSLATI NR 1 TC 1 Z9 1 PU NEW YORK TIMES PI NEW YORK PA 229 W 43RD ST, NEW YORK, NY 10036-3959 USA SN 0028-7806 J9 NY TIMES BK REV JI N. Y. Times Book Rev. PD FEB 5 PY 2006 BP 24 EP 24 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 006WQ UT WOS:000234928800036 ER PT J AU Constantino, JN Lajonchere, C Lutz, M Gray, T Abbacchi, A McKenna, K Singh, D Todd, RD AF Constantino, JN Lajonchere, C Lutz, M Gray, T Abbacchi, A McKenna, K Singh, D Todd, RD TI Autistic social impairment in the siblings of children with pervasive developmental disorders SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID GENERAL-POPULATION; TRAITS AB Objective: Sibling recurrence risk in autism has been estimated to be approximately 10%. This study investigated subsyndromal autistic impairments among siblings of probands with pervasive developmental disorders. Method: The authors used the Social Responsiveness Scale to obtain quantitative assessments of autistic social impairment in three groups of proband-sibling pairs: 1) autistic children from multiple-incidence families and their closest in age nonautistic brothers (N=49 pairs); 2) children with any pervasive developmental disorder, including autism, and their closest-in-age brothers (N=100 pairs), and 3) children with psychopathology unrelated to autism and their closest-in-age brothers (N=45 pairs). Results: Sibling Social Responsiveness Scale scores were continuously distributed and substantially elevated for both the autistic and pervasive developmental disorder groups. Highest scores (i.e., greatest impairment) were seen among siblings of autistic probands from multiple-incidence families, followed by siblings of probands with any pervasive developmental disorder, then siblings of probands with psychopathology unrelated to autism. Conclusions: Taken together with previous findings, these results support the notion that genetic susceptibility factors responsible for common, subsyndromal social impairments may be related to the causes of categorically defined pervasive developmental disorders. C1 Washington Univ, Sch Med, Dept Psychiat Pediat & Genet, St Louis, MO 63110 USA. Austism Genet Resource Exchange, Los Angeles, CA USA. RP Constantino, JN (reprint author), Washington Univ, Sch Med, Dept Psychiat Pediat & Genet, 660 S Euclid Ave,Campus Box 8134, St Louis, MO 63110 USA. EM constantino@wustl.edu CR Constantino JN, 2005, BIOL PSYCHIAT, V57, P655, DOI 10.1016/j.biopsych.2004.12.014 Constantino JN, 2004, J CHILD PSYCHOL PSYC, V45, P719, DOI 10.1111/j.1469-7610.2004.00266.x Constantino JN, 2003, ARCH GEN PSYCHIAT, V60, P524, DOI 10.1001/archpsyc.60.5.524 Lauritsen MB, 2005, J CHILD PSYCHOL PSYC, V46, P963, DOI 10.1111/j.1469-7610.2004.00391.x Murphy M, 2000, PSYCHOL MED, V30, P1411, DOI 10.1017/S0033291799002949 Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 NR 6 TC 131 Z9 133 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 FEB PY 2006 VL 163 IS 2 BP 294 EP 296 DI 10.1176/appi.ajp.163.2.294 PG 3 WC Psychiatry SC Psychiatry GA 008HO UT WOS:000235031000021 PM 16449484 ER PT J AU Benedek, EP AF Benedek, EP TI Autism spectrum disorders: A research review for practitioners SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Book Review CR Ozonoff S, 2003, AUTISM SPECTRUM DISO NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD FEB PY 2006 VL 163 IS 2 BP 332 EP 333 DI 10.1176/appi.ajp.163.2.332-a PG 2 WC Psychiatry SC Psychiatry GA 008HO UT WOS:000235031000040 ER PT J AU Meadan, H Halle, JW Watkins, RV Chadsey, JG AF Meadan, H Halle, JW Watkins, RV Chadsey, JG TI Examining communication repairs of 2 young children with autism spectrum disorder: The influence of the environment SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Article DE nonverbal language; autism; communication repair ID PROFOUND MENTAL-RETARDATION; CONVERSATIONAL REPAIR; CONTINGENT QUERIES; RESPONSES; REQUESTS; DISABILITIES; LANGUAGE; ADULTS; CLARIFICATION; STRATEGIES AB Purpose: The purpose of this study was to examine the repair strategies of 2 young children with autism spectrum disorder from an environmental rather than a developmental perspective. Method: A scripted protocol that included opportunities for requests and repair was followed. The environmental variables investigated were activity type (e.g., puzzle, shapes, book) and breakdown type (i.e., request for clarification, wrong response, and ignore). The sessions were videotaped, and each child's behavior was coded. Results: The results revealed that (a) both participants repaired the majority (70%) of their unsuccessful initial requests and (b) the repair strategies varied across children, activities, and breakdowns. Conclusions: The findings of this study suggest that the 2 young children with autism and limited expressive language discriminated among environmental variables (i.e., type of activity and type of breakdown). The participants modified their repair topographies to correspond to changes in the environment. The findings from this study off er ways to enhance assessment and intervention of early communication. Implications for future research and practice are discussed. C1 Univ Illinois, Dept Special Educ, Champaign, IL 61820 USA. 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PD FEB PY 2006 VL 15 IS 1 BP 57 EP 71 DI 10.1044/1058-0360(2006/007) PG 15 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 027PZ UT WOS:000236428800007 PM 16533093 ER PT J AU Autret-Leca, E Bensouda-Grimaldi, L Jonville-Bera, AP Beau-Salinas, F AF Autret-Leca, E Bensouda-Grimaldi, L Jonville-Bera, AP Beau-Salinas, F TI Pharmacovigilance of vaccines SO ARCHIVES DE PEDIATRIE LA French DT Review DE vaccines; adverse effects; product surveillance; post marketing; adverse drug reaction reporting systems ID INFLAMMATORY-BOWEL-DISEASE; SUDDEN UNEXPECTED DEATH; WHOLE-CELL PERTUSSIS; MEASLES VACCINATION; MULTIPLE-SCLEROSIS; MACROPHAGIC MYOFASCIITIS; RUBELLA VACCINATION; ADVERSE EVENTS; CROHNS-DISEASE; B VACCINATION AB Safety of vaccines must be excellent to make vaccine's strategy acceptable, since it usually has a deferred individual benefit but immediate adverse drug reactions (ADRs). Pharmacovigilance of vaccines after their marketing is crucial because, prior to its availability on the market, the size of clinical trials is insufficient to identify rare or deferred adverse effects. The Pharmacovigilance is based on "spontaneous reporting" of ADRs to the Pharmacovigilance Regional Centre (PVRC) which establishes a relationship between each drug taken by the patient and the ADRs occurrence (imputability). This method is crucial to generate alerts, but under-estimates the real frequency of ADRs (1 to 10% of severe ADRs are reported). Thus pharmacoepidermology studies are necessary to confirm the alerts identified by spontaneous reporting. ADRs can be specific, related to the antigen of an attenuated alive virus vaccine (lymphocyte meningitis after anti-mumps vaccine) or non-specific, related to a component different from the antigen (aluminium hydroxide involved in the "macrophagic myofasciitis", allergic reactions to neomycin, latex, egg or gelatine). Importance of Pharmacovigilance of vaccines is illustrated. Data, especially case-control studies, about the relationship between multiple sclerosis and hepatitis B vaccine are summarised. Data about the relationship between Crohn's disease or autism and MMR vaccine are analysed. As vaccines are used in healthy people, their safety must be excellent to be accepted. To monitor them after their marketing is the unique way to detect rare ADRs. This surveillance is made through reporting of ADRs to the PVRC. However, an active and intensive surveillance of ADRs as the one set up from the marketing of Prevenar (R) should be systematic. (c) 2005 Elsevier SAS. Tons droits reserves. C1 Univ Francois Rabelais Tours, Hop Bretonneau, Serv Pharmacol, Ctr Reg Pharmacovigilance & Informat Med, F-37044 Tours 09, France. CHU Tours, Serv Pharmacol, Hop Bretonneau, Ctr Reg Pharmacovigilance & Informat Medicament, F-37044 Tours, France. RP Autret-Leca, E (reprint author), Univ Francois Rabelais Tours, Hop Bretonneau, Serv Pharmacol, Ctr Reg Pharmacovigilance & Informat Med, 2 Blvd Tonnelle, F-37044 Tours 09, France. 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Pediatr. PD FEB PY 2006 VL 13 IS 2 BP 175 EP 180 DI 10.1016/j.arcped.2005.10.020 PG 6 WC Pediatrics SC Pediatrics GA 011JO UT WOS:000235264600013 PM 16343870 ER PT J AU Bolte, S Hubl, D Feineis-Matthews, S Prvulovic, D Dierks, T Poustka, F AF Bolte, S Hubl, D Feineis-Matthews, S Prvulovic, D Dierks, T Poustka, F TI Facial affect recognition training in autism: Can we animate the fusiform gyrus? SO BEHAVIORAL NEUROSCIENCE LA English DT Article DE autism; fMRI; emotion recognition; face processing; neuropsychotherapy ID COMPUTER-ASSISTED-INSTRUCTION; ASPERGER-SYNDROME; SPECTRUM DISORDER; FACE AREA; CHILDREN; INDIVIDUALS; ACTIVATION; EMOTIONS; THERAPY; SCHIZOPHRENIA AB One of the most consistent findings in the neuroscience of autism is hypoactivation of the fusiform gyrus (FG) during face processing. In this study the authors examined whether successful facial affect recognition training is associated with an increased activation of the FG in autism. The effect of a computer-based program to teach facial affect identification was examined in 10 individuals with high-functioning autism. Blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) changes in the FG and other regions of interest, as well as behavioral facial affect recognition measures, were assessed pre- and posttraining. No significant activation changes in the FG were observed. Trained participants showed behavioral improvements, which were accompanied by higher BOLD fMRI signals in the superior parietal lobule and maintained activation in the right medial occipital gyrus. C1 Klin Psychiat & Psychotherapie Kindes & Jugendalt, D-60528 Frankfurt, Germany. JW Goethe Univ, Dept Child & Adolescent Psychiat, Frankfurt, Germany. Univ Hosp Clin Psychiat, Dept Neurophysiol, Bern, Switzerland. RP Bolte, S (reprint author), Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, D-60528 Frankfurt, Germany. 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Neurosci. PD FEB PY 2006 VL 120 IS 1 BP 211 EP 216 DI 10.1037/0735-7044.120.1.211 PG 6 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 018WE UT WOS:000235794700023 PM 16492133 ER PT J AU Strambi, M Longini, M Hayek, J Berni, S Macucci, F Scalacci, E Vezzosi, P AF Strambi, M Longini, M Hayek, J Berni, S Macucci, F Scalacci, E Vezzosi, P TI Magnesium profile in autism SO BIOLOGICAL TRACE ELEMENT RESEARCH LA English DT Article DE autistic spectrum disorders; autism; erythrocyte; magnesium; plasma; Rett syndrome ID CYTOSOLIC-FREE MG2+; IONIZED MAGNESIUM; PLATELETS; CHILDREN; ADULTS; SERUM; CA2+ AB The aim of the present study was to determine and compare plasma and erythrocyte concentrations of magnesium in 12 autistic children (10 boys, 2 girls), 17 children with other autistic spectrum disorders (14 boys, 3 girls), 5 girls with classic Rett syndrome, and 14 normal children (7 boys, 7 girls) of the same age. No differences in intracellular Mg were found between controls and pathological subjects; however, autistic children and children with other autistic spectrum disorders had significantly lower plasma concentrations of Mg than normal subjects (p = 0.013 and p = 0.02, respectively). Although our study population was small, we conclude that children with autistic spectrum disorders require special dietary management. If these cases are diagnosed at an early stage, they can be helped through diet. C1 Azienda Univ Osped Senese, Policlin Scotte, Dept Paediat Obstet & Reprod Med, Sect Neonatol & Prevent Paediat, Siena, Italy. Azienda Univ Osped Senese, Policlin Scotte, Neuropsychiat Unit, Siena, Italy. RP Strambi, M (reprint author), Azienda Univ Osped Senese, Policlin Scotte, Dept Paediat Obstet & Reprod Med, Sect Neonatol & Prevent Paediat, Siena, Italy. 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L., 2005, NEUROBIOLOGY AUTISM NR 1 TC 0 Z9 0 PU CANADIAN PSYCHIATRIC ASSOC PI OTTAWA PA 141 LAURIER AVENUE WEST, STE 701, OTTAWA, ONTARIO K1P 5J3, CANADA SN 0706-7437 J9 CAN J PSYCHIAT JI Can. J. Psychiat.-Rev. Can. Psychiat. PD FEB PY 2006 VL 51 IS 2 BP 122 EP 122 PG 1 WC Psychiatry SC Psychiatry GA 023AB UT WOS:000236096300009 ER PT J AU Penn, HE AF Penn, HE TI Neurobiological correlates of autism: A review of recent research SO CHILD NEUROPSYCHOLOGY LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; NEONATAL AMYGDALA LESIONS; BRAIN-STEM INVOLVEMENT; INFANTILE-AUTISM; CORPUS-CALLOSUM; SPECTRUM DISORDERS; YOUNG-CHILDREN; MENTAL-RETARDATION; CEREBELLAR ABNORMALITY; BEHAVIORAL TREATMENT AB This review paper integrates recent structural and functional imaging, postmortem, animal lesion, and neurochemical research about the pathophysiology of autism. An understanding of the neurobiological correlates of autism is becoming increasingly important as more children are diagnosed with the condition and funding for well-targeted interventions increases. Converging evidence suggests that autism involves abnormalities in brain volume, neurotransmitter systems, and neuronal growth. In addition, evidence firmly links autism with abnormalities in the cerebellum, the medial temporal lobe, and the frontal lobe. Potential implications of these findings and suggestions for future research are reviewed. C1 York Univ, Dept Psychol BSB, Clin Dev Psychol Program, Toronto, ON M3J 1P3, Canada. RP Penn, HE (reprint author), York Univ, Dept Psychol BSB, Clin Dev Psychol Program, 4700 Keele St, Toronto, ON M3J 1P3, Canada. 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PD FEB PY 2006 VL 12 IS 1 BP 57 EP 79 DI 10.1080/09297040500253546 PG 23 WC Clinical Neurology SC Neurosciences & Neurology GA 011OZ UT WOS:000235279300004 PM 16484102 ER PT J AU Koochek, M Harvard, C Hildebrand, MJ Van Allen, M Wingert, H Mickelson, E Holden, JJA Rajcan-Separovic, E Lewis, MES AF Koochek, M Harvard, C Hildebrand, MJ Van Allen, M Wingert, H Mickelson, E Holden, JJA Rajcan-Separovic, E Lewis, MES TI 15q duplication associated with autism in a multiplex family with a familial cryptic translocation t(14;15)(q11.2;q13.3) detected using array-CGH SO CLINICAL GENETICS LA English DT Article DE autism spectrum disorder (ASD); chromosome 6q, 14q, 15q; comparative genomic hybridization (CGH); cryptic translocation; fluorescent in situ hybridization (FISH); intellectual disability; microarray; microdeletion; microduplication ID COMPARATIVE GENOMIC HYBRIDIZATION; PRADER-WILLI-SYNDROME; INTERSTITIAL DUPLICATIONS; PROXIMAL 15Q; PERICENTROMERIC REGION; CHROMOSOME 15Q; DELETIONS; PHENOTYPE; REARRANGEMENTS; ABNORMALITIES AB Autism spectrum disorders (ASDs) are a group of neurodevelopmental disorders with a strong genetic aetiology. In approximately 1% of cases, duplication of the 15q11-13 region has been reported. We report the clinical, array-comparative genomic hybridization (CGH) and cytogenetic evaluation of two individuals from a multiplex family demonstrating autism due to a maternally inherited gain of 15q11-13. Our findings indicate that unlike most 15q11-13 gains, which are caused by interstitial duplication of this region or supernumerary marker chromosomes deriving from proximal 15q, the 15q gain in this family is the result of abnormal segregation of a cryptic familial translocation with breakpoints at 14q11.2 and 15q13.3. The affected members of this family were found to have a normal karyotype at > 550 band resolution. This translocation was identified using the 1-Mb resolution whole genome array (Spectral Genomics). The affected individuals have a gain of seven clones from proximal 15q, a loss of two clones from proximal 14q and a gain of two clones from 6q. Fluorescent in situ hybridization (FISH) analysis with clones from chromosomes 14 and 15, combined with DAPI reverse banding, showed an abnormal karyotype with one normal chromosome 15 and the der(15) t(14;15)(q11.2.;q13.3), resulting in the gain of proximal 15q and the loss of proximal 14q in affected individuals. The duplication of two clones from 6q in the affected subjects was also found in unaffected members of the family. Our findings suggest that the gain of 15q in autism may in some cases be due to cryptic translocations with breakpoints in the pericentromic regions of chromosome 15 and a different acrocentric chromosome. Variation in the size of pericentromic regions of any acrocentric chromosome may justify karyotype and FISH studies of autistic probands and their parents using probes from the 15q proximal region to determine recurrence risk for autism in some families. C1 Univ British Columbia, Michael Smith Fdn Hlth Res, Dept Med Genet, Child & Family Res Inst,BC Childrens & Womens Hlt, Vancouver, BC V6H 3N1, Canada. Univ British Columbia, Dept Pathol, Vancouver, BC V6H 3N1, Canada. Univ British Columbia, Dept Pediat, Vancouver, BC V6H 3N1, Canada. Queens Univ, Dept Physiol, Kingston, ON K7L 3N6, Canada. Queens Univ, Dept Psychiat, Kingston, ON K7L 3N6, Canada. RP Lewis, MES (reprint author), Univ British Columbia, Michael Smith Fdn Hlth Res, Dept Med Genet, Child & Family Res Inst,BC Childrens & Womens Hlt, 4500 Oak St, Vancouver, BC V6H 3N1, Canada. 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Compared with the controls, the children who had experienced NE were 5.9 times (95% confidence interval 2.0-16.9) more likely to have been diagnosed with an ASD. C1 Childrens Hosp, Dept Neonatol, Westmead, NSW 2145, Australia. Univ Sydney, Hornsby Ku Ring Gai Hosp, Sydney, NSW 2006, Australia. Telethon Inst Child Hlth Res, Subiaco, WA, Australia. Sophia Childrens Univ Hosp, Erasmus MC, Paediat Surg Intens Care Unit, Rotterdam, Netherlands. Univ Oxford, Natl Perinatal Epidemiol Unit, Oxford, England. RP Badawi, N (reprint author), Childrens Hosp, Dept Neonatol, Locked Bag 4001, Westmead, NSW 2145, Australia. 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M., 1997, EXAMINERS MANUAL PEA Elliot C., 1983, BRIT ABILITIES SCALE Felix JF, 2000, DEV MED CHILD NEUROL, V42, P803 FOLSTEIN SE, 1991, PEDIATRICS, V87, P767 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 GILLBERG C, 1983, J AUTISM DEV DISORD, V13, P153, DOI 10.1007/BF01531816 GLASSON E, 2003, REGISTER AUTISM SPEC Glasson EJ, 2004, ARCH GEN PSYCHIAT, V61, P618, DOI 10.1001/archpsyc.61.6.618 Griffiths R, 1970, ABILITIES YOUNG CHIL Hills M., 1993, STAT MODELS EPIDEMIO LEVY S, 1988, J AUTISM DEV DISORD, V18, P573, DOI 10.1007/BF02211875 Moore SJ, 2000, J MED GENET, V37, P489, DOI 10.1136/jmg.37.7.489 NELSON KB, 1991, PEDIATRICS, V87, P761 PICKLES A, 1995, AM J HUM GENET, V57, P717 Risch N, 1999, AM J HUM GENET, V65, P493, DOI 10.1086/302497 SARNAT HB, 1976, ARCH NEUROL-CHICAGO, V33, P696 Sparrow S, 1984, VINELAND ADAPTIVE BE STROMLAND K, 1994, DEV MED CHILD NEUROL, V36, P351 Szatmari P, 1998, J AUTISM DEV DISORD, V28, P351, DOI 10.1023/A:1026096203946 WALKER HA, 1977, J AUTISM CHILD SCHIZ, V7, P165, DOI 10.1007/BF01537727 Webb E, 2003, DEV MED CHILD NEUROL, V45, P377, DOI 10.1017/S001216220300720 *WHO, 1992, INT STAT CLASS DIS H, V1 Williams G, 2001, DEV MED CHILD NEUROL, V43, P202, DOI 10.1017/S001216220100038X Zwaigenbaum L, 2002, J AM ACAD CHILD PSY, V41, P572, DOI 10.1097/00004583-200205000-00015 NR 34 TC 21 Z9 22 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD FEB PY 2006 VL 48 IS 2 BP 85 EP 89 DI 10.1017/S001216220600020X PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 011NK UT WOS:000235274900003 PM 16417661 ER PT J AU Newman, CJ Ziegler, AL Jeannet, PY Roulet-Perez, E Deonna, TW AF Newman, CJ Ziegler, AL Jeannet, PY Roulet-Perez, E Deonna, TW TI Transient dystonic toe-walking: differentiation from cerebral palsy and a rare explanation for some unexplained cases of idiopathic toe-walking SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID CHILDHOOD AUTISM; CHILDREN; WALKERS; FOOT AB We report on seven children (five males, two females) who presented with marked, often asymmetrical, toe-walking from onset of independent walking, associated with abnormal foot postures and increased tone at the ankles with characteristics of dystonia. Most of the children had presented with unusual pre-walking locomotion and a mild delay in independent walking. They did not fit into the usual categories of 'habitual' toe-walking or congenital short tendo calcaneus but nor did they have the clinical signs of spastic diplegia or of a peripheral neuromuscular disease. Normalization occurred progressively in the second to fourth years of life. The children were re-examined several years later (1 to 11y) and were normal. We believe that their persistent toe-walking corresponded to a variant of 'transient focal dystonia of infancy'. Knowledge of its existence may justify a period of observation without special investigations, surgery, or casting. C1 CHU Vaudois, Dept Paediat, Neuropaediat Unit, CH-1010 Lausanne, Switzerland. RP Deonna, TW (reprint author), CHU Vaudois, Dept Paediat, Neuropaediat Unit, CH-1010 Lausanne, Switzerland. EM Thierry.Deonna@chuv.hospvd.ch CR DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 DEONNA TW, 1991, NEUROPEDIATRICS, V22, P220, DOI 10.1055/s-2008-1071445 Engelbert R H, 1999, Eur J Paediatr Neurol, V3, P273, DOI 10.1016/S1090-3798(99)90982-0 FURRER F, 1982, HELV PAEDIATR ACTA, V37, P301 GRIFFIN PP, 1977, J BONE JOINT SURG AM, V59, P97 HALL J. E., 1967, J BONE JOINT SURG B BRIT, V49, P695 KALEN V, 1986, J PEDIATR ORTHOPED, V6, P31 Kelly IP, 1997, J PEDIATR ORTHOPED, V17, P478, DOI 10.1097/00004694-199707000-00013 Mosca VS, 2001, J PEDIATR ORTHOPED, V21, P423, DOI 10.1097/00004694-200107000-00001 Policy JF, 2001, J PEDIATR ORTHOPED, V21, P784, DOI 10.1097/00004694-200111000-00016 REIMERS J, 1995, J PEDIATR ORTHOP B, V4, P71 Sanger T. D., 2003, PEDIATRICS, V111, P89 Stricker SJ, 1998, J PEDIATR ORTHOPED, V18, P289, DOI 10.1097/00004694-199805000-00003 Taussig G, 2001, Ann Readapt Med Phys, V44, P333, DOI 10.1016/S0168-6054(01)00110-6 VILENSKY JA, 1981, ARCH NEUROL-CHICAGO, V38, P646 WEBER D, 1978, ACTA PAEDOPSYCHIATR, V43, P73 WILLEMSE J, 1986, DEV MED CHILD NEUROL, V28, P355 NR 17 TC 6 Z9 6 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD FEB PY 2006 VL 48 IS 2 BP 96 EP 102 DI 10.1017/S0012162206000223 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 011NK UT WOS:000235274900005 PM 16417663 ER PT J AU Harjutsalo, V Tuomilehto, J AF Harjutsalo, V Tuomilehto, J TI Type 1 diabetes and autism: Is there a link? Response SO DIABETES CARE LA English DT Letter ID RISK-FACTORS; DISORDERS; SPECTRUM C1 Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Diabet & Genet Epidemiol Unit, FIN-00300 Helsinki, Finland. Univ Helsinki, Dept Publ Hlth, Helsinki, Finland. S Ostrobohtnia Cent Hosp, Seinajoki, Finland. RP Harjutsalo, V (reprint author), Natl Publ Hlth Inst, Dept Epidemiol & Hlth Promot, Diabet & Genet Epidemiol Unit, Mannerheimintie 166, FIN-00300 Helsinki, Finland. EM valmaharjutsalo@ktl.fi CR Comi AM, 1999, J CHILD NEUROL, V14, P388, DOI 10.1177/088307389901400608 Croen LA, 2005, ARCH PEDIAT ADOL MED, V159, P151, DOI 10.1001/archpedi.159.2.151 Freeman SJ, 2005, DIABETES CARE, V28, P925, DOI 10.2337/diacare.28.4.925 Hultman CM, 2002, EPIDEMIOLOGY, V13, P417, DOI 10.1097/01.EDE.0000016968.14007.E6 Kielinen M, 2000, EUR CHILD ADOLES PSY, V9, P162 Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 NR 6 TC 3 Z9 3 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD FEB PY 2006 VL 29 IS 2 BP 484 EP 485 DI 10.2337/diacare.29.02.06.dc05-1552 PG 2 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 011KJ UT WOS:000235266700084 PM 16482712 ER PT J AU Daneman, D AF Daneman, D TI Type 1 diabetes and autism: Is there a link? Response SO DIABETES CARE LA English DT Letter C1 Hosp Sick Children, Div Endocrinol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Toronto, ON, Canada. RP Daneman, D (reprint author), Hosp Sick Children, Div Endocrinol, Room 5110,555 Univ Ave, Toronto, ON M5G 1X8, Canada. EM denis.daneman@sickkids.on.ca CR Freeman SJ, 2005, DIABETES CARE, V28, P925, DOI 10.2337/diacare.28.4.925 GILLESPIE KM, 2004, LANCET, V364, P1645 HARJUTSALO V, 2005, DIABETES CARE, V29, P484 NR 3 TC 2 Z9 2 PU AMER DIABETES ASSOC PI ALEXANDRIA PA 1701 N BEAUREGARD ST, ALEXANDRIA, VA 22311-1717 USA SN 0149-5992 J9 DIABETES CARE JI Diabetes Care PD FEB PY 2006 VL 29 IS 2 BP 485 EP 485 DI 10.2337/diacare.29.02.06.dc05-2094 PG 1 WC Endocrinology & Metabolism SC Endocrinology & Metabolism GA 011KJ UT WOS:000235266700085 ER PT J AU Kim, HL Donnelly, JH Tournay, AE Book, TM Filipek, P AF Kim, HL Donnelly, JH Tournay, AE Book, TM Filipek, P TI Absence of seizures despite high prevalence of epileptiform EEG abnormalities in children with autism monitored in a tertiary care center SO EPILEPSIA LA English DT Article DE autism; seizures; EEG; video-EEG monitoring ID DEVELOPMENTAL DISORDERS; EPILEPSY; REGRESSION; CHILDHOOD; ELECTROENCEPHALOGRAM; SPIKES AB Purpose: Children with autism are commonly referred for video-EEG monitoring to determine the precise nature of their seizure-like events. Methods: We studied 32 children with autism by using continuous video-EEG telemetry ( VEEG) monitoring at a tertiary care referral center. Results: Of the 32 total patients, 22 were primarily referred for seizure evaluation and 10 for 24-h interictal EEG recording. Studies in two additional patients were prematurely terminated because of intolerance ( they are not included in the analyses). The median monitoring duration was 1 day ( range, 1-7 days). Of 22 patients referred for seizure evaluation, 15 had recorded events, but none was an epileptic seizure; the other seven patients had no recorded events. Interictal epileptiform EEG abnormalities were detected in 19 ( 59%) of 32 patients. These abnormalities included focal sharp waves ( in eight patients), multifocal sharp waves ( in six patients), generalized spike-wave complexes ( in 11 patients), and generalized paroxysmal fast activity/polyspikes ( in two patients). Focal/multifocal and generalized epileptiform abnormalities coexisted in six patients. Notably, 11 ( 73%) of the 15 patients with nonepileptic events had interictal epileptiform EEG abnormalities. Conclusions: Video-EEG evaluation of children with autism reveals epileptiform EEG abnormalities in the majority. However, many recorded seizure-like events are not epileptic, even in children with epileptiform EEG abnormalities. C1 Univ Calif Irvine, Med Ctr, Dept Neurol, Orange, CA 92868 USA. Univ Calif Irvine, Med Ctr, Dept Pediat, Orange, CA 92868 USA. For OC Kids, Orange, CA USA. RP Kim, HL (reprint author), Univ Calif Irvine, Med Ctr, Dept Neurol, 101 City Dr,Bldg 22C,Route 13, Orange, CA 92868 USA. EM kimhl@uci.edu CR AARTS JHP, 1984, BRAIN, V107, P293, DOI 10.1093/brain/107.1.293 Aldenkamp T, 2004, EPILEPSIA, V45, P54 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, P65 Binnie C D, 1991, Adv Neurol, V55, P113 Canitano R, 2005, J CHILD NEUROL, V20, P27, DOI 10.1177/08830738050200010401 CAVAZZUTI GB, 1980, EPILEPSIA, V21, P43, DOI 10.1111/j.1528-1157.1980.tb04043.x DEYKIN EY, 1979, AM J PSYCHIAT, V136, P1310 Doose H, 1996, NEUROPEDIATRICS, V27, P227, DOI 10.1055/s-2007-973771 DUCHOWNY MS, 1988, PEDIATR NEUROL, V4, P162, DOI 10.1016/0887-8994(88)90004-5 EEGOLOFS.O, 1971, NEUROPADIATRIE, V2, P375, DOI 10.1055/s-0028-1091791 ELIA M, 1995, AM J MENT RETARD, V100, P6 GUBBAY SS, 1970, DEV MED CHILD NEUROL, V12, P422 HIRSCH E, 1990, EPILEPSIA, V31, P756, DOI 10.1111/j.1528-1157.1990.tb05517.x International Federation of Societies for Clinical Neurophysiology, 1974, ELECTROENCEPHALOGR C, V37, P538, DOI DOI 10.1016/0013-4694(74)90099-6 Kanner AM, 2000, J AUTISM DEV DISORD, V30, P491, DOI 10.1023/A:1005524212271 Kawasaki Y, 1997, J AUTISM DEV DISORD, V27, P605, DOI 10.1023/A:1025886228387 BANCAUD J, 1981, EPILEPSIA, V22, P489 METRICK ME, 1991, EPILEPSIA, V32, P322, DOI 10.1111/j.1528-1157.1991.tb04658.x Nass R, 1998, DEV MED CHILD NEUROL, V40, P453 OLSSON I, 1988, ARCH NEUROL-CHICAGO, V45, P666 PATRY G, 1971, ARCH NEUROL-CHICAGO, V24, P242 ROSSI PG, 1995, BRAIN DEV-JPN, V17, P169, DOI 10.1016/0387-7604(95)00019-8 RUTTER M, 1970, SEMIN PSYCHIAT, V2, P435 SMALL JG, 1975, BIOL PSYCHIAT, V10, P385 TUCHMAN R, 1998, CNS SPECTRUMS, V3, P65 Tuchman R, 2002, LANCET NEUROL, V1, P352, DOI 10.1016/S1474-4422(02)00160-6 TUCHMAN RF, 1991, PEDIATRICS, V88, P1219 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 Valente KD, 2003, PEDIATR NEUROL, V28, P285, DOI 10.1016/S0887-8994(03)00002-X VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 WONG V, 1993, J CHILD NEUROL, V8, P316 Yung AWY, 2000, PEDIATR NEUROL, V23, P391, DOI 10.1016/S0887-8994(00)00220-4 NR 32 TC 37 Z9 37 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PD FEB PY 2006 VL 47 IS 2 BP 394 EP 398 DI 10.1111/j.1528-1167.2006.00434.x PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 014HI UT WOS:000235470000021 PM 16499766 ER PT J AU Chez, MG Chang, M Krasne, V Coughlan, C Kominsky, M Schwartz, A AF Chez, MG Chang, M Krasne, V Coughlan, C Kominsky, M Schwartz, A TI Frequency of epileptiform EEG abnormalities in a sequential screening of autistic patients with no known clinical epilepsy from 1996 to 2005 SO EPILEPSY & BEHAVIOR LA English DT Article DE autism; autism spectrum disorders; epilepsy; electroencephalogram abnormalities; autistic regression; ambulatory electroencephalogram ID SPECTRUM DISORDERS; CHILDREN; REGRESSION; SEIZURES; PATTERNS AB Autism spectrum disorders (ASDs) affect 1 in 166 births. Although electroencephalogram (EEG) abnormalities and clinical seizures may play a role in ASDs, the exact frequency of EEG abnormalities in an ASD population that has not had clinical seizures or prior abnormal EEGs is unknown. There is no current consensus on whether treatment of EEG abnormalities may influence development. This retrospective review of 24-hour ambulatory digital EEG data collected from 889 ASD patients presenting between 1996 and 2005 (with no known genetic conditions, brain malformations, prior medications, or clinical seizures) shows that 540 of 889 (60.7%) subjects had abnormal EEG epileptiform activity in sleep with no difference based on clinical regression. The most frequent sites of epileptiform abnormalities were localized over the right temporal region. Of 176 patients treated with valproic acid, 80 normalized on EEG and 30 more showed EEG improvement compared with the first EEG (average of 10.1 months to repeat EEG). (c) 2005 Elsevier Inc. All rights reserved. C1 Rosalind Franklin Univ Hlth Sci, Chicago Med Sch, Dept Neurol, N Chicago, IL USA. RP Chez, MG (reprint author), Rosalind Franklin Univ Hlth Sci, Chicago Med Sch, Dept Neurol, N Chicago, IL USA. 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PD FEB PY 2006 VL 8 IS 1 BP 267 EP 271 DI 10.1016/j.yebeh.2005.11.001 PG 5 WC Behavioral Sciences; Clinical Neurology; Psychiatry SC Behavioral Sciences; Neurosciences & Neurology; Psychiatry GA 010VL UT WOS:000235225900031 PM 16403678 ER PT J AU Mooney, EL Gray, KM Tonge, BJ AF Mooney, EL Gray, KM Tonge, BJ TI Early features of autism - Repetitive behaviours in young children SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; early features; repetitive behaviours ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; PRESCHOOL-CHILDREN; SPECTRUM DISORDER; EARLY RECOGNITION; EARLY SYMPTOMS; ADI-R; DIAGNOSIS; INFANTS; EPIDEMIOLOGY AB This study examined whether repetitive behaviours were a differentiating feature of autism in children aged less than 51 months. The study also examined the relationship between age (chronological and developmental) and repetitive behaviours in young children with autism. Standardised developmental and diagnostic assessments were conducted on 55 children aged between 22 and 51 months, consisting of 40 developmentally delayed children with DSM-IV-TR Autistic Disorder and 15 developmentally delayed children without Autistic Disorder. Results indicated that several measures of repetitive behaviour, particularly more complex high-level ones, were significantly positively associated with the probability of receiving a diagnosis of autism. No significant relationships were found between developmental age and the presence of repetitive behaviours in children with autism, but younger chronological age was associated more with simple or low-level repetitive behaviours. C1 Monash Univ, Ctr Dev Psychiat & Psychol, Dept Child & Adolescent Psychiat, Clayton, Vic 3168, Australia. RP Gray, KM (reprint author), Monash Univ, Ctr Dev Psychiat & Psychol, Dept Child & Adolescent Psychiat, 246 Clayton Rd, Clayton, Vic 3168, Australia. EM kylie.gray@med.monash.edu.au RI Gray, Kylie/H-3345-2014 OI Gray, Kylie/0000-0001-6518-4240 CR ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 ADRIEN JL, 1992, J AUTISM DEV DISORD, V22, P375, DOI 10.1007/BF01048241 American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 Einfeld S. 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L., 1997, HDB AUTISM PERVASIVE Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 STONE WL, 1994, ARCH PEDIAT ADOL MED, V148, P174 Tabachnick B., 2001, USING MULTIVARIATE S THELEN E, 1979, ANIM BEHAV, V27, P699, DOI 10.1016/0003-3472(79)90006-X Turner M, 1999, J CHILD PSYCHOL PSYC, V40, P839, DOI 10.1017/S0021963099004278 Vig S, 1999, J AUTISM DEV DISORD, V29, P235, DOI 10.1023/A:1023084106559 Vostanis P., 1998, AUTISM, V2, P229, DOI 10.1177/1362361398023002 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 37 TC 25 Z9 25 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD FEB PY 2006 VL 15 IS 1 BP 12 EP 18 DI 10.1007/s00787-006-0499-6 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 018EY UT WOS:000235748000002 PM 16514505 ER PT J AU Nagaraj, A AF Nagaraj, A TI Does qualitative synthesis of anecdotal evidence with that from scientific research help in understanding public health issues: a review of low MMR uptake SO EUROPEAN JOURNAL OF PUBLIC HEALTH LA English DT Article DE complementary medicine and MMR vaccination; MMR vaccination uptake; MMR vaccine; religion and MMR; review ID CHILDHOOD IMMUNIZATION; RUBELLA VACCINATION; MEASLES OUTBREAK; MUMPS; CHILDREN; PERSPECTIVES; CAMPAIGN; IRELAND; REASONS; PARENTS AB Study objective: To explore the professional and parental factors underlying low MMR uptake by qualitative synthesis of evidence from technical and non-technical anecdotal literature. Methods: An intensive investigation of literature covering research, press, online, E groups and grey literature was carried out using devised search strategies. Key themes were identified from both the research and anecdotal evidence, which were merged to form common themes. Results: The review of technical literature identified media scare and inadequate information from health professionals as the main reasons for non-uptake of MMR. The non-technical anecdotal evidence showed that professionals' belief in parental right to choose, target payments and fear of autism were the major factors. Conclusions: Anecdotal evidence may contribute to evidence-based public health practice, especially in widely debated public health issues. C1 Specialist Reg Publ Hlth, Hereford HR1 1UX, England. RP Nagaraj, A (reprint author), Specialist Reg Publ Hlth, 38 Hampton Dene Rd, Hereford HR1 1UX, England. EM Anandhi.Nagaraj@wyreforest-pct.nhs.uk CR Alderson P, 1997, EUR J PUBLIC HEALTH, V7, P95, DOI 10.1093/eurpub/7.1.95 Bedford H, 2000, BRIT MED J, V320, P240, DOI 10.1136/bmj.320.7229.240 Bozosky Zoltan, 1998, BRIT MED J, V316, P561 BURNETT V, 2001, BMJ 0113 Conway SP, 1999, ARCH DIS CHILD, V81, P422 Coughlan S, 2002, CLIN INFECT DIS, V35, P84, DOI 10.1086/340708 CUNINGHAME CJ, 1994, J PUBLIC HEALTH MED, V16, P314 Duffell E, 2001, J EPIDEMIOL COMMUN H, V55, P685, DOI 10.1136/jech.55.9.685 Elliman David A C, 2002, Paediatr Drugs, V4, P631 Evans M, 2001, BRIT J GEN PRACT, V51, P904 Evans MR, 1998, ARCH DIS CHILD, V79, P141 Fry R, 2002, BRIT MED J, V324, P733 GHEBREHEWET S, 1999, INVESTIGATION LOW 2 HODES DT, 1990, PUBLIC HEALTH, V104, P27, DOI 10.1016/S0033-3506(05)80342-7 Jarmulowicz M, 2002, BRIT MED J, V324, P734 Johnson A, 2001, BRIT J GEN PRACT, V51, P408 JOHNSON H, 1995, VACCINE, V13, P533, DOI 10.1016/0264-410X(94)00021-E Lewendon CL, 2002, HLTH ED J, V61, P212, DOI 10.1177/001789690206100303 LI J, 1993, BRIT MED J, V307, P168 LOCHHEAD YJ, 1991, J ADV NURS, V16, P130, DOI 10.1111/j.1365-2648.1991.tb01616.x Mason B W, 2000, Commun Dis Public Health, V3, P67 Mason BW, 2000, J EPIDEMIOL COMMUN H, V54, P473, DOI 10.1136/jech.54.6.473 Mayor Susan, 2002, BMJ, V324, P1118 MORETON J, J FAM HLTH CARE, V12, P31 Moreton J, 2001, Br J Community Nurs, V6, P199 *NHS LOND REG OFF, 2002, MEASL LOND INC CURR Pareek M, 2000, BRIT J GEN PRACT, V50, P969 Petrovic M, 2001, BRIT MED J, V322, P82, DOI 10.1136/bmj.322.7278.82 Roberts KA, 2002, LANCET, V360, P1596, DOI 10.1016/S0140-6736(02)11560-1 ROBERTS RJ, 1995, BRIT MED J, V310, P1629 Sharland M, 1997, Commun Dis Rep CDR Rev, V7, pR169 SIMPSON N, 1995, BRIT MED J, V310, P227 Smith A, 2001, Commun Dis Public Health, V4, P273 SUTTON GC, 1991, PUBLIC HEALTH, V105, P133, DOI 10.1016/S0033-3506(05)80287-2 Swennen B, 2001, VACCINE, V20, pS5, DOI 10.1016/S0264-410X(01)00307-3 Thomas D R, 1998, Commun Dis Public Health, V1, P44 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 2000, MMWR WEEKLY, V49, P299 NR 38 TC 7 Z9 7 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 1101-1262 J9 EUR J PUBLIC HEALTH JI Eur. 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Public Health PD FEB PY 2006 VL 16 IS 1 BP 85 EP 88 DI 10.1093/eurpub/cki058 PG 4 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 011OQ UT WOS:000235278300016 PM 16446303 ER PT J AU Nelson, PG Kuddo, T Song, EY Dambrosia, JM Kohler, S Satyanarayana, G VanDunk, C Grether, JK Nelson, KB AF Nelson, PG Kuddo, T Song, EY Dambrosia, JM Kohler, S Satyanarayana, G VanDunk, C Grether, JK Nelson, KB TI Selected neurotrophins, neuropeptides, and cytokines: developmental trajectory and concentrations in neonatal blood of children with autism or Down syndrome SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article DE autism; Down syndrome; neurotrophin; neuropeptide; cytokine; luminex ID VASOACTIVE-INTESTINAL-PEPTIDE; CENTRAL-NERVOUS-SYSTEM; MENTAL-RETARDATION; RAT-BRAIN; INTERLEUKIN-8; CHEMOKINE; NEURONS; MOUSE; TRANSCRIPTION; NEUROGENESIS AB Using a double-antibody immunoaffinity assay (Luminex) and ELISA technology, we measured concentrations of certain neurotrophins, neuropeptides, and cytokines in pooled samples (one to three subjects per sample) eluted from archived neonatal blood of children with later-diagnosed autism, Down syndrome, very preterm birth, or term control infants. We also measured analytes in blood from healthy adult controls. Case or control status for infant Subjects was ascertained by retrospective review of service agency medical records. We observed inhibitory substances in eluates from archived bloodspots, especially marked for measurement of BDNR Concentrations in control subjects differed by age: BDNF rose markedly with age, while NT-3 and NT-4/5 concentrations were lower in adults than in newborn infants. IL-8 concentrations were higher in newborn infants, preterm and term, than in adults. Considered by diagnostic group, total protein was higher in Down syndrome than in either autism or control subjects. In infants with Down syndrome, concentrations of IL-8 levels were higher than in controls, whether or not corrected for total protein; NT-3 and CGRP were lower and VIP higher. In samples from autistic subjects, NT-3 levels were significantly lower than controls and an increase in VIP approached statistical significance. Concentrations of NT-4/5 and CGRP were correlated in infants with autism but not in Down syndrome or controls. Some of these result, differ front earlier findings using a single-antibody recycling immunoaffinity chromatography (RIC) system. We discuss interrelationships of VIP, NF-3 and IL-8 and their potential relevance to features of the neuropathology of autism or Down syndrome. (c) 2005 ISDN. Published by Elsevier Ltd. All rights reserved. C1 NICHHD, Bethesda, MD 20892 USA. NINDS, Bethesda, MD 20892 USA. RP Nelson, PG (reprint author), NICHHD, Bldg 31,Room 2A25, Bethesda, MD 20892 USA. EM nelsonp@mail.nih.gov CR ADES AM, 2000, SOC PED RES, V79, P472 Anderson GM, 2002, J AM ACAD CHILD PSY, V41, P1513, DOI 10.1097/01.CHI.0000024874.60748.28 Anderson LE, 2004, J NEUROCHEM, V91, P1417, DOI 10.1111/j.1471-4159.2004.02833.x ARAUJO DM, 1993, BRAIN RES, V600, P49, DOI 10.1016/0006-8993(93)90400-H Bauman ML, 2005, INT J DEV NEUROSCI, V23, P183, DOI 10.1016/j.ijdevneu.2004.09.006 BECKER LE, 1991, CAN J NEUROL SCI, V18, P170 Blondel O, 2000, J NEUROSCI, V20, P8012 Brenneman DE, 1999, ANN NY ACAD SCI, V897, P17, DOI 10.1111/j.1749-6632.1999.tb07875.x BRENNEMAN DE, 1995, INT J DEV NEUROSCI, V13, P187, DOI 10.1016/0736-5748(95)00014-8 Courchesne E, 2005, INT J DEV NEUROSCI, V23, P153, DOI 10.1016/j.ijdevneu.2005.01.003 Croonenberghs J, 2002, NEUROPSYCHOBIOLOGY, V45, P1, DOI 10.1159/000048665 Danik M, 2003, J NEUROSCI RES, V74, P286, DOI 10.1002/jnr.10744 Delgado M, 2003, BIOCHEM BIOPH RES CO, V302, P275, DOI 10.1016/S0006-291X(03)00149-9 Desbaillets I, 1997, J EXP MED, V186, P1201, DOI 10.1084/jem.186.8.1201 Franciosi S, 2005, J NEUROIMMUNOL, V159, P66, DOI 10.1016/j.jneuroim.2004.10.006 GOLDEN JA, 1994, J NEUROPATH EXP NEUR, V53, P513, DOI 10.1097/00005072-199409000-00011 GRESSENS P, 1993, NATURE, V362, P155, DOI 10.1038/362155a0 Grether JK, 2003, ARCH PEDIAT ADOL MED, V157, P26 Griffin WST, 2002, J LEUKOCYTE BIOL, V72, P233 GRIFFIN WST, 1989, P NATL ACAD SCI USA, V86, P7611 Hagberg H, 2005, CURR OPIN NEUROL, V18, P117, DOI 10.1097/01.wco.0000162851.44897.8f Hesselgesser J, 1999, J NEUROVIROL, V5, P13, DOI 10.3109/13550289909029741 Hill JM, 2003, EXP NEUROL, V183, P56, DOI 10.1016/S0014-4886(03)00164-X Jyonouchi H, 2001, J NEUROIMMUNOL, V120, P170, DOI 10.1016/S0165-5728(01)00421-0 Karege F, 2002, NEUROSCI LETT, V328, P261, DOI 10.1016/S0304-3940(02)00529-3 LARKFORS L, 1996, J NEUROCHEM, V66, P1262 Miyazaki K, 2004, BRAIN DEV-JPN, V26, P292, DOI 10.1016/S0387-7604(03)00168-2 MOUNT HTJ, 1994, NEUROREPORT, V5, P2497, DOI 10.1097/00001756-199412000-00023 Mrak RE, 2004, J NEUROPATH EXP NEUR, V63, P679 Murphy M, 2000, PSYCHOL MED, V30, P1411, DOI 10.1017/S0033291799002949 Nelson K. 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PD FEB PY 2006 VL 24 IS 1 BP 73 EP 80 DI 10.1016/j.ijdevneu.2005.10.003 PG 8 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 025XX UT WOS:000236302000012 PM 16289943 ER PT J AU Diehl, JJ Bennetto, L Young, EC AF Diehl, JJ Bennetto, L Young, EC TI Story recall and narrative coherence of high-functioning children with autism spectrum disorders SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article DE autism spectrum disorders; language; narratives; coherence; pragmatics ID INFANTILE-AUTISM; LANGUAGE; INDIVIDUALS; ADOLESCENTS; IMMEDIATE; EVENTS; INTACT AB Previous research has found few quantitative differences between children with high-functioning autism spectrum disorders (ASDs) and well-matched controls in the length, complexity, and structure of their narratives. Researchers have noted, however, that narratives of children with ASDs have an unusual and idiosyncratic nature. This study provides an analysis of narratives in 17 children with high-functioning ASDs and 17 typically developing children matched on age, gender, language abilities, and cognitive abilities. We examined story recall and narrative coherence. The study revealed no group differences in story length or syntactic complexity. Children with ASDs also did not differ from controls in their use of the gist of a story to aid recall, or in their sensitivity to the importance of story events. Children with ASDs did, however, produce narratives that were significantly less coherent than the narratives of controls. Children with ASDs appeared less likely to use the gist of the story to organize their narratives coherently. These findings are discussed with regard to their relationship to other cognitive and linguistic difficulties of children with ASDs. C1 Univ Rochester, Dept Clin & Social Sci Psychol, Rochester, NY 14627 USA. Univ Rochester, Sch Med & Dent, Dept Surg, Rochester, NY USA. RP Bennetto, L (reprint author), Univ Rochester, Dept Clin & Social Sci Psychol, RC Box 270266, Rochester, NY 14627 USA. 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Abnorm. Child Psychol. PD FEB PY 2006 VL 34 IS 1 BP 87 EP 102 DI 10.1007/s10802-005-9003-x PG 16 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 046EZ UT WOS:000237795500007 PM 16485176 ER PT J AU Konstantareas, MM Stewart, K AF Konstantareas, MM Stewart, K TI Affect regulation and temperament in children with autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism Spectrum Disorder; emotion regulation; temperament; effortful control; negative affectivity; extraversion ID EMOTION REGULATION; DOWN-SYNDROME; PSYCHOPATHOLOGY; EXPRESSION; RATINGS AB Affect regulation (AR) and temperament were examined in children with Autism Spectrum Disorder (ASD). To determine AR, children were exposed to a mildly frustrating situation. Temperament was assessed by the Children's Behavior Questionnaire (CBQ). Children with ASD showed greater variability in AR and used less effective AR strategies compared to controls. Lower academic ability was associated with less effective AR strategies for the ASD while for the controls older age predicted more effective AR strategies. Those with ASD were lower than controls in Attention Focusing, Inhibitory Control, and Soothability. Of the three overarching temperament factors of the CBQ, only Effortful Control but not Negative Affectivity and Surgency/Extraversion distinguished those with ASD from controls. For the ASD group, higher academic ability predicted higher Negative Affectivity. Fewer symptoms and older chronological age predicted higher Effortful Control. C1 Univ Guelph, Coll Social & Appl Human Sci, Dept Psychol, Guelph, ON N1G 2W1, Canada. RP Konstantareas, MM (reprint author), Univ Guelph, Coll Social & Appl Human Sci, Dept Psychol, Guelph, ON N1G 2W1, Canada. 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PD FEB PY 2006 VL 36 IS 2 BP 143 EP 154 DI 10.1007/s10803-005-0051-4 PG 12 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400002 PM 16456727 ER PT J AU Kamio, Y Wolf, J Fein, D AF Kamio, Y Wolf, J Fein, D TI Automatic processing of emotional faces in high-functioning Pervasive Developmental Disorders: An affective priming study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high-functioning Pervasive Developmental Disorders; autism; social deficit; facial emotions; affective priming ID AUTISTIC CHILDS APPRAISAL; FACIAL EXPRESSIONS; HUMAN AMYGDALA; SPECTRUM DISORDER; EARLY RECOGNITION; ASPERGER-SYNDROME; SOCIAL COGNITION; JOINT ATTENTION; STIMULI; DISCRIMINATION AB This study examined automatic processing of emotional faces in individuals with high-functioning Pervasive Developmental Disorders (HFPDD) using an affective priming paradigm. Sixteen participants (HFPDD and matched controls) were presented with happy faces, fearful faces or objects in both subliminal and supraliminal exposure conditions, followed by Japanese ideographs for which the participants provided liking ratings. In the HFPDD group, affective priming was not found in either condition; the control group showed affective priming for both emotional faces under the subliminal condition and only for happy faces under the supraliminal condition. Results suggest that the social deficit in autism may derive in part from a failure in evaluating the emotional significance of emotional faces, a function for which the amygdala plays an important role. C1 Kyushu Univ, Grad Sch Human Environm Studies, Dept Psychol, Fukuoka 8128581, Japan. Univ Connecticut, Dept Psychol, Storrs, CT USA. RP Kamio, Y (reprint author), Kyushu Univ, Grad Sch Human Environm Studies, Dept Psychol, Hakozaki 6-19-1, Fukuoka 8128581, Japan. 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Disord. PD FEB PY 2006 VL 36 IS 2 BP 155 EP 167 DI 10.1007/s10803-005-0056-z PG 13 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400003 PM 16523242 ER PT J AU Golan, O Baron-Cohen, S Hill, J AF Golan, O Baron-Cohen, S Hill, J TI The Cambridge mindreading (CAM) face-voice battery: Testing complex emotion recognition in adults with and without Asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE emotion recognition; complex emotions; face perception; voice perception; theory of mind; Asperger Syndrome; autism spectrum; psychometrics ID HIGH-FUNCTIONING ADULTS; AUTISTIC CHILDS APPRAISAL; MIND; EXPRESSIONS; INFORMATION; DECEPTION; DISGUST; EYES AB Adults with Asperger Syndrome (AS) can recognise simple emotions and pass basic theory of mind tasks, but have difficulties recognising more complex emotions and mental states. This study describes a new battery of tasks, testing recognition of 20 complex emotions and mental states from faces and voices. The battery was given to males and females with AS and matched controls. Results showed the AS group performed worse than controls overall, on emotion recognition from faces and voices and on 12/20 specific emotions. Females recognised faces better than males regardless of diagnosis, and males with AS had more difficulties recognising emotions from faces than from voices. The implications of these results are discussed in relation to social functioning in AS. C1 Univ Cambridge, Autism Res Ctr, Dept Psychiat, Cambridge CB2 2AH, England. RP Golan, O (reprint author), Univ Cambridge, Autism Res Ctr, Dept Psychiat, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. 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Autism Dev. Disord. PD FEB PY 2006 VL 36 IS 2 BP 169 EP 183 DI 10.1007/s10803-005-0057-y PG 15 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400004 PM 16477515 ER PT J AU Leekam, SR Ramsden, CAH AF Leekam, SR Ramsden, CAH TI Dyadic orienting and joint attention in preschool children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; joint attention; dyadic orienting ID DIAGNOSTIC INTERVIEW; COMMUNICATION DISORDERS; SPECTRUM DISORDER; SOCIAL COMPETENCE; LANGUAGE; MIND; BEHAVIORS; STIMULI; INFANCY; DELAY AB Acts of dyadic orienting (responses to attention bids by a researcher) and acts of joint attention (e.g. pointing and showing behaviors) were observed in preschool children with autism and children with developmental delay. Children with autism responded to fewer adult vocal and non-vocal attention bids that were made singly and by combining modalities (e.g. name call plus touch). 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Autism Dev. Disord. PD FEB PY 2006 VL 36 IS 2 BP 185 EP 197 DI 10.1007/s10803-005-0054-1 PG 13 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400005 PM 16502142 ER PT J AU Davis, RAO Bockbrader, MA Murphy, RR Hetrick, WP O'Donnell, BF AF Davis, RAO Bockbrader, MA Murphy, RR Hetrick, WP O'Donnell, BF TI Subjective perceptual distortions and visual dysfunction in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Conference of the Society-of-Biological-Psychiatry CY MAR, 2002 CL Philadelphia, PA SP Soc Biolog Psychiatry DE autism; visual system; contrast sensitivity; sensory profile; motion processing; subjective distortions ID LATERAL GENICULATE LESIONS; CONTRAST SENSITIVITY; WORKING-MEMORY; MOTION; ABNORMALITIES; CEREBELLAR; DEFICIT; VARIABILITY; DISORDERS; ATTENTION AB Case reports and sensory inventories suggest that autism involves sensory processing anomalies. Behavioral tests indicate impaired motion and normal form perception in autism. The present study used first-person accounts to investigate perceptual anomalies and related subjective to psychophysical measures. Nine high-functioning children with autism and nine typically-developing children were given a questionnaire to assess the frequency of sensory anomalies, as well as psychophysical tests of visual perception. Results indicated that children with autism experience increased perceptual anomalies, deficits in trajectory discrimination consistent with dysfunction in the cortical dorsal pathway or in cerebellar midsagittal vermis, and high spatial frequency contrast impairments consistent with dysfunctional parvocellular processing. Subjective visual hypersensitivity was significantly related to greater deficits across vision tests. C1 Indiana Univ, Dept Psychol, Bloomington, IN 47401 USA. Indiana Univ, Sch Med, Dept Otolaryngol, Indianapolis, IN 46204 USA. 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Autism Dev. Disord. PD FEB PY 2006 VL 36 IS 2 BP 199 EP 210 DI 10.1007/s10803-005-0055-0 PG 12 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400006 PM 16453070 ER PT J AU Eldevik, S Eikeseth, S Jahr, E Smith, T AF Eldevik, S Eikeseth, S Jahr, E Smith, T TI Effects of low-intensity behavioral treatment for children with autism and mental retardation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE behavioral intervention; eclectic treatment; autism; intensity ID PERVASIVE DEVELOPMENTAL DISORDER; EARLY INTERVENTION; YOUNG-CHILDREN AB We retrospectively compared 2 groups of children receiving either behavioral treatment (n = 13) or eclectic treatment (n = 15) for an average of 12 hours per week. Children were assessed on intelligence, language, adaptive functioning and maladaptive behavior at pretreatment and 2 years into treatment. The groups did not differ significantly at pretreatment. 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Autism Dev. Disord. PD FEB PY 2006 VL 36 IS 2 BP 211 EP 224 DI 10.1007/s10803-005-0058-x PG 14 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400007 PM 16477514 ER PT J AU Milne, E White, S Campbell, R Swettenham, J Hansen, P Ramus, F AF Milne, E White, S Campbell, R Swettenham, J Hansen, P Ramus, F TI Motion and form coherence detection in autistic spectrum disorder: Relationship to motor control and 2 : 4 digit ratio SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE motion detection; motor control; foetal testosterone; autistic spectrum disorder ID DORSAL STREAM FUNCTION; DEVELOPMENTAL DYSLEXIA; ASPERGER SYNDROME; VISUAL-MOTION; MAGNOCELLULAR DEFICIT; WILLIAMS-SYNDROME; CHILDREN; CEREBELLAR; IMPAIRMENT; PERCEPTION AB Children with autistic spectrum disorder and controls performed tasks of coherent motion and form detection, and motor control. Additionally, the ratio of the 2nd and 4th digits of these children, which is thought to be ail indicator of foetal testosterone. was measured. Children in the experimental group were impaired at tasks of motor control, and had lower 2D:4D than controls. There were no group differences in motion or form detection. However a sub-group of children with autism were selectively impaired at motion detection. There were significant relationships between motion coherence detection and motor control in both groups of children, and also between motion detection, fine motor control and 2D:4D in the group of children with autistic spectrum disorder. C1 UCL, Dept Human Commun Sci, London, England. UCL, Inst Cognit Neurosci, London, England. Physiol Lab, Oxford, England. ENS, CNRS, EHESS, Lab Sci Cognit & Psycholinguist, F-75230 Paris 05, France. RP Milne, E (reprint author), Univ Sheffield, Dept Psychol, Sheffield S10 2TP, S Yorkshire, England. 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Autism Dev. Disord. PD FEB PY 2006 VL 36 IS 2 BP 225 EP 237 DI 10.1007/s10803-005-0052-3 PG 13 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400008 PM 16477516 ER PT J AU Mottron, L Lemmens, K Gagnon, L Seron, X AF Mottron, L. Lemmens, K. Gagnon, L. Seron, X. TI Non-algorithmic access to calendar information in a calendar calculator with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; calendar calculation; savant syndrome; autistic intelligence; perception ID IDIOT SAVANT; MEMORY; SUBJECT AB The possible use of a calendar algorithm was assessed in DBC, an autistic "savant" of normal measured intelligence. Testing of all the dates in a year revealed a random distribution of errors. Re-testing DBC on the same dates one year later shows that his errors were not stable across time. Finally, DBC was able to answer "reversed" questions that cannot be solved by a classical algorithm. These findings favor a non-algorithmic retrieval of calendar information. It is proposed that multidirectional, non-hierarchical retrieval of information, and solving problems in a non-algorithmic way, are involved in savant performances. The possible role of a functional rededication of low-level perceptual systems to the processing of symbolic information in savants is discussed. C1 Hop Riviere Des Prairies, Clin Specialisee Autisme, Montreal, PQ H1E 1A4, Canada. Hop Riviere Des Prairies, Dept Psychiat, Montreal, PQ H1E 1A4, Canada. Maastricht Univ, Maastricht, Netherlands. Hop St Justine, Montreal, PQ H3T 1C5, Canada. Univ Louvain, B-1348 Louvain La Neuve, Belgium. RP Mottron, L (reprint author), Hop Riviere Des Prairies, Clin Specialisee Autisme, 7070 Blvd Perras, Montreal, PQ H1E 1A4, Canada. 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Autism Dev. Disord. PD FEB PY 2006 VL 36 IS 2 BP 239 EP 247 DI 10.1007/s10803-005-0059-9 PG 9 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400009 PM 16453069 ER PT J AU Holzer, L Mihaileseu, R Rodrigues-Degaeff, C Junier, L Muller-Nix, C Halfon, O Ansermet, F AF Holzer, L Mihaileseu, R Rodrigues-Degaeff, C Junier, L Muller-Nix, C Halfon, O Ansermet, F TI Community introduction of practice parameters for autistic spectrum disorders: Advancing early recognition SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Pervasive Developmental Disorder; early detection; community; quality of care ID PERVASIVE DEVELOPMENTAL DISORDERS; CLINICAL-PRACTICE GUIDELINES; CHILDHOOD AUTISM; MENTAL-HEALTH; RATING-SCALE; CHILDREN; CLASSIFICATION; INTERVENTION; DIAGNOSIS AB Objectives: Within a strong interdisciplinary framework, improvement in the quality of care for children with autistic spectrum disorders through a 2 year implementation program of Practice Parameters, aimed principally at improving early detection and intervention. Method We developed Practice Parameters (PPs) for Pervasive Developmental Disorders and circulated the PPs to all child and adolescent psychiatrists practicing in the region. Results: PP development and parallel information strategies resulted in a significant decrease of 1.5 years in the mean-age-at-diagnosis. However, further analysis indicated that improvement was only transient. Conclusion: Despite the encouraging improvement in mean-age-at-diagnosis 2 years after PP implementation, other indicators showed a failure to maintain the improvements. A systematic screening program would be the most reliable method to reinforce the PPs. C1 SUPEA, Hop Nestle, CH-1012 Lausanne, Switzerland. Univ Geneva, Dept Psychol, Geneva, Switzerland. RP Holzer, L (reprint author), SUPEA, Hop Nestle, CTJA 48 Ave Beaumont, CH-1012 Lausanne, Switzerland. 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Autism Dev. Disord. PD FEB PY 2006 VL 36 IS 2 BP 249 EP 262 DI 10.1007/s10803-005-0053-2 PG 14 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400010 PM 16447011 ER PT J AU Wakabayashi, A Baron-Cohen, S Wheelwright, S Tojo, Y AF Wakabayashi, A Baron-Cohen, S Wheelwright, S Tojo, Y TI The Autism-Spectrum Quotient (AQ) in Japan: A cross-cultural comparison SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism Spectrum Quotient; Asperger syndrome; high-functioning autism; normal intelligence; adults with autism; self-administered ID FUNCTIONING AUTISM AB The AQ (Autism-Spectrurn Quotient) is a self-administered instrument for measuring the degree to which an adult with normal intelligence has the traits associated with the autistic spectrum. The AQ was administered in Japan to test whether the UK results would generalize to a very different culture. Three groups of subjects, adults with AS or HFA (n = 57), adult controls (n = 194), and University students (n = 1050) were assessed. The adults with AS/HFA had a mean AQ score which was significantly higher than both the controls and the University students. Among the controls, males scored significantly higher than females. The similarity of results in both the general population and the clinical group across the two cultures was remarkable. C1 Chiba Univ, Dept Psychol, Chiba 2638522, Japan. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge, England. Natl Inst Special Educ, Sect Educ Children Autism, Musashino, Tokyo, Japan. RP Wakabayashi, A (reprint author), Chiba Univ, Dept Psychol, 1-33 Yayoi Cho, Chiba 2638522, Japan. EM akiowcam@mac.com CR APA, 1994, DSMIV DIAGN STAT MAN BAILEY A, 1995, PSYCHOL MED, V25, P63 Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Baron-Cohen S, 1997, ADV INFANCY RES, V11, P193 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BARONCOHEN S, UNPUB AUTISM SPECTRU Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY FRITH U, 1991, AUTISM APERGERS SYND Rutter M., 1978, AUTISM REAPPRAISAL C Wing L, 1988, ASPECTS AUTISM BIOL WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1992, INT CLASS DIS NR 15 TC 71 Z9 71 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 FEB PY 2006 VL 36 IS 2 BP 263 EP 270 DI 10.1007/s10803-005-0061-2 PG 8 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400011 PM 16586157 ER PT J AU Gadow, KD DeVincent, CJ Pomeroy, J AF Gadow, KD DeVincent, CJ Pomeroy, J TI ADHD symptom subtypes in children with pervasive developmental disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; PDDNOS; pervasive developmental disorder; attention-deficit/hyperactivity disorder; oppositional defiant disorder; DSM-IV; diagnosis ID DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DSM-IV ADHD; AUTISTIC DISORDER; MENTAL-RETARDATION; PRESCHOOL-CHILDREN; ASPERGER-SYNDROME; FIELD TRIAL; BEHAVIORAL-ADJUSTMENT; PSYCHIATRIC-DISORDERS AB Objective: Compares DSM-IV ADHD subtypes in large samples of 3-to-5 and 6-to-12 year old children with pervasive developmental disorder (PDD) vs. nonPDD clinic referrals. Method: Parents and teachers completed a DSM-IV-referenced rating scale. Results: ADHD subtypes were clearly differentiated from the nonADHD group and showed a differential pattern of co-occurring psychiatric symptoms (more pronounced for teacher- than parent-defined subtypes and older than younger children) that was similar in both PDD and nonPDD samples. The Combined type had more severe oppositional, aggressive and PDD symptoms than Inattentive type and were from less advantaged homes than other subtypes. Hyperactive-Impulsive type was least impaired. Conclusion: Findings support the notion that ADHD may be a clinically meaningful syndrome in children with PDD. C1 SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA. SUNY Stony Brook, Dept Pediat, Stony Brook, NY 11794 USA. RP Gadow, KD (reprint author), SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA. EM kenneth.gadow@stonybrook.edu CR Achenbach T. 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K., 1978, J PEDIATR PSYCHOL, V3, P177, DOI 10.1093/jpepsy/3.4.177 WHALEN CK, 1979, J APPL BEHAV ANAL, V12, P65, DOI 10.1901/jaba.1979.12-65 Willcutt EG, 1999, J AM ACAD CHILD PSY, V38, P1355, DOI 10.1097/00004583-199911000-00009 Wolraich ML, 1996, J AM ACAD CHILD PSY, V35, P319, DOI 10.1097/00004583-199603000-00013 Wozniak J, 1997, J AM ACAD CHILD PSY, V36, P1552, DOI 10.1016/S0890-8567(09)66564-3 NR 75 TC 93 Z9 94 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 FEB PY 2006 VL 36 IS 2 BP 271 EP 283 DI 10.1007/s10803-005-0060-3 PG 13 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400012 PM 16477513 ER PT J AU Pickett, JA Paculdo, DR Shavelle, RM Strauss, DJ AF Pickett, JA Paculdo, DR Shavelle, RM Strauss, DJ TI 1998-2002 Update on "Causes of death in autism" SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter C1 Autism Tissue Program, Princeton, NJ 08540 USA. Life Expectancy Project, San Francisco, CA USA. RP Pickett, JA (reprint author), Autism Tissue Program, 99 Wall St, Princeton, NJ 08540 USA. EM atp@brainbank.org CR *CA DDS, 2002, BIANN SUMM COMM BAS Shavelle RM, 2001, J AUTISM DEV DISORD, V31, P569, DOI 10.1023/A:1013247011483 NR 2 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 FEB PY 2006 VL 36 IS 2 BP 287 EP 288 DI 10.1007/s10803-005-0066-x PG 2 WC Psychology, Developmental SC Psychology GA 041RC UT WOS:000237472400014 PM 16565885 ER PT J AU Posey, DJ Erickson, CA Stigler, KA McDougle, CJ AF Posey, DJ Erickson, CA Stigler, KA McDougle, CJ TI The use of selective serotonin reuptake inhibitors in autism and related disorders SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; OPEN-LABEL; FLUOXETINE TREATMENT; REPETITIVE THOUGHTS; DOUBLE-BLIND; CHILDREN; ADULTS; BEHAVIOR; PAROXETINE AB This paper reviews the published literature on the use of selective serotonin reuptake inhibitors (SSRIs) for the treatment of symptoms associated with autistic disorder and other pervasive developmental disorders (PDDs) in both children and adults. To date, placebo-controlled studies of SSRIs have involved only fluvoxamine (in children and adults) and fluoxetine (in children). Open-label and retrospective studies of all other SSRIs in PDDs have also been published that suggest effectiveness. Despite these positive reports, there continues to be questions about the tolerability and appropriate dosing of SSRIs in children with PDDs. Because of the limited number of placebo-controlled studies, definitive conclusions about the role SSRIs should play in the clinical treatment of children with PDDs cannot be drawn. Larger, placebo-controlled studies of SSRIs are needed to guide clinical treatment. C1 James Whitcomb Riley Hosp Children, Christian Sarkine Autism Treatment Ctr, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46204 USA. RP Posey, DJ (reprint author), James Whitcomb Riley Hosp Children, Christian Sarkine Autism Treatment Ctr, Room 4300,702 Barnhill Dr, Indianapolis, IN 46202 USA. EM dposey@iupui.edu CR AMAN MG, 1985, AM J MENT DEF, V89, P485 Aman MG, 2005, J CHILD ADOL PSYCHOP, V15, P116, DOI 10.1089/cap.2005.15.116 AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 Branford D, 1998, J INTELL DISABIL RES, V42, P301, DOI 10.1046/j.1365-2788.1998.00144.x BRASIC JR, 1998, CNS SPECTRUMS, V3, P39 COOK EH, 1992, J AM ACAD CHILD PSY, V31, P739, DOI 10.1097/00004583-199207000-00024 Couturier JL, 2002, J CHILD ADOL PSYCHOP, V12, P243, DOI 10.1089/104454602760386932 Damore J, 1998, J AM ACAD CHILD PSY, V37, P248, DOI 10.1097/00004583-199803000-00006 Davanzo PA, 1998, AM J MENT RETARD, V102, P427 DeLong GR, 2002, DEV MED CHILD NEUROL, V44, P652 DeLong GR, 1998, DEV MED CHILD NEUROL, V40, P551 Fukuda Tokiko, 2001, No To Hattatsu, V33, P314 GORDON CT, 1993, ARCH GEN PSYCHIAT, V50, P441 Hellings JA, 1996, J CLIN PSYCHIAT, V57, P333 Hollander E, 2005, NEUROPSYCHOPHARMACOL, V30, P582, DOI 10.1038/sj.npp.1300627 Langworthy-Lam KS, 2002, J CHILD ADOL PSYCHOP, V12, P311, DOI 10.1089/104454602762599853 Martin A, 2003, J AUTISM DEV DISORD, V33, P77, DOI 10.1023/A:1022234605695 McDougle C. 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Child Adolesc. Psychopharmacol. PD FEB-APR PY 2006 VL 16 IS 1-2 BP 181 EP 186 DI 10.1089/cap.2006.16.181 PG 6 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 030HJ UT WOS:000236624900017 PM 16553538 ER PT J AU Levy, Y Gottesman, R Borochowitz, Z Frydman, M Sagi, M AF Levy, Y Gottesman, R Borochowitz, Z Frydman, M Sagi, M TI Language in boys with fragile X syndrome SO JOURNAL OF CHILD LANGUAGE LA English DT Article ID INVERSE CORRELATION; WILLIAMS-SYNDROME; CHILDREN; AUTISM; MALES; ACQUISITION; IMPAIRMENT; PHENOTYPE; LENGTH; MLU AB The current paper reports of language production in 15 Hebrew-speaking boys, aged 9;0-13;0, with fully methylated, non-mosaic fragile X syndrome and no concomitant diagnosis of autism. Contrary to expectations, seven children were non-verbal. Language production in the verbal children was studied in free conversations and in context-bound speech. Despite extra caution in calculating MLU, participants' larigUage level was not predicted by mean utterance length. Context bound speech resulted In grammatically more advanced performance than free conversation, and performance in both contexts differed in important ways from performance of typically developing MLU-matched controls. The relevance of MLU as a predictor of productive grammar in disordered populations is briefly discussed. C1 Hebrew Univ Jerusalem, Dept Psychol, Hadassah Med Sch, IL-91905 Jerusalem, Israel. Hebrew Univ Jerusalem, Dept Psychol, Jerusalem, Israel. Technion Israel Inst Technol, Rapport Sch Med, IL-32000 Haifa, Israel. Bnai Zion Med Ctr, Simon Winter Inst Human Genet, Haifa, Israel. Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel. Hebrew Univ Jerusalem, Hadassah Med Ctr, Dept Human Genet, IL-91905 Jerusalem, Israel. RP Levy, Y (reprint author), Hebrew Univ Jerusalem, Dept Psychol, Hadassah Med Sch, IL-91905 Jerusalem, Israel. 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PD FEB PY 2006 VL 33 IS 1 BP 125 EP 144 DI 10.1017/S030500090500718X PG 20 WC Psychology, Developmental; Linguistics; Psychology, Experimental SC Psychology; Linguistics GA 026LX UT WOS:000236341500006 PM 16566323 ER PT J AU Wong, V Khong, PL AF Wong, V Khong, PL TI Tuberous sclerosis complex: Correlation of magnetic resonance imaging (MRI) findings with comorbidities SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; CLINICORADIOLOGICAL EVALUATION; INFANTILE SPASMS; AUTISM; POPULATION; EPILEPSY; CHILDREN; SEIZURES AB We studied the magnetic resonance imaging (MRI) findings in a cohort of Chinese children with tuberous sclerosis complex to determine the relationship between age, sex, mental retardation, autism, epilepsy, infantile spasm, and early age at onset of seizures and the numbers and locations of tubers detected. We searched our tuberous sclerosis registry, established in 1985 (N = 44), and performed an analysis of children who had MRIs of the brain performed (n = 22). A neuroradiologist blinded to the clinical findings scored the MRIs according to the total number and site of the tubers. The following factors were analyzed: age, sex, presence of autism (n = 7), presence (n = 19) and severity of mental retardation (mild [n = 121, moderate to severe [n = 7]), presence of epilepsy (n = 21) or infantile spasm (n = 8), and age at onset of seizures less than 1 year (n = 10). There was no significant relationship between the number and site of tubers and the following factors: sex, autism, mental retardation, degree of mental retardation, epilepsy, history of infantile spasm, or age at onset of seizures less than 1 year. Only the presence of cortical tubers in the parietal regions had a significant relationship with the history of infantile spasm (P = .012). Using multiple regression analysis of all of the risk factors, only age is related to the number of tubers in the MRI (P = .047), and a history of infantile spasm is related to the presence of tubers in the parietal (P = .009) and occipital (P = .031) lobes. The associated comorbidities in tuberous sclerosis complex might be explained by more complex underlying genetic or pathologic issues rather than purely by the site of the cortical tubers. We suggest that a developmental approach, by analyzing the age at the appearance of tubers in both symptomatic and asymptomatic cases with the development of other neuropsychiatric comorbidities, should be undertaken to assess the causal relationship. C1 Univ Hong Kong, Div Neurodev Paediat, Dept Paediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China. Univ Hong Kong, Dept Diagnost Radiol, Hong Kong, Hong Kong, Peoples R China. RP Wong, V (reprint author), Univ Hong Kong, Div Neurodev Paediat, Dept Paediat & Adolescent Med, Hong Kong, Hong Kong, Peoples R China. 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Child Neurol. PD FEB PY 2006 VL 21 IS 2 BP 99 EP 105 DI 10.2310/7010.2006.00027 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 046SS UT WOS:000237831900002 PM 16566871 ER PT J AU Braddock, BA Farmer, JE Deidrick, KM Iverson, JM Maria, BL AF Braddock, BA Farmer, JE Deidrick, KM Iverson, JM Maria, BL TI Oromotor and communication findings in Joubert syndrome: Further evidence of multisystem apraxia SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT Annual Symposium on Research in Child Language Disorders CY JUN, 2004 CL Madison, WI ID ABNORMAL EYE-MOVEMENTS; MOLAR TOOTH SIGN; EPISODIC HYPERPNEA; CEREBELLAR VERMIS; AUTISM; CHILDREN; RETARDATION; BEHAVIOR; ATAXIA AB This study provides descriptive information in the areas of oromotor abilities and communication to better understand the spectrum of disability in individuals with Joubert syndrome. Participants included 21 individuals with the diagnosis of Joubert syndrome (mean age 10.45 years). Participants completed oromotor and receptive language measures. In addition, all of the participants' speech and gesture communication from a narrative task was coded and analyzed from videotape. Caregivers reported the participants' level of fine and gross motor function. The results show that individuals with Joubert syndrome exhibit a distinct oromotor pattern consistent with verbal and lingual apraxias. Despite significant motor skills deficits and oculomotor apraxia, persons with Joubert syndrome produced gestures when communicating, and those whose speech was less intelligible used a higher rate of gesture compared with those with greater verbal output. These findmgs suggest a new form of apraxia not previously described in the condition and are consistent with previous research that suggests that persons with Joubert syndrome typically do not exhibit classic symptoms of autism spectrum disorder. C1 Univ Missouri, Dept Hlth Psychol, Columbia, MO 65212 USA. Univ Missouri, Dept Psychol Sci, Columbia, MO USA. Univ Pittsburgh, Dept Psychol, Pittsburgh, PA USA. Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA. RP Farmer, JE (reprint author), Univ Missouri, Dept Hlth Psychol, 1 Hosp Dr,DC116-88, Columbia, MO 65212 USA. EM farmerje@health.missouri.edu CR Andermann F, 1999, J CHILD NEUROL, V14, P565, DOI 10.1177/088307389901400903 BOLTSHAUSER E, 1977, NEUROPADIATRIE, V8, P57, DOI 10.1055/s-0028-1091505 Bruininks R., 1996, SCALES INDEPENDENT B Butcher C., 2000, LANGUAGE GESTURE, P235, DOI DOI 10.1017/CBO9780511620850.015 Charman T, 2003, J CHILD LANG, V30, P213, DOI 10.1017/S0305000902005482 DARLEY FL, 1975, MOTOR SPEECH DISORDE, V4, P69 Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd Farmer JE, 2003, PEDIATR RES, V53, p69A Fennell EB, 1999, J CHILD NEUROL, V14, P592, DOI 10.1177/088307389901400907 FLETCHER SG, 1972, J SPEECH HEAR RES, V15, P760 GITTEN JC, 1997, J CHILD NEUROL, V13, P391 Gleeson JG, 2004, AM J MED GENET A, V125A, P125, DOI 10.1002/ajmg.a.20437 JOUBERT M, 1969, NEUROLOGY, V19, P813 Lord C., 1999, AUTISM DIAGNOSTIC OB LOVELAND KA, 1990, BRIT J DEV PSYCHOL, V8, P9 Maria BL, 1999, J CHILD NEUROL, V14, P368, DOI 10.1177/088307389901400605 Maria BL, 1997, J CHILD NEUROL, V12, P423 MILLER J, 1985, ASESSING LANGUAGE PR MOROZUMI A, 1997, MY FRIEND GORILA OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Ozonoff S, 1999, J CHILD NEUROL, V14, P636, DOI 10.1177/088307389901401003 Takahashi TN, 2005, AM J MED GENET A, V132A, P347, DOI 10.1002/ajmg.a.30500 NR 22 TC 11 Z9 11 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD FEB PY 2006 VL 21 IS 2 BP 160 EP 163 DI 10.2310/7010.2006.00021 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 046SS UT WOS:000237831900015 PM 16566884 ER PT J AU Poling, JS Frye, RE Shoffner, J Zimmerman, AW AF Poling, JS Frye, RE Shoffner, J Zimmerman, AW TI Developmental regression and mitochondrial dysfunction in a child with autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID SPECTRUM DISORDERS; RETT-SYNDROME; ABNORMALITIES AB Autistic spectrum disorders can be associated with mitochondrial dysfunction. We present a singleton case of developmental regression and oxidative phosphorylation disorder in a 19-month-old girl. Subtle abnormalities in the serum creatine kinase level, aspartate aminotransferase, and serum bicarbonate led us to perform a muscle biopsy, which showed type I myofiber atrophy, increased lipid content, and reduced cytochrome c oxidase activity. There were marked reductions in enzymatic activities for complex I and III. Complex IV (cytochrome c oxidase) activity was near the 5% confidence level. To determine the frequency of routine laboratory abnormalities in similar patients, we performed a retrospective study including 159 patients with autism (Diagnostic and Statistical Manual of Mental Disorders-Nand Childhood Autism Rating Scale) not previously diagnosed with metabolic disorders and 94 age-matched controls with other neurologic disorders. Aspartate aminotransferase was elevated in 38% of patients with autism compared with 15% of controls (P <.0001). The serum creatine kinase level also was abnormally elevated in 22 (47%) of 47 patients with autism. These data suggest that further metabolic evaluation is indicated in autistic patients and that defects of oxidative phosphorylation might be prevalent. C1 Johns Hopkins Univ Hosp, Kennedy Krieger Inst, Dept Neurol & Neurosurg, Baltimore, MD 21205 USA. Boston Childrens Hosp, Dept Neurol, Boston, MA USA. Georgia State Univ, Atlanta, GA 30303 USA. RP Zimmerman, AW (reprint author), Johns Hopkins Univ Hosp, Kennedy Krieger Inst, Dept Neurol & Neurosurg, 707 N Broadway, Baltimore, MD 21205 USA. EM zimmerman@kennedykrieger.org CR CORNFORD ME, 1994, J CHILD NEUROL, V9, P424 Filipek PA, 2003, ANN NEUROL, V53, P801, DOI 10.1002/ana.10596 Fillano James J, 2002, J Child Neurol, V17, P435 Graf WD, 2000, J CHILD NEUROL, V15, P357, DOI 10.1177/088307380001500601 Heilstedt HA, 2002, AM J MED GENET, V111, P238, DOI 10.1002/ajmg.10633 Lerman-Sagie T, 2004, J CHILD NEUROL, V19, P379, DOI 10.1177/088307380401900510 Pons R, 2004, J PEDIATR-US, V144, P81, DOI 10.1016/j.jpeds.2003.10.023 Rogers SJ, 2004, MENT RETARD DEV D R, V10, P139, DOI 10.1002/mrdd.20027 SHOFFNER JM, 2001, METABOLIC MOL BASES, P2367 WALLACE DC, 1988, CELL, V55, P601, DOI 10.1016/0092-8674(88)90218-8 ZHENG XX, 1990, BIOCHIM BIOPHYS ACTA, V1019, P1, DOI 10.1016/0005-2728(90)90118-N NR 11 TC 60 Z9 62 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD FEB PY 2006 VL 21 IS 2 BP 170 EP 172 DI 10.2310/7010.2006.00032 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 046SS UT WOS:000237831900018 PM 16566887 ER PT J AU Posserud, MB Lundervold, AJ Gillberg, C AF Posserud, MB Lundervold, AJ Gillberg, C TI Autistic features in a total population of 7-9-year-old children assessed by the ASSQ (Autism Spectrum Screening Questionnaire) SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; child psychiatry; ASSQ; Asperger syndrome; screening ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME; FUNCTIONING AUTISM; GENERAL-POPULATION; SEX-DIFFERENCES; MALE BRAIN; EPIDEMIOLOGY; PREVALENCE; PARENTS; INFORMANT AB Background: The prevalence of autism is reported to be on the rise worldwide. Change of diagnostic criteria and a broadening of the concept of autism have been mentioned as contributing factors. Further studies of general populations are needed. The present study assessed the distribution of autistic features in a total population of children 7-9 years of age, and explored the impact of age, gender, informant, and participation bias on symptom report. Methods: Teacher and parent forms of the Autism Spectrum Screening Questionnaire (ASSQ) were used in the 'Bergen Child Study', a total population study of 9430 children aged 7-9 years. Completed teacher forms were returned for 97% and parent forms for 71% of the children. High-scorers were defined according to the ASSQ validation study by Ehlers, Gillberg, and Wing (1999). Results: The distribution of ASSQ scores was found to be almost continuous. Of the children with both a teacher and a parent form, 2.1% were defined as high-scorers. Children without parent informed consent (i.e., anonymous children) obtained significantly higher teacher scores than those who had questionnaires completed by both parent and teacher. Adjusting prevalence for the anonymous children, the prevalence of high-scorers was 2.7% of the total population. Age did not affect symptom scores. Boys scored higher and parents reported more symptoms, particularly in girls. Agreement between informants was low to moderate. Conclusions: Autism symptoms are not uncommon in the general population of children. Our findings are consistent with the concept of autism as a spectrum. Non-responders had a higher load of autism symptoms than identified children, indicating that reports on the prevalence of autism in a responder group underestimate true prevalence. Large differences across informants suggested the need to gather information both from families and from schools when screening for autism spectrum disorders. C1 Univ Bergen, Ctr Child & Adolescent Mental Hlth, N-5020 Bergen, Norway. Univ Bergen, Dept Biol & Med Psychol, Bergen, Norway. Sahlgrens Univ Hosp, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. St George Hosp, Med Sch, London, England. RP Posserud, MB (reprint author), Univ Bergen, Ctr Child & Adolescent Mental Hlth, Box 7800, N-5020 Bergen, Norway. 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Child Psychol. Psychiatry PD FEB PY 2006 VL 47 IS 2 BP 167 EP 175 DI 10.1111/j.1469-7610.2005.01462.x PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 003GL UT WOS:000234669700008 PM 16423148 ER PT J AU Attwood, T AF Attwood, T TI Autism and Asperger syndrome: preparing for adulthood, 2nd edn SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Book Review CR HOWLIN P, 2004, AUTSIM ASPERGER SYND NR 1 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD FEB PY 2006 VL 47 IS 2 BP 223A EP 224 PG 2 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 003GL UT WOS:000234669700014 ER PT J AU Dyck, MJ Piek, JP Hay, D Smith, L Hallmayer, J AF Dyck, MJ Piek, JP Hay, D Smith, L Hallmayer, J TI Are abilities abnormally interdependent in children with autism? SO JOURNAL OF CLINICAL CHILD AND ADOLESCENT PSYCHOLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; MIND; INDIVIDUALS; DISCRIMINATION; INTELLIGENCE; RECOGNITION; CEREBELLUM; ATTENTION AB We propose that stronger than usual correlations between abilities indicate which cognitive processes are impaired in autism. Study 1 compared partial correlations (controlling age) between intelligence and social cognition in children with autism (n = 18), mental retardation (MR; n = 34), or no psychological disorder (n = 37). Correlations were stronger in the autism group. Study 2 compared correlations between measures of perceptual organization and verbal comprehension, receptive and expressive language, fine and gross motor coordination, and theory of mind, emotion recognition, and emotion understanding abilities in children with autism (n = 30) or MR (n = 24) and in a large representative sample of children (n = 449). 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PD FEB PY 2006 VL 26 IS 1 BP 90 EP 92 DI 10.1097/01.jcp.0000196114.93376.86 PG 3 WC Pharmacology & Pharmacy; Psychiatry SC Pharmacology & Pharmacy; Psychiatry GA 004SY UT WOS:000234773700020 PM 16415715 ER PT J AU Hagerman, RJ AF Hagerman, RJ TI Lessons from fragile X regarding neurobiology, autism, and neurodegeneration SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Review DE fragile X; neurobiology; autism; neurodegeneration ID MENTAL-RETARDATION PROTEIN; TREMOR/ATAXIA-SYNDROME FXTAS; WILLI-LIKE PHENOTYPE; FMR1 GENE; PREMUTATION CARRIERS; YOUNG-CHILDREN; FULL MUTATION; DEVELOPMENTAL DISORDERS; INOSITOL TRISPHOSPHATE; CYTOGENETIC ANALYSES AB The fragile X mental retardation 1 gene (FMR1) mutation causes two disorders: fragile X syndrome (FXS) in those with the full mutation and the fragile X-associated tremor/ataxia syndrome (FXTAS) in some older individuals with the premutation. FXS is caused by a deficiency of the FMR1 protein (FMRP) leading to dysregulation of many genes that create a phenotype with ADHD, anxiety, and autism. FXTAS is caused by the elevation of FMR1-mRNA to levels 2 to 8 times normal in the premutation. This causes an RNA gain of function toxicity leading to brain atrophy, white matter disease, neuronal and astrocytic inclusion formation, and subsequent ataxia, intention tremor, peripheral neuropathy, and cognitive decline. The neurobiology and pathophysiology of FXS and FXTAS are described in detail. C1 Univ Calif Davis Hlth Syst, Dept Pediat, MIND, Sacramento, CA 95817 USA. RP Hagerman, RJ (reprint author), Univ Calif Davis Hlth Syst, Dept Pediat, MIND, 2825 50th St, Sacramento, CA 95817 USA. 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Dev. Behav. Pediatr. PD FEB PY 2006 VL 27 IS 1 BP 63 EP 74 DI 10.1097/00004703-200602000-00012 PG 12 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 016MH UT WOS:000235623800011 PM 16511373 ER PT J AU Pivalizza, PJ AF Pivalizza, PJ TI Autism spectrum disorders in children, pediatric habilitation, vol 12 SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review C1 Texas Childrens Hosp, Baylor Coll Med, Houston, TX 77030 USA. RP Pivalizza, PJ (reprint author), Texas Childrens Hosp, Baylor Coll Med, Houston, TX 77030 USA. CR GUPTA V, 2004, AUTISM SPECTRUM DISO, V12 NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD FEB PY 2006 VL 27 IS 1 BP 75 EP 76 DI 10.1097/00004703-200602000-00015 PG 2 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 016MH UT WOS:000235623800014 ER PT J AU Sally, D Hill, E AF Sally, D Hill, E TI The development of interpersonal strategy: Autism, theory-of-mind, cooperation and fairness SO JOURNAL OF ECONOMIC PSYCHOLOGY LA English DT Article DE autism; bargaining; cooperation; dilemmas; theory-of-mind ID OTHER-REGARDING BEHAVIOR; PRISONERS-DILEMMA; DICTATOR GAMES; ULTIMATUM GAMES; SOCIAL DILEMMAS; CHILDREN; PRESCHOOLERS; METAANALYSIS; PREFERENCES; INFORMATION AB Mentalising is assumed to be involved in decision-making that is necessary to social interaction. We investigated the relationship between mentalising and three types of strategic games Prisoners' Dilemma, Dictator and Ultimatum - in children with and without autistic spectrum disorders. Overall, the results revealed less dramatic differences than expected among the normally developing age groups and the children with autism, suggesting that in these laboratory tasks, mentalising skills are not always necessary. There were, nonetheless, some important findings. Young children were more Cautious about initiating cooperation than their older peers and, in bargaining Situations, they were less generous in their opening unilateral grants and over-solicitous of an empowered receiver. Participants with autism did have a harder time shifting strategy between versions of the Prisoners' Dilemma, and they were much more likely to accept low initial offers in the Ultimatum game and to refuse fair proposals. In addition, participants' measured mentalising abilities explain intentional and strategic behaviour within the Prisoners' dilemma and the avoidance of unsuccessful ultimatum proposals. (c) 2005 Elsevier B.V. All rights reserved. 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PD FEB PY 2006 VL 27 IS 1 BP 73 EP 97 DI 10.1016/j.joep.2005.06.015 PG 25 WC Economics; Psychology, Multidisciplinary SC Business & Economics; Psychology GA 011EJ UT WOS:000235250500006 ER PT J AU Poo-Arguelles, P Arias, A Vilaseca, MA Ribes, A Artuch, R Sans-Fito, A Moreno, A Jakobs, C Salomons, G AF Poo-Arguelles, P Arias, A Vilaseca, MA Ribes, A Artuch, R Sans-Fito, A Moreno, A Jakobs, C Salomons, G TI X-Linked creatine transporter deficiency in two patients with severe mental retardation and autism SO JOURNAL OF INHERITED METABOLIC DISEASE LA English DT Article ID GENE SLC6A8; INBORN ERROR; DEFECT; GUANIDINOACETATE; BRAIN; METABOLISM; MUTATION AB We describe the first two unrelated Spanish patients with creatine transporter deficiency initially identified by brain proton magnetic resonance spectroscopy (MRS). The clinical phenotype was characterized by severe mental retardation, epilepsy, autism, severe speech delay and absence of brain creatine by MRS. Urine creatine/creatinine ratio was increased and creatine uptake in fibroblasts was impaired in both patients. On DNA sequence analysis of the SLC6A8/creatine transporter gene, one hemizygous mutation was found in each patient: one mutation was novel and consisted of a deletion of two nucleotides c.878-879delTC in exon 5, resulting in a frameshift (p.Lys293fsX3), and in the other patient a known deletion of three nucleotides 1222-1224delTTC in exon 8 resulting in p.Phe408del. Creatine treatment for one year failed to improve the neurological symptoms and was associated with a striking increase in body weight in both patients (13 and 16 kg, respectively). C1 Hosp St Joan de Deu, Dept Biochem, Barcelona, Spain. Hosp St Joan de Deu, Dept Neuropediat, Barcelona, Spain. Corp Sanitaria Clin, Inst Bioquim Clin, Barcelona, Spain. CDP Unitat Esplugues, Grp Med, CETIR, Barcelona, Spain. VU Univ Med Ctr, Dept Clin Chem, Metab Unit, Amsterdam, Netherlands. RP Artuch, R (reprint author), Hosp St Joan de Deu, Dept Biochem, Barcelona, Spain. EM rartuch@hsjdbcn.org CR Almeida LS, 2004, MOL GENET METAB, V82, P214, DOI 10.1016/j.ymgme.2004.05.001 Arias A, 2004, MOL GENET METAB, V82, P220, DOI 10.1016/j.ymgme.2004.04.009 Bianchi MC, 2000, ANN NEUROL, V47, P511 Bizzi A, 2002, ANN NEUROL, V52, P227, DOI 10.1002/ana.10246 Cecil KM, 2001, ANN NEUROL, V49, P401, DOI 10.1002/ana.79 DeGrauw TJ, 2002, NEUROPEDIATRICS, V33, P232, DOI 10.1055/s-2002-36743 deGrauw TJ, 2003, MOL CELL BIOCHEM, V244, P45, DOI 10.1023/A:1022487218904 Hahn KA, 2002, AM J HUM GENET, V70, P1349, DOI 10.1086/340092 Kutz MR, 2003, J STRENGTH COND RES, V17, P817 Mancini GMS, 2005, AM J MED GENET A, V132A, P288, DOI 10.1002/ajmg.a.30473 Rosenberg EH, 2004, AM J HUM GENET, V75, P97, DOI 10.1086/422102 Salomons GS, 2001, AM J HUM GENET, V68, P1497, DOI 10.1086/320595 Salomons GS, 2003, J INHERIT METAB DIS, V26, P309, DOI 10.1023/A:1024405821638 Stockler S, 1996, LANCET, V348, P789, DOI 10.1016/S0140-6736(96)04116-5 STOCKLER S, 1994, PEDIATR RES, V36, P409 NR 15 TC 31 Z9 35 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0141-8955 J9 J INHERIT METAB DIS JI J. Inherit. Metab. Dis. PD FEB PY 2006 VL 29 IS 1 BP 220 EP 223 DI 10.1007/s10545-006-0212-4 PG 4 WC Endocrinology & Metabolism; Genetics & Heredity SC Endocrinology & Metabolism; Genetics & Heredity GA 030IC UT WOS:000236627000037 PM 16601898 ER PT J AU Greaves, N Prince, E Evans, DW Charman, T AF Greaves, N Prince, E Evans, DW Charman, T TI Repetitive and ritualistic behaviour in children with Prader-Willi syndrome and children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; Prader-Willi syndrome (PWS); repetitive behaviour; rigid behaviour; ritualistic behaviour ID PERVASIVE DEVELOPMENTAL DISORDERS; MATERNAL UNIPARENTAL DISOMY; OBSESSIVE COMPULSIVE SCALE; MALADAPTIVE BEHAVIOR; DIAGNOSTIC-CRITERIA; MENTAL-RETARDATION; YOUNG-CHILDREN; POPULATION; PEOPLE; ADULTS AB Background Recent research has shown that the range of repetitive behaviour seen in individuals with Prader-Willi syndrome (PWS) extends beyond food-related behaviour. Methods The presence and intensity of repetitive, rigid and routinized behaviour in children with PWS was compared with that seen in children with another neurodevelopmental condition in which repetitive behaviour is common: children with autism. Parents completed the Childhood Routines Inventory (CRI). Results Contrary to our predictions, controlling for developmental level, children with PWS and children with autism showed similar levels of repetitive and ritualistic behaviour overall and on the two CRI factors measuring 'just right' and 'repetitive' behaviour. Indeed, the majority of the sample of parents of children with PWS endorsed most items on the CRI. However there was some specificity at the level of individual items with parents of children with PWS more frequently endorsing an item on 'collecting and storing objects' and parents of children with autism more frequently endorsing 'lining up objects', 'has a strong preference for certain foods' and 'seems aware of detail at home'. Conclusions These findings confirm the range of repetitive behaviours that form part of the behavioural phenotype of PWS, including insistence on sameness and 'just right' behaviours, and uncover a surprising overlap with those seen in children with autism. Clinical management for children with PWS should include advice and education regarding management of repetitive and rigid behaviour. Future research should investigate whether the repetitive behaviours that form part of the behavioural phenotype of both PWS and autism are associated with a common neuropsychological, neurotransmitter or genetic origin. C1 UCL, Behav & Brain Sci Unit, Inst Child Hlth, London WC1N 1EH, England. Islington Primary Care NHS Trust, London, England. Bucknell Univ, Lewisburg, PA 17837 USA. RP Charman, T (reprint author), UCL, Behav & Brain Sci Unit, Inst Child Hlth, 30 Guilford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson GM, 1997, HDB AUTISM PERVASIVE, P325 BENJAMIN E, 1993, J AM ACAD CHILD PSY, V32, P870, DOI 10.1097/00004583-199307000-00025 BOER H, 2004, BEHAV STUDIES PRADER Boer H, 2002, LANCET, V359, P135, DOI 10.1016/S0140-6736(02)07340-3 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Charman T, 2004, AUTISM, V8, P89, DOI 10.1177/1362361304040641 Clarke DJ, 2002, BRIT J PSYCHIAT, V180, P358, DOI 10.1192/bjp.180.4.358 COOK EH, 1992, J AM ACAD CHILD PSY, V31, P739, DOI 10.1097/00004583-199207000-00024 Dimitropoulos A, 2000, MENT RETARD DEV D R, V6, P125, DOI 10.1002/1098-2779(2000)6:2<125::AID-MRDD6>3.0.CO;2-T Dykens EM, 2001, J CHILD PSYCHOL PSYC, V42, P49, DOI 10.1017/S0021963001006540 Dykens EM, 1996, J CHILD PSYCHOL PSYC, V37, P995, DOI 10.1111/j.1469-7610.1996.tb01496.x DYKENS EM, 1992, J AM ACAD CHILD PSY, V31, P1131, DOI 10.1097/00004583-199211000-00023 Dykens EM, 1995, AM J MED GENET, V60, P546, DOI 10.1002/ajmg.1320600612 Dykens EM, 1999, AM J MENT RETARD, V104, P67, DOI 10.1352/0895-8017(1999)104<0067:MBDIPS>2.0.CO;2 Evans DW, 2000, CHILD DEV, V71, P288, DOI 10.1111/1467-8624.00144 Evans DW, 1997, CHILD DEV, V68, P58, DOI 10.2307/1131925 Feurer ID, 1998, J INTELL DISABIL RES, V42, P472, DOI 10.1046/j.1365-2788.1998.4260472.x Fombonne E, 2003, J AUTISM DEV DISORD, V33, P365, DOI 10.1023/A:1025054610557 GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P489, DOI 10.1097/00004583-199105000-00022 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1012 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1006 Gunay-Aygun M, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.5.e92 Holland AJ, 2003, PSYCHOL MED, V33, P141, DOI 10.1017/S0033291702006736 HOLM VA, 1993, PEDIATRICS, V91, P398 Horner RH, 2002, J AUTISM DEV DISORD, V32, P423, DOI 10.1023/A:1020593922901 Jacobsen J, 1998, J MED GENET, V35, P534, DOI 10.1136/jmg.35.7.534 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 MCDOUGLE CJ, 1993, BIOL PSYCHIAT, V33, P547, DOI 10.1016/0006-3223(93)90011-2 MCDOUGLE CJ, 1995, AM J PSYCHIAT, V152, P772 Roof E, 2000, J INTELL DISABIL RES, V44, P25, DOI 10.1046/j.1365-2788.2000.00250.x Shao YJ, 2003, AM J HUM GENET, V72, P539, DOI 10.1086/367846 Sparrow S, 1984, VINELAND ADAPTIVE BE Sparrow SS, 2000, VINELAND ADAPTIVE BE Thomas JA, 2003, AM J MED GENET A, V119A, P111, DOI 10.1002/ajmg.a.10176 Turner M, 1999, J CHILD PSYCHOL PSYC, V40, P839, DOI 10.1017/S0021963099004278 Veltman MWM, 2004, EUR CHILD ADOLES PSY, V13, P42, DOI 10.1007/s00787-004-0354-6 WHITMAN BY, 1987, AM J MED GENET, V28, P897, DOI 10.1002/ajmg.1320280415 Whittington J, 2004, J INTELL DISABIL RES, V48, P172, DOI 10.1111/j.1365-2788.2004.00556.x Whittington J, 2004, PRADER WILLI SYNDROM Whittington J, 2002, J MED GENET, V39, P926, DOI 10.1136/jmg.39.12.926 WINGREN M, 2003, J INTELL DISABIL RES, V47, P428 World Health Organization, 1993, MENT DIS GLOSS GUID NR 44 TC 45 Z9 45 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD FEB PY 2006 VL 50 BP 92 EP 100 DI 10.1111/j.1365-2788.2005.00726.x PN 2 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 999QI UT WOS:000234404600002 PM 16403198 ER PT J AU Kroeger, KA Nelson, WM AF Kroeger, KA Nelson, WM TI A language programme to increase the verbal production of a child dually diagnosed with Down syndrome and autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE applied behaviour analysis design; autism; Down syndrome; dual diagnoses; language programme; spontaneous language ID ADAPTIVE-BEHAVIOR; COMMUNICATION; INTERVENTION; DISORDERS AB Background The incidence of children dually diagnosed with Down syndrome and autism is estimated to be as high as 11%. There is a paucity of research investigating linguistic treatment interventions for such children. This single-subject experiment examined a programme designed to increase the language production and verbal behaviour of a 9-year-old dually diagnosed boy who had been receiving a 15-h/week home-based applied behaviour analysis (ABA) programme. Methods Training principles were derived from previously empirically validated research in discrete trail learning and natural environment teaching, as well as modified incidental teaching procedures. The crux of the language programme involved withholding reinforcement until a spoken request was made. Results Language production noticeably increased for each target area after the introduction of the language programme and was maintained at a 9-month follow-up session. Conclusions A combined treatment approach incorporating direct instruction, natural environment teaching and incidental teaching can be effective in increasing and maintaining responsive and spontaneous speech in a child with Down syndrome diagnosed with autism. Replication studies are needed with such multiple dually diagnosed children to further evaluate the effectiveness and generalizability of this combined language programme. C1 Childrens Hosp, Med Ctr, Kelly O Leary Ctr Autism Spectrum Disorders, Div Dev Disabil, Cincinnati, OH 45229 USA. Xavier Univ, Dept Psychol, Cincinnati, OH 45207 USA. RP Kroeger, KA (reprint author), Childrens Hosp, Med Ctr, Kelly O Leary Ctr Autism Spectrum Disorders, Div Dev Disabil, MLC 4002,3333 Burnet Ave, Cincinnati, OH 45229 USA. 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Intell. Disabil. Res. PD FEB PY 2006 VL 50 BP 101 EP 108 DI 10.1111/j.1365-2788.2005.00734.x PN 2 PG 8 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 999QI UT WOS:000234404600003 PM 16403199 ER PT J AU Seung, HK Ashwell, S Elder, JH Valcante, G AF Seung, HK Ashwell, S Elder, JH Valcante, G TI Verbal communication outcomes in children with autism after in-home father training SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; communication; communication outcome; father training; social reciprocity intervention ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; DIAGNOSTIC INTERVIEW; SPECTRUM DISORDERS; PRESCHOOL-CHILDREN; INTERVENTION; DISABILITIES; PARENTS; PREVALENCE; EFFICACY AB Background This retrospective study examined the efficacy of in-home father training on the communicative outcomes of children with autism. The in-home training consisted of two components: (1) expectant waiting; and (2) imitation with animation. Methods Efficacy of parent training was examined by measuring the ratio of utterances produced by the parents to the utterances produced by the children and the number of verbal imitation by the parents. Outcomes of the children's verbal production were examined by measuring the number of (1) single word utterances; (2) different words produced; and (3) verbal response to questions. Results Following training there was a decrease in the ratio of parent to child utterances and an increase in (1) the use of imitation by the parents; and (2) the number of single words and different words produced by the children. Discussion Results of this study suggested that the parents had learned to wait for their children to communicate verbally during communicative interactions and to interact more efficiently with their children by using verbal imitation. Overall, the results of this study support the efficacy of parent training that focuses on promotion of social reciprocity, and have important implications for clinicians and future research. C1 Univ Florida, Coll Hlth Profess, Dept Commun Disorders, Gainesville, FL 32610 USA. RP Seung, HK (reprint author), Univ Florida, Coll Hlth Profess, Dept Commun Disorders, 1600 SW Archer Rd DG 78,POB 100174, Gainesville, FL 32610 USA. 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PD FEB PY 2006 VL 50 BP 139 EP 150 DI 10.1111/j.1365-2788.2005.00767.x PN 2 PG 12 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 999QI UT WOS:000234404600006 PM 16403202 ER PT J AU Rehnstrom, K Ylisaukko-oja, T Nieminene-von Wendt, T Sarenius, S Kallman, T Kempas, E von Wendt, L Peltonen, L Jarvela, I AF Rehnstrom, K Ylisaukko-oja, T Nieminene-von Wendt, T Sarenius, S Kallman, T Kempas, E von Wendt, L Peltonen, L Jarvela, I TI Independent replication and initial fine mapping of 3p21 24 in Asperger syndrome SO JOURNAL OF MEDICAL GENETICS LA English DT Article ID MULTILOCUS LINKAGE ANALYSIS; MAJOR SUSCEPTIBILITY LOCUS; AUTISM-SPECTRUM DISORDERS; GENOMEWIDE SCREEN; GENETIC DISORDER; GENOMIC SCREEN; DISEQUILIBRIUM; SCHIZOPHRENIA; CHILDREN; LOCATION AB Background: Asperger syndrome is characterised by abnormalities in social interaction as well as repetitive and stereotyped behaviours and interests. The trait is thought to display complex inheritance, but in a subset of families the inheritance resembles the autosomal dominant model. Linkage to 3p14 - 24 has recently been reported in Asperger syndrome in Finnish families with a maximum multipoint NPLall of 3.32 at D3S2432. Methods: We have replicated linkage findings to 3p21 - 24 in 12 new extended Asperger syndrome families. Linkage analyses were performed separately for the 12 new families, and linkage and association analyses were also performed jointly with data from the original genome- wide screen. Results: Best two point and multipoint logarithm of the odds (LOD) scores in analyses of both data sets were obtained at D3S2432 (NPLall = 3.83) with both subsets of families contributing to linkage. Association analysis of the combined data set produced a trend towards association with D3S2432 and D3S1619. Conclusions: This study further validates 3q21 - 24 as a candidate region for Asperger syndrome. C1 Univ Helsinki, Cent Hosp, Genet Mol Lab, Helsinki 00029, Finland. Univ Helsinki, Dept Med Genet, FIN-00014 Helsinki, Finland. Natl Publ Hlth Inst, Dept Mol Med, Biomedicum, Helsinki 00251, Finland. Helsinki Hosp Children & Adolescents, Unit Child Neurol, Helsinki 00029, Finland. Dextra Med Ctr, Helsinki 00350, Finland. RP Jarvela, I (reprint author), Univ Helsinki, Cent Hosp, Genet Mol Lab, Haartmaninkatu 2, Helsinki 00029, Finland. 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Med. Genet. PD FEB PY 2006 VL 43 IS 2 AR e6 DI 10.1136/jmg.2005.033621 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 010IZ UT WOS:000235182900020 PM 16467216 ER PT J AU Rajendran, G Mitchell, P AF Rajendran, G Mitchell, P TI Text chat as a tool for referential questioning in Asperger syndrome SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE Asperger syndrome; referential communication; computer; text chat; telephone ID HIGH-FUNCTIONING AUTISM; COMMUNICATION IMPAIRMENTS; DYSEXECUTIVE SYNDROME; EXECUTIVE FUNCTIONS; ROUTE DIRECTIONS; CHILDREN; INDIVIDUALS; ADULTS; MIND; SYMPTOMATOLOGY AB Purpose: This article reports a study in which referential communication in 11 individuals with Asperger syndrome (AS) and 11 controls was compared between text chat and telephone, using a route-solving task. Method: Participants deduced routes by asking closed questions, and the dependent variables were (a) accuracy in working out the route, (b) number of questions posed (turns taken), and (c) time taken to complete the task. Results: Generally, individuals with AS were equally competent in solving the task in both media but less efficient than the typically developing comparison group. Individuals with AS who had higher measured executive ability adopted a similar approach to the comparison group, asking about landmarks on the map to deduce the route taken. In contrast, AS participants with lower executive ability used an inefficient left/right questioning strategy, which occupied more time, required more conversational turns, and was associated with a higher rate of error. Conclusion: Individuals with AS, who also have problems of executive functioning, may have difficulty communicating with others to use a route-solving task. C1 Univ Edinburgh, Sch Educ, Edinburgh EH8 8AG, Midlothian, Scotland. Univ Nottingham, Nottingham NG7 2RD, England. RP Rajendran, G (reprint author), Univ Edinburgh, Sch Educ, Edinburgh EH8 8AG, Midlothian, Scotland. 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Speech Lang. Hear. Res. PD FEB PY 2006 VL 49 IS 1 BP 102 EP 112 DI 10.1044/1092-4388(2006/008) PG 11 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 030JZ UT WOS:000236632000008 PM 16533076 ER PT J AU Oestreich, AE AF Oestreich, AE TI Danger of multiple magnets beyond the stomach in children SO JOURNAL OF THE NATIONAL MEDICAL ASSOCIATION LA English DT Article; Proceedings Paper CT Annual Scientific Assembly of the Section on Radiology of the National-Medical-Association CY JUL 28, 2005 CL New York, NY SP Natl Med Assoc, Sect Radiol DE small-bowel perforation; foreign bodies; autism ID INGESTION AB Examples from our recent experience, as well as several reports in surgical and pediatric journals, proclaim the danger in children whenever more than one swallowed magnet travels beyond the stomach. They may attract across the thin walls of small bowel, causing ischemia, necrosis and perforation into the peritoneum. The radiologist or other healthcare worker seeing magnets in the abdomen on radiographs should consider the situation an emergency and recommend surgical treatment as soon as possible. C1 CCHMC, Cincinnati, OH 45229 USA. RP Oestreich, AE (reprint author), CCHMC, Radiol 5031,3333 Burnet Ave, Cincinnati, OH 45229 USA. EM oestreich.ae@cchmc.org CR Cauchi JA, 2002, ARCH DIS CHILD, V87, P539, DOI 10.1136/adc.87.6.539 Chung JH, 2003, J PEDIATR SURG, V38, P1548, DOI 10.1016/S0022-3468(03)00514-1 OESTREICH AE, 2004, 2004 YB DIAGNOSTIC R, P155 Oestreich AE, 2004, RADIOLOGY, V233, P615, DOI 10.1148/radiol.2332041446 2004, ZEIT, V53, P33 NR 5 TC 12 Z9 14 PU NATL MED ASSOC PI WASHINGON PA 1012 10TH ST, N W, WASHINGON, DC 20001 USA SN 0027-9684 J9 J NATL MED ASSOC JI J. Natl. Med. Assoc. PD FEB PY 2006 VL 98 IS 2 BP 277 EP 279 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 017AA UT WOS:000235665300021 PM 16708516 ER PT J AU de Ledesma, AMR Desai, AN Bolivar, VJ Symula, DJ Flaherty, L AF de Ledesma, AMR Desai, AN Bolivar, VJ Symula, DJ Flaherty, L TI Two new behavioral QTLs, Emo4 and Reb1, map to mouse Chromosome 1: Congenic strains and candidate gene identification studies SO MAMMALIAN GENOME LA English DT Article ID QUANTITATIVE TRAIT LOCI; LABORATORY MICE; OPEN-FIELD; WD-REPEAT; ANXIETY; LINKAGE; RGS2 AB By use of newly developed subcongenic strains of mice from a parental B6.129-IL10(-/-) knockout/congenic strain, we have narrowed the critical region for a new behavioral QTL, called Emo4, for open-field activity to a segment of Chromosome 1 between Erbb4 (68.4Mb) and B3gnt7 (86.2 Mb). We have also uncovered an additional QTL governing repetitive beam breaks in the open field. This QTL, called Reb1, maps to the interval between Asb1 (91.4 Mb) and NM_172851 (100.0 Mb) and is one of the first QTLs mapped for this type of behavior. Genome-wide microarray expression analyses were then undertaken to help to identify candidate genes that may be the cause of these genetic differences in open-field performance. In this effort, we analyzed global gene expression differences in the amygdalae by use of Affymetrix GeneChips between B6, B6.129-Il10(-/-), and B6.129R4. Several probe sets representing target Chr 1 genes were found that showed significantly differential expression in the subcongenic and congenic strains. Several candidate genes have been identified. One of these regions coincides with an homologous region in humans that has been associated with autism, a disease whose symptoms include repetitive actions. This study illustrates that the use of congenic strains combined with global gene expression analyses can produce a list of viable candidates. 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Genome PD FEB PY 2006 VL 17 IS 2 BP 111 EP 118 DI 10.1007/s00335-005-0107-y PG 8 WC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Genetics & Heredity GA 010SW UT WOS:000235219200003 PM 16465591 ER PT J AU Gauthier, J Joober, R Dube, MP St-Onge, J Bonnel, A Gariepy, D Laurent, S Najafee, R Lacasse, H St-Charles, L Fombonne, E Mottron, L Rouleau, GA AF Gauthier, J Joober, R Dube, MP St-Onge, J Bonnel, A Gariepy, D Laurent, S Najafee, R Lacasse, H St-Charles, L Fombonne, E Mottron, L Rouleau, GA TI Autism spectrum disorders associated with X chromosome markers in French-Canadian males SO MOLECULAR PSYCHIATRY LA English DT Article DE autism spectrum disorders; French-Canadian; association study; X chromosome; haplotype analysis ID PERVASIVE DEVELOPMENTAL DISORDERS; GENOMEWIDE SCREEN; MULTILOCUS HAPLOTYPES; SUSCEPTIBILITY LOCI; MENTAL-RETARDATION; QUEBEC POPULATION; GENES; IDENTIFICATION; HIPPOCAMPUS; MUTATIONS AB It is now well established that genetic factors play an important role in the pathogenesis of autism disorder and converging lines of evidence suggest the implication of the X chromosome. Using a sample of subjects diagnosed with autism spectrum disorders, exclusively composed of males from French-Canadian (FC) origin, we tested markers covering the entire X chromosome using a family-based association study. Our initial analysis revealed the presence of association at two loci: DXS6789 (P=0.026) and DXS8043 (P=0.0101). In a second step, we added support to the association at DXS8043 using additional markers, additional subjects and a haplotype-based analysis (best obtained P-value 0.00001). These results provide support for the existence of a locus on the X chromosome that predisposes the FC to autism spectrum disorders. C1 Notre Dame Hosp, CHUM Res Ctr, Ctr Study Brain Dis, Montreal, PQ H2L 4M1, Canada. McGill Univ, Dept Biol, Montreal, PQ H3A 1B1, Canada. McGill Univ, Dept Psychiat, Montreal, PQ, Canada. Douglas Hosp, Res Ctr, Montreal, PQ, Canada. Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada. Inst Cardiol Montreal, Montreal, PQ, Canada. Ctr Readaptat Deficience Intellectuelle Bas St La, Riviere Du Loup, PQ, Canada. Montreal Childrens Hosp, Montreal, PQ H3H 1P3, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. Rivieres Prairies Hosp, Montreal, PQ, Canada. Univ Montreal, Dept Med, Montreal, PQ H3C 3J7, Canada. RP Rouleau, GA (reprint author), Notre Dame Hosp, CHUM Res Ctr, Ctr Study Brain Dis, JA de Seve Pavillon,Room Y-3633, Montreal, PQ H2L 4M1, Canada. 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Psychiatr. PD FEB PY 2006 VL 11 IS 2 BP 206 EP 213 DI 10.1038/sj.mp.4001756 PG 8 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 007FJ UT WOS:000234953700015 PM 16261168 ER PT J AU Chen, GK Kono, N Geschwind, DH Cantor, RM AF Chen, GK Kono, N Geschwind, DH Cantor, RM TI Quantitative trait locus analysis of nonverbal communication in autism spectrum disorder SO MOLECULAR PSYCHIATRY LA English DT Article DE autism; nonverbal communication; QTL analysis ID OBSESSIVE-COMPULSIVE BEHAVIORS; BIPOLAR AFFECTIVE-DISORDER; LINKAGE ANALYSIS; SUSCEPTIBILITY GENE; GENOMEWIDE SCREEN; BROADER PHENOTYPE; CHROMOSOME 16P13; COMPLEX TRAITS; FAMILIES; SUPPORT AB Autism spectrum disorder (ASD) is a neurodevelopmental syndrome marked by impairments in social interactive functioning and communication skills, and the presence of repetitive and restrictive behaviors. Twin and linkage studies provide evidence that ASD is heritable and genetically complex. Genetic analyses of familial quantitative traits in those with ASD may help to reveal underlying risk genes. We report a quantitative trait locus (QTL) analysis of nonverbal communication (NVC) in 228 families from the autism genetics resource exchange (AGRE) ascertained for at least two siblings with ASD. QTL at 1p13-q12, 4q21-25, 7q35, 8q23-24, and 16p12-13 indicate that genes at these loci may contribute to the variation in NVC among those with ASD. Using the criteria of Lander and Kruglyak, the QTL at 1p13-q12 is 'suggestive', while the other four are 'possible'. To assess whether these QTL are likely to harbor genes contributing specifically to the deficits in NVC, linkage analysis of ASD sibships with the most severe NVC scores was conducted. The sibships were identified by ordered-subset analyses (OSA), and families with the most severe NVC scores displayed lod scores of 3.4 at 8q23-24 and 3.8 at 16p12-13, indicating that these two regions are likely to harbor gene(s) contributing to ASD by predisposing to deficits in NVC. C1 Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, David Geffen Sch Med, Ctr Autism Res, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Program Neurogenet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, David Geffen Sch Med, Ctr Neurobehav Genet, Inst Neuropsychiat, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Pediat, Los Angeles, CA 90095 USA. RP Cantor, RM (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Human Genet, 695 Charles E Young Dr S, Los Angeles, CA 90095 USA. 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Psychiatr. PD FEB PY 2006 VL 11 IS 2 BP 214 EP 220 DI 10.1038/sj.mp.4001753 PG 7 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 007FJ UT WOS:000234953700016 PM 16189504 ER PT J AU Kayser, N Sarfati, Y Besche, C Hardy-Bayle, MC AF Kayser, N Sarfati, Y Besche, C Hardy-Bayle, MC TI Elaboration of a rehabilitation method based on a pathogenetic hypothesis of "theory of mind" impairment in schizophrenia SO NEUROPSYCHOLOGICAL REHABILITATION LA English DT Article ID COMMUNICATION DISORDERS; COGNITIVE REMEDIATION; TEACHING THEORY; RATING-SCALE; PEOPLE; SKILLS; SYMPTOMATOLOGY; AUTISM; DISORGANIZATION; VERBALIZATION AB "Theory of mind" skills have repeatedly been shown to be impaired in schizophrenic patients. The purpose of this paper is to develop a therapeutic intervention targeting schizophrenic patients' abilities to attribute mental states to others. This preliminary study tried to test the hypothesis that this kind of intervention should improve patients' communication abilities; we also wondered if this would have a positive impact on their more general psychopathology. Eight chronic schizophrenic patients were asked to analyse video scenes (showing interactions between two or more persons), with particular attention being paid to the characters' mental states. Their clinical assessments (general clinical symptoms, communication, and the ability to attribute intentions to others, rated before and after two training sessions, over a one-week period) were compared with those of a control group of six chronic schizophrenic patients. The results support our hypothesis of a possible improvement of patients' communication disorders and an improvement of their abilities to attribute intentions to others. The more general psychopathology ratings, however, remained unchanged. Although these results need further development and confirmation, they suggest a possible promising approach for psychosocial rehabilitation therapies based on "theory of mind" skills. C1 Hop Versailles, Psychiat Serv, F-78157 Le Chesnay, France. RP Sarfati, Y (reprint author), Hop Versailles, Psychiat Serv, 177 Rue Versailles, F-78157 Le Chesnay, France. EM ysarfarti@ch-versailles.fr CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDREASEN NC, 1979, ARCH GEN PSYCHIAT, V36, P1315 Bark N, 2003, SCHIZOPHR RES, V63, P229, DOI 10.1016/S0920-9964(02)00374-2 Bedell J, 1998, PSYCHIAT RES, V78, P197, DOI 10.1016/S0165-1781(98)00018-3 BELLACK AS, 1994, J ABNORM PSYCHOL, V103, P371, DOI 10.1037/0021-843X.103.2.371 Binois R., 1947, TEST VOCABULAIRE Bustillo JR, 2001, AM J PSYCHIAT, V158, P163, DOI 10.1176/appi.ajp.158.2.163 Corcoran R, 1997, SCHIZOPHR RES, V24, P319, DOI 10.1016/S0920-9964(96)00117-X CORCORAN R, 1995, SCHIZOPHR RES, V17, P5, DOI 10.1016/0920-9964(95)00024-G CORRIGAN PW, 1993, AM J PSYCHIAT, V150, P589 CRAMER P, 1992, BRIT J PSYCHIAT, V160, P481, DOI 10.1192/bjp.160.4.481 DONAHOE CP, 1990, PSYCHIATRY, V53, P329 Doody GA, 1998, PSYCHOL MED, V28, P397, DOI 10.1017/S003329179700648X Drury VM, 1998, PSYCHOL MED, V28, P1101, DOI 10.1017/S0033291798006850 Frith CD, 1996, PSYCHOL MED, V26, P521 Garson V, 1997, EUR REV APPL PSYCHOL, V47, P23 Greig TC, 2004, J NERV MENT DIS, V192, P12, DOI 10.1097/01.nmd.0000105995.67947.fc Hadwin J, 1997, J AUTISM DEV DISORD, V27, P519, DOI 10.1023/A:1025826009731 Hardy-Bayle MC, 2003, SCHIZOPHRENIA BULL, V29, P459 KAY SR, 1987, SCHIZOPHRENIA BULL, V13, P261 Keefe RSE, 1999, SCHIZOPHRENIA BULL, V25, P201 Krabbendam L, 2003, PSYCHOL MED, V33, P756 LIBERMAN RP, 1992, SCHIZOPHRENIA BULL, V18, P27 Mazza M, 2001, SCHIZOPHR RES, V47, P299, DOI 10.1016/S0920-9964(00)00157-2 Meltzer HY, 1999, SCHIZOPHRENIA BULL, V25, P233 Olivier V, 1997, EUR PSYCHIAT, V12, P352, DOI 10.1016/S0924-9338(97)80005-3 OVERALL JE, 1962, PSYCHOL REP, V10, P799 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 Pickup GJ, 2001, PSYCHOL MED, V31, P207 Pilling S, 2002, PSYCHOL MED, V32, P783, DOI 10.1017/S0033291702005640 Sarfati Y, 1999, PSYCHOL MED, V29, P613, DOI 10.1017/S0033291799008326 Sarfati Y, 2000, PSYCHOPATHOLOGY, V33, P246, DOI 10.1159/000029153 Sarfati Y, 1997, SCHIZOPHR RES, V25, P199, DOI 10.1016/S0920-9964(97)00025-X Sarfati Y, 1999, SCHIZOPHR RES, V37, P183, DOI 10.1016/S0920-9964(98)00154-6 Sarfati Y, 1997, Cogn Neuropsychiatry, V2, P1, DOI 10.1080/135468097396388 Swettenham J, 1996, J CHILD PSYCHOL PSYC, V37, P157, DOI 10.1111/j.1469-7610.1996.tb01387.x NR 36 TC 36 Z9 38 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0960-2011 J9 NEUROPSYCHOL REHABIL JI Neuropsychol. Rehabil. PD FEB PY 2006 VL 16 IS 1 BP 83 EP 95 DI 10.1080/09602010443000236 PG 13 WC Neurosciences; Psychology SC Neurosciences & Neurology; Psychology GA 014NG UT WOS:000235486300004 PM 16509520 ER PT J AU Goodman, MJ Nordin, J AF Goodman, MJ Nordin, J TI Vaccine Adverse Event Reporting System reporting source: A possible source of bias in longitudinal studies SO PEDIATRICS LA English DT Article DE VAERS; adverse event reporting systems ID VAERS; AUTISM; SAFETY AB OBJECTIVE. The US Vaccine Adverse Event Reporting System (VAERS) is a passive reporting system to which anyone can report an event. Publicity related to potential adverse events may change reporting patterns. The objective of this paper is to show how litigation-related reports have influenced the trends in possible adverse event reports to VAERS. METHODS. The VAERS public-use data files were downloaded in July 2004 and translated into identical SAS data sets for analysis. Cases that were related to litigation were identified using a word search algorithm. All cases for the most frequently reported symptoms in litigation (overdose, neuropathy, autism, "mental retardation," arthralgia, and "speech disorder") were reviewed. RESULTS. In recent years, most case reports to VAERS that were related to overdose, neuropathy, and thimerosal were related to litigation. Many cases that were related to autism and mental retardation were as well. CONCLUSIONS. This review shows a previously undisclosed rise in the number of reports to the VAERS related to pending litigation for vaccine injury. The implications of this for understanding longitudinal reporting patterns are discussed. C1 HealthParners Res Fdn, Minneapolis, MN 55440 USA. RP Goodman, MJ (reprint author), HealthParners Res Fdn, 8100 34th Ave S, Minneapolis, MN 55440 USA. EM michael.j.goodman@healthpartners.com CR American Academy of Pediatrics and the Public Health Service, 1999, MMWR-MORBID MORTAL W, V48, P563 BRAUN MM, 2000, PEDIATRICS, V106 CHEN RT, 1994, VACCINE, V12, P542, DOI 10.1016/0264-410X(94)90315-8 Ellenberg SS, 2002, DRUG SAFETY, V25, P145, DOI 10.2165/00002018-200225030-00001 Geier David A, 2003, Pediatr Rehabil, V6, P97, DOI 10.1080/1363849031000139315 Geier DA, 2004, MED SCI MONITOR, V10, pPI33 Geier M.R., 2003, J AM PHYS SURG, V8, P6 Geier MR, 2003, EXP BIOL MED, V228, P660 Niu MT, 2001, VACCINE, V19, P4627, DOI 10.1016/S0264-410X(01)00237-7 Singleton JA, 1999, VACCINE, V17, P2908, DOI 10.1016/S0264-410X(99)00132-2 Varricchio F, 2004, PEDIATR INFECT DIS J, V23, P287, DOI 10.1097/00006454-200404000-00002 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Woo EJ, 2004, AM J PUBLIC HEALTH, V94, P990, DOI 10.2105/AJPH.94.6.990 Zhou Weigong, 2003, MMWR Surveill Summ, V52, P1 NR 14 TC 14 Z9 16 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 FEB PY 2006 VL 117 IS 2 BP 387 EP 390 DI 10.1542/peds.2004-2687 PG 4 WC Pediatrics SC Pediatrics GA 014PC UT WOS:000235491100016 PM 16452357 ER PT J AU Sergeant, MJT Dickins, TE Davies, MNO Griffiths, MD AF Sergeant, MJT Dickins, TE Davies, MNO Griffiths, MD TI Aggression, empathy and sexual orientation in males SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE direct aggression; indirect aggression; empathy; sexual orientation; Internet-based research ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; MEN; WOMEN; QUOTIENT; HOMOSEXUALITY; ADULTS AB Homosexual males are reported to be less physically aggressive than heterosexual males (Ellis, Hoffman, & Burke, 1990; Gladue & Bailey, 1995). Previous aggression studies have not, however, compared all forms of direct aggression, indirect aggression and empathy among these populations. Empathy is a significant factor to consider since it both mitigates the expression of aggression (Kaukiainen et al., 1998) and differs between heterosexual and homosexual males (Salais & Fischer, 1995). This study therefore evaluated levels of direct and indirect aggression and empathy among homosexual (n = 9 1) and heterosexual (n = 9 1) males. Data was collected from an Internet-based sample of the two groups using self-report psychometric measures in order to reduce social desirability effects. Homosexual males reported significantly lower levels of physical aggression and higher levels of empathy but report similar levels of indirect aggression, and other forms of direct aggression, to heterosexual males. (c) 2005 Elsevier Ltd. All rights reserved. C1 Nottingham Trent Univ, Div Psychol, Nottingham NG1 4BU, England. 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PD FEB PY 2006 VL 40 IS 3 BP 475 EP 486 DI 10.1016/j.paid.2005.07.002 PG 12 WC Psychology, Social SC Psychology GA 013DU UT WOS:000235390600008 ER PT J AU Ferris, CF Lu, SF Messenger, T Guillon, CD Heindel, N Miller, M Koppel, G Bruns, FR Simon, NG AF Ferris, CF Lu, SF Messenger, T Guillon, CD Heindel, N Miller, M Koppel, G Bruns, FR Simon, NG TI Orally active vasopressin V1a receptor antagonist, SRX251, selectively blocks aggressive behavior SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE arginine vasopressin; hamster; serenic; impulsive aggression; violence; resident-intruder; flank marking; sexual motivation ID ANDROGENIC STEROID TREATMENT; MALE GOLDEN-HAMSTERS; ANTERIOR HYPOTHALAMUS; OFFENSIVE AGGRESSION; SPECIES-DIFFERENCES; SYRIAN-HAMSTERS; INCREASES; BINDING; MICE; IMMUNOREACTIVITY AB Arginine vasopressin functions as a neurochemical signal in the brain to affect social behavior. There is an expanding literature from animal and human studies showing that vasopressin, through the vasopressin 1A receptor (V1A), can stimulate aggressive behavior. Using a novel monocylic beta lactam platform, a series of orally active vasopressin V1a antagonists was developed with high affinity for the human receptor. SRX251 was chosen from this series of V1a antagonists to screen for effects on serenic activity in a resident-intruder model of offensive aggression. Resident, male Syrian golden hamsters were given oral doses of SRX251 or intraperitoneal Manning compound, a selective V1a receptor antagonist with reduced brain penetrance, at doses of 0.2 mu g, 20 mu g, 2 mg/kg or vehicle. When tested 90-120 min later, SRX251, but not Manning compound, caused a significant dose-dependent reduction in offensive aggression toward intruders as measured by latency to bite and number of bites. The reduction in aggression persisted for over 6 h and was no longer present 12 h post treatment. SRX251 did not alter the amount of time the resident investigated the intruder, olfactory communication, general motor activity, or sexual motivation. These data corroborate previous studies showing a role for vasopressin neurotransmission in aggression and suggest that V1 a receptor antagonists may be used to treat interpersonal violence co-occurring with such illness as ADHD, autism, bipolar disorder, and substance abuse. (c) 2006 Elsevier Inc. All rights reserved. C1 Univ Massachusetts, Dept Psychiat, Sch Med, Ctr Comparat Neuroimaging, Worcester, MA 01605 USA. Lehigh Univ, Dept Biol Sci, Bethlehem, PA 18015 USA. Lehigh Univ, Dept Chem, Bethlehem, PA USA. Univ Notre Dame, Dept Chem & Biochem, South Bend, IN USA. Azevan Pharmaceut Inc, Bethlehem, PA USA. Eli Lilly & Co, Indianapolis, IN 46285 USA. RP Ferris, CF (reprint author), Univ Massachusetts, Dept Psychiat, Sch Med, Ctr Comparat Neuroimaging, 55 Lake Ave N, Worcester, MA 01605 USA. 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Biochem. Behav. PD FEB PY 2006 VL 83 IS 2 BP 169 EP 174 DI 10.1016/j.pbb.2006.01.001 PG 6 WC Behavioral Sciences; Neurosciences; Pharmacology & Pharmacy SC Behavioral Sciences; Neurosciences & Neurology; Pharmacology & Pharmacy GA 037SS UT WOS:000237167900001 PM 16504276 ER PT J AU Miguez, MJP Garcia, CS AF Miguez, MJP Garcia, CS TI Pretend play: an application of on intervention program in autism SO PSICOTHEMA LA Spanish DT Article ID VERBAL-ABILITY; CHILDS THEORY; MIND; KNOWLEDGE; LANGUAGE; BELIEF; UNDERSTAND; SKILLS; STATE AB Methodologically and theoretically based on metarrepresentational deficit hypothesis, we design an intervention to teach the mental state of pretense to an autistic boy. The production and comprehension of symbolic play by means of the use of two specific strategies founded on pictorial analogy of the mental representation and process, was the focus of the learning. The efficiency and efectiveness of the program is reflected in the results that indicated the subject's competence to generate and comprehend the pretense as well as to generalize the acquired knowledge into other areas of mentalistic functioning. We discuss the possibility to develop a metarrepresentational knowledge based on the internalizing of the strategies of conceptual support. C1 Univ Santiago de Compostela, Fac Psicol, Santiago De Compostela 15706, Spain. RP Miguez, MJP (reprint author), Univ Santiago de Compostela, Fac Psicol, Santiago De Compostela 15706, Spain. 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DEL RIO, 4-1 B, 33001 OVIEDO, SPAIN SN 0214-9915 J9 PSICOTHEMA JI Psicothema PD FEB PY 2006 VL 18 IS 1 BP 9 EP 17 PG 9 WC Psychology, Multidisciplinary SC Psychology GA 005TO UT WOS:000234846900002 ER PT J AU Richler, E Reichert, JG Buxbaum, JD McInnes, LA AF Richler, E Reichert, JG Buxbaum, JD McInnes, LA TI Autism and ultraconserved non-coding sequence on chromosome 7q SO PSYCHIATRIC GENETICS LA English DT Article DE autistic disorder; conserved sequence; evolution; genetic variation; molecular; nucleic acid; polymorphism; regulatory sequences; single nucleotide ID SUSCEPTIBILITY GENE; TRANSLOCATION BREAKPOINT; CANDIDATE GENES; HUMAN GENOME; FOXP2; IDENTIFICATION; MUTATIONS; DISORDER; REGION; SPEECH AB Objective Autism has been linked to a broad region on chromosome 7q that contains a large number of genes involved in transcription and development. This region is also enriched for ultraconserved non-coding elements, defined as human-rodent sequences that are 100% aligned over;>= 200 base pairs, which have a high likelihood of being functional. Therefore, as only a few rare coding variants have been detected in the autism candidate genes on 7q examined to date, we decided to screen these ultraconserved elements for possible autism susceptibility alleles. Methods We used denaturing high-performance liquid chromatography, and DNA sequencing, to perform variant detection in a total of 146 cases with autism, 96 from the Autism Genetic Resource Exchange and 50 from the Central Valley of Costa Rica, as well as 124 controls from the Polymorphism Discovery Resource Panel. We screened 10 consecutive ultraconserved elements in, or flanking, the genes DLX5/6, AUTS2 and FOXP2 on chromosome 7q. Results Although we did find several rare variants in autism cases that were not present in controls, we also observed rare variants present in controls and not cases. The most common variant occurred in controls at a frequency of 3.3%. Interestingly, two ultraconserved elements each harbored three independent variants and one ultraconserved element harbored two independent variants, suggesting that ultraconservation is maintained chiefly by a decreased tendency toward fixation, rather than a significantly lower mutation rate. Conclusions Our results show that these sequences are unlikely to harbor major autism susceptibility alleles. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. RP McInnes, LA (reprint author), 1 Gustave L Levy Pl,Box 1229, New York, NY 10029 USA. 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Genet. PD FEB PY 2006 VL 16 IS 1 BP 19 EP 23 DI 10.1097/01.ypg.0000180683.18665.ef PG 5 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 012AO UT WOS:000235310800004 PM 16395125 ER PT J AU Yonan, AL Palmer, AA Gilliam, TC AF Yonan, AL Palmer, AA Gilliam, TC TI Hardy-Weinberg disequilibrium identified genotyping error of the serotonin transporter (SLC6A4) promoter polymorphism SO PSYCHIATRIC GENETICS LA English DT Article DE autism; genotyping; method; error; bias ID ASSOCIATION ANALYSIS; AUTISTIC DISORDER; GENE; LINKAGE; REGION; SCREEN AB We analyzed the putative functional promoter polymorphism of the serotonin transporter (5-HTTLPR) in two large autism spectrum disorder samples and a control sample. A Hardy-Weinberg disequilibrium was detected for 5-HTTLPR in the unaffected founders of both autism spectrum disorder samples and control samples. When we lowered the total magnesium concentration in the polymerase chain reaction below levels reported in previously published studies, we observed a shift in relative allele frequencies and restoration of the Hardy-Weinberg equilibrium. Our data suggest that higher magnesium concentrations caused allele-dependent, non-random genotyping errors. Genotyping data obtained from the 2mM magnesium protocol increased the significance of linkage and gave suggestive (P=0.06) association with autism spectrum disorder, whereas the corrected genotypes of 5-HTTLPR provide no linkage information beyond the results we have previously published and no evidence of association with autism spectrum disorder. We present details regarding appropriate polymerase chain reaction conditions for the accurate genotyping of this polymorphism. C1 Columbia Univ, Dept Genet & Dev, New York, NY USA. Columbia Univ, Genome Ctr, New York, NY USA. Columbia Univ, Dept Psychiat, New York, NY USA. 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Genet. PD FEB PY 2006 VL 16 IS 1 BP 31 EP 34 DI 10.1097/01.ypg.0000174393.79883.05 PG 4 WC Genetics & Heredity; Neurosciences SC Genetics & Heredity; Neurosciences & Neurology GA 012AO UT WOS:000235310800006 PM 16395127 ER PT J AU Eaves, RC Williams, TO AF Eaves, RC Williams, TO TI The reliability and construct validity of ratings for the autism behavior checklist SO PSYCHOLOGY IN THE SCHOOLS LA English DT Article ID COVARIANCE STRUCTURE-ANALYSIS; CONFIRMATORY FACTOR-ANALYSIS; ISSUES; SCALES AB The reliability and construct validity of ratings for the Autism Behavior Checklist were examined with a sample of 198 children diagnosed with autistic disorder and conditions often confused with autism. Alpha coefficients for the five scales of the ABC as well as the Total Score were reported and the factor structure of the ABC was examined through confirmatory factor analysis. 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G., 1995, STRUCTURAL EQUATION, P56 Wothke Werner, 1993, TESTING STRUCTURAL E, P256 NR 31 TC 8 Z9 8 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 FEB PY 2006 VL 43 IS 2 BP 129 EP 142 DI 10.1002/pits.20122 PG 14 WC Psychology, Educational SC Psychology GA 013DA UT WOS:000235388600001 ER PT J AU Wallace, C Leask, J Trevena, LJ AF Wallace, C Leask, J Trevena, LJ TI Effects of a web based decision aid on parental attitudes to MMR vaccination: a before and after study SO BRITISH MEDICAL JOURNAL LA English DT Article ID IMMUNIZE AB Objective To determine whether an evidence based decision aid on the measles, mumps, and rubella (MMR) vaccine changed parents' attitudes towards vaccination. Design Before and after study. Setting Website promoted through search engines and online parenting and health websites. Participants 158 people completing offline questions out of 1277 who accessed the website. Intervention Evidence based decision aid with text and graphical representation of the possible outcomes of measles, mumps, and rubella diseases compared with MMR vaccination. Main outcome measures Attitudes towards MMR vaccination. Results Significantly more participants indicated they were "leaning towards" vaccination after using the decision aid (39% before v 55% after, P<0.001). Compared with those who were undecided or "leaning away from" vaccination after using the decision aid, participants "leaning towards" it were more likely to strongly value its potential to protect their children from the serious side effects of disease (98% v 84%) and other children who could not be vaccinated for medical reasons (68% v 25%). Participants with an unfavourable attitude to vaccination were more likely to be very concerned about die rare side effects of vaccination (78% v 57%), have residual concerns about autism and bowel disease (78% v 27%), and anticipate guilt should their child have an adverse reaction (77% v 50%). Those with a positive attitude to vaccination after using the decision aid were also more likely to feel well informed (83% v 48%). Conclusions A web based decision aid significantly improved parental attitudes to MMR vaccination. Residual concerns about autism and bowel disease and the rare chance of serious complications remained as attitudinal barriers to some parents. C1 Univ Sydney, Childrens Hosp Westmead, Natl Ctr Immunisat Res & Surveillance, Westmead, NSW 2145, Australia. Univ Sydney, Sch Publ Hlth, Westmead, NSW 2145, Australia. RP Leask, J (reprint author), Univ Sydney, Childrens Hosp Westmead, Natl Ctr Immunisat Res & Surveillance, Locked Bag 4001, Westmead, NSW 2145, Australia. 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PD JAN 21 PY 2006 VL 332 IS 7534 BP 146 EP + DI 10.1136/bmj.38678.681840.68 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 006OC UT WOS:000234905800016 PM 16352657 ER PT J AU Gomot, M Bernard, FA Davis, MH Belmonte, MK Ashwin, C Bullmore, ET Baron-Cohen, S AF Gomot, M Bernard, FA Davis, MH Belmonte, MK Ashwin, C Bullmore, ET Baron-Cohen, S TI Change detection in children with autism: An auditory event-related fMRI study SO NEUROIMAGE LA English DT Article DE autism; fMRI; deviance detection; novelty detection; auditory; oddball; anterior cingulate cortex; children ID CEREBRAL-BLOOD-FLOW; MISMATCH NEGATIVITY MMN; POSITRON-EMISSION-TOMOGRAPHY; ANTERIOR CINGULATE CORTEX; BRAIN POTENTIALS; INVOLUNTARY ATTENTION; CORTICAL NETWORK; SENSORY MEMORY; ELECTROPHYSIOLOGICAL EVIDENCE; FUNCTIONAL NEUROANATOMY AB Autism involves impairments in communication and social interaction, as well as high levels of repetitive, stereotypic, and ritualistic behaviours, and extreme resistance to change. This latter dimension, whilst required for a diagnosis, has received less research attention. We hypothesise that this extreme resistance to change in autism is rooted in atypical processing of unexpected stimuli. We tested this using auditory event-related fMRI to determine regional brain activity associated with passive detection of infrequently occurring frequency-deviant and complex novel sounds in a no-task condition. Participants were twelve 10- to 15-year-old children with autism and a group of 12 age- and sex-matched healthy controls. During deviance detection, significant activation common to both groups was located in the superior temporal and inferior frontal gyri. During 'novelty detection', both groups showed activity in the superior temporal gyrus, the temporo-parietal junction, the superior and inferior frontal gyri, and the cingulate gyrus. Children with autism showed reduced activation of the left anterior cingulate cortex during both deviance and novelty detection. During novelty detection, children with autism also showed reduced activation in the bilateral temporo-parietal region and in the right inferior and middle frontal areas. This study confirms previous evidence from ERP studies of atypical brain function related to automatic change detection in autism. Abnormalities involved a cortical network known to have a role in attention switching and attentional resource distribution. These results throw light on the neurophysiological processes underlying autistic 'resistance to change'. (c) 2005 Elsevier Inc. All rights reserved. C1 INSERM, U619, Serv Explorat Fonctionnelles & Pedopsychiat, F-37044 Tours, France. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 1TN, England. CHRU Bretonneau, Tours, France. Univ Cambridge, Brain Mapping Unit, Cambridge CB2 1TN, England. Univ Cambridge, Wolfson Brain Imaging Ctr, Cambridge CB2 1TN, England. Addenbrookes Hosp, Cambridge, England. MRC Cognit & Brain Sci Unit, Cambridge, England. RP Gomot, M (reprint author), INSERM, U619, Serv Explorat Fonctionnelles & Pedopsychiat, 2 Bd Tonnelle, F-37044 Tours, France. 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PM 16115783 ER PT J AU Casiday, R Cresswell, T Wilson, D Panter-Brick, C AF Casiday, R Cresswell, T Wilson, D Panter-Brick, C TI A survey of UK parental attitudes to the MMR vaccine and trust in medical authority SO VACCINE LA English DT Article DE vaccination; trust; risk information ID RUBELLA VACCINE; IMMUNIZATION; MUMPS; RISK; COMMUNICATION; MEASLES AB Contested reports associating the MMR vaccine with autism have resulted in diminished confidence and uptake of the vaccine in the UK. This postal survey of parent's decisions, attitudes and use of information about MMR immunisation was constructed from questions derived from in-depth qualitative work. The setting was a Primary Care Trust in northeast England (N = 996). Both MMR-accepting and refusing parents were supportive of immunisation, yet the high level of concern about the safety of the vaccine expressed even by parents who had immunised their children is worrying in its implications for public confidence and trust in health care. The findings suggest that the ability of practitioners to provide effective professional advice about MMR vaccine could be undermined if a government were to directly promote the vaccine to parents. Practitioners should continue to provide parents with accurate information, while communicating respect for parents' intentions to protect their children's health. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Durham, Dept Anthropol, Durham DH1 3HN, England. Durham & Chester Le St Primary Care Trust, Durham DH1 3YG, England. Cty Durham & Tees Valley Hlth Protect Unit, Durham DH1 5XZ, England. RP Casiday, R (reprint author), Univ Durham, Dept Anthropol, 43 Old Elvet, Durham DH1 3HN, England. 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Among the genes involved in this process are cell adhesion molecules, such as protocadherins and neuroligins, which are essential factors for the identification of the appropriate partner cell and the formation of synapses. In this work, we studied the expression and the genetic variability of two closely related members of the protocadherin family PCDH11X/Y, located on the X and the Y chromosome, respectively. PCDH11Y is one of the rare genes specific to the hominoid lineage, being absent in other primates. Expression analysis indicated that transcripts of the PCDH11X/Y genes are mainly detected in the cortex of the human brain. Mutation screening of 30 individuals with autism identified two PCDH11Y polymorphic amino acid changes, F885V and K980N. These variations are in complete association, appeared during human evolution approximately 40,000 years ago and represent informative polymorphisms to study Y chromosome variability in populations. We studied the frequency of these variants in males with autism spectrum disorders (n = 110), attention deficit hyperactivity disorder (ADHD; n = 61), bipolar disorder (n = 61), obsessive-compulsive disorder (n = 51), or schizophrenia (n = 61) and observed no significant differences when compared to ethnically-matched control populations. or more generally of a frequent specific Y chromosome, in the susceptibility to these neuropsychiatric disorders. (C) 2005 Wiley-Liss, Inc. C1 Inst Pasteur, F-75724 Paris 15, France. Univ Paris 12, Fac Med, INSERM, Creteil, France. Gothenburg Univ, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Hop Robert Debre, Assistance Publ Hop Paris, Serv Psychopathol Enfant & Adolescent, F-75019 Paris, France. Hop Henri Mondor & Albert Chenevier, Assistance Publ Hop Paris, Psychiat Serv, Creteil, France. St George Hosp, Sch Med, London, England. Univ Denis Diderot Paris, Paris, France. RP Bourgeron, T (reprint author), Inst Pasteur, 25 Rue Dr Roux, F-75724 Paris 15, France. EM thomasb@pasteur.fr RI Anckarsater, Henrik/C-2244-2009 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Blanco P, 2000, MAMM GENOME, V11, P906, DOI 10.1007/s003350010177 Blanco-Arias P, 2004, MAMM GENOME, V15, P41, DOI 10.1007/s00335-003-3028-7 Bray NJ, 2002, GENES BRAIN BEHAV, V1, P187, DOI 10.1034/j.1601-183X.2002.10307.x CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1006/abio.1987.9999 Crow TJ, 1999, SCHIZOPHR RES, V39, P219, DOI 10.1016/S0920-9964(99)00076-6 Esumi S, 2005, NAT GENET, V37, P171, DOI 10.1038/ng1500 Giouzeli M, 2004, AM J MED GENET B, V129B, P1, DOI 10.1002/ajmg.b.30036 Hilschmann N, 2001, NATURWISSENSCHAFTEN, V88, P2 Jamain S, 2003, NAT GENET, V34, P27, DOI 10.1038/ng1136 Jamain S, 2002, MOL PSYCHIATR, V7, P217, DOI 10.1038/sj.mp.4000968 Lopes AM, 2004, MOL BIOL EVOL, V21, P2092, DOI 10.1093/molbev/msh218 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 NURNBERGER JI, 1994, ARCH GEN PSYCHIAT, V51, P849 Wells RS, 2001, P NATL ACAD SCI USA, V98, P10244, DOI 10.1073/pnas.171305098 Ellis N, 2002, GENOME RES, V12, P339 NR 16 TC 29 Z9 31 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 JAN 5 PY 2006 VL 141B IS 1 BP 67 EP 70 DI 10.1002/ajmg.b.30229 PG 4 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 001DS UT WOS:000234514400012 PM 16331680 ER PT J AU Allik, H Larsson, JO Smedje, H AF Allik, Hiie Larsson, Jan-Olov Smedje, Hans TI Health-related quality of life in parents of school-age children with Asperger syndrome or high-functioning autism SO HEALTH AND QUALITY OF LIFE OUTCOMES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTAL-HEALTH; BEHAVIOR PROBLEMS; DIFFICULTIES QUESTIONNAIRE; PSYCHOMETRIC PROPERTIES; SPECTRUM DISORDERS; CAREGIVER BURDEN; SWEDISH VERSION; DOWNS-SYNDROME; STRESS AB Background: The estimated prevalence rate of Pervasive Developmental Disorders (PDD) in children is 6 per 1.000. Parenting children who are intellectually impaired and have PDDs is known to be linked to the impaired well-being of the parents themselves. However, there is still little available data on health-related quality of life (HRQL) in parents of children with Asperger Syndrome ( AS) and High-Functioning Autism (HFA), or other PDD diagnoses in children of normal intelligence. The present study aimed to evaluate aspects of HRQL in parents of school-age children with AS/HFA and the correlates with child behaviour characteristics. Methods: The sample consisted of 31 mothers and 30 fathers of 32 children with AS/HFA and 30 mothers and 29 fathers of 32 age and gender matched children with typical development. Parental HRQL was surveyed by the use of the 12 Item Short Form Health Survey (SF-12) which measures physical and mental well-being. The child behaviour characteristics were assessed using the structured questionnaires: The High-Functioning Autism Spectrum Screening Questionnaire (ASSQ) and The Strengths and Difficulties Questionnaire (SDQ). Results: The mothers of children with AS/HFA had lower SF-12 scores than the controls, indicating poorer physical health. The mothers of children with AS/HFA also had lower physical SF-12 scores compared to the fathers. In the AS/HFA group, maternal health was related to behaviour problems such as hyperactivity and conduct problems in the child. Conclusion: Mothers but not fathers of children with AS/HFA reported impaired HRQL, and there was a relationship between maternal well-being and child behaviour characteristics. C1 Karolinska Inst, Dept Woman & Child Hlth, Child & Adolescent Psychiat Unit, Astrid Lindgren Childrens Hosp, SE-17176 Stockholm, Sweden. Uppsala Univ, Dept Neurosci, Child & Adolescent Psychiat Unit, SE-75185 Uppsala, Sweden. RP Allik, H (reprint author), Karolinska Inst, Dept Woman & Child Hlth, Child & Adolescent Psychiat Unit, Astrid Lindgren Childrens Hosp, SE-17176 Stockholm, Sweden. 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Life Outcomes PD JAN 4 PY 2006 VL 4 AR 1 DI 10.1186/1477-7525-4-1 PG 8 WC Health Care Sciences & Services; Health Policy & Services SC Health Care Sciences & Services GA 090QS UT WOS:000240966500001 PM 16393335 ER PT J AU Kuehn, BM AF Kuehn, BM TI Studies probe autism anatomy, genetics SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT News Item AB Advanced imaging technologies and techniques that allow scientists to efficiently comb through the genome for rare gene variants are helping researchers better understand autism and identify its genetic basis. Magnetic resonance imaging has identified abnormalities in regions of the brains of parents whose children are autistic. Abnormalities in the serotonin system may also be involved in autism, as 19 variants of the gene encoding the serotonin transporter have been identified and 4 have mutations in the protein-coding region. This indicates that serotonin may be important in the treatment of autism. 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PD JAN 4 PY 2006 VL 295 IS 1 BP 19 EP 20 DI 10.1001/jama.295.1.19 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 999HT UT WOS:000234381100001 PM 16391205 ER PT J AU Moretti, P Levenson, JM Battaglia, F Atkinson, R Teague, R Antalffy, B Armstrong, D Arancio, O Sweatt, JD Zoghbi, HY AF Moretti, P Levenson, JM Battaglia, F Atkinson, R Teague, R Antalffy, B Armstrong, D Arancio, O Sweatt, JD Zoghbi, HY TI Learning and memory and synaptic plasticity are impaired in a mouse model of Rett syndrome SO JOURNAL OF NEUROSCIENCE LA English DT Article DE Rett syndrome; neurodevelopmental disorders; autism; synaptic plasticity; LTP; LTD; epigenetics; MeCP2; learning and memory ID LONG-TERM DEPRESSION; HIPPOCAMPAL EXCITATORY SYNAPSES; X-CHROMOSOME INACTIVATION; SEVERE MENTAL-RETARDATION; PROTEIN-SYNTHESIS; MECP2 MUTATIONS; AREA CA1; GENE; DUPLICATION; EXPRESSION AB Loss-of-function mutations or abnormal expression of the X-linked gene encoding methyl CpG binding protein 2 (MeCP2) cause a spectrum of postnatal neurodevelopmental disorders including Rett syndrome (RTT), nonsyndromic mental retardation, learning disability, and autism. Mice expressing a truncated allele of Mecp2 (Mecp2(308)) reproduce the motor and social behavior abnormalities of RTT; however, it is not known whether learning deficits are present in these animals. We investigated learning and memory, neuronal morphology, and synaptic function in Mecp2308 mice. Hippocampus-dependent spatial memory, contextual fear memory, and social memory were significantly impaired in Mecp2308 mutant males (Mecp2(308/Y)). The morphology of dendritic arborizations, the biochemical composition of synaptosomes and postsynaptic densities, and brain- derived neurotrophic factor expression were not altered in these mice. However, reduced postsynaptic density cross-sectional length was identified in asymmetric synapses of area CA1 of the hippocampus. In the hippocampus of symptomatic Mecp2(308/Y) mice, Schaffer-collateral synapses exhibited enhanced basal synaptic transmission and decreased paired-pulse facilitation, suggesting that neurotransmitter release was enhanced. Schaffer-collateral long- term potentiation (LTP) was impaired. LTP was also reduced in the motor and sensory regions of the neocortex. Finally, very early symptomatic Mecp2(308/Y) mice had increased basal synaptic transmission and deficits in the induction of long-term depression. These data demonstrate a requirement for MeCP2 in learning and memory and suggest that functional and ultrastructural synaptic dysfunction is an early event in the pathogenesis of RTT. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurosci, Houston, TX 77030 USA. Baylor Coll Med, Dept Pathol, Houston, TX 77030 USA. Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. Baylor Coll Med, Howard Hughes Med Inst, Houston, TX 77030 USA. NYU, Ctr Dementia Res, Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA. RP Zoghbi, HY (reprint author), Baylor Coll Med, Dept Mol & Human Genet, Mail Stop,1 Baylor Plaza, Houston, TX 77030 USA. 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Neurosci. PD JAN 4 PY 2006 VL 26 IS 1 BP 319 EP 327 DI 10.1523/JNEUROSCI.2623-05.2006 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 999LM UT WOS:000234390800038 PM 16399702 ER PT J AU Vlavianou, K AF Vlavianou, K TI Autism in schizophrenia SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Meeting Abstract C1 Agia Olga Hosp, Athens, Greece. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0001-690X J9 ACTA PSYCHIAT SCAND JI Acta Psychiatr. Scand. PY 2006 VL 114 SU 431 BP 67 EP 67 PG 1 WC Psychiatry SC Psychiatry GA 046KX UT WOS:000237811600303 ER PT J AU Maestro, S Muratori, F Cesari, A Pecini, C Apicella, F Stern, D AF Maestro, S Muratori, F Cesari, A Pecini, C Apicella, F Stern, D TI A view to regressive autism through home movies. Is early development really normal? SO ACTA PSYCHIATRICA SCANDINAVICA LA English DT Article DE autism; retrospective study; regression; child development ID 1ST YEAR; LIFE; DISORDERS; CHILDREN AB Objective: To describe early development of children with regressive autism. Method: Home movies from the first 18 months of life of three groups of children with early onset autism (EOA), regressive autism (RA) and typical development (TD) were rated through the Grid for Attention in Infants in three age ranges. Different ANOVA and post hoe t-tests were conducted on frequencies of behaviours. Results: Differently from TD, for both RA and EOA non-social attention is higher than social attention across ages. While EOA is characterized by an early deficit in social attention, in RA social attention increases until the first birthday when its decrease proceeds at the same rate as the increase of non-social attention. 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PD JAN PY 2006 VL 113 IS 1 BP 68 EP 72 DI 10.1111/j.1600-0447.2005.00695.x PG 5 WC Psychiatry SC Psychiatry GA 008IS UT WOS:000235034600012 PM 16390373 ER PT J AU Omura, Y AF Omura, Yoshiaki TI Asbestos as a possible major cause of malignant lung tumors (including Small Cell Carcinoma, Adenocarcinoma & Mesothelioma), brain tumors (i.e. Astrocytoma & Glioblastoma Multiforme), many other malignant tumors, intractable pain including fibromyalgia, & some cardio-vascular pathology: Safe & effective methods of reducing Asbestos from normal & pathological areas SO ACUPUNCTURE & ELECTRO-THERAPEUTICS RESEARCH LA English DT Article DE Asbestos; telomere; Mesothelioma; malignant tumors (Lung, brain, breast, ovary, esophagus & colon); Astrocytoma; Glioblastoma Multiforme; intractable pain; intractable itchiness; cardio-vascular diseases; Fibromyalgia; TXB2; DHEA; acupuncture; Qi Gong (Qigong) or Solar Energy Stored Paper ID O-RING TEST; PLEURAL MESOTHELIOMA; INTERNAL ORGANS; MOLECULAR INFORMATION; MERCURY DEPOSITS; CANCER; EXPOSURE; TRANSMISSION; WELL; LOCALIZATION AB High incidences of Small Cell Carcinoma & Adenocarcinoma of the lung, Astrocytoma & Glioblastoma Multiforme of the brain and Mesothelioma of the lung were found in those who had a high accumulation of Asbestos in the eyes and upper respiratory system (nose, larynx, trachea, etc.). When measured noninvasively using the Bi-Digital O-Ring Test (BDORT), brain tumors had the highest concentration of Asbestos (0.2-2.1 mg BDORT units). Relatively high levels of Asbestos (0.2-0.6 mg BDORT units) were found in: Squamous Cell Carcinoma of the lungs & esophagus, Adenocarcinoma of the larynx & breast, myelogenic leukemia, arteries of these cancers, left ventricle of failing heart, myocardial infarction, some of the narrowed arteries, varicose veins, cataracts, balding heads, hot flashes, Alzheimer's Disease and Autism. A small, round or ellipsoidal area, with diameter of 5 mm or less, was found near the center of every cancer tissue with a higher level of Asbestos (1-3 mg), As, Zn, Cr and Se, thanin the rest of the tumor; this small area may be where the cancer initiated. Among areas of intractable pain with frequent recurrence and gradual worsening, about 0.2-0.5 mg BDORT units (or higher) of Asbestos were found. The author found that in the Astrocytoma and many other cancer patients, the optimal dose of DHEA produced very significant reductions of cancer cell telomere from over 1400 ng in the brain tumors (and over 900 ng in other cancers) to close to or less than 1 yg (=10(-24) g), with circulatory improvement by reduction of TXB2. Unlike the standard, widely used treatment with DHEA 25-50 mg daily, which is an overdose; we only gave one optimal dose (1.5-12.5 mg) and the beneficial effects usually lasted anywhere between 3-6 months, unless inhibiting factors were introduced. In addition, once one optimal dose of DHEA was given, the amount of Asbestos from these tumors decreased very significantly (30-99% reduction) with marked increase in urine Asbestos. One optimal dose of special Cilantro tablet reduced more Asbestos than DHEA or (+) Qi Gong Energy Stored Paper. 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Child Develop. Behav. PY 2006 VL 34 BP 207 EP 246 DI 10.1016/S0065-2407(06)80008-X PG 40 WC Psychology, Developmental SC Psychology GA BFI01 UT WOS:000241946100006 PM 17120806 ER PT J AU Spencer, KC Turkett, A Vaughan, R Koenig, S AF Spencer, KC Turkett, A Vaughan, R Koenig, S TI School-based practice patterns: A survey of occupational therapists in Colorado SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article ID DISABILITIES; STUDENTS; CHILDREN; PARTICIPATION; PERCEPTIONS; TEACHERS AB OBJECTIVE. This purpose of this study was to describe school-based occupational therapy practice for kindergarten through twelfth-grade students in Colorado and to examine occupational therapy practice in light of current education policy and published views of best practice. METHOD. Study data were provided by 105 occupational therapists and occupational therapy assistants who completed a 24-item questionnaire. RESULTS. Occupational therapists carried an average caseload of 43.68 students; most frequently served kindergarten through third-grade students with perceptual or communicative disabilities;, and delivered services most often in pullout treatment areas. Practitioners spent most of their work week providing direct services. Remedial or developmental approaches were used 62% of the time and compensatory and educational approaches 37% of the time. Individualized education program goals addressed by occupational therapists were most frequently developed by the occupational therapist and targeted students' sensory or motor impairments. Workshops on autism and sensorimotor intervention techniques were reported as the primary and preferred forms of professional development. CONCLUSION. The strong majority of reported occupational therapy services contrasted with emerging views of best practice. They were, however, consistent with the Colorado Department of Education's guidelines for "motor specialists" that address occupational therapy, physical therapy, and adaptive physical educators working in schools. Study findings are discussed. C1 Colorado State Univ, Dept Occupat Therapy, Ft Collins, CO 80523 USA. Laradon Community Sch, Denver, CO USA. Maxim Hlth Care & Preferred Home Hlth Care, Ft Collins, CO USA. Marion Cty Sch, Gainesville, FL USA. RP Spencer, KC (reprint author), Colorado State Univ, Dept Occupat Therapy, Ft Collins, CO 80523 USA. 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It has been generally accepted that endocrinological differences are involved in the sexual dimorphism of complex disease; however, specific molecular mechanisms of such hormonal effects have not been elucidated yet. This paper will review evidence that sex hormone action may be mediated via gene-specific epigenetic modifications of DNA and histones. The epigenetic modifications can explain sex effects at DNA sequence polymorphisms and haplotypes identified in gender-stratified genetic linkage and association studies. Hormone-induced DNA methylation and histone modification changes at specific gene regulatory regions may increase or reduce the risk of a disease. The epigenetic interpretation of sexual dimorphism fits well into the epigenetic theory of complex disease, which argues for the primary pathogenic role of inherited and/or acquired epigenetic misregulation rather than DNA sequence variation. 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TI Serum antibrain antibodies in mothers of children with autism: A study with fetal human and rodent tissue 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. PY 2006 VL 60 SU 10 BP S124 EP S124 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 091ON UT WOS:000241038300424 ER PT J AU Mostofsky, SH Dziuk, M Larson, JCG Apostu, A Mahone, EM Denckla, M AF Mostofsky, S. H. Dziuk, M. Larson, J. C. Gidley Apostu, A. Mahone, E. M. Denckla, M. TI Motor deficits contribute to, but do not entirely account for, dyspraxia in autism 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. PY 2006 VL 60 SU 10 BP S123 EP S123 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 091ON UT WOS:000241038300422 ER PT J AU Mostofsky, SH Larson, JCG Bastian, AJ Donchin, O Shadmehr, R AF Mostofsky, S. H. Larson, J. C. Gidley Bastian, A. J. Donchin, O. Shadmehr, R. TI Normal adaptation in children with autism in tasks requiring the cerebellum 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. PY 2006 VL 60 SU 10 BP S124 EP S124 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 091ON UT WOS:000241038300425 ER PT J AU Williams, DL Kana, RK Keller, TA Minshew, NJ Just, AM AF Williams, D. L. Kana, R. K. Keller, T. A. Minshew, N. J. Just, A. M. TI Functional neuroimaging of irony comprehension in children with autism: Role of medial frontal gyrus 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. PY 2006 VL 60 SU 10 BP S141 EP S141 DI 10.1002/ana.11480 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 091ON UT WOS:000241038300486 ER PT J AU Zihlif, M Kaleyias, J Adams, R Legido, A Kothare, S AF Zihlif, M. Kaleyias, J. Adams, R. Legido, A. Kothare, S. TI Insomnia as a presenting manifestation of autism in children 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. PY 2006 VL 60 SU 10 BP S130 EP S130 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 091ON UT WOS:000241038300447 ER PT J AU Ylisaukko-oja, T Alarcon, M Cantor, RM Auranen, M Vanhala, R Kempas, E von Wendt, L Jarvela, I Geschwind, DH Peltonen, L AF Ylisaukko-oja, T Alarcon, M Cantor, RM Auranen, M Vanhala, R Kempas, E von Wendt, L Jarvela, I Geschwind, DH Peltonen, L TI Search for autism loci by combined analysis of Autism Genetic Resource Exchange and Finnish families SO ANNALS OF NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; ASPERGER-SYNDROME; LINKAGE ANALYSIS; GENOMEWIDE SCREEN; SUSCEPTIBILITY LOCUS; CHROMOSOME 3Q25-27; SOCIAL DEFICITS; COMPLEX TRAITS; OXYTOCIN AB Objective: Several genome-wide screens have been performed in autism spectrum disorders resulting in the identification Of numerous putative susceptibility loci. Analyses of pooled primary data should result in an increased sample size and the different study samples have a potential to strengthen the evidence for some earlier identified loci, reveal novel loci, and even to provide information of the general significance of the locus. The objective of this study was to search for potential susceptibility loci for autism, which are supported by two independent samples. Methods. We performed a combined analysis of the primary genome scan data of the Autism Genetic Resource Exchange (AGRE) and Finnish autism samples to reveal susceptibility loci potentially shared by these study samples. Results: In the initial combined data analysis, the best loci (p < 0.05) were observed at Ip12-q25, 3p24-26, 4q21-31, 5p15-q12, 6q14-21, 7q33-36, 8q22-24, 17p12-q21, and 19p13-q13. The combined analysis of Finnish and AGRE families showed the most promising shared locus on 3p24-26 with nonparametric logarithm of odds (NPL) score of 2.20 (p = 0.011). The combined data analysis did not provide increased linkage evidence for the earlier identified loci on 3q25-27 or 17p12-q21. However, the 17pI2-q21 locus remained promising also in the combined sample (NPLall = 2.38, p = 0.0076). Interpretation: Our study of 314 autism families highlights the importance of further analyses on 3p24-26 locus involving comprehensive molecular genetic analyses of oxytocin receptor gene (OXTR), a positional and functional candidate gene for autism. C1 Natl Publ Hlth Inst, Dept Mol Med, Helsinki, Finland. Univ Helsinki, Dept Med Genet, Helsinki, Finland. Univ Calif Los Angeles, Ctr Neurobehav Genet, Los Angeles, CA USA. Univ Calif Los Angeles, Neuropsychiat Res Inst, Los Angeles, CA USA. Univ Calif Los Angeles, Program Neurogenet, Dept Neurol, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Human Genet, David Geffen Sch Med, Los Angeles, CA USA. Univ Helsinki, Cent Hosp, Unit Child Neurol, Hosp Children & Adolescents, Helsinki, Finland. Univ Helsinki, Cent Hosp, Genet Mol Lab, Helsinki, Finland. RP Peltonen, L (reprint author), Biomedicum, Dept Mol Med, Natl Publ Hlth Inst, POB 104, Helsinki 00251, Finland. 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Ting TI Autism from developmental and neuropsychological perspectives SO ANNUAL REVIEW OF CLINICAL PSYCHOLOGY SE Annual Review of Clinical Psychology LA English DT Review; Book Chapter DE developmental disabilities; psychopathology; social/communicative development ID HIGH-FUNCTIONING AUTISM; THIMEROSAL-CONTAINING VACCINES; PERINATAL RISK-FACTORS; CEREBRAL-BLOOD-FLOW; FUSIFORM FACE AREA; SPECTRUM DISORDER; ASPERGER-SYNDROME; JOINT ATTENTION; NEURODEVELOPMENTAL DISORDERS; INFANTILE-AUTISM AB In this review of the research literature on autism, we argue that the application of developmental and neuropsychological perspectives has contributed importantly to the understanding of the core deficits in autism and their underlying neural bases. The three classes of theories postulated to explain the developmental and neuropsychological deficits in autism are considered in terms of the specificity, uniqueness, and universality of these impairments in autism. Because we believe that a primary reason for our lack of understanding of the developmental trajectory in autism stems from our inability to diagnose the syndrome in the first three years of life, research approaches to early identification are discussed, as are longitudinal studies aimed at identifying later-life outcomes and their predictors. In contrast to the progress made in defining the core deficits and arriving at criteria for diagnosis, less progress has been made in identifying the causes of autism and in creating and testing interventions aimed at ameliorating the impairments of autism, possibly because these activities have been less tied to the developmental and neuropsychological models that have enlightened the investigation of core deficits. C1 [Sigman, Marian; Spence, Sarah J.] Univ Calif Los Angeles, Dept Psychiat & Biobehav Sci, David Geffen Sch Med, Los Angeles, CA 90095 USA. [Sigman, Marian] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. 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Rev. Clin. Psychol. PY 2006 VL 2 BP 327 EP 355 DI 10.1146/annurev.clinpsy.2.022305.095210 PG 29 WC Psychology, Clinical; Psychology SC Psychology GA 295QD UT WOS:000255488100012 PM 17716073 ER PT J AU Baron-Cohen, S AF Baron-Cohen, S TI Two new theories of autism: hyper-systemising and assortative mating SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID ASPERGER-SYNDROME; COGNITIVE PHENOTYPE; FUNCTIONING AUTISM; VISUAL-SEARCH; CHILDREN; PSYCHOLOGY; SCIENTISTS; QUOTIENT; PARENTS; ADULTS C1 Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 2AH, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Psychiat, Autism Res Ctr, Douglas House,18B Trumpington Rd, Cambridge CB2 2AH, England. EM sb205@cam.ac.uk CR American Psychiatric Association [APA], 1994, DSM 4 DIAGN STAT MAN Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 BAILEY A, 1995, PSYCHOL MED, V25, P63 Baron-Cohen S., 2001, J DEV LEARNING DISOR, V5, P47 Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S, 1999, NEUROCASE, V5, P475, DOI 10.1080/13554799908402743 BaronCohen S, 1997, J COGNITIVE NEUROSCI, V9, P548, DOI 10.1162/jocn.1997.9.4.548 Baron-Cohen S, 1999, BRIT J PSYCHIAT, V175, P484, DOI 10.1192/bjp.175.5.484 Baron-Cohen S., 1998, AUTISM, V2, P296, DOI 10.1177/1362361398023008 Baron-Cohen S., 2005, ORIGINS SOCIAL MIND BARONCOHEN S, 1986, BRIT J DEV PSYCHOL, V4, P113 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206 BARONCOHEN S, 1994, CAH PSYCHOL COGN, V13, P724 BARONCOHEN S, 2005, NAT AUT SOC C LOND S Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Baron-Cohen S, 1997, AUTISM INT J RES PRA, V1, P153 BARONCOHEN S, IN PRESS NEUROPSYCHO BARONCOHEN S, IN PRESS HUMAN NATUR Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY COURCHESNE E, 2002, MOL PSYCHIATR, V7, P21 Fitzgerald M., 2005, GENESIS ARTISTIC CRE Fitzgerald M, 2000, EUR CHILD ADOLES PSY, V9, P61 Frith CD, 1999, SCIENCE, V286, P1692, DOI 10.1126/science.286.5445.1692 FRITH U, 1970, J EXP CHILD PSYCHOL, V10, P120, DOI 10.1016/0022-0965(70)90049-4 Frith U, 1991, AUTISM ASPERGERS SYN Happe F, 2001, J CHILD PSYCHOL PSYC, V42, P299, DOI 10.1111/1469-7610.00723 HAPPE F, 1996, AUTISM Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 HARRISON MJ, 2005, ARCH DIS CHILD, V90, P16 Heider F, 1944, AM J PSYCHOL, V57, P243, DOI 10.2307/1416950 Hermelin B, 2002, BRIGHT SPLINTERS MIN James I, 2003, J ROY SOC MED, V96, P36, DOI 10.1258/jrsm.96.1.36 Jolliffe T, 1997, J CHILD PSYCHOL PSYC, V38, P527, DOI 10.1111/j.1469-7610.1997.tb01539.x Kanner L, 1943, NERV CHILD, V2, P217 Kimura D., 1999, SEX COGNITION Lawson J, 2004, J AUTISM DEV DISORD, V34, P301, DOI 10.1023/B:JADD.0000029552.42724.1b LESLIE AM, 1992, COGNITION, V43, P225, DOI 10.1016/0010-0277(92)90013-8 MYERS P, 2004, EXACT MIND O'Riordan MA, 2001, J EXP PSYCHOL HUMAN, V27, P719, DOI 10.1037//0096-1523.27.3.719 PERRETT DI, 1985, PROC R SOC SER B-BIO, V223, P293, DOI 10.1098/rspb.1985.0003 Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P777, DOI 10.1017/S0021963098002613 Plaisted K. C., 2001, DEV AUTISM PERSPECTI SHAH A, 1983, J CHILD PSYCHOL PSYC, V24, P613, DOI 10.1111/j.1469-7610.1983.tb00137.x WILLIAMS JO, 2005, ARCH DIS CHILD, V90, P8 NR 46 TC 25 Z9 26 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD JAN PY 2006 VL 91 IS 1 BP 2 EP 5 PG 4 WC Pediatrics SC Pediatrics GA 995MD UT WOS:000234103500002 PM 16371371 ER PT J AU Williams, JG Higgins, JPT Brayne, CEG AF Williams, JG Higgins, JPT Brayne, CEG TI Systematic review of prevalence studies of autism spectrum disorders SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; CHILDHOOD AUTISM; EPIDEMIOLOGIC SURVEY; CHANGING PREVALENCE; PRESCHOOL-CHILDREN; TOTAL POPULATION; JAPAN; FRENCH; DISTRICT AB Aim: To quantitatively examine the influence of study methodology and population characteristics on prevalence estimates of autism spectrum disorders. Methods: Electronic databases and bibliographies were searched and identified papers evaluated against inclusion criteria. Two groups of studies estimated the prevalence of typical autism and all autism spectrum disorders (ASD). The extent of variation among studies and overall prevalence were estimated using meta-analysis. The influence of methodological factors and population characteristics on estimated prevalence was investigated using meta-regression and summarised as odds ratios (OR). Results: Forty studies met inclusion criteria, of which 37 estimated the prevalence of typical autism, and 23 the prevalence of all ASD. A high degree of heterogeneity among studies was observed. The overall random effects estimate of prevalence across studies of typical autism was 7.1 per 10 000 (95% Cl 1.6 to 30.6) and of all ASD was 20.0 per 10000 (95% Cl 4.9 to 82.1). Diagnostic criteria used (ICD-10 or DSM-IV versus other; OR = 3.36, 95% Cl 2.07 to 5.46), age of the children screened (OR = 0.91 per year, 95% Cl 0.83 to 0.99), and study location ( e. g. Japan versus North America; OR = 3.60, 95% Cl 1.73 to 7.46) were all significantly associated with prevalence of typical autism. Diagnostic criteria, age of the sample, and urban or rural location were associated with estimated prevalence of all ASD. Conclusions: Sixty one per cent of the variation in prevalence estimates of typical autism was explained by these models. Diagnostic criteria used, age of children screened, and study location may be acting as proxies for other study characteristics and require further investigation. C1 Univ Cambridge, Dept Publ Hlth & Primary Care, Cambridge CB2 2SR, England. Univ Cambridge, Publ Hlth Genet Unit, Cambridge CB2 2SR, England. Biostat Unit, Cambridge, England. RP Williams, JG (reprint author), Univ Cambridge, Dept Publ Hlth & Primary Care, Forvie Site,Robinson Way, Cambridge CB2 2SR, England. 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Dis. Child. PD JAN PY 2006 VL 91 IS 1 BP 8 EP 15 DI 10.1136/adc.2004.062083 PG 8 WC Pediatrics SC Pediatrics GA 995MD UT WOS:000234103500004 PM 15863467 ER PT J AU Harrison, MJ O'Hare, AE Campbell, H Adamson, A McNeillage, J AF Harrison, MJ O'Hare, AE Campbell, H Adamson, A McNeillage, J TI Prevalence of autistic spectrum disorders in Lothian, Scotland: an estimate using the "capture-recapture" technique SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID CHILDHOOD AUTISM; PRESCHOOL-CHILDREN; RATING-SCALE; CLASSIFICATION; EPIDEMIOLOGY; POPULATION; DIAGNOSIS; UK AB Aims: To determine the prevalence of autistic spectrum disorder in a geographically defined population for children receiving services and compare this to the estimated prevalence based on a two source "capture recapture'' technique previously employed in biological populations to give a "true'' prevalence with full ascertainment. Methods: Information on gender, age, and postcode sector was determined from nine different datasets maintained for children with autistic spectrum disorder and point prevalence was calculated. Data from the diagnostic services and the Special Needs System were entered into the two source "capture-recapture'' calculation. Results: Of a total population of 134 661 under 15 year olds resident in Lothian in southeast Scotland, 443 were known to autism services, with a point prevalence of 32.9 per 10000 (95% Cl 29.8 to 36.0). The estimated prevalence using a capture-recapture method was 44.2 (95% Cl 39.5 to 48.9), which suggests that 74% of affected children were registered with services in some way. The age distribution was similar to that of the background population under the age of 12 years and there was no indication of a rising prevalence. The ratio of boys to girls was 7:1. Conclusions: The prevalence of autistic spectrum disorder in a geographically based population employing two source capture-recapture analysis is comparable to that quoted for the best active ascertainment studies. This technique offers a tool for establishing the prevalence of this condition in health service populations to assist in planning clinical services. C1 Univ Edinburgh, Dept Publ Hlth Sci & Child Life & Hlth Reprod & D, Edinburgh EN9 1TS, Midlothian, Scotland. Royal Hosp Sick Children, Edinburgh EH9 1LF, Midlothian, Scotland. RP O'Hare, AE (reprint author), Univ Edinburgh, Dept Child Life & Hlth, 10 Chalmers Crescent, Edinburgh EN9 1TS, Midlothian, Scotland. 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SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract EM jason.low@vuw.ac.nz NR 0 TC 0 Z9 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2006 VL 58 SU S BP 158 EP 159 PG 2 WC Psychology, Multidisciplinary SC Psychology GA 112QJ UT WOS:000242541400574 ER PT J AU Rinehart, NJ AF Rinehart, NJ. TI Autism and Asperger's disorder: A neurobehavioural approach to clinical definition SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Monash Univ, Clayton, Vic 3168, Australia. EM nicole.rinehart@med.monash.edu.au NR 0 TC 0 Z9 0 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2006 VL 58 SU S BP 186 EP 186 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 112QJ UT WOS:000242541400680 ER PT J AU Williams, J Brayne, C AF Williams, J Brayne, C TI Screening for autism spectrum disorders - What is the evidence? SO AUTISM LA English DT Review DE autistic disorders; childhood development disorders; literature review; pervasive disorders; screening ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; SOCIAL-BEHAVIOR QUESTIONNAIRE; SCHOOL-AGE-CHILDREN; FOLLOW-UP; ASPERGER-SYNDROME; INFANTILE-AUTISM; COMMUNICATION DISORDERS; INTERRATER RELIABILITY; PRESCHOOL-CHILDREN AB This review examines the evidence for screening for autism spectrum disorders in the general population and the information needed to inform screening policy. The UK National Screening Committee criteria are taken as the framework. These criteria cover the condition, the screening test, the treatment and the screening programme as a whole. With respect to the condition, reasons for variation in prevalence estimates for autism spectrum disorders need to be resolved and there are few longitudinal studies to describe the natural history of autism spectrum disorders that include data on children identified at an early age. There is no screening test suitable for use in a population setting that has been fully validated. There is insufficient evidence regarding the effectiveness of interventions. This review supports the current policy position of the National Screening Committee, that on the basis of existing evidence, screening for autism spectrum disorders cannot be recommended. C1 Univ Cambridge, Inst Publ Hlth, Dept Publ Hlth & Primary Care, Cambridge, England. RP Williams, J (reprint author), Univ Cambridge, Inst Publ Hlth, Dept Publ Hlth & Primary Care, Forvie Site,Robinson Way, Cambridge, England. 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In this study, we examined whether attention to emotion cues in others could be enhanced in children with autism, by varying the relevance of children's attention to emotion expressions. Twenty-eight high-functioning boys with autism and 31 boys from a control group were asked to sort photos depicting smiling or frowning faces of adults. As found in earlier studies, in neutral conditions children with autism were less attentive to emotion expressions than children from a control group. This difference disappeared when children were explicitly asked to make a socially relevant decision. These findings suggest that the attention of children with autism to emotion expressions in others is influenced by situational factors. Theoretical implications of these findings are discussed. C1 Free Univ Amsterdam, Dept Psychol, NL-1081 BT Amsterdam, Netherlands. PI Res, Duivendrecht, Netherlands. Leiden Univ, Leiden, Netherlands. Ctr Autisme, Oegstgeest, Netherlands. RP Begeer, S (reprint author), Free Univ Amsterdam, Dept Psychol, Van Boecharststr 1, NL-1081 BT Amsterdam, Netherlands. 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SO AUTISM LA English DT Article DE Asperger's disorder; executive dysfunction; high-functioning autism; number generation ID BASAL GANGLIA; INDIVIDUALS; ADULTS; PERFORMANCE; TASK; ATTENTION; HISTORY; CORTEX; BRAIN; MIND AB The repetitive, stereotyped and obsessive behaviours, which are core diagnostic features of autism, are thought to be underpinned by executive dysfunction. This study examined executive impairment in individuals with autism and Asperger's disorder using a verbal equivalent of an established pseudo-random number generating task. Different patterns of disinhibition emerged in the autism (n = 12) and Asperger's disorder (n = 12) groups. Consistent with previous research, the autism group repeated single numbers (e.g. 2, 2, 2) more frequently than the control group. In contrast to past research suggesting intact executive abilities, this study found that the Asperger's disorder group generated more repetitive number patterns (e.g. 45, 45) than the controls. Executive functioning in children with Asperger's disorder may be particularly vulnerable to a lack of visual cueing and concrete rules. Qualitative differences in executive dysfunction between these groups may implicate differential disruption within the fronto-striatal circuitry. C1 Monash Univ, Sch Psychol Psychiat & Psychol Med, Med Ctr, Dept Psychol Med, Clayton, Vic 3168, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Sch Psychol Psychiat & Psychol Med, Med Ctr, Dept Psychol Med, 246 Clayton Rd, Clayton, Vic 3168, Australia. 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This study collected such data longitudinally in relation to the Son-Rise Program (R), a home-based parent-run intervention for autism. Questionnaires and interview data on family demographics, implementation patterns, and perceived treatment fidelity were gathered three times over the course of a year from families who had attended a Son-Rise (R) initial training course. Although it proved possible to produce a profile of intervention use, findings indicated that the programme is not always implemented as it is typically described in the literature. The study also highlighted methodological challenges likely to be encountered in any future evaluation of this and similar interventions for autism. C1 Univ Edinburgh, Moray Houst Sch Educ, Edinburgh EH8 8AQ, Midlothian, Scotland. RP Williams, KR (reprint author), Univ Edinburgh, Moray Houst Sch Educ, Simon Laurie House,Holyrood Rd, Edinburgh EH8 8AQ, Midlothian, Scotland. 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This review considers the current literature on the prevalence, presentation, treatment and assessment of depression in autism and Asperger syndrome. There are diagnostic difficulties when considering depression in autism and Asperger syndrome, as the characteristics of these disorders, such as social withdrawal and appetite and sleep disturbance, are. also core symptoms of depression. Impaired verbal and non-verbal communication can mask the symptoms of depression. Symptoms associated with autism and Asperger syndrome such as obsessionality and self-injury may be increased during an episode of depression. There is a clear need to develop specific tools both for diagnostic purposes and for measurement of depression in autism and Asperger syndrome in order to help alleviate the distress caused by this treatable illness. C1 Heriot Watt Univ, Edinburgh EH14 4AS, Midlothian, Scotland. Univ Newcastle Upon Tyne, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. 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RP Tregay, J (reprint author), UCL, Inst Child Hlth, London, England. CR BOGDASHINA O, 2004, SENSORY PERCEPTUAL I 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 JAN PY 2006 VL 10 IS 1 BP 117 EP 118 DI 10.1177/1362361306062016 PG 2 WC Psychology, Developmental SC Psychology GA 031KM UT WOS:000236703500009 ER PT J AU Wyver, S AF Wyver, S TI Autism spectrum disorders: Interventions and treatments for children and youth SO AUTISM LA English DT Book Review C1 Macquarie Univ, Inst Early Childhood, Sydney, NSW, Australia. RP Wyver, S (reprint author), Macquarie Univ, Inst Early Childhood, Sydney, NSW, Australia. CR Simpson R. L., 2005, AUTISM SPECTRUM DISO 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 JAN PY 2006 VL 10 IS 1 BP 118 EP 119 DI 10.1177/136236130601000110 PG 2 WC Psychology, Developmental SC Psychology GA 031KM UT WOS:000236703500010 ER PT J AU Davies, W Isles, AR Burgoyne, PS Wilkinson, LS AF Davies, W Isles, AR Burgoyne, PS Wilkinson, LS TI X-linked imprinting: effects on brain and behaviour SO BIOESSAYS LA English DT Review ID TURNER-SYNDROME; GENE-EXPRESSION; SEX-DIFFERENCES; CHROMOSOME INACTIVATION; EPIGENETIC REGULATION; DNA RECOMBINATION; MOUSE-BRAIN; FEMALE; AUTISM; LOCUS AB Imprinted genes are monoallelically expressed in a parent-of-origin-dependent manner and can affect brain and behavioural phenotypes. The X chromosome is enriched for genes affecting neurodevelopment and is donated asymmetrically to male and female progeny. Hence, X-linked imprinted genes could potentially influence sexually dimorphic neurobiology. Consequently, investigations into such loci may provide new insights into the biological basis of behavioural differences between the sexes and into why men and women show different vulnerabilities to certain mental disorders. In this review, we summarise recent advances in our knowledge of X-linked imprinted genes and the brain substrates that they may act upon. In addition, we suggest strategies for identifying novel X-linked imprinted genes and their downstream effects and discuss evolutionary theories regarding the origin and maintenance of X-linked imprinting. C1 Babraham Inst, Lab Cognit & Behav Neurosci, Cambridge CB2 4AT, England. Babraham Inst, Lab Dev Genet & Imprinting, Cambridge CB2 4AT, England. Univ Cambridge, Cambridge, England. Natl Inst Med Res, Div Stem Cell Biol & Dev Genet, London NW7 1AA, England. RP Davies, W (reprint author), Babraham Inst, Lab Cognit & Behav Neurosci, Babraham Res Campus, Cambridge CB2 4AT, England. 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adults with autism SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; MRI; brain; tissue volume; neuroimaging; adolescent/adult ID HEAD CIRCUMFERENCE; SPECTRUM DISORDER; MATTER VOLUME; CHILDREN; MRI; CLASSIFICATION; LIFE; AGE AB Background: A number of studies have found brain enlargement in autism, but there is disagreement as to whether this enlargement is limited to earl); development or continues into adulthood. In this study, cortical gray and white tissue volumes were examined in a sample of adolescents and adults with autism who bad demonstrated total brain enlargement in a previous magnetic resonance imaging (MRI) study. Methods: An automated tissue segmentation program was applied to structural M-RI scans to obtain volumes of gray, white, and cerebrospinal fluid (CSF) tissue on a sample of adolescent and adult males ages 13-29 with autism (h = 23) and controls (n = 15). Regional differences for brain lobes and brain hemispheres were also examined. Results: Significant enlargement in gray matter volume was found for the individuals with autism, with a disproportionate increase in left-sided gray matter volume. Lobe volume enlargements were detected for frontal and temporal, but not parietal or occipital lobes, in the subjects with autism. Age and nonverbal IQ effects on tissue volume were also observed. Conclusions: These findings give evidence for left-lateralized gray tissue enlargement in adolescents and adults with autism, and demonstrate a regional pattern of cortical lobe volumes underlying this effect. C1 Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. Univ N Carolina, Neurodev Disorders Res Ctr, Sch Med, Chapel Hill, NC 27599 USA. Univ N Carolina, Frank Porter Graham Child Dev Ctr, Chapel Hill, NC 27599 USA. RP Hazlett, HC (reprint author), Univ N Carolina, Dept Psychiat, CB 3367, Chapel Hill, NC 27599 USA. 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Psychiatry PD JAN 1 PY 2006 VL 59 IS 1 BP 1 EP 6 DI 10.1016/j.biopsych.2005.06.015 PG 6 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 996TN UT WOS:000234197800001 PM 16139816 ER PT J AU Schmitz, N Rubia, K Daly, E Smith, A Williams, S Murphy, DGM AF Schmitz, N Rubia, K Daly, E Smith, A Williams, S Murphy, DGM TI Neural correlates of executive function in autistic spectrum disorders SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autistic spectrum disorder; executive function; frontal cortex; functional magnetic resonance imaging; fMRI; voxel based morphometry; VBM ID PERVASIVE DEVELOPMENTAL DISORDERS; SPATIAL WORKING-MEMORY; RESPONSE-INHIBITION; ASPERGERS-SYNDROME; CHILDHOOD AUTISM; FRONTAL-CORTEX; IN-VIVO; BRAIN; FMRI; CHILDREN AB Background: Some clinical characteristics of high-functioning individuals with autistic spectrum disorder (ASD) such as repetitive stereotyped behaviors, perseveration, and obsessionality have been related to executive function (EF) deficits, more specifically); to deficits in inhibitory control and set shifting and mediating frontostriatal neural pathways. however, to date, no functional imaging study on ASD has investigated inhibition and cognitive,flexibility and no one has related EF brain activation to brain structure. Methods: We compared brain activation (using functional magnetic resonance imaging) in 10 normal intelligence adults with ASD and 12 healthy control subjects during three different EF tasks: 1) motor-inhibition (GO/NO-GO); 2) cognitive interference-inhibition (spatial STROOP); and 3) set shifting (SWITCH). Using voxel-based morphometry, we investigated if cortical areas which were functionally different in people with ASD were also anatomatically abnormal. Results: Compared with control subjects, ASD individuals showed significantly increased brain activation in 1) left inferior and orbital frontal gyrus (motor inhibition); 2) left insula (interference-inhibition),- and 3) parietal lobes (set shifting). Moreover, in individuals with ASD, increased frontal gray matter density and increased functional activation shared the same anatomical location. 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Psychiatry PD JAN 1 PY 2006 VL 59 IS 1 BP 7 EP 16 DI 10.1016/j.biopsych.2005.06.007 PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 996TN UT WOS:000234197800002 PM 16140278 ER PT J AU Allik, H Larsson, JO Smedje, H AF Allik, Hiie Larsson, Jan-Olov Smedje, Hans TI Insomnia in school-age children with Asperger syndrome or high-functioning autism SO BMC PSYCHIATRY LA English DT Article ID SLEEP PROBLEMS; DIFFICULTIES QUESTIONNAIRE; ACTIGRAPHIC MEASUREMENT; SPECTRUM DISORDERS; PEDIATRIC INSOMNIA; DISTURBED SLEEP; STRENGTHS; PARENTS; ADULTS; PREVALENCE AB Background: Asperger syndrome (AS) and high-functioning autism (HFA) are pervasive developmental disorders (PDD) in individuals of normal intelligence. Childhood AS/HFA is considered to be often associated with disturbed sleep, in particular with difficulties initiating and/or maintaining sleep (insomnia). However, studies about the topic are still scarce. The present study investigated childhood AS/HFA regarding a wide range of parent reported sleep-wake behaviour, with a particular focus on insomnia. Methods: Thirty-two 8-12 yr old children with AS/HFA were compared with 32 age and gender matched typically developing children regarding sleep and associated behavioural characteristics. Several aspects of sleep-wake behaviour including insomnia were surveyed using a structured paediatric sleep questionnaire in which parents reported their children's sleep patterns for the previous six months. Recent sleep patterns were monitored by use of a one-week sleep diary and actigraphy. Behavioural characteristics were surveyed by use of information gleaned from parent and teacher-ratings in the High-Functioning Autism Spectrum Screening Questionnaire, and in the Strengths and Difficulties Questionnaire. Results: Parent-reported difficulties initiating sleep and daytime sleepiness were more common in children with AS/HFA than in controls, and 10/32 children with AS/HFA (31.2%) but none of the controls fulfilled our definition of paediatric insomnia. The parent-reported insomnia corresponded to the findings obtained by actigraphy. Children with insomnia had also more parent-reported autistic and emotional symptoms, and more teacher-reported emotional and hyperactivity symptoms than those children without insomnia. Conclusion: Parental reports indicate that in childhood AS/HFA insomnia is a common and distressing symptom which is frequently associated with coexistent behaviour problems. Identification and treatment of sleep problems need to be a routine part of the treatment plan for children with AS/HFA. C1 [Allik, Hiie; Larsson, Jan-Olov] Karolinska Inst, Dept Woman & Child Hlth, Child & Adolescent Psychiat Unit, Astrid Lindgren Childrens Hosp, SE-17176 Stockholm, Sweden. 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Peterson, Eric Winterrowd, Erin Reite, Martin L. Rogers, Sally J. Tregellas, Jason R. TI Regional gray matter volumetric changes in autism associated with social and repetitive behavior symptoms SO BMC PSYCHIATRY LA English DT Article AB Background: Although differences in brain anatomy in autism have been difficult to replicate using manual tracing methods, automated whole brain analyses have begun to find consistent differences in regions of the brain associated with the social cognitive processes that are often impaired in autism. We attempted to replicate these whole brain studies and to correlate regional volume changes with several autism symptom measures. Methods: We performed MRI scans on 24 individuals diagnosed with DSM-IV autistic disorder and compared those to scans from 23 healthy comparison subjects matched on age. All participants were male. Whole brain, voxel-wise analyses of regional gray matter volume were conducted using voxel-based morphometry (VBM). Results: Controlling for age and total gray matter volume, the volumes of the medial frontal gyri, left pre-central gyrus, right post-central gyrus, right fusiform gyrus, caudate nuclei and the left hippocampus were larger in the autism group relative to controls. Regions exhibiting smaller volumes in the autism group were observed exclusively in the cerebellum. Significant partial correlations were found between the volumes of the caudate nuclei, multiple frontal and temporal regions, the cerebellum and a measure of repetitive behaviors, controlling for total gray matter volume. Social and communication deficits in autism were also associated with caudate, cerebellar, and precuneus volumes, as well as with frontal and temporal lobe regional volumes. Conclusion: Gray matter enlargement was observed in areas that have been functionally identified as important in social-cognitive processes, such as the medial frontal gyri, sensorimotor cortex and middle temporal gyrus. Additionally, we have shown that VBM is sensitive to associations between social and repetitive behaviors and regional brain volumes in autism. C1 [Rojas, Donald C.; Peterson, Eric; Reite, Martin L.; Tregellas, Jason R.] Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80220 USA. [Winterrowd, Erin] Colorado State Univ, Dept Psychol, Ft Collins, CO 80523 USA. [Rogers, Sally J.] Univ Calif Davis, Dept Psychiat, Sacramento, CA 95817 USA. [Rogers, Sally J.] Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. RP Rojas, DC (reprint author), Univ Colorado, Hlth Sci Ctr, Dept Psychiat, 4200 E 9th Ave, Denver, CO 80220 USA. EM don.rojas@uchsc.edu; Eric.Peterson@unco.edu; ewinterr@lamar.colostate.edu; Martin.Reite@uchsc.edu; Sally.Rogers@ucdmc.ucdavis.edu; Jason.Tregellas@uchsc.edu RI Rojas, Don/F-4296-2012 FU Public Health Service [P01 HD35468]; National Alliance for Autism Research FX Funding for this study was provided by Public Health Service grant P01 HD35468 (SJ Rogers) and the National Alliance for Autism Research (DC Rojas). 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SO BRAIN INJURY LA English DT Article; Proceedings Paper CT Conference on Day of Spring CY JUN 04-05, 2004 CL Angers, FRANCE DE traumatic brain injury; theory of mind; executive functions; social cognition ID CLOSED-HEAD INJURY; ASPERGER-SYNDROME; SOCIAL COGNITION; NORMAL ADULTS; AUTISM; IMPAIRMENTS; ATTRIBUTION; SCHIZOPHRENIA; DISTURBANCE; INTENTIONS AB Background: Behavioural changes are often reported after a severe traumatic brain injury (TBI). These changes are usually a greater burden for relatives than physical or cognitive impairments. This study investigated social cognition in TBI patients using two theory of mind (TOM) tasks. Method: The performances of 17 patients with severe TBI and 17 matched controls were compared on two tasks designed to investigate understanding of other people's mental states: The 'Reading the Mind in the Eyes' test (RME) and the 'Character Intention Task' (CIT). TBI patients and controls were also given several executive function tasks. Results: Compared to healthy controls, patients were impaired in most executive tests and in both TOM tasks. No relationship was found between TOM and executive measures. This is consistent with Rowe's position, who suggested an independence between executive functioning and social cognition. These data suggest that TBI patients may have specific social intelligence disturbances. Conclusion: Future work should employ additional tests of TOM and behavioural ratings and recruit more patients in order to complete analysis. C1 Univ & Hosp Ctr Angers, Dept Psychol, Angers, France. RP Le Gall, D (reprint author), Univ Angers, Ctr Hosp, Dept Neurol, Unite Neuropsychol, 4 Rue Larrey, F-49933 Angers 01, France. 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PD DEC 31 PY 2006 VL 20 IS 1 BP 83 EP 91 DI 10.1080/02699050500340655 PG 9 WC Neurosciences; Rehabilitation SC Neurosciences & Neurology; Rehabilitation GA 001AQ UT WOS:000234505000009 PM 16403703 ER PT J AU Mascha, K Boucher, J AF Mascha, K Boucher, J TI Preliminary investigation of a qualitative method of examining siblings' experiences of living with a child with ASD SO BRITISH JOURNAL OF DEVELOPMENTAL DISABILITIES LA English DT Article ID BEHAVIORAL-ADJUSTMENT; EARLY INTERVENTION; AUTISM; SUPPORT; DISABILITIES; BROTHERS; FAMILIES; SISTERS; STRESS; HOME C1 Univ Crete, Dept Psychol, Rethimnon 74100, Crete, Greece. Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. RP Mascha, K (reprint author), Univ Crete, Dept Psychol, Rethimnon 74100, Crete, Greece. 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PD JAN PY 2006 VL 52 IS 102 BP 73 EP 73 PN 1 PG 1 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 020OI UT WOS:000235918800007 ER PT J AU Neumarker, KJ AF Neumarker, KJ TI Classification matters for catatonia and autism in children SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID CHILDHOOD-ONSET SCHIZOPHRENIA; KLEIST-LEONHARD SCHOOL; ANOREXIA-NERVOSA; DISORDERS; SYMPTOMS; ADOLESCENCE; COMORBIDITY; DENSITY; NEURONS AB Despite its chequered history, Kahlbaum's 1874 description of catatonia (tension insanity) and its categorization as a clinical illness is in outline still valid. Kahlbaum also acknowledged the existence of catatonia in children. Corresponding case studies have also been analyzed. The originators and disciples of the Wernicke-Kleist-Leonhard school proved catatonia in early childhood as a discrete entity with specific psychopathology. This does not mean that catatonic symptoms do not occur in other illnesses and in particular in organic psychoses. These are, however, of a totally different nature. Autism, as first described in connection with schizophrenic negativism by Bleuler in 1910, is one of the key symptoms of schizophrenia. As identified by Kanner in 1943, abnormal social interaction and communication, together with retarded development, are the main characteristics of autism in early childhood. Asperger's concept of autistic disorder (1944), although based on psychopathological theory, did not include retardation in development as an aspect. Consequently, autistic behavior can occur in a variety of mental disorders. Research into possible etiological and pathogenetic factors has been undertaken, but no clear link found as yet. C1 Humboldt Univ, Dept Child & Adolescent Psychiat & Psychotherapy, DRK Hosp, Charite, Berlin, Germany. 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CHILD ADOLES PSY, V13, P201, DOI 10.1007/s00787-004-0363-5 ZIEHEN T, 2004, AM J PSYCHIAT, V161, P1369 ZIEHEN T, 1915, GEISTESKRANKHEITEN K 2000, CNS SPECTRUMS, V5, P25 2000, CNS SPECTRUMS, V5, P10 NR 110 TC 3 Z9 3 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7742 J9 INT REV NEUROBIOL PY 2006 VL 72 BP 3 EP 19 DI 10.1016/S0074-7742(05)72001-8 PG 17 WC Neurosciences SC Neurosciences & Neurology GA BEH50 UT WOS:000237270600001 PM 16697288 ER PT J AU Wing, L Shah, A AF Wing, L Shah, A TI A systematic examination of catatonia-like clinical pictures in autism spectrum disorders SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID COMMUNICATION DISORDERS; DIAGNOSTIC INTERVIEW; CHILDHOOD AUTISM; CHILDREN AB Three studies concerning catatonia-like clinical pictures in people with autism spectrum disorders (ASDs) referred to clinics are described. The first investigated the frequencies, in children and adults with autistic disorders, of 28 specific disorders of movement, speech, and behavior similar to those occurring in chronic catatonia spectrum conditions. The second compared the frequency of these items among groups of children with, ASDs, learning disabilities, specific language impairment, and a group with typical development, respectively. The third study examined the pattern of catatonia-like deterioration occurring in a minority of adolescents and adults with ASDs. The studies demonstrated the high frequency of catatonia-like features in people with autistic disorders. There was some tendency for improvement with increasing age, especially for those with IQ 70 or over. The items were also found in children with learning disabilities and specific language disorders but significantly less often. They occurred least often in the children with typical development. Severe catatonia-like deterioration occurred in 17% of those with autistic disorders, who were aged 15 years or over when assessed at a diagnostic center. A history of passivity in social interaction and impairment of expressive language were associated with the deterioration. No clear relationship was found between a history of catatonia-like features, singly or combined, and catatonia-like deterioration. The findings pose questions for future research. C1 Ctr Social & Commun Disorders, Bromley BR2 9HT, Kent, England. Leading Edge Psychol, Purley CR8 2EA, England. RP Wing, L (reprint author), Ctr Social & Commun Disorders, Bromley BR2 9HT, Kent, England. CR American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th Billstedt E, 2005, J AUTISM DEV DISORD, V35, P351, DOI 10.1007/s10803-005-3302-5 Brasic J. R., 2000, GERMAN J PSYCHIAT, V3, P13 Bush G, 1996, ACTA PSYCHIAT SCAND, V93, P129, DOI 10.1111/j.1600-0447.1996.tb09814.x CREAK M, 1964, DEV MED CHILD NEUROL, V4, P530 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 DeSanctis S, 1908, FOLIA NEUROBIOLOGICA, V2, P9 Dhossche D, 1998, J AUTISM DEV DISORD, V28, P329, DOI 10.1023/A:1026064720287 DHOSSCHE DM, 2004, MED SCI MONITOR, V10, P31 Earl CJC, 1934, BRIT J MED PSYCHOL, V14, P230 Fink M, 2003, CATATONIA CLIN GUIDE Ghaziuddin M, 2005, J INTELL DISABIL RES, V49, P102, DOI 10.1111/j.1365-2788.2005.00666.x Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 Hare DJ, 2004, AUTISM, V8, P183, DOI 10.1177/1362361304042722 Haw CM, 1996, MOVEMENT DISORD, V11, P395, DOI 10.1002/mds.870110408 HOWLIN P, 1995, DEV MED CHILD NEUROL, V37, P406 JOSEPH AB, 1992, MOVEMENT DISORDERS N, P335 Kanner L, 1943, NERV CHILD, V2, P217 Leary MR, 1996, MENT RETARD, V34, P39 Leekam SR, 2002, J CHILD PSYCHOL PSYC, V43, P327, DOI 10.1111/1469-7610.00024 Maudsley H., 1867, PHYSL PATHOLOGY MIND, P259, DOI 10.1037/12216-011 Northoff G, 2002, BEHAV BRAIN SCI, V25, P578 REALMUTO GM, 1991, J AUTISM DEV DISORD, V21, P517, DOI 10.1007/BF02206874 Rogers D. M., 1992, MOTOR DISORDER PSYCH Rollin HR, 1946, AM J MENT DEF, V51, P219 WING L, 1987, HDB AUTISM PERVASIVE, P15 Wing L, 2002, J CHILD PSYCHOL PSYC, V43, P307, DOI 10.1111/1469-7610.00023 Wing L, 2000, BRIT J PSYCHIAT, V176, P357, DOI 10.1192/bjp.176.4.357 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 World Health Organization, 1993, ICD10 CLASS MENT BEH Zaw FKM, 1999, DEV MED CHILD NEUROL, V41, P843, DOI 10.1017/S001216229900167X NR 31 TC 13 Z9 13 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7742 J9 INT REV NEUROBIOL PY 2006 VL 72 BP 21 EP 39 DI 10.1016/S0074-7742(05)72002-X PG 19 WC Neurosciences SC Neurosciences & Neurology GA BEH50 UT WOS:000237270600002 PM 16697289 ER PT J AU Ohta, M Kano, Y Nagai, Y AF Ohta, M Kano, Y Nagai, Y TI Catatonia in individuals with autism spectrum disorders in adolescence and early adulthood: A long-term prospective study SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID OBSESSIVE COMPULSIVE SCALE; INFANTILE-AUTISM AB The objective is to cast light on diagnosis and catastasis, course, and comorbidity as concerned with catatonia in patients with autism spectrum disorders (ASDs) with respect to long-term prospective follow-up. Eleven patients (all male) were enrolled. The mean age and the mean follow-up duration were 27.6 years (standard deviation (SD) 5.5) and 18.7 ycars (SD 8.7), respectively. The mean IQ was 27 (SD 16.4). Information was garnered from medical case records; current examination and observation of patients, interview of parents, and questionnaires completed by parents or other caretakers. Informed consent was obtained from the parents. Criteria for catatonia in this study were: (1) abrupt stop of movements and maintenance of immobility or bizarre posture beginning in adolescence and early adult life, (2) such a cataleptic state had continued for at least several minutes and appeared many times a day to the point of interfering with daily activities. We described two typical catatonic cases of ASDs. The average onset age was 19 years (SD 6). In all cases, our diagnostic criteria of catatonia evaluating at worse are fully compatible with those of Diagnostic and Statistical Manual of Mental Disorders, 4th ed. (DSM-IV). In 8 out of 11, the onset of catatonia was clearly preceded by the appearance of slowness in movements accompanying the exacerbation of obsessive-compulsive symptoms. Catatonia was also found to have some connection with Tourette syndrome (3 cases), adjustment disorders (N = 1), and depressive mood disorders (N = 1). In one case, the manifestations of catatonia had to be distinguished from parkinsonism caused by antipsychotics. Catatonia in ASDs seems to be a chronic condition in most cases. However, there were also a few cases in which catatonia repeatedly aggravated over short spans of time. Catatonia in ASDs may be considered an epiphenomenon of ASDs or a manifestation of comorbidity in adolescence or early adulthood. C1 Tokyo Gakugei Univ, Ctr Res & Support Educ Practice, Koganei, Tokyo 184, Japan. Kitasato Univ, Grad Sch Med Sci, Sagamihara, Kanagawa 228, Japan. Univ Shizuoka, Sch Nursing, Shizuoka, Japan. RP Ohta, M (reprint author), Tokyo Gakugei Univ, Ctr Res & Support Educ Practice, Koganei, Tokyo 184, Japan. 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A few working hypotheses involving gaba, purkinje cell survival, neurogenesis, and ECT SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID GAMMA-AMINOBUTYRIC-ACID; RECEPTOR SUBUNIT GENES; CHILDHOOD DISINTEGRATIVE DISORDER; LANDAU-KLEFFNER-SYNDROME; INFANTILE-AUTISM; ELECTROCONVULSIVE-THERAPY; DEPRESSED-PATIENTS; NEONATAL SEIZURES; ANGELMAN-SYNDROME; RAT-BRAIN AB Autistic regression seems to occur in about a quarter of children with autism. Its cause is unknown. Late-onset autistic regression, that is, after 2 years of age, shares some features with catatonic regression. A working hypothesis is developed that some children with autistic regression suffer from early-onset catatonic regression. This hypothesis cannot be answered from current data and is difficult to address in clinical studies in the absence of definite markers of autistic and catatonic regression. Treatment implications are theoretical and involve the potential use of anticatatonic treatments for autistic regression. Focus is on electroconvulsive therapy (ECT)-an established but controversial treatment that is viewed by many, but not all, as the most effective treatment for severe, life-threaten in g catatonic regression. Clinical trials of ECT in early-or late-onset autistic regression in children have not been done yet. The effects of electroconvulsive seizures-the experimental analogue of ECT-should also be tested in gamma-aminobutyric acid-ergic animal models of autistic regression, autism, catatonia, and other neurodevelopmental disorders. Purkinje cell survival and neurogenesis are putative outcome measures in these models. C1 Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, Jackson, MS 39216 USA. Univ Mississippi, Med Ctr, Dept Surg, Jackson, MS 39216 USA. 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0074-7742 J9 INT REV NEUROBIOL PY 2006 VL 72 BP 55 EP 79 DI 10.1016/S0074-7742(05)72004-3 PG 25 WC Neurosciences SC Neurosciences & Neurology GA BEH50 UT WOS:000237270600004 PM 16697291 ER PT J AU Stoppelbein, L Greening, L Kakooza, A AF Stoppelbein, L Greening, L Kakooza, A TI The importance of catatonia and stereotypies in autistic spectrum disorders SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; SELF-INJURIOUS-BEHAVIOR; DIAGNOSTIC-ASSESSMENT; MENTAL-RETARDATION; DASH-II; CHILDREN; SCHIZOPHRENIA; INDIVIDUALS; SYMPTOMS; FEATURES AB Motor disturbances are often observed in individuals with autistic spectrum disorders (ASDs) and recognized as diagnostic features of these disorders. The movement disorders characteristically associated with autism include stereotypics and self-injurious behavior. Yet, Individuals with ASD may also be at the risk for catatonia. Although not as frequent as stereotypics, up to 17% of older adolescents and adults with autistic disorder may have severe catatonic-like symptoms. Catatonia may be a comorbid risk factor of autism that warrants further empirical and clinical evaluations. Clinicians may need to be attentive to more subtle signs of catatonic-like symptoms in individuals diagnosed with ASDs, especially as they enter adolescence and young adulthood. Stress has been implicated as a possible precursor for symptoms; however, its role has not been empirically proven as a potential risk factor. Clinicians might also need to assess for signs of significant declines in motor movements, as this appears to be a useful diagnostic indicator of catatonic-like symptoms. The literature on stereotypies and autism is more extensive than for catatonia and ASDs, probably because of the higher rate of stereotypies with autism. Explanations for the occurrence of stereotypies range from genetic to behavioral contingencies, with evidence for a multifactor explanation. Assessment measures often include items that assess for stereotypies to aid with diagnosing these symptoms in individuals with autism. Treatment for stereotypies is largely behavioral at the present time and requires consistent reinforcement of treatment gains to manage the symptoms successfully. An important area of future research in autism is the relation among different types of motor abnormalities, including stereotypies and catatonia. C1 Univ Mississippi, Med Ctr, Ctr Psychiat Neurosci, Dept Psychiat & Human Behav, Jackson, MS 39216 USA. Makerere Univ, Kampala, Uganda. 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R., 1989, AUTISM NATURE DIAGNO, P208 VOLKMAR FR, 1986, J AM ACAD CHILD PSY, V25, P190, DOI 10.1016/S0002-7138(09)60226-0 Volkmar FR, 1998, AUTISM PERVASIVE DEV, P1 Wing L, 2000, BRIT J PSYCHIAT, V176, P357, DOI 10.1192/bjp.176.4.357 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Zaw FKM, 1999, DEV MED CHILD NEUROL, V41, P843, DOI 10.1017/S001216229900167X NR 66 TC 11 Z9 11 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7742 J9 INT REV NEUROBIOL PY 2006 VL 72 BP 103 EP 118 DI 10.1016/S0074-7742(05)72006-7 PG 16 WC Neurosciences SC Neurosciences & Neurology GA BEH50 UT WOS:000237270600006 PM 16697293 ER PT J AU Dhossche, DM Carroll, BT Carroll, TD AF Dhossche, DM Carroll, BT Carroll, TD TI Is there a common neuronal basis for autism and catatonia? SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID SPECTRUM DISORDERS; CEREBELLAR MUTISM; BIPOLAR DISORDER; EXECUTIVE FUNCTION; CHILDHOOD AUTISM; CHILDREN; SCHIZOPHRENIA; VULNERABILITY; PARENTS; ACQUISITION AB Neuronal bases for autism and catatonia are unknown although integrative theories may soon become feasible as research in autism and catatonia advances. Catatonia and autism may both qualify as neurobiological syndromes in their own light. There is emerging evidence that catatonia may be a common syndrome in autism. Although the relation between autism and catatonia is unclear, coexpression of autism and catatonia may be due to abnormalities in common neuronal circuitries. This possibility constitutes another level of complexity, to neurobiological inquiry, but also provides an opportunity to advance our understanding of both disorders. There is a great potential benefit in studying the relation between catatonia and autism in order to focus future research on subtype-specific causes and treatments. Future research avenues are outlined. C1 Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, Jackson, MS 39216 USA. Univ Cincinnati, Dept Psychiat, Cincinnati, OH USA. VA Med Ctr, Psychiat Serv, Chillicothe, OH 43162 USA. Neurosci Alliance, W Jefferson, OH 43162 USA. RP Dhossche, DM (reprint author), Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, Jackson, MS 39216 USA. 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Localization of the markers has been updated across the studies using the same cytological (Genetic Location Database), physical (National Center for Biological information), and genetic (Marshfield) maps. Eight autosomal chromosomes (1, 2, 3 7, 9, 13, 15, and 17) showed significant linkages with ASD, and one with catatonia (15). Chromosome 15 was further characterized for SZ genome scans (N = 4) since catatonia was observed in SZ patients, for candidate genes for ASD and catatonia, and for the numerous chromosomal rearrangement and abnormalities associated to ASD. From these results, we observed that four potential susceptibility regions for ASD could be observed on chromosome 15 at 15q11-q13 15q14-q21, 15q22-q23, and 15q26, respectively. All the four regions were shared between ASD and SZ, with 15q15-q21 being also shared with catatonia. Strong candidate genes, such as gamma-aminobutyric acid receptor B3, A5, and G3, have shown associations with ASD at 15q11-q13 susceptibility region where the majority of the chromosomal rearrangements are also found. On the other hand, negative association results were observed at 15q14-q21 susceptibility region for catatonia with the genes encoding the zinc transporter SLC30A4, the cholinergic receptor nicotinic alpha poly-peptide 7, and the delta-like 4 Drosophila. Further, fine mapping and candidate gene analyses are needed to highlight potential common genes between ASD and catatonia for this chromosome. C1 Univ Laval, Robert Giffard Res Ctr, Beauport, PQ, Canada. RP Chagnon, YC (reprint author), Univ Laval, Robert Giffard Res Ctr, Beauport, PQ, Canada. 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Literature and Outcome data are reviewed with respect to three categories: language, social skills, and self-management. Generalization of results is somewhat problematic, as all of the interventions discussed consist of relatively small sample sizes and utilize single case design methodology. However, expansion and refinement of research methodology over the last decade, with more researchers replicating previous studies, may make broader application of research findings possible. C1 Univ Mississippi, Med Ctr, Dept Pediat, Div Child Dev & Behav Med, Jackson, MS 39216 USA. Univ Mississippi, Med Ctr, Dept Pediat, Mississippi Child Dev Inst, Jackson, MS 39216 USA. RP Scattone, D (reprint author), Univ Mississippi, Med Ctr, Dept Pediat, Div Child Dev & Behav Med, Jackson, MS 39216 USA. 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L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Thiemann KS, 2001, J APPL BEHAV ANAL, V34, P425, DOI 10.1901/jaba.2001.34-425 Tincani M., 2004, FOCUS AUTISM OTHER D, V19, P152, DOI DOI 10.1177/10883576040190030301 Zanolli K, 1996, J AUTISM DEV DISORD, V26, P407, DOI 10.1007/BF02172826 NR 32 TC 1 Z9 1 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7742 J9 INT REV NEUROBIOL PY 2006 VL 72 BP 181 EP 193 DI 10.1016/S0074-7742(05)72011-0 PG 13 WC Neurosciences SC Neurosciences & Neurology GA BEH50 UT WOS:000237270600011 PM 16697298 ER PT J AU Schieveld, JNM AF Schieveld, JNM TI Case reports with a child psychiatric exploration of catatonia, autism, and delirium SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID ELECTROCONVULSIVE-THERAPY; SPECTRUM DISORDERS; ADOLESCENTS; CLOZAPINE AB This chapter starts with some remarks on the conceptual history of catatonia, which begins with Kahlbaum and continues Kraeplin, Bleuler, and Leonhard. The Diagnostic and Statistical Manual, 4th ed.,Text Revision, criteria for catatonia and the multicausal origin of the disorder are discussed. So, not only schizophrenia and mood disorders associated with catatonia, which is the primary form, are introduced but also an extensive list of somatic disorders-resulting in secondary catatonia-along with the work of Gelenberg and Wing. Next, two very difficult cases, of boys with autism, catatonia, and one of them with mental retardation as well, are presented. Major textbooks, PubMed, and Medline were used for a select literature search. The results show the main and really relevant but scarce data concerning primary and secondary catatonia. In the discussion the topics are this dearth in knowledge, the concept of catatonia and its similarities with delirium, and the relation catatonia-autism, and where to find the data. The conclusions summarize the main points and end with a gentle reminder, or is it an appeal? C1 State Univ Limburg Hosp, Dept Psychiat & Neuropsychol, NL-6201 BX Maastricht, Netherlands. RP Schieveld, JNM (reprint author), State Univ Limburg Hosp, Dept Psychiat & Neuropsychol, NL-6201 BX Maastricht, Netherlands. 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S., 2005, KAPLAN SADOCKS COMPR, V8th Schieveld JNM, 2005, J AM ACAD CHILD PSY, V44, P392, DOI 10.1097/01.chi.0000153231.64968.1a SCHMIDT AMG, 1971, PLUK PETTEFLET, P145 Slooter AJC, 2005, PEDIATR NEUROL, V32, P190, DOI 10.1016/j.pediatrneurol.2004.10.004 Taylor MA, 2003, AM J PSYCHIAT, V160, P1233, DOI 10.1176/appi.ajp.160.7.1233 UNGVARI GS, 1994, ACTA PSYCHIAT SCAND, V89, P285, DOI 10.1111/j.1600-0447.1994.tb01515.x VAN DER HEIJDEN F, 2005, PSYCHOPATHOLOGY, V15, P3 VANDERHEIJDEN F, 2004, THESIS U UTRECHT NET WILLIAMS DT, 2002, CHILD ADOLESCENT PSY Wing L, 2000, BRIT J PSYCHIAT, V177, P180 Wing L., 1987, HDB AUTISM PERVASIVE, P3 Wing L, 2000, BRIT J PSYCHIAT, V176, P357, DOI 10.1192/bjp.176.4.357 WISE MG, 1987, TXB NEUROPSYCHIATRY Zaw FKM, 1999, DEV MED CHILD NEUROL, V41, P843, DOI 10.1017/S001216229900167X Zuddas A, 1996, AM J PSYCHIAT, V153, P738 NR 42 TC 6 Z9 6 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7742 J9 INT REV NEUROBIOL PY 2006 VL 72 BP 195 EP 206 DI 10.1016/S0074-7742(05)72012-2 PG 12 WC Neurosciences SC Neurosciences & Neurology GA BEH50 UT WOS:000237270600012 PM 16697299 ER PT J AU Zaw, FKM AF Zaw, FKM TI ECT and the youth: Catatonia in context SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID NEUROLEPTIC MALIGNANT SYNDROME; ELECTROCONVULSIVE-THERAPY; UNITED-STATES; ADOLESCENTS; DEPRESSION; PHARMACOTHERAPY; ATTITUDES; CHILDREN; AUTISM; EXPERIENCES AB Electroconvulsive therapy (ECT) has been in psychiatric practice for well over half a century, but it continues to incite controversy. However, it is regarded amongst psychiatrists as a safe and effective treatment and at times even a lifesaver. It offers a fairly swift but a time-limited response, opening up opportunities for initiation of more longer lasting treatments. The use of ECT in the youth is limited, and as such good studies are few and far between. The recent Practice Parameters by the American Academy of Child and Adolescent Psychiatry, specifically addressing ECT in adolescents, is indeed a welcome addition. Electrocovulsive therapy is as effective in the youth as it is in the adults, and the indications and contraindication are the same. The administration of ECT follows the same general principles in all age groups. One particular indication is of the use in catatonia, a motor syndrome that could occur with affective disorders, schizophrenia or medical conditions, in which it is considered to be extremely effective. The association between catatonia and autism and spectrum disorders has been noted, and in this situation, ECT is considered by some to be effective. Ethical considerations and that of capacity and informed consent are of paramount importance as are the human rights. Working in partnership with the parents/carers all the way is a must. The lack of information leaflets on ECT especially designed for young patients and their parents has to be rectified soon. Registers based on geographical health regions for those below the age of 18 will assist tremendously in epidemiological studies as well as pave the way toward more evidence-based studies that are essential. C1 Univ Birmingham, Dept Psychiat, Div Neurosci, Birmingham B15 2TT, W Midlands, England. RP Zaw, FKM (reprint author), Huntercombe Stafford Hosp, Ivetsey Bank, Wheaton Aston ST19 9QT, Staffs, England. 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Assessing the elements of the Syndrome for the presence of depression, psychosis, mania, or catatonia, offers opportunities for systematic intervention. Since almost all descriptions of autism highlight the presence of motor symptoms that characterize catatonia, an assessment for this eminently treatable syndrome is recommended for all patients considered to be autistic. A minimum examination includes a catatonia rating scale and for those patients with defined catatonia, a lorazepam test. For those whose catatonia responds to lorazepam, high dose lorazepam therapy is recommended. If this falls, electroconvulsive therapy is recommended. The assessment and treatment of catatonia offers positive medical therapy for the victims of autism and their families. C1 SUNY Stony Brook, Sch Med, Stony Brook, NY 11794 USA. Rosalind Franklin Univ Med & Sci, N Chicago, IL 60064 USA. Univ Michigan, Sch Med, Ann Arbor, MI 48109 USA. RP Fink, M (reprint author), SUNY Stony Brook, Sch Med, Stony Brook, NY 11794 USA. 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Clinical observation suggests that an important factor is ongoing stress. The evidence for this from research and clinical observation is considered. The lack of evidence concerning the most appropriate medical treatments is discussed. A psychological approach designed for individual needs by relevant professionals and applied by parents and/or caregivers is described. This can be helpful whether or not medical treatments are used. It involves detailed holistic assessment of the individual and their circumstances to highlight possible precipitating stress factors in view of their underlying autism and cognitive/psychological functioning. The overall aim of this approach is to restructure the individual's lifestyle, environment and resolve cognitive/psychological factors to reduce the stress. An eclectic approach is used to find individual strategies in order to provide external goals and stimulation to increase motivation and keep the person engaged and active in meaningful and enjoyable pursuits. The approach describes ways of using verbal and physical prompts as external stimuli to overcome the movement difficulties and emphasizes maintaining a predictable structure and routine for each day. The importance of educating caregivers and service providers to understand the catatonia-like behavior is emphasized. Advice is given on management of specific problems such as incontinence, freezing in postures, eating problems, and episodes of excitement. C1 Leading Edge Psychol, Purley CR8 2EA, England. Ctr Social & Commun Disorders, Bromley BR2 9HT, Kent, England. RP Shah, A (reprint author), Leading Edge Psychol, Purley CR8 2EA, England. CR Brasic J. 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M., 1992, MOTOR DISORDER PSYCH SHAH A, 1985, J AUTISM DEV DISORD, V15, P195, DOI 10.1007/BF01531605 Ungvari GS, 1999, PSYCHOPHARMACOLOGY, V142, P393, DOI 10.1007/s002130050904 VENABLES PH, 1962, ARCH GEN PSYCHIAT, V7, P114 Wechsler D., 1992, WECHSLER INTELLIGENC Wechsler D, 1997, WECHSLER ADULT INTEL, V3rd Williams D, 2003, EXPOSURE ANXIETY INV Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 Wing L, 2002, J CHILD PSYCHOL PSYC, V43, P307, DOI 10.1111/1469-7610.00023 Wing L, 2000, BRIT J PSYCHIAT, V176, P357, DOI 10.1192/bjp.176.4.357 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Zaw FKM, 1999, DEV MED CHILD NEUROL, V41, P843, DOI 10.1017/S001216229900167X NR 30 TC 8 Z9 8 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7742 J9 INT REV NEUROBIOL PY 2006 VL 72 BP 245 EP 264 DI 10.1016/S0074-7742(05)72015-8 PG 20 WC Neurosciences SC Neurosciences & Neurology GA BEH50 UT WOS:000237270600015 PM 16697302 ER PT J AU Dhossche, DM Shah, A Wing, L AF Dhossche, DM Shah, A Wing, L TI Blueprints for the assessment, treatment, and future study of catatonia in autism spectrum disorders SO CATATONIA IN AUTISM SPECTRUM DISORDERS SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review AB The blueprints for the assessment, treatment, and future study of catatonia in autism spectrum disorders (ASDs), which are submitted in this chapter aim to increase early recognition and treatment of catatonia in ASDs, show the urgency of controlled treatment trials, and increase collaborative and interdisciplinary research into the co-occurrence of these two enigmatic disorders. Catatonia should be assessed in any patient with ASDs when there is an obvious and marked deterioration in movement, pattern of activities, self-care, and practical skills, compared with previous levels, through a comprehensive diagnostic evaluation of medical and psychiatric symptoms. A formal diagnosis should be ascertained using ASD specific criteria for catatonia that takes into account baseline symptoms like muteness, echophenomena, stereotypy, negativism, or other psychomotor abnormalities. Any underlying medical and neurological conditions should be treated, and culprit medications or other substances that may cause catatonia should be eliminated. Separate treatment blueprints are presented for mild, moderate, and severe catatonia, featuring combinations of a psychological approach developed by Shah and Wing and medical treatments that have shown efficacy in catatonia: lorazepam challenge, lorazepam trial, lorazepam continuation, and bilateral electroconvulsive therapy (ECT). These treatment modalities in themselves are well established. Side effects and complications are known and manageable. Legal, ethical, and practice guidelines governing all treatment aspects should be followed. The treatment blueprints should be viewed as best estimates pending future controlled studies. The blueprint for the future study of catatonia in ASDs describes promising clinical and preclinical research avenues. Longitudinal studies need to assess the possible effect of early recognition and adequate treatment of catatonia in ASDs in order to avoid the impairment associated with chronicity. Effects of current and new anticatatonic treatments should be examined in experimental models of autism and catatonia. Finally, the role of gamma-aminobutyric acid (GABA) dysfunction in autism, catatonia, and abnormal stress responses in these disorders should be further assessed. C1 Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, Jackson, MS 39216 USA. 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Mack, Andreas F. Ma, Zhan-Lu Hollmann, Michael Lang, Florian Seebohm, Guiscard TI Functional significance of the kainate receptor GluR6(M836I) mutation that is linked to autism SO CELLULAR PHYSIOLOGY AND BIOCHEMISTRY LA English DT Article DE kainate receptor; glutamate receptor; GLUR(6); Rab11; Rab5; recycling; expression ID GLUR6-DEFICIENT MICE; RAB PROTEINS; ION CHANNELS; WILD-TYPE; SUBUNITS; GLYCOSPHINGOLIPIDS; TRAFFICKING; ASSOCIATION; CONDUCTANCE; HIPPOCAMPUS AB Previous studies revealed a linkage of the kainate receptor GluR6 with autism, a pervasive developmental disorder. Mutational screening in autistic patients disclosed the amino acid exchange M836I in a highly conserved domain of the cytoplasmic C-terminal region of GluR6. Here, we show that this mutation leads to GluR6 gain-of-function. By using the two-electrode voltage clamp technique we observed a significant increase of current amplitudes of mutant GluR6 compared to wild type GluR6. Western blotting of oocytes injected with mutant or wild type GluR6 cRNA and transfection of EGFP-tagged GluR6 receptors into COS-7 cells revealed an enhanced plasma membrane expression of GluR6(M836I) compared to wild type GluR6. Membrane expression of GluR6(M836I) but not of wild type GluR6 seems to be regulated by Rab11 as indicated by our finding that GluR6(M836I) but not wild type GluR6 showed increased current amplitudes and protein expression when coexpressed with Rab11. Furthermore, injection of GTP plus Rab11A protein into oocytes increased current amplitudes in GluR6(M836I) but not in wild type GluR6. By contrast, Rab5 downregulated the currents in oocytes expressing wild type GluR6 but had only little, statistically not significant effects on currents in oocytes expressing GluR6(M836I). Our data on altered functional properties of GluR6(M836I) provide a functional basis for the postulated linkage of GluR6 to autism. Furthermore, we identified new mechanisms determining the plasma membrane abundance of wild type GluR6 and GluR6(M836I). C1 Univ Tubingen, Dept Physiol 1, D-72076 Tubingen, Germany. Univ Tubingen, Dept Anat, D-72076 Tubingen, Germany. Ruhr Univ Bochum, Dept Biochem 1, D-4630 Bochum, Germany. RP Lang, F (reprint author), Univ Tubingen, Dept Physiol 1, Gmelinstr 5, D-72076 Tubingen, Germany. 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PY 2006 VL 18 IS 4-5 BP 287 EP 294 DI 10.1159/000097675 PG 8 WC Cell Biology; Physiology SC Cell Biology; Physiology GA 130IO UT WOS:000243793500012 PM 17167233 ER PT J AU King, BH Bostic, JQ AF King, BH Bostic, JQ TI An update on pharmacologic treatments for autism spectrum disorders SO CHILD AND ADOLESCENT PSYCHIATRIC CLINICS OF NORTH AMERICA LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; OPEN-LABEL; DOUBLE-BLIND; RETROSPECTIVE ASSESSMENT; ADOLESCENT AUTISM; BRAIN OVERGROWTH; CASE SERIES; OPEN-PILOT; CHILDREN; RISPERIDONE AB Autism spectrum disorders (ASDs) are a heterogeneous group of conditions that include autism, Asperger disorder, Rett disorder, childhood disintegrative disorder, and sometimes less severe or otherwise atypical presentations currently diagnosed as pervasive developmental disorder (PDD) not otherwise specified. By definition, the diagnosis of an ASD indicates that the affected individual will experience significant difficulty in reciprocal social interactions and communication and will exhibit repetitive or nonfunctional stereotyped behaviors or preoccupations. Affected individuals commonly avoid eye contact, do not develop normal social relationships appropriate for their age, do not seem to show interest in others' thoughts or feelings, and have difficulty understanding or seeing the world through the perspective of others. Affected individuals may have restricted speech or even be nonverbal, may use language unusually (invert pronouns, repeat phrases over and over), and frequently have difficulty sustaining conversations with others. Persons who have autism are often quite concrete and may be preoccupied with parts of objects or use objects in unusual ways. 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Psychiatr. N. Am. PD JAN PY 2006 VL 15 IS 1 BP 161 EP + DI 10.1016/j.chc.2005.08.005 PG 16 WC Psychiatry SC Psychiatry GA 001GU UT WOS:000234522400009 PM 16321729 ER PT J AU Blackledge, JT Hayes, SC AF Blackledge, JT Hayes, SC TI Using acceptance and commitment training in the support of parents of children diagnosed with autism SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Article DE autism; parental stress; acceptance; defusion; Acceptance and Commitment Therapy ID DEPRESSION; FAMILIES; STRESS; HEALTH AB Parents of autistic children face enormous challenges, but very little attention has been paid to their psychological needs. Acceptance and Commitment Therapy (ACT) has previously been tested with parents as part of a comprehensive package, but not yet alone. The present study used a within-subject, repeated measures design to test the effects of a 2-day (14 hour) group ACT workshop on 20 normal parents/guardians of children diagnosed with autism. Parents were assessed three weeks before the workshop, one week before, one week after, and three months after. No significant change occurred while waiting for treatment, but pre to post improvements were found on the Beck Depression Inventory-II (BDI-II), and the Global Severity Index (GSI) of the Brief Symptom Inventory (BSI). Significant pre to follow-up improvements were observed on the BDI-II, BSI, and the General Health Questionnaire-12. Processes measures of experiential avoidance and cognitive fusion also changed and there was some evidence that these changes mediated outcomes seen. Results suggest that ACT may have promise in helping parents better adjust to the difficulties in raising children diagnosed with autism. C1 Univ Wollongong, Dept Psychol, Wollongong, NSW 2522, Australia. Univ Nevada, Reno, NV 89557 USA. RP Blackledge, JT (reprint author), Univ Wollongong, Dept Psychol, Northfields Ave, Wollongong, NSW 2522, Australia. 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TI A modularized cognitive-behavioral intervention for water phobia in an adolescent with childhood-onset schizophrenia SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Article DE modular cognitive-behavior therapy; childhood-onset schizophrenia; specific phobia; multiple baseline ID TREATING ANXIETY DISORDERS; RANDOMIZED CLINICAL-TRIAL; CHILDREN; AUTISM AB The current study evaluated the effectiveness of a modularized treatment of a specific fear of water for a 14-year-old youth with childhood onset schizophrenia using a multiple-baseline across behaviors design. Treatment included gradual exposure to a hierarchy of feared water-related situations with rewards for Successful approximations ranging from looking at water to swimming in a pool. Both parent and youth fear ratings, as well as behavioral observation, were used to monitor treatment progress over the course of 22 weeks. Consistent and repeated exposure successfully reduced fear and avoidance of the swimming pool over time. C1 Univ Hawaii Manoa, Dept Psychol, Honolulu, HI 96822 USA. RP Nakamura, BJ (reprint author), Univ Hawaii Manoa, Dept Psychol, 2430 Campus Rd, Honolulu, HI 96822 USA. 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Behav. Ther. PY 2006 VL 28 IS 3 BP 29 EP 41 DI 10.1300/J019v28n03_02 PG 13 WC Psychology, Clinical; Family Studies SC Psychology; Family Studies GA 096JB UT WOS:000241372300002 ER PT J AU Martins, MP Harris, SL AF Martins, MP Harris, SL TI Teaching children with autism to respond to joint attention initiations SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Article DE joint attention; autism; applied behavior analysis; children ID EARLY LANGUAGE; INTERVENTION; ACQUISITION; PLAY AB Children with autism fail to develop joint attention skills appropriate to developmental age. Joint attention is a predictor of ability in several core domains of autism including language, social development, affective sharing, and theory oh mind capacity, thus establishing the significance of teaching joint attention. However, there is limited research to assist clinicians with methods to teach this skill. The present study used a multiple baseline with reversal design across three children to examine the effectiveness of a training program to teach children with autism to respond to successively more demanding joint attention initiations given by adults. Consistent with previous research, during baseline, all participants demonstrated low levels of joint attention skills. Following intervention, independent responses to joint attention bids were observed for all three participants. These findings support previous reports suggesting that behavioral intervention may facilitate the development of joint attention skills. An assessment before baseline and following treatment indicated no change in initiating joint attention skills, indicating that clinicians may have to teach these skills independently. C1 Rutgers State Univ, Douglass Dev Disabilities Ctr, Dept Psychol, New Brunswick, NJ 08901 USA. Rutgers State Univ, Grad Sch Appl & Profess Psychol, New Brunswick, NJ 08901 USA. RP Martins, MP (reprint author), Rutgers State Univ, Douglass Dev Disabilities Ctr, Dept Psychol, 151 Ryders Lane, New Brunswick, NJ 08901 USA. 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Behav. Ther. PY 2006 VL 28 IS 1 BP 51 EP 68 DI 10.1300/J019v28n01_04 PG 18 WC Psychology, Clinical; Family Studies SC Psychology; Family Studies GA 049CI UT WOS:000237992700004 ER PT J AU Lopez-Rangel, E Lewis, MES AF Lopez-Rangel, E Lewis, MES TI Loud and clear evidence for gene silencing by epigenetic mechanisms in autism spectrum and related neurodevelopmental disorders SO CLINICAL GENETICS LA English DT Editorial Material C1 BC Children & Womens Hlth Ctr, Dept Med Genet, Vancouver, BC V6H 3N1, Canada. Univ British Columbia, Vancouver, BC V6H 3N1, Canada. RP Lopez-Rangel, E (reprint author), BC Children & Womens Hlth Ctr, Dept Med Genet, Rm C234,4500 Oak St, Vancouver, BC V6H 3N1, Canada. EM elopez@cw.bc.ca NR 0 TC 23 Z9 24 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2006 VL 69 IS 1 BP 21 EP 22 DI 10.1111/j.1399-0004.2006.00543a.x PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 008IR UT WOS:000235034500004 PM 16451129 ER PT J AU [Anonymous] AF [Anonymous] TI Multiple pathways lead to MeCP2 in the aetiology of autism spectrum-associated neurodevelopmental disorders SO CLINICAL GENETICS LA English DT Editorial Material CR Samaco RC, 2004, HUM MOL GENET, V13, P629, DOI 10.1093/hmg/ddh063 NR 1 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2006 VL 69 IS 1 BP 22 EP 23 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 008IR UT WOS:000235034500005 ER PT J AU [Anonymous] AF [Anonymous] TI Further evidence for epigenetic influence of MECP2 in Rett, autism and Angelman's syndromes SO CLINICAL GENETICS LA English DT Editorial Material CR SAMACO, 2005, HUMAN MOL GENETICS, V14, P483 THATCHER, 2005, HUMAN MOL GENETICS, V14, P785 NR 2 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2006 VL 69 IS 1 BP 23 EP 25 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 008IR UT WOS:000235034500006 ER PT J AU [Anonymous] AF [Anonymous] TI Do other methyl-binding proteins play a role in autism? SO CLINICAL GENETICS LA English DT Editorial Material CR LI, 2005, BRAIN DEV, V27, P321 NR 1 TC 0 Z9 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0009-9163 EI 1399-0004 J9 CLIN GENET JI Clin. Genet. PD JAN PY 2006 VL 69 IS 1 BP 25 EP 25 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 008IR UT WOS:000235034500007 ER PT J AU Melamed, I McDonald, A Gonzalez, M AF Melamed, Isaac McDonald, Angela Gonzalez, Monica TI Autism as a neuro-immune disease - the benefit effect of IVIG. SO CLINICAL IMMUNOLOGY LA English DT Meeting Abstract CT 6th Annual Meeting of the Federation-of-Clinical-Immunology-Societies CY JUN 01-05, 2006 CL San Francisco, CA SP Federat Clin Immunol Soc C1 1st Hlth Ctr, Centennial, CO USA. NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1521-6616 J9 CLIN IMMUNOL JI Clin. Immunol. PY 2006 VL 119 SU S BP S121 EP S121 DI 10.1016/j.clim.2006.04.278 PG 1 WC Immunology SC Immunology GA 048CD UT WOS:000237924300320 ER PT J AU Baxter, AJ Krenzelok, EP AF Baxter, A. J. Krenzelok, E. P. TI Pediatric fatality secondary to 'EDTA' chelation therapy for autism SO CLINICAL TOXICOLOGY LA English DT Meeting Abstract C1 Pittsburght Poison Ctr, Pittsburgh, PA USA. Univ Pittsburgh, Sch Pharm, Pittsburgh, PA USA. Sch Med, Pittsburgh, PA USA. NR 0 TC 0 Z9 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0731-3810 J9 CLIN TOXICOL JI Clin. Toxicol. PY 2006 VL 44 IS 5 MA 112 BP 680 EP 680 PG 1 WC Toxicology SC Toxicology GA 072RJ UT WOS:000239690400117 ER PT J AU Soden, SE Lowry, JA Garrison, CB Wasserman, GS AF Soden, S. E. Lowry, J. A. Garrison, C. B. Wasserman, G. S. TI Provoked urinary excretion testing for heavy metals in children with autism SO CLINICAL TOXICOLOGY LA English DT Meeting Abstract C1 Childrens Mercy Hosp & Clin, Kansas City, MO USA. Univ Kansas, Mid Amer Poison Control Ctr, Med Ctr, Kansas City, KS 66103 USA. NR 0 TC 0 Z9 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 0731-3810 J9 CLIN TOXICOL JI Clin. Toxicol. PY 2006 VL 44 IS 5 MA 329 BP 783 EP 783 PG 1 WC Toxicology SC Toxicology GA 072RJ UT WOS:000239690400334 ER PT J AU Skwerer, DP Verbalis, A Schofield, C Faja, S Tager-Flusberg, H AF Skwerer, DP Verbalis, A Schofield, C Faja, S Tager-Flusberg, H TI Social-perceptual abilities in adolescents and adults with Williams syndrome SO COGNITIVE NEUROPSYCHOLOGY LA English DT Article ID ASPERGER-SYNDROME; GENETIC SYNDROME; MIND; PERSONALITY; HYPERSOCIABILITY; LANGUAGE; CHILDREN; AUTISM AB People with Williams syndrome (WMS) have a unique social phenotype characterised by unusually strong interest in other people and an engaging and empathic personality. Two experiments were designed to test whether this phenotype is associated with relatively spared abilities to decode mental-state information from nonverbal cues. The first experiment involved a modified version of the revised Eyes Test. The second experiment probed the ability to label emotions from brief dynamic facial displays. Adolescents and adults with WMS were compared to age-, IQ-, and language-matched participants with learning/intellectual disabilities, and age- matched normal controls. In both experiments the WMS group performed at a significantly lower level than the normal controls, and no different from the well-matched comparison-group with intellectual disabilities. These findings, contradicting earlier reports in the literature, argue against the view that in WMS social-perceptual abilities are relatively spared and can explain the social profile associated with this neurodevelopmental disorder. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Skwerer, DP (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St L-814, Boston, MA 02118 USA. EM dplesas@bu.edu RI Tager-Flusberg, Helen/D-5265-2009 CR Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 Baron-Cohen S, 2003, MIND READING INTERAC BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Bates EA, 2004, BRAIN LANG, V88, P248, DOI 10.1016/S0093-934X(03)00102-0 Beardsmore A, 1998, J INTELL DISABIL RES, V42, P463, DOI 10.1046/j.1365-2788.1998.4260463.x Bellugi U., 1988, LANGUAGE DEV EXCEPTI, P177 BELLUGI U, 1992, MINN SYM CHILD PSYCH, V24, P201 Bellugi U, 1999, NEUROREPORT, V10, P1653, DOI 10.1097/00001756-199906030-00006 Benton A. 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L., 1994, ATYPICAL COGNITIVE D, P23 Jones W, 2000, J COGNITIVE NEUROSCI, V12, P30, DOI 10.1162/089892900561968 Karmiloff-Smith A, 1998, NEUROPSYCHOLOGIA, V36, P343, DOI 10.1016/S0028-3932(97)00133-4 KARMILOFFSMITH A, 1995, J COGNITIVE NEUROSCI, V7, P196, DOI 10.1162/jocn.1995.7.2.196 KAUFMAN A, 1990, MANAUL KAUFMAN BRIEF Klein-Tasman BP, 2003, DEV NEUROPSYCHOL, V23, P269, DOI 10.1207/S15326942DN231&2_12 KOENIG K, IN PRESS J AUTISM DE Mervis CB, 2000, MENT RETARD DEV D R, V6, P148 SKWERER P, IN PRESS WILLIAMS BE Sullivan K, 2003, DEV NEUROPSYCHOL, V23, P85, DOI 10.1207/S15326942DN231&2_5 Sullivan K, 1999, AM J MENT RETARD, V104, P523, DOI 10.1352/0895-8017(1999)104<0523:SBAIWS>2.0.CO;2 Tager-Flusberg H, 1998, J COGNITIVE NEUROSCI, V10, P631, DOI 10.1162/089892998563031 Tager-Flusberg H, 2003, COGNITION, V89, P11, DOI 10.1016/S0010-0277(03)00049-0 TAGERFLUSBERG H, DEV SOCIAL ENGAGEMEN Tager-Flusberg H, 2000, COGNITION, V76, P59, DOI 10.1016/S0010-0277(00)00069-X THOMAS ML, 2002, DEV EMPATHY 4 YEAR O UDWIN O, 1987, J CHILD PSYCHOL PSYC, V28, P297, DOI 10.1111/j.1469-7610.1987.tb00212.x WANG PP, 1995, BRAIN COGNITION, V29, P54, DOI 10.1006/brcg.1995.1267 WHITMAN BY, 1987, AM J MED GENET, V28, P897, DOI 10.1002/ajmg.1320280415 NR 34 TC 14 Z9 14 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0264-3294 J9 COGN NEUROPSYCHOL JI Cogn. Neuropsychol. PY 2006 VL 23 IS 2 BP 338 EP 349 PG 12 WC Psychology; Psychology, Experimental SC Psychology GA 026OI UT WOS:000236348100006 PM 21049334 ER PT J AU Stein, D Weizman, A Ring, A Barak, Y AF Stein, D Weizman, A Ring, A Barak, Y TI Obstetric complications in individuals diagnosed with autism and in healthy controls SO COMPREHENSIVE PSYCHIATRY LA English DT Article ID INFANTILE-AUTISM; PERINATAL FACTORS; SCHIZOPHRENIA; TWIN; POPULATION; OPTIMALITY; PREGNANCY; ETIOLOGY; CHILDREN; RISK AB The aim of the present study was to investigate birth complications in Israeli autistic probands. We interviewed 206 mothers of autistic probands and 152 healthy control mothers with a structured tool encompassing prenatal, perinatal, and neonatal complications. Analysis of obstetric suboptimality, derived by summing all positive items of each of the 3 categories and dividing them by the number of patients analyzed, revealed no prenatal between-group difference. The controls had a somewhat elevated perinatal suboptimality score, whereas the autistic probands had a significantly greater neonatal suboptimality score. These differences in obstetric suboptimality were retained after controlling for the demographic parameters found different between the 2 groups (sex of participants and mothers' years of schooling). Our findings suggest that the presence of nonspecific neonatal factors, rather than the specific influence of individual severe insults, may account for the elevated neonatal suboptimality found in probands diagnosed with autism compared with healthy controls. (c) 2005 Elsevier Inc. All rights reserved. C1 Geha Psychiat Hosp, Petah Tiqwa, Israel. Felsenstein Med Res Ctr, Petah Tiqwa, Israel. Chaim Sheba Med Ctr, Pediat Psychosomat Dept, IL-52621 Tel Hashomer, Israel. Ababanel Mental Hlth Ctr, Bat Yam, Israel. Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel. RP Weizman, A (reprint author), Geha Psychiat Hosp, Rabin Campus, Petah Tiqwa, Israel. 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Psychiat. PD JAN-FEB PY 2006 VL 47 IS 1 BP 69 EP 75 DI 10.1016/j.comppsych.2005.01.001 PG 7 WC Psychiatry SC Psychiatry GA 996MM UT WOS:000234178000010 PM 16324905 ER PT S AU Davis, M Dautenhahn, K Nehaniv, C Powell, SD AF Davis, Megan Dautenhahn, Kerstin Nehaniv, Chrystopher Powell, Stuart D. BE Miesenberger, K Klaus, J Zagler, W Karshmer, A TI TouchStory: Towards an interactive learning environment for helping children with autism to understand narrative SO COMPUTERS HELPING PEOPLE WITH SPECIAL NEEDS, PROCEEDINGS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 10th International Conference on Computers Helping People with Special Needs CY JUL 11-13, 2006 CL Linz, AUSTRIA SP DG Informat Soc, European Commiss, Fed Minist Educ, Sci & Culture, Fed Minist Transport, Innovat & Technol, Reg Govt Upper Austria, Governor, Reg Govt Upper Austria, Dept Social Affairs, Austrian Comp Soc AB Children with autism exhibit a deficit in the comprehension and creation of narrative which impacts their social world. Our ongoing research agenda is to find ways of developing interactive learning environments which enhance the ability of individual children with autism to deal with narrative and thus the social world. The study reported here involved 12 children in a longitudinal study which focussed on identifying the particular aspects of narrative which individual children found difficult. Our aim was to investigate each individual child's understanding of 'primitive' components of narrative by means of an interactive software game called TouchStory which we developed for this purpose. Our results show, for most of the children, an ongoing and clear distinction in their understanding of the various narrative components, which relates their narrative comprehension as shown by a picture-story based narrative comprehension task. C1 Univ Hertfordshire, Sch Comp Sci, Adapt Syst Res Grp, Hatfield AL10 9AB, Herts, England. Univ Hertfordshire, Dept Educ, Hatfield AL10 9AB, Herts, England. RP Davis, M (reprint author), Univ Hertfordshire, Sch Comp Sci, Adapt Syst Res Grp, Hatfield AL10 9AB, Herts, England. 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Recently, a relationship between disease risk and consumption of a specific bovine beta-case infraction either A(1) or A(2) genetic variants has been identified. Populations, which consume milk containing high levels of beta-casein A(2) variant, have a lower incidence of cardiovascular disease and type 1 diabetes. Furthermore, consumption of milk with the A(2) variant may be associated with less severe symptoms of autism and schizophrenia. The mechanism of action focuses oil beta-casein A(1) and related forms preferentially that are able to produce a bioactive opioid peptide, beta-casomorphin-7 (beta-CM-7) during digestion. Infants may absorb beta-CM-7 due to an immature gastrointestinal tract. Adults, on the other hand, appear to reap the biological activity locally on the intestinal brush boarder. beta-CM-7 can potentially affect numerous opioid receptors in the nervous, endocrine, and immune systems. Whether there is a definite health benefit to milk containing the A(2) genetic variant is unknown and requires further investigation. C1 Res & Dev Ideasphere Inc, Belmont, MA 02478 USA. Ideasphere Inc, Grand Rapids, MI 49546 USA. A2 Corp Ltd, Auckland 1001, New Zealand. RP Bell, SJ (reprint author), Res & Dev Ideasphere Inc, 56 Amherst Rd, Belmont, MA 02478 USA. 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PY 2006 VL 46 IS 1 BP 93 EP 100 DI 10.1080/10408390591001144 PG 8 WC Food Science & Technology; Nutrition & Dietetics SC Food Science & Technology; Nutrition & Dietetics GA 005EE UT WOS:000234804600004 PM 16403684 ER PT J AU Mandelbaum, DE Stevens, M Rosenberg, E Wiznitzer, M Steinschneider, M Filipek, P Rapin, I AF Mandelbaum, DE Stevens, M Rosenberg, E Wiznitzer, M Steinschneider, M Filipek, P Rapin, I TI Sensorimotor performance in school-age children with autism, developmental language disorder, or low IQ SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID INHERITED SPEECH; NEUROLOGICAL EXAMINATION; MOVEMENTS; GENE AB The purpose of the study was to determine the prevalence of 'soft' motor deficits in school-aged children with either developmental language disorder (DLD), autism (with high IQ [HiAD] or low IQ [LoAD]), or low IQ without autism (LoIQ), and to evaluate the utility of a refined neurological examination to discriminate between these groups. A total of 242 children (74% male), aged 7 or 9 years, were evaluated as part of a longitudinal, multi-institutional study, with a standardized neurological examination that included Denckla's Physical and Neurological Examination for Soft Signs. Most of the scores separated children into two groups defined by nonverbal IQ, with the DLD and HiAD groups performing better than the LoAD and LoIQ groups. Exceptions included motor impersistence and stereotypies, which were more likely in the autistic groups. The neurologists' summary clinical impressions indicated better sensory/motor skills, oromotor skills, and praxis in the HiAD than in the DLD children. Inability/unwillingness to perform tasks was much more frequent in LoAD than LoIQ children. C1 Brown Med Sch, Dept Clin Neurosci, Providence, RI USA. Brown Med Sch, Dept Pediat, Providence, RI USA. Hartford Hosp, Olin Neuropsychiat Res Ctr, Clin Cognit Neurosci Lab, Hartford, CT 06115 USA. Independent Stat Consultant, New York, NY USA. Rainbow Babies & Childrens Hosp, Dept Neurol, Cleveland, OH 44106 USA. Case Western Reserve Univ, Sch Med, Cleveland, OH USA. Albert Einstein Coll Med, Saul R Korey Dept Neurol, Bronx, NY 10467 USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. RP Mandelbaum, DE (reprint author), 110 Lockwood St,Suite 342, Providence, RI 02903 USA. EM David_Mandelbaum@brown.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bauman M. L., 1992, MOVEMENT DISORDERS N, P660 Bodfish JW, 2000, J AUTISM DEV DISORD, V30, P237, DOI 10.1023/A:1005596502855 Brasic JR, 1999, MED HYPOTHESES, V53, P48, DOI 10.1054/mehy.1997.0711 Cohen J., 1988, STAT POWER ANAL BEHA, V2nd DENCKLA MB, 1977, TOPICS CHILD NEUROLO, P243 DENCKLA MB, 1985, PSYCHOPHARMACOL BULL, V21, P773 DENHOFF E, 1968, DEV MED CHILD NEUROL, V10, P220 Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 FLETCHER SG, 1972, J SPEECH HEAR RES, V15, P763 GARDNER RA, 1979, J CLIN CHILD PSYCHOL, V8, P156 Hresko W. P., 1981, TEST EARLY LANGUAGE HURST JA, 1990, DEV MED CHILD NEUROL, V32, P352 KINSBOURNE M, 1964, QUART J EXPT PSYCHOL, V15, P132 Lai CSL, 2001, NATURE, V413, P519, DOI 10.1038/35097076 McCreary AC, 1999, EUR J PHARMACOL, V369, P1, DOI 10.1016/S0014-2999(99)00039-4 MILLER JF, 1981, P S RES CHILD LANG D, V2, P130 MUNDY P, 1990, J AUTISM DEV DISORD, V20, P115, DOI 10.1007/BF02206861 Naidoo S., 1991, CHILDREN SPECIFIC SP PETERS JE, 1975, DEV MED CHILD NEUROL, V17, P63 POLLACK M, 1957, ARCH NEURO PSYCHIATR, V77, P635 RAPIN I, 1996, CLIN DEV MED, V139, P98 Rapin I., 1996, PRESCHOOL CHILDREN I Rapin I, 2003, BRAIN DEV-JPN, V25, P166, DOI 10.1016/S0387-7604(02)00191-2 STEVENS MC, 2000, J AM ACAD CHILD ADOL, V39, P399 Tan A, 1997, MOVEMENT DISORD, V12, P47, DOI 10.1002/mds.870120109 TOUWEN BCL, 1970, NEUROLOGICAL EXAMINA Waterhouse L, 1996, PSYCHOL REV, V103, P457, DOI 10.1037/0033-295X.103.3.457 Watkins KE, 2002, BRAIN, V125, P452, DOI 10.1093/brain/awf058 Watkins KE, 2002, BRAIN, V125, P465, DOI 10.1093/brain/awf057 Wing L., 1996, PRESCHOOL CHILDREN I, P247 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 32 TC 30 Z9 30 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD JAN PY 2006 VL 48 IS 1 BP 33 EP 39 DI 10.1017/S0012162206000089 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 002EM UT WOS:000234594300008 PM 16359592 ER PT J AU Johansson, M Rastam, M Billstedt, E Danielsson, S Stromland, K Miller, M Gillberg, C AF Johansson, M Rastam, M Billstedt, E Danielsson, S Stromland, K Miller, M Gillberg, C TI Autism spectrum disorders and underlying brain pathology in CHARGE association SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID MOBIUS SEQUENCE; CHILDREN; MALFORMATIONS; INDIVIDUALS; BEHAVIOR; POPULATION; ANOMALIES; PATTERNS; FEATURES; DEFICITS AB The rate of autism spectrum disorders (ASDs) and brain abnormalities was analyzed in 31 individuals (15 males, 16 females; age range 1mo to 31y, mean age 8y 11mo) with CHARGE association, as part of a multidisciplinary study. A meticulous neuropsychiatric examination was performed, including standardized autism diagnostic interviews. Judgement regarding ASDs was impossible in three infants and three patients who were deaf and blind. Five individuals met diagnostic criteria for autism, five for an autistic-like condition, and seven for autistic traits. Brain abnormalities were indicated in almost three-quarters of examined individuals, and midline abnormalities of the forebrain in one-third. Awareness of the coexistence of CHARGE and ASDs is important in habilitation care in CHARGE. Moreover, the results indicate that a subgroup of ASDs may be associated with errors in early embryonic brain development. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, SE-41119 Gothenburg, Sweden. Univ Gothenburg, Dept Ophthalmol, Gothenburg, Sweden. Univ Illinois, Eye & Ear Infirm, Dept Ophthalmol & Visual Sci, Chicago, IL 60612 USA. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. RP Johansson, M (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Kungsgatan 12, SE-41119 Gothenburg, Sweden. EM maria.johansson@pediat.gu.se CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Aronson M, 1997, DEV MED CHILD NEUROL, V39, P583 Bandim JM, 2003, ARQ NEURO-PSIQUIAT, V61, P181, DOI 10.1590/S0004-282X2003000200004 Blake KD, 1998, CLIN PEDIATR, V37, P159, DOI 10.1177/000992289803700302 BYERLY KA, 1993, AM J MED GENET, V45, P751, DOI 10.1002/ajmg.1320450617 CHAMBERLAIN RS, 1990, BIOL PSYCHIAT, V28, P773, DOI 10.1016/0006-3223(90)90513-2 DAVENPORT SLH, 1986, CLIN GENET, V29, P298 Ek U, 1998, DEV MED CHILD NEUROL, V40, P297 Fernell E, 1999, DEV MED CHILD NEUROL, V41, P270, DOI 10.1017/S0012162299000572 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x Gillberg C, 2000, BIOL AUTISTIC SYNDRO, V153, P291 Good P., 2000, PERMUTATION TESTS Graham JM, 2001, AM J MED GENET, V99, P120, DOI 10.1002/1096-8628(2000)9999:999<00::AID-AJMG1132>3.0.CO;2-J GRIX A, 1982, BIRTH DEFECTS-ORIG, V18, P55 HAGBERG G, 1988, NEUROPEDIATRICS, V19, P16, DOI 10.1055/s-2008-1052395 HARVEY AS, 1991, AM J MED GENET, V39, P48, DOI 10.1002/ajmg.1320390112 Hindley PA, 2000, MENTAL HLTH DEAFNESS, P42 Hobson R. Peter, 1993, PERCEIVED SELF ECOLO, P254 Johansson M, 2001, DEV MED CHILD NEUROL, V43, P338, DOI 10.1017/S0012162201000627 JURE R, 1991, DEV MED CHILD NEUROL, V33, P1062 Kallen K, 1999, TERATOLOGY, V60, P334 Karlberg P, 1976, ACTA PAEDIATR SC S, V258, P7 Karlberg P, 1988, Lakartidningen, V85, P3452 KNUDTZON J, 1988, Tidsskrift for den Norske Laegeforening, V108, P2125 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x LANDGREN M, 1992, DEV MED CHILD NEUROL, V34, P999 LIN AE, 1990, AM J MED GENET, V37, P304, DOI 10.1002/ajmg.1320370303 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MENENZES M, 1990, PEDIATR NEUROL, V6, P428, DOI 10.1016/0887-8994(90)90015-S Minter M, 1998, BRIT J DEV PSYCHOL, V16, P183 Muller F, 2003, CELLS TISSUES ORGANS, V173, P1, DOI 10.1159/000068214 Niklasson L, 2002, DEV MED CHILD NEUROL, V44, P44, DOI 10.1017/S0012162201001645 Nordin V, 1996, DEV MED CHILD NEUROL, V38, P297 OLEY CA, 1988, J MED GENET, V25, P147, DOI 10.1136/jmg.25.3.147 Ozonoff S, 1999, J CHILD NEUROL, V14, P636, DOI 10.1177/088307389901401003 PAGON RA, 1981, J PEDIATR-US, V99, P223, DOI 10.1016/S0022-3476(81)80454-4 Peterson CC, 1999, PSYCHOL SCI, V10, P126, DOI 10.1111/1467-9280.00119 RAPIN I, 1976, LARYNGOSCOPE, V86, P1469, DOI 10.1288/00005537-197610000-00003 Raqbi F, 2003, DEV MED CHILD NEUROL, V45, P483, DOI 10.1017/S0012162203000896 Rodier PM, 2004, BIRTH DEFECTS RES A, V70, P1, DOI 10.1002/bdra.10152 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Sparrow S, 1984, VINELAND ADAPTIVE BE Stromland K, 2005, AM J MED GENET A, V133A, P331, DOI 10.1002/ajmg.a.30563 STROMLAND K, 1994, DEV MED CHILD NEUROL, V36, P351 Tellier AL, 1998, AM J MED GENET, V76, P402, DOI 10.1002/(SICI)1096-8628(19980413)76:5<402::AID-AJMG7>3.0.CO;2-O VISSERS L, 2004, NAT GENET, V9, P955 Wechsler D., 1992, WECHSLER INTELLIGENC WING L, 1981, J AUTISM DEV DISORD, V11, P31, DOI 10.1007/BF01531339 WIZNITZER M, 1987, INT J PEDIATR OTORHI, V13, P41, DOI 10.1016/0165-5876(87)90006-1 Zhou FC, 2003, DEV BRAIN RES, V144, P43, DOI 10.1016/S0165-3806(03)00158-5 NR 51 TC 19 Z9 19 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD JAN PY 2006 VL 48 IS 1 BP 40 EP 50 DI 10.1017/S0012162206000090 PG 11 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 002EM UT WOS:000234594300009 PM 16359593 ER PT J AU Porter, MA Coltheart, M AF Porter, Melanie A. Coltheart, Max TI Global and local processing in Williams syndrome, autism, and Down syndrome: Perception, attention, and construction SO DEVELOPMENTAL NEUROPSYCHOLOGY LA English DT Article ID VISUOSPATIAL COGNITION; SELECTIVE ATTENTION; DIVIDED ATTENTION; PRECEDENCE; CHILDREN; PERFORMANCE; FREQUENCY; DELETIONS; DEFICIT; PROFILE AB Global and local processing was studied in Williams Syndrome (WS), autism (AS), and Down Syndrome (DS) using perception, attention, and construction tasks. Past research has suggested an abnormal bias toward global processing in DS and, in contrast, an abnormal local bias in both WS and AS. Until now, no study has investigated whether the local processing bias in WS and AS has a different or similar underlying cause. Findings here suggest a common underlying mechanism, namely a bias in attention toward local processing. Results also indicate a global bias in attention in DS. This study finds no evidence to support predictions of the hierarchical deficit theory (Mottron & Belleville, 1993) as an explanation of hierarchical processing deficits in AS or DS, but does find support for hierarchical deficit theory in a subset of WS individuals. This study finds evidence of cognitive heterogeneity in WS, consistent with Porter and Coltheart (2005). C1 Macquarie Univ, Macquarie Ctr Cognit Sci, Sydney, NSW 2109, Australia. RP Porter, MA (reprint author), Macquarie Univ, Macquarie Ctr Cognit Sci, Sydney, NSW 2109, Australia. EM mporter@maccs.mq.edu.au CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Atkinson J, 2003, DEV NEUROPSYCHOL, V23, P139, DOI 10.1207/S15326942DN231&2_7 BADCOCK JC, 1990, PERCEPTION, V19, P617, DOI 10.1068/p190617 BELLUGI U, 1988, P273 Bellugi U, 1990, Am J Med Genet Suppl, V6, P115 Bellugi U, 2000, J COGNITIVE NEUROSCI, V12, P1, DOI 10.1162/089892900561940 BIHRLE AM, 1989, BRAIN COGNITION, V11, P37, DOI 10.1016/0278-2626(89)90003-1 Deruelle C, 1997, Laterality, V2, P233, DOI 10.1080/713754268 Edgington E, 1995, RANDOMISATION TESTS Farran EK, 2003, DEV NEUROPSYCHOL, V23, P173, DOI 10.1207/S15326942DN231&2_8 Farran EK, 2003, NEUROPSYCHOLOGIA, V41, P676, DOI 10.1016/S0028-3932(02)00219-1 Forster KI, 2003, BEHAV RES METH INS C, V35, P116, DOI 10.3758/BF03195503 Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x Hubner R, 1997, PERCEPT PSYCHOPHYS, V59, P187, DOI 10.3758/BF03211888 LOWERY MC, 1995, AM J HUM GENET, V57, P49 McKusick V., 1988, MENDELIAN INHERITANC Mervis C. B., 1999, NEURODEVELOPMENTAL D Mervis CB, 2000, BRAIN COGNITION, V44, P604, DOI 10.1006/brcg.2000.1232 MORRIS CA, 1988, J PEDIATR-US, V113, P318, DOI 10.1016/S0022-3476(88)80272-5 Mottron L, 1999, J CHILD PSYCHOL PSYC, V40, P743, DOI 10.1017/S0021963098003795 MOTTRON L, 1993, BRAIN COGNITION, V23, P279, DOI 10.1006/brcg.1993.1060 NAVON D, 1977, COGNITIVE PSYCHOL, V9, P353, DOI 10.1016/0010-0285(77)90012-3 NAVON D, 1983, J EXP PSYCHOL HUMAN, V9, P955, DOI 10.1037//0096-1523.9.6.955 NICKERSON E, 1995, AM J HUM GENET, V56, P1156 Plaisted K, 1999, J CHILD PSYCHOL PSYC, V40, P733, DOI 10.1111/1469-7610.00489 Porter MA, 2005, DEV NEUROPSYCHOL, V27, P275, DOI 10.1207/s15326942dn2702_5 RIMLAND B, 1971, J AUTISM CHILD SCHIZ, V1, P161, DOI 10.1007/BF01537955 Rinehart NJ, 2000, J CHILD PSYCHOL PSYC, V41, P769, DOI 10.1017/S002196309900596X ROBERTSON LC, 1991, COGNITIVE PSYCHOL, V23, P299, DOI 10.1016/0010-0285(91)90012-D Ropar D, 2001, J CHILD PSYCHOL PSYC, V42, P539, DOI 10.1111/1469-7610.00748 SNODGRASS JG, 1980, J EXP PSYCHOL-HUM L, V6, P174, DOI 10.1037/0278-7393.6.2.174 WANG PP, 1995, BRAIN COGNITION, V29, P54, DOI 10.1006/brcg.1995.1267 WILLIAMS JC, 1961, CIRCULATION, V24, P1311 Woodcock R. 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PY 2006 VL 30 IS 3 BP 771 EP 789 DI 10.1207/s15326942dn3003_1 PG 19 WC Psychology, Developmental; Psychology; Psychology, Experimental SC Psychology GA 113OM UT WOS:000242607200001 PM 17083292 ER PT J AU Einav, S Hood, BA AF Einav, S Hood, BA TI Children's use of the temporal dimension of gaze for inferring preference SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article DE gaze perception; mental state attribution; attention; nonverbal cues; social cognition ID JOINT VISUAL-ATTENTION; LOOKING BEHAVIOR; EYE CONTACT; EMOTIONAL EXPRESSION; INFANTS; AUTISM; ABILITY; DESIRES; ADULTS; CUES AB This study examined 4- and 5-year-olds' ability to spontaneously use the relative duration and frequency of another's object-directed gaze for inferring that person's preference. In Experiment 1, analysis revealed a strong age effect for judgment accuracy, which could not be accounted for by cue-monitoring proficiency. Reducing the saliency of the objects in Experiment 2 yielded significant improvement in the younger children's performance. Thus, at 4 years, children already show signs of attending to the temporal dimension of gaze for making mentalistic inferences of preferential liking, but their competence may be undermined by the object choices themselves. By 5 years, they appear to overcome this competition. The obtained developmental difference is discussed in terms of concurrent transitions in attention regulation. C1 Univ Bristol, Dept Expt Psychol, Bristol Cognit Dev Ctr, Bristol BS8 1TN, Avon, England. RP Hood, BA (reprint author), Univ Bristol, Dept Expt Psychol, Bristol Cognit Dev Ctr, 8 Woodland Rd, Bristol BS8 1TN, Avon, England. EM Bruce.Hood@bristol.ac..uk CR Argyle Michael, 1976, GAZE AND MUTUAL GAZE Baldwin D. 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D., 1997, REV GEN PSYCHOL, V1, P198, DOI DOI 10.1037/1089-2680.1.2.198 NR 39 TC 10 Z9 11 PU AMER PSYCHOLOGICAL ASSOC/EDUCATIONAL PUBLISHING FOUNDATION PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0012-1649 J9 DEV PSYCHOL JI Dev. Psychol. PD JAN PY 2006 VL 42 IS 1 BP 142 EP 152 DI 10.1037/0012-1649.42.1.142 PG 11 WC Psychology, Developmental SC Psychology GA 005SM UT WOS:000234844100011 PM 16420124 ER PT J AU Keay-Bright, W AF Keay-Bright, Wendy TI ReActivities (c): autism and play SO DIGITAL CREATIVITY LA English DT Article; Proceedings Paper CT Mindplay 2006 Conference CY JAN 20, 2006 CL London, ENGLAND SP Grp Res Interact Med, Dept Appl Social Sci HO London Metropolitan Univ DE autism spectrum differences; collaborative design; digital environments; interaction; monotropism ID CHILDREN; MIND AB ReActivities (c) are digital play sequences which encourage the integration of social, emotional and cognitive development in children on the autistic spectrum. High levels of anxiety in autistic children can inhibit playful experiences and increase the rigid, stereotypical and challenging behaviours which have a negative effect in social situations. Interactions with objects that offer repetition, pattern and similarity combined with colour and rhythm are regularly used by autistic children as methods to reduce anxiety. However little has been done to interpret these sensations in digital environments. The aim of ReActivities (c) has been to offer a rich physical and cognitive experience which simulates the perceptible characteristics of phenomena such as elasticity, velocity, gravity and inertia. This is an advanced form of cause and effect that promises a unique form of expression in response to exploration with computer technology. There are numerous thoughtful and engaging websites designed and maintained by autistic people which are testimony to the theory that computers, and particularly electronic networks, offer enormous possibilities for creativity, communication and fun. The project is utilising open source technology to enable autistic users, many of whom are already conversant with programming languages, to adapt and re-generate the software. Fostering a community approach to development affords further opportunities to explore an innovative, inclusive design method that, should it prove successful, could provide a model for other marginalised groups. C1 Univ Wales Inst, Cardiff, Wales. RP Keay-Bright, W (reprint author), Univ Wales Inst, Cardiff, Wales. EM wkbright@uwic.ac.uk CR BARONCOHEN S, 1989, BRIT J DISORD COMMUN, V24, P199 BEYER J, 2000, AUTISM PLAY Boucher J., 1999, CHILD LANG TEACH THE, V15, P1, DOI 10.1191/026565999676029298 Jarrold C, 1996, BRIT J DEV PSYCHOL, V14, P275 Jordan R., 1997, AUTISM LEARNING GUID Laurel B., 2003, DESIGN RES METHODS P LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 Lessig Lawrence, 2001, FUTURE IDEAS FATE CO Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 MOOR J, 2002, PLAYING LAUGHING LEA Murray D., 1997, AUTISM LEARNING GUID MURRAY D, 1997, AUTISM COMPUTING MURRAY D, 2005, AUTISM, V9 SEIGAL B, 1996, WORLD AUTISTIC CHILD Sherratt D., 2002, DEV PLAY DRAMA CHILD SHERRATT D, 1999, GOOD AUTISM PRAC SEP, P23 Shields J., 1999, AUTISTIC SPECTRUM HD Stahmer A. C., 1999, CHILD LANG TEACH THE, V15, P29, DOI 10.1191/026565999672332808 Vygotsky Lev Semyonovitch, 1978, MIND SOC DEV HIGHER Williams E, 2001, J AUTISM DEV DISORD, V31, P67, DOI 10.1023/A:1005665714197 WING L, 1975, AUTISTIC CHILDREN Wolfberg P. J., 1999, PLAY IMAGINATION CHI NR 22 TC 3 Z9 3 PU ROUTLEDGE JOURNALS, TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXFORDSHIRE, ENGLAND SN 1462-6268 J9 DIGIT CREAT JI Digit. Creat. PY 2006 VL 17 IS 3 BP 149 EP 156 DI 10.1080/14626260600882414 PG 8 WC Art SC Art GA 080QM UT WOS:000240262600004 ER PT J AU Baker, DL AF Baker, DL TI Neurodiversity, neurological disability and the public sector: notes on the autism spectrum SO DISABILITY & SOCIETY LA English DT Article ID RIGHTS MOVEMENT; UPDATE AB Neurodiversity and neurological disabilities reflect rising public sector challenges. Both refer to the same set of medical conditions, but speak to different aspects of diversity affecting the public sector. Neurodiversity describes features of neurological difference associated with individual or community identity that is a more or less elective choice of those experiencing neurological difference. Neurological disability refers to impairment of socially determined major life functions caused by observable, diagnosable difference in an individual's brain. Both neurodiversity and neurological disability produce challenges and opportunities for public programs and societies. This article employs findings from a survey of families with children with autism to examine administrative implications of neurodiversity and neurological disability. The findings suggest that in managing new (and rising) kinds of diversity, public administrators must navigate sharpening divides between interests related to inclusion and those related to identity. 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, 14204 NE Salmon Creek Ave, Vancouver, WA 98686 USA. 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Soc. PD JAN PY 2006 VL 21 IS 1 BP 15 EP 29 DI 10.1080/09687590500373734 PG 15 WC Rehabilitation; Social Sciences, Interdisciplinary SC Rehabilitation; Social Sciences - Other Topics GA 993AB UT WOS:000233924000002 ER PT J AU Casiday, RE Cox, AR AF Casiday, Rachel E. Cox, Anthony R. TI Restoring confidence in vaccines by explaining vaccine safety monitoring - Is a targeted approach needed? SO DRUG SAFETY LA English DT Editorial Material ID ADVERSE DRUG-REACTIONS; MEASLES-VIRUS; MMR VACCINE; CHILDREN; UK; IMMUNIZATION; DISORDER; RUBELLA; AUTISM; BLOOD AB Public trust in childhood vaccines is crucial to achieving adequate immunisation coverage to ensure population-level immunity. However, in the UK, immunisation uptake has been adversely affected by vaccine safety scares, such as those surrounding whooping cough and measles, mumps and rubella (MMR). It is our belief that greater public awareness of safety surveillance schemes may play a key role in improving trust in vaccine safety. Many parents of vaccination-age children are unaware of the procedures in place for postmarketing surveillance of vaccines. Thus, we propose specific steps for generating such awareness, such as assisting parents to report suspected adverse reactions directly to the Medicines and Healthcare products Regulatory Agency (MHRA) via the Yellow Card scheme, providing information about adverse reaction reporting with vaccination information packs, and displaying posters and leaflets to convey the message that patient concerns and experiences are taken seriously by the MHRA and to generate further awareness about the scheme. In addition, healthcare staff should be encouraged to report suspected adverse reactions relating to vaccine products. Unresolved issues about the scientific usefulness of data reported by parents and the potential for these steps to increase parental concern and expectations require further investigation. 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Using an antibody specific to acetylated histone H3 lysine 9 (H3K9ac), a bright punctate nuclear staining pattern was observed as MECP2 expression increased in early post-natal neuronal nuclei. As neurons matured in juvenile and adult brain samples, the intensity of H3K9ac staining was reduced. Mecp2-deficient mouse and RTT cerebral neurons lacked this developmental reduction in H3K9ac staining compared to age-matched controls, resulting in a significant increase in neuronal nuclei with bright H3K9ac punctate staining. In contrast, trimethylated histone H3 lysine 9 (H3K9me3) localized to heterochromatin independent of Mecp3, but showed significantly reduced levels in Mecp2 deficient mouse and RTT brain. Autism brain with reduced MECP2 expression displayed similar histone H3 alterations as RTT human brain. These observations suggest that MeCP2 regulates global histone modifications during a critical post-natal stage of neuronal maturation. 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Knowing that cognitive and/or behavioral abnormalities can be the presenting and sometimes the only symptom of an epileptic disorder or can even be caused by paroxysmal EEG abnormalities without recognized seizures, the possibility that this may apply to autism has given rise to much debate. Epilepsy and/or epileptic EEG abnormalities are frequently associated with autistic disorders in children but this does not necessarily imply that they are the cause; great caution needs to be exercised before drawing any such conclusions. So far, there is no evidence that typical autism can be attributed to an epileptic disorder, even in those children with a history of regression after normal early development. Nevertheless, there are several early epilepsies (late infantile spasms, partial complex epilepsies, epilepsies with CSWS, early forms of Landau-Kleffner syndrome) and with different etiologies (tuberous sclerosis is an important model of these situations) in which a direct relationship between epilepsy and some features of autism may be suspected. In young children who primarily have language regression (and who may have autistic features) without evident cause, and in whom paroxysmal focal EEG abnormalities are also found, the possible direct role of epilepsy can only be evaluated in longitudinal studies. C1 CHU Vaudois, Neuropediat Unit, CH-1011 Lausanne, Switzerland. RP Deonna, T (reprint author), CHU Vaudois, Neuropediat Unit, Rue Bugnon, CH-1011 Lausanne, Switzerland. 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Univ Oslo, Norwegian Radium Hosp, Dept Neurol, Div Clin Neurosci, Oslo, Norway. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2006 VL 47 SU 4 BP 122 EP 122 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 096OA UT WOS:000241385500341 ER PT J AU Romero-Andujar, F Garcia-Penas, J Gutierrez-Solana, LG Ruiz-Falco, M Alcami, M Rodriguez, AD Lopez-Marin, L AF Romero-Andujar, F. Garcia-Penas, J. Gutierrez-Solana, L. Gonzalez Ruiz-Falco, M. Alcami, M. Rodriguez, A. Duat Lopez-Marin, L. TI Autism spectrum disorders and temporal lobe epilepsy: Report of 30 paediatric patients SO EPILEPSIA LA English DT Meeting Abstract CT 7th European Congress on Epileptology CY JUL 02-06, 2006 CL Helsinki, FINLAND C1 Hosp Infantil Universitario Nino Jesus, Pediat Neurol Unit, Madrid, Spain. Hosp Infantil Universitario Nino Jesus, Pervas Depelopmental Disorders Unit, Madrid, Spain. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2006 VL 47 SU 3 BP 178 EP 178 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 119OO UT WOS:000243021800692 ER PT J AU Stobbe, GA Eileen, K Davies, JM Malmquist, S AF Stobbe, Gary A. Eileen, Kathy Davies, Julie M. Malmquist, Susan TI Use of levetiracetam in children with autism spectrum disorders and EEG epileptiform abnormalities SO EPILEPSIA LA English DT Meeting Abstract CT 60th Annual Meeting of the American-Epilepsy-Society CY DEC 01-05, 2006 CL San Diego, CA SP Amer Epilepsy Soc C1 Autism Spectrum Treatment & Res Ctr, Seattle, WA USA. Seattle Pacific Univ, Dept Psychol, Seattle, WA USA. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2006 VL 47 SU 4 BP 285 EP 286 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 096OA UT WOS:000241385501290 ER PT J AU Blasi, F Bacchelli, E Carone, S Toma, C Monaco, AP Bailey, AJ Maestrini, E AF Blasi, F Bacchelli, E Carone, S Toma, C Monaco, AP Bailey, AJ Maestrini, E CA IMGSAC TI SLC25A12 and CMYA3 gene variants are not associated with autism in the IMGSAC multiplex family sample SO EUROPEAN JOURNAL OF HUMAN GENETICS LA English DT Article DE autism; chromosome 2q; association; SLC25A12; CMYA3; SNPs ID LINKAGE; DISEQUILIBRIUM; CHROMOSOME-2 AB Autism is a severe neurodevelopmental disorder with a complex genetic predisposition. Linkage findings from several genome scans suggest the presence of an autism susceptibility locus on chromosome 2q24-q33, making this region the focus of candidate gene and association studies. Recently, significant association with autism has been reported for single-nucleotide polymorphisms (SNPs) in the SLC25A12 and CMYA3 genes on chromosome 2q. We attempted to replicate these findings in the collection of families from the International Molecular Genetic Study of Autism Consortium (IMGSAC), using the transmission disequilibrium test and case-control comparison. Our study failed to reveal any significant association for the SNPs tested at either locus, suggesting that these variants are unlikely to play a major role in genetic susceptibility to autism in our sample. C1 Univ Bologna, Dept Biol, I-40126 Bologna, Italy. Policlin S Orsola, Med Genet Lab, Bologna, Italy. Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. Univ Oxford, Pk Hosp Children, Dept Psychiat, Sect Child Adolescent Psychiat, Oxford, England. RP Maestrini, E (reprint author), Dipartimento Biol Evoluz Sperimentale, Via Selmi 3, I-40126 Bologna, Italy. 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J. Hum. Genet. PD JAN PY 2006 VL 14 IS 1 BP 123 EP 126 DI 10.1038/sj.ejhg.5201444 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 995MA UT WOS:000234103200021 PM 16205742 ER PT J AU Josselin, F AF Josselin, F TI Genius of the autism - On the ..."distinction of autism" by Rosine and Robert Lefort SO EVOLUTION PSYCHIATRIQUE LA French DT Editorial Material C1 EPS Paul Guiraud Villejuif, F-75004 Paris, France. RP Josselin, F (reprint author), EPS Paul Guiraud Villejuif, 5 Rue Tournelles, F-75004 Paris, France. EM francoise-josselin@wanadoo.fr CR JOSSELIN F, 2006, AUTISME PROPOS DISTI, P71 NR 1 TC 0 Z9 0 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD JAN-MAR PY 2006 VL 71 IS 1 BP 146 EP 151 DI 10.1016/j.evopsy.2005.10.003 PG 6 WC Psychiatry SC Psychiatry GA 036TH UT WOS:000237097900014 ER PT J AU Clements, CJ McIntyre, PB AF Clements, CJ McIntyre, PB TI When science is not enough - a risk/benefit profile of thiomersal-containing vaccines SO EXPERT OPINION ON DRUG SAFETY LA English DT Review DE autism; autistic spectrum disorder (ASD); ethyl mercury; methyl mercury; neurodevelopmental abnormality; thimerosal; thiomersal; vaccine adverse event reporting system (VAERS); vaccine preservative ID THIMEROSAL-CONTAINING VACCINES; FOLLOW-UP ANALYSIS; CHILDHOOD VACCINES; UNITED-KINGDOM; NEURODEVELOPMENTAL DISORDERS; DEVELOPMENTAL DISORDERS; CAUSAL ASSOCIATION; MERCURY; AUTISM; METHYLMERCURY AB Without a preservative, such as thiomersal (known as thimerosal in the US), multi-dose liquid presentations of vaccine are vulnerable to bacteriological contamination that can result in death or serious illness of the recipient. Concerns about levels of mercury exposure from thiomersal-containing vaccines were first raised in the US during 1999 in the context of Hepatitis B vaccine for newborns. Since then, a large body of evidence from animal and epidemiological studies has accumulated on the safety of thiomersal. ironically, these data have become largely irrelevant in wealthy countries, where mono-dose, thiomersal-free vaccines have been introduced as a precautionary measure in almost all childhood vaccines, in part related to residual public scepticism. In poor countries, multi-dose vials remain important for vaccine delivery. There is a real danger that this controversy may result in the loss to the world of thiomersal as a preservative, simply from popular pressure. In reality, it would be impossible to cease overnight using thiomersal and maintain the supply of vital vaccines. This paper reviews and summarises the data available from published studies on mercury toxicity, and thiomersal in vaccines in particular that overwhelmingly indicate continued use of thiomersal is safe in those countries where it is most needed. C1 Macfarlane Burnet Inst Med Res & Publ Hlth Ltd, Ctr Int Hlth, Melbourne, Vic 3004, Australia. Childrens Hosp, Natl Ctr Immunisat Res & Surveillance Vaccine Pre, Westmead, NSW, Australia. Univ Sydney, Sydney, NSW 2006, Australia. RP Clements, CJ (reprint author), Macfarlane Burnet Inst Med Res & Publ Hlth Ltd, Ctr Int Hlth, GPO Box 2284,Commercial Rd, Melbourne, Vic 3004, Australia. 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Drug Saf. PD JAN PY 2006 VL 5 IS 1 BP 17 EP 29 DI 10.1517/14740338.5.1.17 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 034RK UT WOS:000236948100008 PM 16370953 ER PT J AU Plichtova, J AF Plichtova, Jana TI The concept of cultural evolution: Its cognitive and social preconditions SO FILOZOFIA LA Czech DT Article ID JOINT ATTENTION; AUTISM; BEHAVIOR; ORIGINS; CHIMPANZEES; INTENTIONS; IMITATION; LANGUAGE; CHILDREN; INFANTS AB The explanation of human nature exclusively from the perspective of biological evolution (as for example in sociobiology) faces two paradoxes. The core of the first one can be summarized as follows: The characteristics of the specifically human behavior, such as symbolic thinking, intentional and planned activity, cooperative work distribution, creation of cultural artifacts and social institutions, needed an incommensurable shorter time to develop when compared with the changes effected by the selection of random mutations. 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S., 1978, MIND SOC DEV HIGHER Watson J., 1999, EARLY SOCIAL COGNITI White R., 1993, LASCAUX COMPLEX RECO, P277 Wrangham RW, 1999, CURR ANTHROPOL, V40, P567, DOI 10.1086/300083 NR 75 TC 0 Z9 0 PU FILOZOFIA PI BRATISLAVA 1 PA KLEMENSOVA 19, 813 64 BRATISLAVA 1, SLOVAKIA SN 0046-385X J9 FILOZOFIA JI Filozofia PY 2006 VL 61 IS 9 BP 726 EP 742 PG 17 WC Philosophy SC Philosophy GA 113JP UT WOS:000242594500004 ER PT J AU Abdul-Rahman, OA Hudgins, L AF Abdul-Rahman, OA Hudgins, L TI The diagnostic utility of a genetics evaluation in children with pervasive developmental disorders SO GENETICS IN MEDICINE LA English DT Article DE pervasive developmental disorder; autism; autistic features; chromosomal abnormalities; Rett syndrome ID AUTISTIC SPECTRUM DISORDERS; DELETION SYNDROME; 15Q; DUPLICATIONS AB Purpose: A genetics evaluation of children with pervasive developmental disorders (PDDs) identifies a diagnosis in 6% to 15% of cases. However, previous studies have not measured the incidence of genetic disorders among children with autistic-like features who do not necessarily meet the Diagnostic and Statistical Manual for Mental Disorders, Fourth Edition criteria for PDD. Methods: We identified 101 patients at our institution referred for PDD, autism, Asperger syndrome, or autistic features. Seventy-eight were males and 23 were females, giving a male-to-female ratio of 3.4:1. No diagnosis was identified on examination alone, although Rett syndrome was suspected in six females. Seventeen patients did not undergo any type of testing because of noncompliance. Results: Of the remaining 84 patients analyzed, seven (8.3%) were found to have abnormalities on testing. Three chromosomal anomalies were found: one with 5p duplication, one with low-level mosaicism for trisomy 21, and one with an unbalanced 10;22 translocation. Three females were diagnosed with Rett syndrome after MECP2 analysis identified a disease-causing mutation. The remaining patient was found to have an elevated urine orotic acid, with a normal ammonia level, of unknown significance. Conclusion: On the basis of our series, the yield of a genetics evaluation in patients with features of PDD who do not necessarily meet the Diagnostic and Statistical Manual for Mental Disorders, Fourth Edition criteria is 8.3%. Approximately half of these were the result of a chromosomal abnormality. Three cases of Rett syndrome were identified for which autistic behaviors are a well-described feature. These findings suggest that a high-resolution karyotype provides the greatest diagnostic yield for patients with autistic-like features. MECP2 analysis should be considered for females who present with autistic behaviors. C1 Stanford Univ, Dept Pediat, Div Med Genet, Stanford, CA 94305 USA. RP Abdul-Rahman, OA (reprint author), 300 Pasteur Dr,H-315, Stanford, CA 94305 USA. 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PY 2006 VL 39 IS 2 BP 72 EP 72 PG 1 WC Chemistry, Inorganic & Nuclear; Chemistry, Physical; Materials Science, Multidisciplinary SC Chemistry; Materials Science GA 062SV UT WOS:000238965700008 ER PT J AU Schauder, S Palm, H AF Schauder, S Palm, H TI Superficial X-ray therapy of lip cancer after chronic excessive sun exposure of a 47-year-old autistic painter SO HAUTARZT LA English DT Article DE superficial X-ray therapy; carcinoma of the lip; autism; "Sun addict"; chronic actinic AB A 47-year-old autistic painter developed lip cancer after chronic excessive sun exposure. As she feared sun withdrawal during inpatient surgical excision, she refused this first-line treatment and therefore received outpatient X-ray therapy. The reason why she developed premature lip cancer and refused to stay in a hospital and the way she illustrated her "sun addiction" in her pictures is presented. Two years later she was free of recurrence. She has remained a sun worshipper until now, but after X-ray therapy she used daily sunscreens with very high sun protection factors, which attenuated the actinic damage. Considering the specific personality of the autistic painter, outpatient radiation therapy was a good alternative to inpatient surgery. C1 Univ Gottingen, D-3400 Gottingen, Germany. RP Schauder, S (reprint author), Univ Klinikum Gottingen, Hautklin, Von Siebold Str 3, D-37075 Gottingen, Germany. EM schauder@med.uni-goettingen.de CR BREUNINGER H, 2003, DERMATOLOGISCHE QUAL, V3, pS165 HEUER M, 1997, HEXEN FLIEGEN UNSTER HOHENLEUTNER U, 1996, STRAHLENTHERAPIE DER, pS163 NICOLAUS F, 1991, ART, V8, P60 ROSENTHAL NE, 1993, JAMA-J AM MED ASSOC, V270, P2717, DOI 10.1001/jama.270.22.2717 SUTER KW, 1990, DERMATOLOGISCHE RONT, V36, P1182 NR 6 TC 0 Z9 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0017-8470 J9 HAUTARZT JI Hautarzt PD JAN PY 2006 VL 57 IS 1 BP 51 EP 54 DI 10.1007/s00105-004-0887-0 PG 4 WC Dermatology SC Dermatology GA 013RQ UT WOS:000235427400008 PM 15657731 ER PT J AU Geier, DA Geier, MR AF Geier, David A. Geier, Mark R. TI A clinical and laboratory evaluation of methionine cycle-transsulfuration and androgen pathway markers in children with autistic disorders SO HORMONE RESEARCH LA English DT Article DE precocious puberty; pervasive developmental delay; sex steroid hormones; sexual development ID PLASMA TOTAL HOMOCYSTEINE; INDIVIDUALS; PREVALENCE; STEROIDS AB Background/Aims: The prevalence of autism spectrum disorders (ASDs) is 1 in 300 children in the US. ASDs are characterized by impairments in social relatedness and communication, repetitive behaviors, abnormal movement patterns, and sensory dysfunction. Pre-pubertal age children with ASDs were assessed for metabolites in the methionine cycle-transsulfuration and androgen pathways, and for present physical development/behaviors indicative of hyperandrogenicity. Methods: The Institutional Review Board of the Institute for Chronic Illnesses (Office for Human Research Protections, US Department of Health and Human Services IRB number: IRB00005375) approved the present study. Sixteen consecutive pre-pubertal age children (<= 11 years old; mean SD: 5.9 +/- 2.1 years old) with previously diagnosed ASDs that presented to the Genetic Centers of America for outpatient care were evaluated. Results: Significantly (p < 0.01) increased levels of serum/plasma dehydroepiandrosterone and serum total testosterone relative to the age- and sex-specific normal laboratory reference ranges were observed. Conversely, serum follicle-stimulating hormone levels were significantly (p < 0.01) decreased. Plasma-reduced glutathione (p < 0.01), plasma cysteine (p < 0.01), plasma methionine (p < 0.01), serum cystathionine (p < 0.05), and serum homocysteine (p < 0.01) were all significantly decreased. Conclusion: The results suggest a possible cyclical interaction between the methionine cycle-transsulfuration and androgen pathways in some children with ASDs. Copyright (c) 2006 S. Karger AG, Basel. C1 Genet Ctr Amer, Silver Spring, MD 20905 USA. MedCon Inc, Silver Spring, MD 20905 USA. RP Geier, DA (reprint author), Genet Ctr Amer, 14 Redgate Ct, Silver Spring, MD 20905 USA. 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Although a definite genetic cause has not yet been fully demonstrated, family based studies suggest that a multigenic pattern may be responsible for susceptibility, but most results are conflicting and have yet to be replicated. The purpose of this investigation was to analyze the linkage of the human leukocyte antigen (HLA) and the human serotonin transporter coding (5-HTTLPR) genes with ASD in a group of 37 families of Sardinian ethnicity in insular Italy. In 50% of these families, ASD is linked to HLA, and in the other 50% it is linked to 5-HTTLPR polymorphic genes; in other words, linkage to one or the other was evident in all cases. Despite a very homogenous genetic pattern being generally reported for Sardinians, the linkage observed with HLA and 5-HTTLPR genetic regions indicated a statistically defined heterogeneity (p = 0.002). No allelic HLA or 5-HTTLPR polymorphisms were specifically associated with ASD, suggesting these loci as markers of other genes mapped in their close proximity that may be more directly involved and thus may merit further analytical studies. C1 Don Gnocchi Fdn, IRCCS S Maria Nascent, Lab Mol Med & Biotechnol, I-20148 Milan, Italy. Univ Sassari, Inst Child Neuropsychiat, I-07100 Sassari, Italy. Univ Sassari, Inst Clin Neurol, I-07100 Sassari, Italy. Policlin San Matteo, IRCCS, Unit Clin Epidemiol & Biometry, I-27100 Pavia, Italy. Univ Milan, Dept Biomed Sci & Technol, Chair Virol, I-20133 Milan, Italy. RP Ferrante, P (reprint author), Don Gnocchi Fdn, IRCCS S Maria Nascent, Lab Mol Med & Biotechnol, Via Capecelatro 66, I-20148 Milan, Italy. 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TI Deafness and theory of mind: The role of task format in understanding false belief in deaf children and adolescents SO INFANCIA Y APRENDIZAJE LA Spanish DT Article DE hearing deficiency; theory of mind; false belief; task format ID 2ND-ORDER BELIEFS; NORMAL-HEARING; ATTRIBUTION; AUTISM AB The study investigates whether certain type of tasks makes it easier for deaf children and adolescents to comprehend false belief Fifty four pre-lingual deaf subjects (6-19 years old), late-signers born to hearing parents, were tested with two types of false belief tasks, These are adaptations of Baron-Cohen, Leslie, and Firth's change of location task, and Hogrefe, Wimmer and Perner's unexpected content task. The results show that the unexpected content task significantly facilitates performance in 11-13 year-old children. 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Aprendiz. PY 2006 VL 29 IS 4 BP 471 EP 484 PG 14 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 114HB UT WOS:000242656200007 ER PT J AU Robins, B Dautenhahn, K Dubowski, J AF Robins, Ben Dautenhahn, Kerstin Dubowski, Janek TI Does appearance matter in the interaction of children with autism with a humanoid robot? SO INTERACTION STUDIES LA English DT Article DE Human-Robot Interaction; robot appearance; assistive technology; autism ID IMITATION; RESPONSIVENESS; TOYS; MIND AB This article studies the impact of a robot's appearance on interactions involving four children with autism. This work is part of the Aurora project with the overall aim to support interaction skills in children with autism, using robots as 'interactive toys' that can encourage and mediate interactions. We follow an approach commonly adopted in assistive robotics and work with a small group of children with autism. This article investigates which robot appearances are suitable to encourage interactions between a robot and children with autism. The children's levels of interaction with and response to different appearances of two types of robots are compared: a small humanoid doll, and a life-sized 'Theatrical Robot' (a mime artist behaving like a robot). The small humanoid robot appeared either as a human-like 'pretty doll' or as a 'robot' with plain features. The Theatrical Robot was presented either as an ordinary human, or with plain clothing and a featureless, masked face. The results of these trials clearly indicate the children's preference in their initial response for interaction with a plain, featureless robot over the interaction with a human-like robot. In the case of the life-size Theatrical Robot, the response of children towards the plain/robotic robot was notably more social and pro-active. 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Stud. PY 2006 VL 7 IS 3 BP 479 EP 512 PG 34 WC Communication; Linguistics SC Communication; Linguistics GA 146NZ UT WOS:000244942600012 ER PT J AU Adams, C Lloyd, J Aldred, C Baxendale, J AF Adams, C Lloyd, J Aldred, C Baxendale, J TI Exploring the effects of communication intervention for developmental pragmatic language impairments: a signal-generation study SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE pragmatic language impairment; intervention; language disorder; single case series ID IMPAIRED CHILDREN; DISORDER; AUTISM; DIFFICULTIES; CHECKLIST AB Background: The remediation of pragmatic problems forms a significant part of the caseload for professionals working with children with communication problems. There is little systematic evidence that demonstrates the benefits of speech and language therapy for children whose difficulties he primarily within the pragmatic domain or which indicates whether changes in pragmatic behaviours, which are a result of a specific intervention, can be measured over time. Aims: To generate a signal of change in pragmatic and other language behaviours for children with pragmatic language impairments; to gauge the magnitude and nature of the signal and to make recommendations for future studies. Methods and Procedures: A case series of six children with pragmatic language impairments without diagnosis of autism received 8 weeks of individual intensive speech and language therapy supported in a mainstream educational setting in the UK. Measures of pragmatic behaviours in conversation were made at seven data points before and after therapy using Bishop's ALICC procedure. Conversation coders were blind to the point of assessment. Inferential comprehension, narrative, sentence formulation and sentence recall skins were also tested before and after therapy. The opinions of teachers and parents were sought regarding any change in communication and social abilities of the children over time. Outcomes and Results: All children showed change in communication behaviour on some conversational measures, even if the child functioned at the ceiling on standardized language testing. Some conversation measures had more utility as outcome measures than others. Most children showed substantial change on standardized language measures, but there are limitations on the use of these due to heterogeneity within the group. Overall, the intervention produced a signal for change in pragmatics and/or language behaviour in all children. Parent/teacher opinion reported demonstrable change in communication behaviour and engagement in the curriculum. Conclusions: There is a strong signal that change in pragmatic language behaviour can be measured in well-controlled intervention studies but this signal is complex. Outcome measures should take into account changes in language processing skills that are significantly impaired in many children with PLI. For those children within the PLI group who function at ceiling on language tests, conversational measures may have the potential to signal change, but this finding has not been subjected to group study or to testing in generalized settings. Qualitative data regarding behaviour, classroom engagement and generalization of language gains will be an essential supplement to measuring progress in a diverse population. C1 Univ Manchester, Commun & Deafness Grp, Manchester M13 9PL, Lancs, England. RP Adams, C (reprint author), Univ Manchester, Commun & Deafness Grp, Oxford Rd, Manchester M13 9PL, Lancs, England. 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PD JAN-FEB PY 2006 VL 41 IS 1 BP 41 EP 65 DI 10.1080/13693780500179793 PG 25 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 003XY UT WOS:000234717800003 PM 16272002 ER PT J AU Pardo, CA Vargas, DL Zimmerman, AW AF Pardo, CA Vargas, DL Zimmerman, AW TI Immunity, neuroglia and neuroinflammation in autism SO INTERNATIONAL REVIEW OF PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; INFANTILE-AUTISM; RISK-FACTORS; AUTOIMMUNE-DISEASES; CEREBROSPINAL-FLUID; MULTIPLE-SCLEROSIS; LANGUAGE DISORDER; MEASLES-VIRUS; TGF-BETA AB Autism is a complex neurodevelopmental disorder of early onset that is highly variable in its clinical presentation. Although the causes of autism in most patients remain unknown, several lines of research support the view that both genetic and environmental factors influence the development of abnormal cortical circuitry that underlies autistic cognitive processes and behaviors. The role of the immune system in the development of autism is controversial. Several studies showing peripheral immune abnormalities support immune hypotheses, however until recently there have been no immune findings in the CNS. We recently demonstrated the presence of neuroglial and innate neuroimmune system activation in brain tissue and cerebrospinal fluid of patients with autism, findings that support the view that neuroimmune abnormalities occur in the brain of autistic patients and may contribute to the diversity of the autistic phenotypes. The role of neuroglial activation and neuroinflammation are still uncertain but could be critical in maintaining, if not also in initiating, some of the CNS abnormalities present in autism. A better understanding of the role of neuroinflammation in the pathogenesis of autism may have important clinical and therapeutic implications. C1 Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21287 USA. Johns Hopkins Univ, Sch Med, Dept Pathol, Div Neuroimmunol & Infect Disorders, Baltimore, MD 21287 USA. Kennedy Kriegar Inst, Baltimore, MD USA. RP Pardo, CA (reprint author), Johns Hopkins Univ, Sch Med, Dept Neurol, Pathol 627,600 N Wolfe St, Baltimore, MD 21287 USA. 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Rev. Res. Ment. Retard. PY 2006 VL 32 BP 197 EP 227 DI 10.1016/S0074-7750(06)32007-1 PG 31 WC Education, Special; Psychology; Psychology, Multidisciplinary; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA BFJ79 UT WOS:000242402700007 ER PT S AU Avchen, RN Bhasin, TK Braun, KV Yeargin-Allsopp, M AF Avchen, Rachel Nonkin Bhasin, Tanya Karapurkar Braun, Kim Van Naarden Yeargin-Allsopp, Marshalyn BE Urbano, RC Hodapp, RM TI Public health impact: Metropolitan Atlanta Developmental Disabilities Surveillance Program SO INTERNATIONAL REVIEW OF RESEARCH IN MENTAL RETARDATION, VOL 33: DEVELOPMENTAL EPIDEMIOLOGY OF MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES SE International Review of Research in Mental Retardation LA English DT Article; Book Chapter ID CHILDHOOD VISION IMPAIRMENT; MAGNESIUM-SULFATE EXPOSURE; LOW-BIRTH-WEIGHT; MENTAL-RETARDATION; 10-YEAR-OLD CHILDREN; CEREBRAL-PALSY; DESCRIPTIVE EPIDEMIOLOGY; RUBELLA VACCINE; RISK-FACTORS; AUTISM C1 Natl Ctr Birth Defects & Dev Disabil, Ctr Dis Control & Prevent, Atlanta, GA USA. RP Avchen, RN (reprint author), Natl Ctr Birth Defects & Dev Disabil, Ctr Dis Control & Prevent, Atlanta, GA USA. 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Rev. Res. Ment. Retard. PY 2006 VL 33 BP 149 EP 190 DI 10.1016/S0074-7750(06)33007-8 PG 42 WC Education, Special; Psychology, Multidisciplinary; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA BFR31 UT WOS:000243971700007 ER PT J AU Wachtel, LE Hagopian, LP AF Wachtel, Lee E. Hagopian, Louis P. TI Psychopharmacology and applied behavioral analysis: Tandem treatment of severe problem behaviors in intellectual disability and a case series SO ISRAEL JOURNAL OF PSYCHIATRY AND RELATED SCIENCES LA English DT Article ID MENTALLY-RETARDED PERSONS; SELF-INJURIOUS-BEHAVIOR; FUNCTIONAL-ANALYSIS; YOUNG-ADULTS; RETARDATION; PSYCHOPATHOLOGY; CHILDREN; PEOPLE; REINFORCEMENT; ADOLESCENTS AB Many individuals with intellectual disability will at some time in their lives engage in problem behaviors that may place them and others at risk, and reduce their opportunities for healthy psychosocial functioning. These behaviors may reach severe proportions in both intensity and frequency, necessitating intervention. Both psychiatrists and behaviorists are often approached regarding negative behaviors in intellectual disability, and each discipline offers key tools in behavioral assessment and resolution. We believe that the coordinated effort of these two disciplines affords the most comprehensive and efficacious method of assessing, understanding and treating a wide range of problem behaviors and associated psychiatric pathology in individuals with various forms of intellectual disability. This paper briefly reviews the background of problem behaviors in intellectual disability and treatment of such disturbances through separate psychiatric and applied behavioral modalities, followed by the proposed coordinated neurobehavioral model. A case series ensues, describing the successful application of the neurobehavioral model to the severe problem behaviors demonstrated by three individuals with intellectual disability related to autism, Cornelia de Lange syndrome and traumatic brain injury. C1 Kennedy Krieger Inst, Neurobehav Unit, Dept Child & Adolescent Psychiat, Baltimore, MD 21205 USA. Kennedy Krieger Inst, Neurobehav Unit, Dept Behav Psychol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. RP Wachtel, LE (reprint author), Kennedy Krieger Inst, Neurobehav Unit, Dept Child & Adolescent Psychiat, 707 N Broadway St, Baltimore, MD 21205 USA. 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J. Psychiatr. Relat. Sci. PY 2006 VL 43 IS 4 BP 265 EP 274 PG 10 WC Psychiatry SC Psychiatry GA 133DE UT WOS:000243991000006 PM 17338446 ER PT J AU Adams, JB George, F Audhya, T AF Adams, JB George, F Audhya, T TI Abnormally high plasma levels of vitamin B-6 in children with autism not taking supplements compared to controls not taking supplements SO JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE LA English DT Article ID DOUBLE-BLIND CROSSOVER; MAGNESIUM; PYRIDOXINE; DEFICIENCY; SUBGROUP; DISORDER; BEHAVIOR; THERAPY; ACID; TERM AB Background: There have been many studies of the effect of high-dose supplementation of vitamin 136 on children and adults with autism, with all but one reporting benefits. Objective: The aim of this study was to investigate the biochemical basis for vitamin B-6 therapy by measuring the level of total vitamin B-6 in the plasma of unsupplemented children with autism spectrum disorder compared to unsupplemented control subjects. Participants: Children with autism spectrum disorders (n = 35, age 3-9 years) and unrelated typical children (n = 11, age 6-9 years), all from Arizona, were studied. (This includes the data from 24 children with autism from our previous study.) Methodology: A microbiologic assay was used to measure the level of total vitamin 136 (including phosphorylated and unphosphorylated forms), in a blinded fashion. Results: Children with autism had a 75% higher level of total vitamin B-6 than the controls (medians of 56 versus 32 ng/mL, respectively, p = 0.00002). Most of the autistic children (77%) had levels that were more than 2 standard deviations above the median value of the controls. The autistic girls (n = 5) also had elevated levels (mean of 54.6 ng/mL, median of 60 ng/mL). Discussion: These results are consistent with previous studies that found that: (1) pyridoxal kinase had a very low activity in children with autism and (2) pyridoxal 5 phosphate (PLP) levels are unusually low in children with autism. Thus, it appears that the low conversion of pyridoxal and pyridoxine to PLP results in low levels of PLP, which is the active cofactor for 113 known enymatic reactions, including the formation of many key neurotransmitters. Conclusions: Total vitamin B-6 is abnormally high in autism, consistent with previous reports of an impaired pyridoxal kinase for the conversion of pyridoxine and pyridoxal to PLP. This may explain the many published studies of benefits of high-dose vitamin B-6 supplementation in some children and adults with autism. C1 Arizona State Univ, Tempe, AZ 85287 USA. Integrat Med Hlth Care, Scottsdale, AZ USA. Vitamin Diagnost, Clifford Beach, NJ USA. RP Adams, JB (reprint author), Arizona State Univ, POB 876006, Tempe, AZ 85287 USA. 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Autism Dev. Disord. PD JAN PY 2006 VL 36 IS 1 BP 1 EP 3 DI 10.1007/s10803-005-0048-z PG 3 WC Psychology, Developmental SC Psychology GA 034UY UT WOS:000236957300001 ER PT J AU Happe, F Frith, U AF Happe, F Frith, U TI The weak coherence account: Detail-focused cognitive style in autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE autism spectrum disorders; central coherence; cognitive style; individual differences; local-global processing ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; SELECTIVE ATTENTION; GLOBAL PRECEDENCE; NEURAL MECHANISMS; FIELD-DEPENDENCE; SEX-DIFFERENCES; VISUAL-SEARCH; CHILDREN; INDIVIDUALS AB "Weak central coherence" refers to the detail-focused processing style proposed to characterise autism spectrum disorders (ASD). The original suggestion of a core deficit in central processing resulting in failure to extract global form/meaning, has been challenged in three ways. First, it may represent an outcome of superiority in local processing. Second, it may be a processing bias, rather than deficit. Third, weak coherence may occur alongside, rather than explain, deficits in social cognition. A review of over 50 empirical studies of coherence suggests robust findings of local bias in ASD, with mixed findings regarding weak global processing. Local bias appears not to be a mere side-effect of executive dysfunction, and may be independent of theory of mind deficits. Possible computational and neural models are discussed. C1 Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, London SE5 8AF, England. UCL, Inst Cognit Neurosci, London, England. RP Happe, F (reprint author), Kings Coll London, Inst Psychiat, Social Genet & Dev Psychiat Ctr, De Crespigny Pk,Denmark Hill,POB P080, London SE5 8AF, England. 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Increased perceptual expertise may be implicated in the choice of special ability in savant autistics, and in the variability of apparent presentations within PDD (autism with and without typical speech, Asperger syndrome) in non-savant autistics. The overfunctioning of brain regions typically involved in primary perceptual functions may explain the autistic perceptual endophenotype. C1 Hop Riviere Des Prairies, Pervas Dev Disorders Specialized Clin, Montreal, PQ H1E 1A4, Canada. Univ Montreal, Fernand Seguin Res Ctr, Montreal, PQ, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada. Univ Provence Cote Azur, Marseille, France. McGill Univ, Dept Educ Psychol, Montreal, PQ, Canada. RP Mottron, L (reprint author), Hop Riviere Des Prairies, Pervas Dev Disorders Specialized Clin, 7070 Blvd Perras, Montreal, PQ H1E 1A4, Canada. 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Autism Dev. Disord. PD JAN PY 2006 VL 36 IS 1 BP 27 EP 43 DI 10.1007/s10803-005-0040-7 PG 17 WC Psychology, Developmental SC Psychology GA 034UY UT WOS:000236957300003 PM 16453071 ER PT J AU Kemner, C van Engeland, H AF Kemner, C van Engeland, H TI ERPs and eye movements reflect atypical visual perception in pervasive developmental disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE event-related potential; P300; eye movement; perception ID EVENT-RELATED POTENTIALS; AUTISM SPECTRUM DISORDER; SPATIAL-FREQUENCY; GLOBAL PRECEDENCE; FACE PERCEPTION; DIVIDED ATTENTION; BIOLOGICAL MOTION; ASPERGER-SYNDROME; BRAIN POTENTIALS; YOUNG-CHILDREN AB Many studies of eye tracking or event-related brain potentials (ERPs) in subjects with Pervasive Developmental Disorder (PDD) have yielded inconsistent results on attentional processing. 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Autism Dev. Disord. PD JAN PY 2006 VL 36 IS 1 BP 45 EP 54 DI 10.1007/s10803-005-0041-6 PG 10 WC Psychology, Developmental SC Psychology GA 034UY UT WOS:000236957300004 PM 16374670 ER PT J AU Bertone, A Faubert, J AF Bertone, A Faubert, J TI Demonstrations of decreased sensitivity to complex motion information not enough to propose an autism-specific neural etiology SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; low-level information processing; motion processing; form processing; neural networks; lateral inhibition ID FRAGILE-X-SYNDROME; HUMAN VISUAL-SYSTEM; BIOLOGICAL MOTION; 2ND-ORDER MOTION; ASPERGER-SYNDROME; WILLIAMS-SYNDROME; PERCEPTION; CHILDREN; DEFICIT; DORSAL AB Interest regarding neural information processing in autism is growing because atypical perceptual abilities are a characteristic feature of persons with autism. 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SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; audition; perception; complexity; local; global ID EVENT-RELATED POTENTIALS; DEVELOPMENTAL LANGUAGE DISORDER; MISMATCH NEGATIVITY MMN; EVOKED POTENTIALS; ABSOLUTE PITCH; ASPERGER-SYNDROME; CENTRAL COHERENCE; CHILDHOOD AUTISM; N1 WAVE; CHILDREN AB To test the hypothesis that level of neural complexity explain the relative level of performance and brain activity in autistic individuals, available behavioural, ERP and imaging findings related to the perception of increasingly complex auditory material under various processing tasks in autism were reviewed. Tasks involving simple material (pure tones) and/or low-level operations (detection, labelling, chord disembedding, detection of pitch changes) show a superior level of performance and shorter ERP latencies. 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Autism Dev. Disord. PD JAN PY 2006 VL 36 IS 1 BP 91 EP 106 DI 10.1007/s10803-005-0050-5 PG 16 WC Psychology, Developmental SC Psychology GA 034UY UT WOS:000236957300008 PM 16477517 ER PT J AU Plaisted, K Dobler, V Bell, S Davis, G AF Plaisted, K Dobler, V Bell, S Davis, G TI The microgenesis of global perception in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE local; global; attention; perception; feature; configuration ID HIGH-FUNCTIONING AUTISM; HIERARCHICAL PATTERNS; ENHANCED DISCRIMINATION; SELECTIVE ATTENTION; SPATIAL-FREQUENCY; ASPERGER-SYNDROME; CHILDREN; DEFICIT; TASK AB Several studies have reported that individuals with autism and Asperger's syndrome show a local processing bias on tasks involving features and configurations. This study assessed whether this bias results from differences in the perception of features or a cognitive bias to attend to features in autism as a consequence of a deficit in attending to configurations. Children with autism and typically developing children performed a task assessing the initial perceptual representation of features and configurations following a 50 ms stimulus display and the development of the perceptual representation by grouping processes following an 800 ms stimulus display. No differences were observed between the two groups, suggesting that the perceptual and attentional mechanisms marshalled by this task operate typically in children with autism. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP Plaisted, K (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. 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Autism Dev. Disord. PD JAN PY 2006 VL 36 IS 1 BP 107 EP 116 DI 10.1007/s10803-005-0047-0 PG 10 WC Psychology, Developmental SC Psychology GA 034UY UT WOS:000236957300009 PM 16450044 ER PT J AU Iarocci, G Burack, JA Shore, DI Mottron, L Enns, JT AF Iarocci, G Burack, JA Shore, DI Mottron, L Enns, JT TI Global-local visual processing in high functioning children with autism: Structural vs. implicit task biases SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE global and local perception; visual search; attentional bias ID FACE RECOGNITION; PERCEPTION; INDIVIDUALS; ATTENTION; SEARCH; EYES; INFORMATION; PRECEDENCE; ABILITIES; FIXATION AB Global-local processing was examined in high-functioning children with autism and in groups of typically developing children. In experiment 1, the effects of structural bias were tested by comparing visual search that favored access to either local or global targets. The children with autism were not unusually sensitive to either level of visual structure. In experiment 2 a structural global bias was pitted against an implicit task bias favoring the local level. Children with autism were least sensitive to the structural global bias but showed greater sensitivity to the implicit task bias. This suggests that autism is associated with differences in the executive control processes used to guide attention to either the global or local level, and strategies may be more "data driven". C1 Simon Fraser Univ, Dept Psychol, Burnaby, BC V5A 1S6, Canada. McGill Univ, Dept Educ Psychol, Montreal, PQ, Canada. Hop Riviere Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ, Canada. McMaster Univ, Dept Psychol Neurosci & Behav, Hamilton, ON, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. Univ British Columbia, Dept Psychol, Vancouver, BC V5Z 1M9, Canada. RP Iarocci, G (reprint author), Simon Fraser Univ, Dept Psychol, 8888 Univ Dr, Burnaby, BC V5A 1S6, Canada. 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Autism Dev. Disord. PD JAN PY 2006 VL 36 IS 1 BP 117 EP 129 DI 10.1007/s10803-005-0045-2 PG 13 WC Psychology, Developmental SC Psychology GA 034UY UT WOS:000236957300010 PM 16397823 ER PT J AU Bar-Haim, Y Shulman, C Lamy, D Reuveni, A AF Bar-Haim, Y Shulman, C Lamy, D Reuveni, A TI Attention to eyes and mouth in high-functioning children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; attention; face processing; probe detection; eyes; dot probe ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGER-SYNDROME; FACE RECOGNITION; FIXATION; ADULTS; INDIVIDUALS; EXPERTISE; DEFICITS AB In the present study, we used a probe-detection task to compare attentional allocation to the eyes versus mouth regions of the face in high-functioning boys with autism relative to normal control boys matched for chronological age and IQs. We found that with upright faces, children from both groups attended more to the eyes region than to the mouth region, and to the same extent. This pattern of behavior was observed for not only initial orientation of attention, but also when enough time was provided for attention to be disengaged from its initial locus. The present findings suggest that atypical face processing in autism does not result from abnormal attentional allocation to the different face parts. C1 Tel Aviv Univ, Dept Psychol, Adler Ctr Res Child Dev & Psychopathol, IL-69978 Tel Aviv, Israel. Hebrew Univ Jerusalem, Jerusalem, Israel. RP Bar-Haim, Y (reprint author), Tel Aviv Univ, Dept Psychol, Adler Ctr Res Child Dev & Psychopathol, IL-69978 Tel Aviv, Israel. EM yair1@post.tau.ac.il RI Lamy, Dominique/L-5032-2013 CR Achenbach TM, 1991, MANUAL CHILD BEHAV C (APA) APA, 2000, DIAGN STAT MAN MENT BaronCohen S, 1997, VIS COGN, V4, P311, DOI 10.1080/713756761 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Dalton KM, 2005, NAT NEUROSCI, V8, P519, DOI 10.1038/nn1421 DIAMOND R, 1986, J EXP PSYCHOL GEN, V115, P107, DOI 10.1037/0096-3445.115.2.107 Gauthier I, 2001, CURR OPIN NEUROBIOL, V11, P219, DOI 10.1016/S0959-4388(00)00200-2 GOREN CC, 1975, PEDIATRICS, V56, P544 Johnson Mark H., 1991, BIOL COGNITIVE DEV C Joseph RM, 2003, J CHILD PSYCHOL PSYC, V44, P529, DOI 10.1111/1469-7610.00142 Klin A, 2002, ARCH GEN PSYCHIAT, V59, P809, DOI 10.1001/archpsyc.59.9.809 LAHAIE A, IN PRESS NEUROPSYCHO LANGDELL T, 1978, J CHILD PSYCHOL PSYC, V19, P255, DOI 10.1111/j.1469-7610.1978.tb00468.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 Matsumoto D., 1988, JAPANESE CAUCASIAN F NAVON D, 1983, Q J EXP PSYCHOL-A, V35, P497 Nelson CA, 2001, INFANT CHILD DEV, V10, P3, DOI 10.1002/icd.239 Pelphrey KA, 2002, J AUTISM DEV DISORD, V32, P249, DOI 10.1023/A:1016374617369 POSNER MI, 1980, J EXP PSYCHOL GEN, V109, P160, DOI 10.1037//0096-3445.109.2.160 Ristic J, 2005, COGNITIVE BRAIN RES, V24, P715, DOI 10.1016/j.cogbrainres.2005.02.007 Schultz RT, 2005, INT J DEV NEUROSCI, V23, P125, DOI 10.1016/j.ijdevneu.2004.12.012 Tanaka J. 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PD JAN PY 2006 VL 36 IS 1 BP 131 EP 137 DI 10.1007/s10803-005-0046-1 PG 7 WC Psychology, Developmental SC Psychology GA 034UY UT WOS:000236957300011 PM 16402154 ER PT J AU van Lang, NDJ Boomsma, A Sytema, S de Bildt, AA Kraijer, DW Ketelaars, C Minderaa, RB AF van Lang, NDJ Boomsma, A Sytema, S de Bildt, AA Kraijer, DW Ketelaars, C Minderaa, RB TI Structural equation analysis of a hypothesised symptom model in the autism spectrum SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism spectrum disorder; symptom structure; structural equation modelling ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; DIMENSIONAL CLASSIFICATION; FIELD TRIAL; DSM-IV; CHILDREN; DOMAINS AB Background: Several studies showed a different symptom structure underlying the spectrum of autistic-like disorders from the behaviour triad as mentioned in the DSM-IV. In the present study, a hypothesised symptom model for autism was constructed, based on earlier explorative findings, and was put to a confirmatory test. Method: Items from the Autism Diagnostic Interview-Revised (ADI-R) were used to examine the goodness of fit of the DSM-IV model, the hypothesised symptom model, and two additional models for autism. All models were tested in a group of 255 verbal and nonverbal individuals with minor to severe autistic symptomatology. Results: The DSM-IV model encountered estimation problems. Conversely, the hypothesised symptom model had no such problems and proved to have a better fit to the sample data than the two additional models for autism. However, some of the observed variables were weak indicators of the three latent factors in the model. Conclusions: The hypothesised symptom model appeared to be a plausible model in a group of individuals with a broad range of autistic behaviours and levels of functioning. Nevertheless, the stability of the model needs further examination in a larger group of individuals with disorders in the autism spectrum, and with varying degrees of intellectual functioning. C1 Univ Groningen, Dept Stat & Measurement Theory, NL-9712 TG Groningen, Netherlands. Univ Groningen, Dept Child & Adolescent Psychit, NL-9700 AB Groningen, Netherlands. Univ Groningen, Dept Psychiat, NL-9700 AB Groningen, Netherlands. RP Boomsma, A (reprint author), Univ Groningen, Dept Stat & Measurement Theory, Boumangebouw,Grote Rozenstr 31, NL-9712 TG Groningen, Netherlands. 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Child Psychol. Psychiatry PD JAN PY 2006 VL 47 IS 1 BP 37 EP 44 DI 10.1111/j.1469-7610.2005.01434.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 995TP UT WOS:000234127200005 PM 16405639 ER PT J AU Bebko, JM Weiss, JA Demark, JL Gomez, P AF Bebko, JM Weiss, JA Demark, JL Gomez, P TI Discrimination of temporal synchrony in intermodal events by children with autism and children with developmental disabilities without autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE attention; auditory-visual perception; autistic disorder; information processing; intermodal processing; language ID ADAPTIVE-BEHAVIOR SCALES; PERCEPTION; INFANTS; SPEECH; COMPREHENSION; INFORMATION; VALIDITY; SOUNDS; MEMORY AB Background: This project examined the intermodal perception of temporal synchrony in 16 young children (ages 4 to 6 years) with autism compared to a group of children without impairments matched on adaptive age, and a group of children with other developmental disabilities matched on chronological and adaptive age. Method: A preferential looking paradigm was used, where participants viewed non-linguistic, simple linguistic or complex linguistic events on two screens displaying identical video tracks, but one offset from the other by 3 seconds, and with the single audio track matched to only one of the displays. Results: As predicted, both comparison groups demonstrated significant non-random preferential looking to violations of temporal synchrony with linguistic and non-linguistic stimuli. However, the group with autism showed an impaired, chance level of responding, except when presented with non-linguistic stimuli. Conclusions: Several explanations are offered for this apparently autism-specific, language-specific pattern of responding to temporal synchrony, and potential developmental sequelae are discussed. C1 York Univ, Dept Psychol, Toronto, ON M3J 1P3, Canada. RP Bebko, JM (reprint author), York Univ, Dept Psychol, 4700 Keele St, Toronto, ON M3J 1P3, Canada. 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S., 1981, INFANT SOCIAL COGNIT SPELKE ES, 1976, COGNITIVE PSYCHOL, V5, P553 SPELKE ES, 1979, DEV PSYCHOL, V15, P626 Sponheim E, 1996, J AUTISM DEV DISORD, V26, P513, DOI 10.1007/BF02172273 WALKERANDREWS AS, 1994, J AUTISM DEV DISORD, V24, P99, DOI 10.1007/BF02172216 WALKER-ANDREWS A S, 1991, Ecological Psychology, V3, P55, DOI 10.1207/s15326969eco0302_1 Waterhouse L, 1996, PSYCHOL REV, V103, P457, DOI 10.1037/0033-295X.103.3.457 NR 44 TC 46 Z9 46 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD JAN PY 2006 VL 47 IS 1 BP 88 EP 98 DI 10.1111/j.1469-7610.2005.01443.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 995TP UT WOS:000234127200011 PM 16405645 ER PT J AU Baird, G AF Baird, G TI Healthcare for children on the autism spectrum. A guide to medical, nutritional and behavioural issues. SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Book Review CR Volkmar FR, 2004, HEALTHCARE CHILDREN NR 1 TC 0 Z9 0 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry PD JAN PY 2006 VL 47 IS 1 BP 112 EP 112 DI 10.1111/j.1469-7610.2005.01573.x PG 1 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 995TP UT WOS:000234127200013 ER PT J AU Bukach, CM Bub, DN Gauthier, I Tarr, MJ AF Bukach, CM Bub, DN Gauthier, I Tarr, MJ TI Perceptual expertise effects are not all or none: Spatially limited perceptual expertise for faces in a case of prosopagnosia SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Article ID HUMAN EXTRASTRIATE CORTEX; OBJECT RECOGNITION; DEVELOPMENTAL PROSOPAGNOSIA; INFORMATION; MECHANISMS; FUSIFORM; AUTISM; CONFIGURATION; INVERSION; COMPONENT AB We document a seemingly unique case of severe prosopagnosia, L. R., who suffered damage to his anterior and inferior right temporal lobe as a result of a motor vehicle accident. We systematically investigated each of three factors associated with expert face recognition: fine-level discrimination, holistic processing, and configural processing (Experiments 1-3). Surprisingly, L. R. shows preservation of all three of these processes; that is, his performance in these experiments is comparable to that of normal controls. However, L. R. is only able to apply these processes over a limited spatial extent to the fine-level detail within faces. Thus, when the location of a given change is unpredictable (Experiment 3), L. R. exhibits normal detection of features and spatial configurations only for the lower half of each face. Similarly, when required to divide his attention over multiple face features, L. R. is able to determine the identity of only a single feature (Experiment 4). We discuss these results in the context of forming a better understanding of prosopagnosia and the mechanisms used in face recognition and visual expertise. We conclude that these mechanisms are not "all-or-none," but rather can be impaired incrementally, such that they may remain functional over a restricted spatial area. This conclusion is consistent with previous research suggesting that perceptual expertise is acquired in a spatially incremental manner [Gauthier, I., & Tarr, M. J. Unraveling mechanisms for expert object recognition: Bridging brain activity and behavior. Journal of Experimental Psychology: Human Perception & Performance, 28, 431-446, 2002]. C1 Vanderbilt Univ, Dept Psychol, Nashville, TN 37203 USA. Univ Victoria, Victoria, BC V8W 2Y2, Canada. Brown Univ, Providence, RI 02912 USA. RP Bukach, CM (reprint author), Vanderbilt Univ, Dept Psychol, 204 Wilson Hall, Nashville, TN 37203 USA. EM cindy.bukach@vanderbilt.edu RI Bukach, Cindy/E-7057-2010 CR Baddeley AD, 1994, DOORS PEOPLE TEST Barton JJS, 2003, NEUROPSYCHOLOGIA, V41, P1703, DOI 10.1016/S0028-3932(03)00115-5 Barton JJS, 2002, NEUROLOGY, V58, P71 Barton JJS, 2003, PERCEPTION, V32, P15, DOI 10.1068/p3460 Benton A. L., 1983, CONTRIBUTIONS NEUROP Brown J. A., 1993, NELSON DENNY READING BUB D, 1990, PSYCHLAB BUKACH CM, 2002, UNPUB STUDIES CONJUN BUKACH CM, UNPUB PRESERVATION M BUKACH CM, UNPUB LIMITS PERCEPT DAMASIO AR, 1990, TRENDS NEUROSCI, V13, P95, DOI 10.1016/0166-2236(90)90184-C DAMASIO AR, 1982, NEUROLOGY, V32, P331 Davidoff J., 1986, ASPECTS FACE PROCESS, P279 DIAMOND R, 1986, J EXP PSYCHOL GEN, V115, P107, DOI 10.1037/0096-3445.115.2.107 Duchaine BC, 2004, NEURON, V43, P469, DOI 10.1016/j.neuron.2004.08.006 Farah MJ, 1998, PSYCHOL REV, V105, P482, DOI 10.1037//0033-295X.105.3.482 FARAH MJ, 1995, NEUROPSYCHOLOGIA, V33, P661, DOI 10.1016/0028-3932(95)00002-K Gauthier I, 1997, VISION RES, V37, P1673, DOI 10.1016/S0042-6989(96)00286-6 Gauthier I, 2004, NEUROPSYCHOLOGIA, V42, P1961, DOI 10.1016/j.neuropsychologia.2004.04.025 Gauthier I, 2003, NAT NEUROSCI, V6, P428, DOI 10.1038/nn1029 Gauthier I, 1998, VISION RES, V38, P2401, DOI 10.1016/S0042-6989(97)00442-2 Gauthier I, 1999, J COGNITIVE NEUROSCI, V11, P349, DOI 10.1162/089892999563472 Gauthier I, 2002, J EXP PSYCHOL HUMAN, V28, P431, DOI 10.1037//0096-1523.28.2.431 Goldstein A. G., 1961, PSYCHON SCI, V6, P149 HAXBY JV, 1994, J NEUROSCI, V14, P6336 Henke K, 1998, CORTEX, V34, P289, DOI 10.1016/S0010-9452(08)70756-1 HOLE GJ, 1994, PERCEPTION, V23, P65, DOI 10.1068/p230065 Joseph RM, 2003, J CHILD PSYCHOL PSYC, V44, P529, DOI 10.1111/1469-7610.00142 Kanwisher N, 1997, J NEUROSCI, V17, P4302 Klin A, 2002, ARCH GEN PSYCHIAT, V59, P809, DOI 10.1001/archpsyc.59.9.809 LANGDELL T, 1978, J CHILD PSYCHOL PSYC, V19, P255, DOI 10.1111/j.1469-7610.1978.tb00468.x Leder H, 2000, Q J EXP PSYCHOL-A, V53, P513, DOI 10.1080/027249800390583 Leder H, 1998, Q J EXP PSYCHOL-A, V51, P449 Le Grand R, 2001, NATURE, V410, P890, DOI 10.1038/35073749 LEVINE DN, 1989, BRAIN COGNITION, V10, P149, DOI 10.1016/0278-2626(89)90051-1 MARASCUI.LA, 1970, PSYCHOMETRIKA, V35, P237, DOI 10.1007/BF02291265 McCarthy G, 1997, J COGNITIVE NEUROSCI, V9, P605, DOI 10.1162/jocn.1997.9.5.605 MCKELVIE SJ, 1976, AM J PSYCHOL, V89, P311, DOI 10.2307/1421414 MCNEIL JE, 1991, Q J EXP PSYCHOL-A, V43, P267 Moscovitch M, 1997, J COGNITIVE NEUROSCI, V9, P555, DOI 10.1162/jocn.1997.9.5.555 Nunn JA, 2001, NEUROCASE, V7, P15, DOI 10.1093/neucas/7.1.15 PUCE A, 1995, J NEUROPHYSIOL, V74, P1192 ROSCH E, 1976, COGNITIVE PSYCHOL, V8, P382, DOI 10.1016/0010-0285(76)90013-X Searcy JH, 1996, J EXP PSYCHOL HUMAN, V22, P904, DOI 10.1037/0096-1523.22.4.904 SERGENT J, 1984, BRIT J PSYCHOL, V75, P221 Sergent J., 1992, PROCESSING FACIAL IM, P55 SERGENT J, 1992, CEREB CORTEX, V2, P375, DOI 10.1093/cercor/2.5.375 Shallice T., 1988, NEUROPSYCHOLOGY MENT SNODGRASS JG, 1980, J EXP PSYCHOL-HUM L, V6, P174, DOI 10.1037/0278-7393.6.2.174 TANAKA JW, 1993, Q J EXP PSYCHOL-A, V46, P225 Tanaka JW, 1997, MEM COGNITION, V25, P583, DOI 10.3758/BF03211301 VIELE K, 2002, CASE STUDIES BAYESIA, V6, P91 WALKERSMITH GJ, 1978, PERCEPT PSYCHOPHYS, V24, P63, DOI 10.3758/BF03202975 Warrington E. K., 1994, RECOGNITION MEMORY T Warrington EK, 1991, VISUAL OBJECT SPACE Wenger MJ, 2003, J EXP PSYCHOL LEARN, V29, P1106, DOI 10.1037/0278-7393.29.6.1106 YIN RK, 1969, J EXP PSYCHOL, V81, P141, DOI 10.1037/h0027474 YOUNG AW, 1987, PERCEPTION, V16, P747, DOI 10.1068/p160747 NR 58 TC 57 Z9 58 PU M I T PRESS PI CAMBRIDGE PA 238 MAIN STREET, STE 500, CAMBRIDGE, MA 02142-1046 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PD JAN PY 2006 VL 18 IS 1 BP 48 EP 63 DI 10.1162/089892906775250094 PG 16 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 012VE UT WOS:000235368200005 PM 16417682 ER PT J AU Sigafoos, J O'Reilly, M Ma, CH Edrisinha, C Cannella, H Lancioni, GE AF Sigafoos, Jeff O'Reilly, Mark Ma, Chia Hui Edrisinha, Chaturi Cannella, Helen Lancioni, Giulio E. TI Effects of embedded instruction versus discrete-trial training on self-injury, correct responding, and mood in a child with autism SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article DE embedded instruction; discrete; trial training; self-injury; autism AB Background Embedded instruction and discrete-trial training are both recommended for teaching children with autism, but there is little research available comparing the two. The present study compared embedded instruction with discrete-trial training for a 12-year-old boy with autism. Method An initial functional analysis indicated that the boy's self-injury was maintained by escape from task demands. Instructional sessions to teach adaptive behaviours were conducted under two conditions: (i) during embedded instruction, learning trials were inserted into ongoing activities at a rate of approximately 1.5 per minute; (ii) during discrete-trial training, instructional opportunities were incorporated into structured sessions at a rate of 4 per minute. In both conditions, the system of least prompts was used to teach relevant target responses. Effects of the two teaching formats were evaluated using an ABABA design. Results Higher rates of self-injury and fewer correct responses occurred during discrete-trial training. Mood ratings were also lower during discrete-trial training. Conclusions The results suggest that self-injury, correct responding, and mood may be sensitive to the type of instructional format. Although discrete-trial training can be highly effective, it may be preferable to start with embedded instruction when the child presents with self-injurious escape behaviour. C1 Univ Tasmania, Sch Educ, Hobart, Tas 7001, Australia. Univ Texas, Austin, TX 78712 USA. Ohio State Univ, Columbus, OH 43210 USA. Univ Bari, I-70121 Bari, Italy. RP Sigafoos, J (reprint author), Univ Tasmania, Sch Educ, Private Bag 66, Hobart, Tas 7001, Australia. EM Jeff.Sigafoos@utas.edu.au CR CARR EG, 1985, BEHAV MODIF, V9, P403, DOI 10.1177/01454455850094001 Delprato DJ, 2001, J AUTISM DEV DISORD, V31, P315, DOI 10.1023/A:1010747303957 DUKER P, 2004, ONE ONE TRAINING INS Iwata B. A., 1982, ANAL INTERVENTION DE, V2, P1 IWATA BA, 1990, J APPL BEHAV ANAL, V23, P11, DOI 10.1901/jaba.1990.23-11 Johnson JW, 2004, J POSIT BEHAV INTERV, V6, P214, DOI 10.1177/10983007040060040301 Lovaas O. I., 2003, TEACHING INDIVIDUALS MIRENDALINNE F, 1992, RES DEV DISABIL, V13, P191 O'Reilly M, 2005, J AUTISM DEV DISORD, V35, P305, DOI 10.1007/s10803-005-3294-1 RICHARDS SB, 1999, SINGLE SUBJECT RES A Schopler E., 1988, CHILDHOOD AUTISM RAT SIGAFOOS J, 2003, CHALLENGING BEHAV DE Sparrow S, 1984, VINELAND ADAPTIVE BE West EA, 2005, EDUC TRAIN DEV DISAB, V40, P131 NR 14 TC 4 Z9 4 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PY 2006 VL 31 IS 4 BP 196 EP 203 DI 10.1080/1366825060099160 PG 8 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 145KX UT WOS:000244865000002 PM 17178531 ER PT J AU Lindsay, RL Arnold, LE Aman, MG Vitiello, B Posey, DJ McDougle, CJ Scahill, L Pachler, M McCracken, JT Tierney, E Bozzolo, D AF Lindsay, Ronald L. Arnold, L. Eugene Aman, Michael G. Vitiello, Benedetto Posey, David J. McDougle, Christopher J. Scahill, Lawrence Pachler, Maryellen McCracken, James T. Tierney, Elaine Bozzolo, Dawn TI Dietary status and impact of risperidone on nutritional balance in children with autism: A pilot study SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Article DE risperidone; nutrition; autism; children; adolescents AB Background Risperidone may be effective in improving tantrums, aggression, or self- injurious behaviour in children with autism, but often leads to weight gain. Method Using a quantitative Food Frequency Questionnaire (FFQ), we prospectively examined the nutritional intake of 20 children with autism participating in a randomised placebo-controlled trial of risperidone for disruptive behaviours. Results At baseline, the mean intakes for macronutrients, vitamins and minerals exceeded Dietary Reference Intakes (DRIs). However there was substantial inter-participant variability, with individual deficiencies (80% of DRI) in the intake of calcium (9 of 20 participants), pantothenic acid (6 of 20), vitamin D (5 of 20) and vitamin K (8 of 20). For the participants for whom FFQs were available, there was an increase in weight and an increase in vitamin K intake after 2 months of risperidone treatment (n=59) compared to placebo (n=58). An additional 4 months of risperidone treatment (n=58) did not result in significant changes in reported nutritional balance. Conclusion These pilot data suggest that treatment with risperidone did not significantly affect the nutritional balance of this small group of children. C1 St Josephs Hosp, Childrens Hlth Ctr, Arizona Child Study Ctr, Phoenix, AZ 85013 USA. Ohio State Univ, Columbus, OH 43210 USA. NIMH, Bethesda, MD 20892 USA. Indiana Univ, Sch Med, Indianapolis, IN USA. Yale Univ, New Haven, CT 06520 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Kennedy Krieger Inst, Baltimore, MD USA. RP Lindsay, RL (reprint author), St Josephs Hosp, Childrens Hlth Ctr, Arizona Child Study Ctr, 3600 N 3rd Ave, Phoenix, AZ 85013 USA. EM rlindsay@chw.edu CR AHEARN W, 2001, MAKING DIFFERENCE BE *FOOD NUTR BOARD N, 2000, DIET REF INT APPL DI Martin A, 2004, AM J PSYCHIAT, V161, P1125, DOI 10.1176/appi.ajp.161.6.1125 Patterson RE, 1999, ANN EPIDEMIOL, V9, P178, DOI 10.1016/S1047-2797(98)00055-6 RAITEN DJ, 1986, J AUTISM DEV DISORD, V16, P133, DOI 10.1007/BF01531725 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Rothman KJ, 1998, MODERN EPIDEMIOLOGY, V2nd, P115 Scahill L, 2001, J CHILD ADOL PSYCHOP, V11, P377, DOI 10.1089/104454601317261555 SHEARER TR, 1982, J AUTISM DEV DISORD, V12, P25, DOI 10.1007/BF01531671 Stigler Kimberly A, 2004, Paediatr Drugs, V6, P33, DOI 10.2165/00148581-200406010-00003 NR 10 TC 13 Z9 13 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PY 2006 VL 31 IS 4 BP 204 EP 209 DI 10.1080/13668250601006924 PG 6 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 145KX UT WOS:000244865000003 PM 17178532 ER PT J AU Ordog, G AF Ordog, G TI Molybdenum toxicity: Toxic leukoencephalopathy as a cause of autism. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Experimental Biology 2004 Annual Meeting CY APR 17-21, 2004 CL Washington, DC C1 Henry Mayo Hosp, Valencia, CA USA. NR 0 TC 1 Z9 1 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 2006 VL 54 IS 1 SU S MA 477 BP S161 EP S161 PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 011XH UT WOS:000235301500490 ER PT J AU Sikora, DM Pettit-Kekel, K Penfield, J Steiner, RD AF Sikora, DM Pettit-Kekel, K Penfield, J Steiner, RD TI The near-universal prevalence of autism spectrum disorders in children with Smith-Lemli-Opitz syndrome. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Experimental Biology 2004 Annual Meeting CY APR 17-21, 2004 CL Washington, DC C1 Oregon Hlth & Sci Univ, Dept Pediat, Portland, OR USA. Oregon Hlth & Sci Univ, Dept Mol & Med Genet, Portland, OR USA. Oregon Hlth & Sci Univ, Child Dev & Rehabil Ctr, Portland, OR USA. NR 0 TC 0 Z9 0 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 2006 VL 54 IS 1 SU S MA 325 BP S136 EP S136 PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 011XH UT WOS:000235301500338 ER PT J AU Sinha, R Osann, K Flodman, P Spence, MA AF Sinha, R Osann, K Flodman, P Spence, MA TI Investigation of the association between induced birth and autism spectrum disorder. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Experimental Biology 2004 Annual Meeting CY APR 17-21, 2004 CL Washington, DC C1 Western Univ Hlth Sci, Coll Osteopath Med, Pomona, CA USA. Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA USA. Univ Calif Irvine, Irvine, CA USA. NR 0 TC 0 Z9 0 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 2006 VL 54 IS 1 SU S MA 377 BP S144 EP S145 PG 2 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 011XH UT WOS:000235301500390 ER PT J AU Waltereit, R Welzl, H Dichgans, J Lipp, HP Schmidt, WJ Weller, M AF Waltereit, R Welzl, H Dichgans, J Lipp, HP Schmidt, WJ Weller, M TI Enhanced episodic-like memory and kindling epilepsy in a rat model of tuberous sclerosis SO JOURNAL OF NEUROCHEMISTRY LA English DT Article DE epilepsy; hippocampus; learning and memory; mitogen-activated protein kinase; tuberous sclerosis ID TERM SYNAPTIC PLASTICITY; EKER RAT; MAP KINASE; CEREBRAL-LESIONS; COMPLEX; HIPPOCAMPUS; GENE; FACILITATION; MECHANISMS; EXPRESSION AB Tuberous sclerosis complex (TSC) is a common neurological autosomal-dominant syndrome caused by mutations in the TSC1 or TSC2 genes. TSC starts in early childhood and is characterized by cerebral hamartomas (benign tumours), severe epilepsy and cognitive deficits such as mental retardation and autism. The hamartomas are characterized by loss of the remaining wild-type TSC allele, and clinical data implicate cerebral hamartomas in the generation of epileptic seizures, which may play a significant role in the development of mental retardation. The TSC2 mutation predicts alterations in mitogen-associated protein kinase (MAPK) and, together with the TSC1 mutation, in mammalian target of rapamycin (mTOR) signalling pathways. Both pathways are involved in neuronal plasticity. We therefore hypothesized that the heterozygous mutation itself, besides cerebral hamartomas, contributes to the pathogenesis of cognitive deficits and possibly also epilepsy. Here, we show that young adult TSC2+/- rats, which are virtually free of cerebral hamartomas, exhibit enhanced episodic-like memory and enhanced responses to chemically-induced kindling. The activation of cyclic adenosine monophosphate (cAMP) in the hippocampus results in stronger induction of phospho-p42-MAPK in TSC2+/- rats than in wild-type animals. Thus, the cognitive phenotype and, possibly, epilepsy in TSC patients may result not only from the focal hamartomatous lesions but also, from altered neuronal plasticity in the heterozygous tissue. C1 Univ Tubingen, Dept Gen Neurol, Hertie Inst Clin Brain Res, Tubingen, Germany. Univ Zurich, Inst Anat, Zurich, Switzerland. Univ Zurich, Ctr Neurosci, Zurich, Switzerland. Univ Tubingen, Div Neuropharmacol, Tubingen, Germany. RP Waltereit, R (reprint author), Univ Heidelberg, Cent Inst Mental Hlth, Dept Psychiat, J5, D-68159 Mannheim, Germany. 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TI Abnormal N1/PA responses in children with autism elicited by both low and high spatial frequency gratings SO JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Univ Sheffield, Sheffield S10 2TN, S Yorkshire, England. NR 0 TC 0 Z9 0 PU HOGREFE & HUBER PUBLISHERS PI GOTTINGEN PA ROHNSWEG 25, D-37085 GOTTINGEN, GERMANY SN 0269-8803 J9 J PSYCHOPHYSIOL JI J. Psychophysiol. PY 2006 VL 20 IS 4 BP 328 EP 328 PG 1 WC Psychology, Biological; Neurosciences SC Psychology; Neurosciences & Neurology GA 102LU UT WOS:000241813500063 ER PT J AU Costello, EJ Foley, DL Angold, A AF Costello, EJ Foley, DL Angold, A TI 10-year research update review: The epidemiology of child and adolescent psychiatric disorders: II. Developmental epidemiology SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Review DE epidemiology; development; review ID C-REACTIVE PROTEIN; NATIONAL COMORBIDITY SURVEY; LOW-BIRTH-WEIGHT; CORONARY-HEART-DISEASE; THIMEROSAL-CONTAINING VACCINES; LYMPHOID-NODULAR HYPERPLASIA; MAJOR DEPRESSIVE DISORDER; GROWTH-HORMONE-SECRETION; POSTTRAUMATIC-STRESS-DISORDER; INFLAMMATORY-BOWEL-DISEASE AB Objective: To describe the growth of developmental epidemiology in the past decade and to illustrate it with examples of recent studies. Method: A review of publications on developmental epidemiology in the past 10 years and a discussion of some key examples. Results: The authors describe how the interaction between developmental psychopathology and psychiatric epidemiology has produced developmental epidemiology, the study of patterns of distribution of psychiatric disorders in time as well as in space. They give two examples of the kinds of questions that developmental epidemiology can help to answer: (1) Is the prevalence of autism increasing? Does the use of vaccines explain the increase? (2) Is there an epidemic of child and adolescent depression? Finally, they describe two areas of science that are beginning to inform developmental epidemiology: molecular genetics and the use of biological measures of stress. Conclusions: While child and adolescent psychiatric epidemiology continues, as described in the first of these reviews, to address questions of prevalence and burden, it has also expanded into new areas of research in the past decade. In the next decade, longitudinal epidemiological data sets with their rich descriptive data on psychopathology and environmental risk over time and the potential to add biological measures will provide valuable resources for research into gene-environment correlations and interactions. 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Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 2006 VL 45 IS 1 BP 8 EP 25 DI 10.1097/01.chi.0000184929.41423.cO PG 18 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 997BY UT WOS:000234221200003 PM 16327577 ER PT J AU Haskins, BG Silva, JA AF Haskins, Barbara G. Silva, J. Arturo TI Asperger's disorder and criminal behavior: Forensic-psychiatric considerations SO JOURNAL OF THE AMERICAN ACADEMY OF PSYCHIATRY AND THE LAW LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; NEUROPSYCHIATRIC DISORDERS; AUTISM; MIND; VIOLENCE; CHILDREN; CLASSIFICATION; ADOLESCENTS; PERSONALITY; PREVALENCE AB Asperger's Disorder remains an under-diagnosed condition because of clinical unfamiliarity with its adult presentation. As forensic clinicians become familiar with the presentation of Asperger's disorder, it appears that affected individuals are over-represented in forensic criminal settings. 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TI Semiparametric analysis of case series data SO JOURNAL OF THE ROYAL STATISTICAL SOCIETY SERIES C-APPLIED STATISTICS LA English DT Article DE case series; conditional likelihood; epidemiology; external variable; Poisson process; product multinomial; recurrent events; semiparametric model; time-dependent covariate ID CASE-CROSSOVER DESIGN; CAUSAL ASSOCIATION; ADVERSE REACTIONS; RISK; MODEL; VACCINATION; EXPOSURE; AUTISM; COHORT; MMR AB The case series model for estimating the association between an age-dependent exposure and an outcome event requires information only on cases and implicitly adjusts for all age-independent multiplicative confounders, while allowing for an age-dependent base-line incidence. In the paper the model is presented in greater generality than hitherto, including more general discussion of its derivation, underlying assumptions, applicability, limitations and efficiency. 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R. Stat. Soc. Ser. C-Appl. Stat. PY 2006 VL 55 BP 553 EP 580 DI 10.1111/j.1467-9876.2006.00554.x PN 5 PG 28 WC Statistics & Probability SC Mathematics GA 096PV UT WOS:000241390200001 ER PT J AU Clarke, JGI AF Clarke, JGI TI Transcending organisational autism in the UN system response to HIV/AIDS in Africa SO KYBERNETES LA English DT Article; Proceedings Paper CT Annual Conference of the Cybernetics-Society CY SEP 03-04, 2004 CL London, ENGLAND SP Cybernet Soc HO London Sch Econ DE cybernetics; leadership; international organizations; acquired immune deficiency syndrome AB Purpose - To encourage the ongoing transformation of the UN system by conceptualising leadership challenges within a cybernetics/systems paradigm. Design/methodology/approach - A grounded theory methodology was used to explore the "paradox of plenty" within the UN system in Southern Africa - how the system can more effectively metabolise the considerable latent creative synergic potential within it, to respond to the challenges of HIV/AIDS in Africa. Findings - Statements from UN leaders call for a new paradigm of humanitarian assistance if the challenges of HIV and AIDS are to be met. However, conversations with a wide range of people both within the UN system and closely connected to it suggest a disconnect between what the system does and what the system espouses - a bias toward "doing things right" rather than "doing the right thing". Drawing on the writings of Berry (eco-spirituality), Beer (VSM), Argyris and Schon (double loop learning), Hock (chaordic organisation) and Ackoff (corporate planning) the sub-optimal organisational performance is interpreted as an "autistic" condition, whereby organisations become "so locked up inside themselves that nothing and no one can get in". Interactive dialogue with primary health care workers in Swaziland generated five interconnected principles for developing a systemic response to HIV and AIDS. These are proposed as "antidotes" to counteract autistic tendencies within the UN system. Research limitations/implications - The principles are offered for discussion and refinement through further research by cyberneticians; and systems thinkers. Originality/value - If internalised by UN leadership the perplexing challenges that HIV/AIDS is posing could be met with renewed confidence and hope. C1 Icosindaba Dev Associates, Johannesburg, South Africa. 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TI Frequency of reading, math, and writing disabilities in children with clinical disorders SO LEARNING AND INDIVIDUAL DIFFERENCES LA English DT Article DE learning disability; ADHD; autism; mood and behavior disorders ID DEFICIT-HYPERACTIVITY DISORDER; LEARNING-DISABLED STUDENTS; WISC-III; PSYCHIATRIC-DISORDERS; BEHAVIORAL-DISORDERS; AUTISTIC INDIVIDUALS; STRATEGY INSTRUCTION; WRITTEN EXPRESSION; GENETIC ETIOLOGY; PROFILE TYPES AB Learning disabilities (LD) are common in clinical disorders, but no study has compared the relative prevalence in referred children with different diagnoses. Our sample comprised 949 children (6 to 16 years). LD percentages were highest for bipolar disorder (79%), ADHD combined type (71%), autism (67%), ADHD inattentive type (66%), and spina bifida (60%). Children with oppositional-defiant disorder, adjustment disorder, anxiety, and depression had relatively low LD percentages (18-19%). LD in written expression was twice as comition as LD in reading or math. Findings indicate that children with neurogenetic disorders should be assessed for possible LD because of the high potential yield and the need to intervene educationally if learning problems exist. (c) 2005 Elsevier Inc. All rights reserved. C1 Penn State Coll Med, Milton S Hershey Med Ctr, Dept Psychiat, Hershey, PA 17033 USA. RP Mayes, SD (reprint author), Penn State Coll Med, Milton S Hershey Med Ctr, Dept Psychiat, POB 850, Hershey, PA 17033 USA. 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Individ. Differ. PY 2006 VL 16 IS 2 BP 145 EP 157 DI 10.1016/j.lindif.2005.07.004 PG 13 WC Psychology, Educational SC Psychology GA 112BB UT WOS:000242499000004 ER PT J AU Rossignol, DA Rossignol, LW AF Rossignol, DA Rossignol, LW TI Hyperbaric oxygen therapy may improve symptoms in autistic children SO MEDICAL HYPOTHESES LA English DT Review ID CEREBRAL-BLOOD-FLOW; SYSTEMIC-LUPUS-ERYTHEMATOSUS; HERPES-SIMPLEX ENCEPHALITIS; ECD BRAIN SPECT; CHILDHOOD AUTISM; OXIDATIVE STRESS; IMMUNOLOGICAL TREATMENTS; EMISSION-TOMOGRAPHY; ANTIOXIDANT STATUS; ISCHEMIC PENUMBRA AB Autism is a neurodevelopmental disorder that currently affects as many as 1 out of 166 children in the United States. Recent research has discovered that some autistic individuals have decreased cerebral perfusion, evidence of neuroinflammation, and increased markers of oxidative stress. Multiple independent single photon emission computed tomography (SPECT) and positron emission tomography (PET) research studies have revealed hypoperfusion to several areas of the autistic brain, most notably the temporal regions and areas specifically related to language comprehension and auditory processing. Several studies show that diminished blood flow to these areas correlates with many of the clinical features associated with autism including repetitive, self-stimulatory and stereotypical behaviors, and impairments in communication, sensory perception, and social interaction. Hyperbaric oxygen therapy (HBOT) has been used with clinical success in several cerebral hypoperfusion syndromes including cerebral palsy, fetal alcohol syndrome, closed head injury, and stroke. HBOT can compensate for decreased blood flow by increasing the oxygen content of plasma and body tissues and can even normalize oxygen levels in ischemic tissue. In addition, animal studies have shown that HBOT has potent anti-inflammatory effects and reduces oxidative stress. Furthermore, recent evidence demonstrates that HBOT mobilizes stem cells from human bone marrow, which may aid recovery in neurodegenerative diseases. Based upon these findings, it is hypothesized that HBOT will improve symptoms in autistic individuals. A retrospective case series is presented that supports this hypothesis. (c) 2006 Elsevier Ltd. All rights reserved. C1 Blue Ridge Med Ctr, Arrington, VA 22922 USA. Univ Virginia, Charlottesville, VA USA. RP Rossignol, DA (reprint author), Blue Ridge Med Ctr, 4038 Thomas Nelson Highway, Arrington, VA 22922 USA. 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Hypotheses PY 2006 VL 67 IS 2 BP 216 EP 228 DI 10.1016/j.mehy.2006.02.009 PG 13 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 057WD UT WOS:000238625000004 PM 16554123 ER PT J AU Thornton, IM AF Thornton, IM TI Out of time: A possible link between mirror neurons, autism and electromagnetic radiation SO MEDICAL HYPOTHESES LA English DT Article ID SPECTRUM DISORDERS; SPEECH-PERCEPTION; LANGUAGE; INFANTS; FIELD; ABNORMALITIES; IMITATION; BRAIN; EEG AB Recent evidence suggests a link between autism and the human mirror neuron system. In this paper, I argue that temporal disruption from the environment may play an important role in the observed mirror neuron dysfunction, leading in turn to the pattern of deficits associated with autism. I suggest that the developing nervous system of an infant may be particularly prone to temporal noise that can interfere with the initial calibration of brain networks such as the mirror neuron system. The most likely source of temporal noise in the environment is artificially generated electromagnetic radiation. To date, there has been little evidence that electromagnetic radiation poses a direct biological hazard. It is clear, however, that time-varying electromagnetic waves have the potential to temporally modulate the nervous system, particularly when populations of neurons are required to act together. This modulation may be completely harmless for the fully developed nervous system of an adult. For an infant, this same temporal disruption might act to severely delay or disrupt vital calibration processes. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ Coll Swansea, Dept Psychol, Swansea SA2 8PP, W Glam, Wales. RP Thornton, IM (reprint author), Univ Coll Swansea, Dept Psychol, Singleton Pk, Swansea SA2 8PP, W Glam, Wales. 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Hypotheses PY 2006 VL 67 IS 2 BP 378 EP 382 DI 10.1016/j.mehy.2006.01.032 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 057WD UT WOS:000238625000033 PM 16530334 ER PT J AU Good, P AF Good, Peter TI Low-dose naltrexone for multiple sclerosis and autism: Does its benefit reveal a common cause? SO MEDICAL HYPOTHESES LA English DT Letter C1 Multiple Sclerosis Studies, Bend, OR 97708 USA. RP Good, P (reprint author), Multiple Sclerosis Studies, POB 7834, Bend, OR 97708 USA. 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Hypotheses PY 2006 VL 67 IS 3 BP 671 EP 672 DI 10.1016/j.mehy.2006.04.015 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 069RK UT WOS:000239465700042 PM 16759815 ER PT J AU Boso, M di Nemi, SU Barale, F Emanuele, E AF Boso, Marianna di Nemi, Stefania Ucelli Barale, Francesco Emanuele, Enzo TI Targeting cerebral Bcl-2 expression as a potential therapeutic target in autism: Potential usefulness of human recombinant nerve growth factor SO MEDICAL HYPOTHESES LA English DT Letter ID PROTEINS; P53 C1 Univ Pavia, Sect Psychiat, Dept Hlth Sci, I-27100 Pavia, Italy. Univ Pavia, CIRMC, I-27100 Pavia, Italy. RP Boso, M (reprint author), Univ Pavia, Sect Psychiat, Dept Hlth Sci, Via Bassi,21, I-27100 Pavia, Italy. EM m_boso@yahoo.it CR Araghi-Niknam M, 2003, CELL MOL NEUROBIOL, V23, P945, DOI 10.1023/B:CEMN.0000005322.27203.73 Baron CA, 2006, HUM MOL GENET, V15, P853, DOI 10.1093/hmg/ddl004 Fatemi SH, 2001, J AUTISM DEV DISORD, V31, P529, DOI 10.1023/A:1013234708757 Fatemi SH, 2001, SYNAPSE, V42, P281, DOI 10.1002/syn.10002 Freeman R, 1999, EUR NEUROL, V41, P20, DOI 10.1159/000052076 Liu YZ, 1999, NUCLEIC ACIDS RES, V27, P2086, DOI 10.1093/nar/27.10.2086 NR 6 TC 1 Z9 1 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 2006 VL 67 IS 5 BP 1256 EP 1257 DI 10.1016/j.mehy.2006.06.003 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 087LJ UT WOS:000240743600051 PM 16887282 ER PT J AU Tsai, SJ AF Tsai, SJ TI TrkB partial agonists: Potential treatment strategy for epilepsy, mania, and autism SO MEDICAL HYPOTHESES LA English DT Article ID NEUROTROPHIC FACTOR; NERVOUS-SYSTEM; BDNF; EPILEPTOGENESIS; DEPRESSION; MICE AB Brain-derived neurotrophic factor (BDNF) is a member of a family of neurotrophins that, by activating a tyrosine kinase B receptor (TrkB), regulates a wide variety of processes in the nervous system, including neural development, function and survival. Evidence suggests that excess BDNF is involved in the pathogenesis of epilepsy, mania and autism. Thus, agents that can decrease BDNF-TrkB pathway signaling may be therapeutic for these diseases. However, blocking BDNF-TrkB pathways with TrkB antagonists may be harmful, as BDNF-TrkB deficiency has been related to major depression and Alzheimer's disease. A partial agonist is an agent that elicits a maximum response that is Less than that of an agonist (e.g., the physiological ligand), so, in the presence of excess full agonist, a partial agonist would act as an antagonist. Interestingly, a dopaminergic partial agonist, aripiprazole, has been successfully developed for the treatment of psychotic disorders. Recently specific TrkB partial agonists have been synthesized by O'Leary and Hughes; it is proposed that these partial TrkB agonists may provide a novel strategy for the treatment of epilepsy, mania or autism, which may be associated with BDNF-TrkB hyperfunction. (c) 2005 Elsevier Ltd. All rights reserved. C1 Taipei Vet Gen Hosp, Dept Psychiat, Taipei 11217, Taiwan. RP Tsai, SJ (reprint author), Taipei Vet Gen Hosp, Dept Psychiat, 201 Shih Pai Rd,Sec 2, Taipei 11217, Taiwan. 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EM skirmantas.janusonis@yate.edu CR Janusonis S, 2005, MED HYPOTHESES, V64, P742, DOI 10.1016/j.mehy.2004.09.020 Janusonis S, 2005, THEOR BIOL MED MODEL, V2, DOI 10.1186/1742-4682-2-27 Persico AM, 2000, AM J MED GENET, V96, P123, DOI 10.1002/(SICI)1096-8628(20000207)96:1<123::AID-AJMG24>3.0.CO;2-N Wu SP, 2005, NEUROSCI LETT, V381, P1, DOI 10.1016/j.neulet.2005.01.073 NR 4 TC 0 Z9 0 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 2006 VL 66 IS 1 BP 214 EP 214 DI 10.1016/j.mehy.2005.08.024 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 994MR UT WOS:000234036400050 ER PT J AU Bazar, KA Yun, AJ Lee, PY Daniel, SM Doux, JD AF Bazar, KA Yun, AJ Lee, PY Daniel, SM Doux, JD TI Obesity and ADHD may represent different manifestations of a common environmental oversampling syndrome: a model for revealing mechanistic overlap among cognitive, metabolic, and inflammatory disorders SO MEDICAL HYPOTHESES LA English DT Article ID ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEFICIT HYPERACTIVITY DISORDER; LONG-TERM POTENTIATION; BEHAVIORAL TREATMENT; SEX DETERMINATION; WEIGHT-REDUCTION; LIFE-SPAN; CHILDREN; ASSOCIATION; OVERWEIGHT AB Obesity and attention-deficit hyperactivity disorder (ADHD) are both increasing in prevalence. Childhood exposure to television has shown linkage to both AND and obesity with the former ascribed to dysfunctional cognitive hyperstimutation and the tatter to altered patterns of diet and exercise. Empirical evidence has contradicted prior presumptions that the hyperactivity of AND would decrease the risk of obesity. Instead, obesity and AND demonstrate significant comorbidity. We propose that obesity and AND represent different manifestations of the same underlying dysfunction, a phenomenon we term environmental oversampling syndrome. Oversupply of information in the form of nutritional content and sensory content may independently predispose to both obesity and ADHD. Moreover, the pathogenic mechanisms of these conditions may overlap such that nutritional excess contributes to AND and cognitive hyperstimulation contributes to obesity. The overlapping effects of medications provide further evidence towards the existence of shared etiologic pathways. Metabolism and cognition may represent parallel systems of intelligence, and oversampling of content may constitute the source of parallel dysfunctions. The emerging association between psychiatric and metabolic disorders suggests a fundamental biologic link between these two systems. In addition, the immune system may represent yet another form of intelligence. The designation of syndrome X subsumes seemingly unrelated metabolic and inflammatory entities. Environmental oversampling syndrome may represent an even more inclusive concept that encompasses various metabolic, inflammatory, and behavioral conditions. Apparently disparate conditions such as insulin resistance, diabetes, hypertension, syndrome X, obesity, AND, depression, psychosis, steep apnea, inflammation, autism, and schizophrenia may operate through common pathways, and treatments used exclusively for one of these conditions may prove beneficial for the others. (c) 2005 Elsevier Ltd. All rights reserved. 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RP Niederhofer, H (reprint author), Gen Hosp Bolzano, Serv Neuropsyichiatr Infantile, Via Guncina 54-A, I-39100 Bolzano, BZ, Italy. EM helmutniederhofer@yahoo.de CR AISNWORTH WD, 1985, B NY ACAD MED, V61, P792 BRISCH KH, 2005, MMW-FORTSCH MEDIZIN, V24, P39 Glasson EJ, 2004, ARCH GEN PSYCHIAT, V61, P618, DOI 10.1001/archpsyc.61.6.618 NR 3 TC 1 Z9 1 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 2006 VL 66 IS 2 BP 441 EP 442 DI 10.1016/j.mehy.2005.08.034 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 002WS UT WOS:000234643400035 PM 16257128 ER PT J AU Casavant, MJ AF Casavant, MJ TI Antibiotic not linked to autism SO MEDICAL HYPOTHESES LA English DT Letter C1 Childrens Res Inst, Columbus, OH USA. RP Casavant, MJ (reprint author), Childrens Res Inst, Columbus, OH USA. EM casavantm@pediatrics.ohio-state.edu RI Casavant, Marcel/E-2848-2011 NR 0 TC 1 Z9 1 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 2006 VL 66 IS 3 BP 678 EP 678 DI 10.1016/j.mehy.2005.09.034 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 026EF UT WOS:000236319200041 PM 16278050 ER PT J AU Hatfield, JS AF Hatfield, JS TI The genetic basis of hair whorl, handedness, and other phenotypes SO MEDICAL HYPOTHESES LA English DT Article ID SEXUAL ORIENTATION; LATERAL PREFERENCE; HOMOSEXUAL-MEN; BIRTH-ORDER; 4 INDEXES; SCHIZOPHRENIA; AUTISM; MECHANISM; WOMEN AB Evidence is presented that RHD, RHCE, and other RH genes, may be interesting candidates to consider when searching for the genetic basis of hair whorl rotation (i.e., clockwise or counterclockwise), handedness (i.e., right handed, left handed or ambidextrous), speech laterality (i.e., right brained or left brained), speech dyslexia (e.g., stuttering), sexual orientation (i.e., heterosexual, homosexual, bisexual, or transsexual), schizophrenia, bipolar disorder, and autism spectrum disorder. Such evidence involves the need for a genetic model that includes maternal immunization to explain some of the empirical results reported in the literature. The complex polymorphisms present among the maternally immunizing RH genes can then be used to explain other empirical results. Easily tested hypotheses are suggested, based upon genotypic (but not phenotypic) frequencies of the RH genes. In particular, homozygous dominant individuals are expected to be less common or tacking entirety among the alternative phenotypes. If it is proven that RH genes are involved in brain architecture, it will have a profound effect upon our understanding of the development and organization of the asymmetrical vertebrate brain and may eventually Lead to a better understanding of the developmental processes which occur to produce the various alternative phenotypes discussed here. In addition, if RH genes are shown to be involved in the production of these phenotypes, then the evolutionary studies can be performed to demonstrate the beneficial effect of the recessive alleles of RHD and RHCE, and why human evolution appears to be selecting for the recessive alleles even though an increase in the frequency of such alleles may imply lower average fecundity among some individuals possessing them. Published by Elsevier Ltd. C1 USGS Patuxent Wildlife Res Ctr, Laurel, MD 20708 USA. RP Hatfield, JS (reprint author), USGS Patuxent Wildlife Res Ctr, 12100 Beech Forest Rd, Laurel, MD 20708 USA. 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Hypotheses PY 2006 VL 66 IS 4 BP 708 EP 714 DI 10.1016/j.mehy.2005.10.010 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 024KS UT WOS:000236194500006 PM 16337093 ER PT J AU Dickinson, MJ Eva, FJ AF Dickinson, MJ Eva, FJ TI Anxiety and depression may have an evolutionary role as negative reinforcers, encouraging sociallisation SO MEDICAL HYPOTHESES LA English DT Article ID FEAR; DEPENDENCE; DISORDER; BRAIN AB Anxiety and depression are both very common mental states and both are quite unpleasant. Their high prevalence and preservation make it likely they have considerable evolutionary significance and in some way improve the chances of an individual's survival. The following article proposes that much of the anxiety and depression we experience is primarily acting as a negative reinforcer, encouraging socialisation. These feelings are experienced most intensely when we are isolated and have evolved to discourage this highly maladaptive behaviour, there being major advantages for being with other people. Particular problems are considered, including aspects of autism and alcohol and tranquilliser abuse. How the presence of other people may alter the expression of anxiety and depression is considered, in addition to implications for psychiatry. (c) 2005 Elsevier Ltd. All rights reserved. C1 Chase Farm Hosp, Cumbira Villa, Enfield EN2 8JL, Middx, England. RP Dickinson, MJ (reprint author), Chase Farm Hosp, Cumbira Villa, Ridgeway, Enfield EN2 8JL, Middx, England. 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Hypotheses PY 2006 VL 66 IS 4 BP 796 EP 800 DI 10.1016/j.mehy.2005.10.008 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 024KS UT WOS:000236194500017 PM 16359828 ER PT J AU Lippiello, PM AF Lippiello, PM TI Nicotinic cholinergic antagonists: A novel approach for the treatment of autism SO MEDICAL HYPOTHESES LA English DT Article ID SPECTRUM DISORDERS; MECAMYLAMINE; RECEPTORS; ATTENTION; CHILDREN; SMOKING; ADOLESCENTS; DIRECTIONS; PREVALENCE; MECHANISMS AB Evidence supports the hypothesis that normalization of cholinergic tone by selective antagonism of neuronal nicotinic acetylcholine receptors (NNRs) may ameliorate the core symptoms of autism. As often is the case, epidemiology has provided the first important clues. It is well recognized that psychiatric patients are significantly more often smokers than the general population. The only known exceptions are obsessive-compulsive disorder (OCD), catatonic schizophrenia and interestingly, autism. In this regard, clinical studies with nicotine have demonstrated amelioration of symptoms of a number of diseases and disorders, including Alzheimer's disease, Parkinson's disease, ADHD and Tourette's syndrome. Nicotine's agonist properties at CNS NNRs have been implicated in these effects and support the concept of self-medication as a strong motivation for smoking in cognitively compromised individuals. On the other hand, the inverse correlation between autism and smoking suggests that smoking does not provide symptomatic relief and may actually be indicative of an active avoidance of nicotine's agonist effects in this disorder. Neuroanatomical evidence is consistent with this idea based on the presence of hypercholinergic architecture in the autistic brain, particularly during the first few years of development, making the avoidance of further stimulation of an already hyperactive cholinergic system plausible. This may also explain why stimulants (known to increase dopamine levels as do NNR agonists) appear to aggravate autistic symptoms and why Studies with cholinesterase inhibitors that increase acetylcholine levels in the brain have yielded variable effects in autism. Taken together, the evidence suggests the possibility that nicotinic cholinergic antagonism may in fact be palliative. Pharmacological evidence supports this hypothesis. For example, antidepressants, many of which are now known to be non-competitive NNR antagonists, have been used successfully to treat a number of autistic symptoms. More specifically, there is anecdotal evidence from at least one medical practitioner that mecamylamine, a non-selective NNR antagonist, is effective in treating many autistic symptoms, particularly those that are refractory to most other treatments. Clearly there is a need for carefully controlled clinical studies with novel selective NNR antagonists to explore their potential as a new and exciting approach for the treatment of autism. (c) 2005 Elsevier Ltd. All rights reserved. C1 Targacept Inc, Preclin Res, Winston Salem, NC 27101 USA. RP Lippiello, PM (reprint author), Targacept Inc, Preclin Res, 200 E 1st St,Suite 300, Winston Salem, NC 27101 USA. 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Hypotheses PY 2006 VL 66 IS 5 BP 985 EP 990 DI 10.1016/j.mehy.2005.11.015 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 028BA UT WOS:000236459100024 PM 16406687 ER PT J AU Chen, F Lemonnier, E Lazartigues, A Planche, P AF Chen, F Lemonnier, E Lazartigues, A Planche, P TI Sleep problems and information processing, a "disconnection effect" in autism? SO MEDICAL HYPOTHESES LA English DT Letter C1 CHU Brest, Hop Bohars, Serv Pedopsychiat, F-29280 Bohars, France. Univ Bretagne Occidentale, Fac Lettres & Sci Sociales, Dept Psychol, F-29200 Brest, France. RP Chen, F (reprint author), CHU Brest, Hop Bohars, Serv Pedopsychiat, BP 17, F-29280 Bohars, France. EM pierre.fei.chen@gmail.com; eric.lemonnier@chu-brest.fr; alain.lazartigues@chu-brest.fr; pascale.planche@univ-brest.fr CR Anisimov SV, 2004, REV NEUROSCIENCE, V15, P209 Bertone A, 2005, BRAIN, V128, P2430, DOI 10.1093/brain/awh561 Frank MG, 2001, NEURON, V30, P275, DOI 10.1016/S0896-6273(01)00279-3 Massimini M, 2005, SCIENCE, V309, P2228, DOI 10.1126/science.1117256 Planche P, 2002, ANN MED-PSYCHOL, V160, P559, DOI 10.1016/S0003-4487(02)00231-7 Ritvo E. R., 1993, EUROPEAN CHILD ADOLE, V2, P75 NR 6 TC 4 Z9 4 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 2006 VL 66 IS 6 BP 1245 EP 1246 DI 10.1016/j.mehy.2006.01.004 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 037UB UT WOS:000237171700040 PM 16503096 ER PT J AU Emanuele, E AF Emanuele, E TI Autism conceptualized as a vasopressin resistance syndrome SO MEDICAL HYPOTHESES LA English DT Letter C1 Univ Pavia, Interdept Ctr Res Mol Med, I-27100 Pavia, Italy. RP Emanuele, E (reprint author), Univ Pavia, Interdept Ctr Res Mol Med, Viale Taramelli 24, I-27100 Pavia, Italy. EM enzo.em@libero.it CR Bielsky IF, 2004, NEUROPSYCHOPHARMACOL, V29, P483, DOI 10.1038/sj.npp.1300360 Momeni N, 2005, BMC PSYCHIATRY, V5, DOI 10.1186/1471-244X-5-27 Morello JP, 2001, ANNU REV PHYSIOL, V63, P607, DOI 10.1146/annurev.physiol.63.1.607 Ring RH, 2005, CURR PHARM DESIGN, V11, P205, DOI 10.2174/1381612053382241 Wassink TH, 2004, MOL PSYCHIATR, V9, P968, DOI 10.1038/sj.mp.4001503 NR 5 TC 4 Z9 4 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 2006 VL 66 IS 6 BP 1245 EP 1245 DI 10.1016/j.mehy.2006.01.011 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 037UB UT WOS:000237171700039 PM 16504417 ER PT S AU Styner, M Gorczowski, K Fletcher, T Jeong, JY Pizer, SM Gerig, G AF Styner, Martin Gorczowski, Kevin Fletcher, Tom Jeong, Ja Yeon Pizer, Stephen M. Gerig, Guido BE Yang, GZ Jiang, T Shen, DG Gu, L Yang, J TI Statistics of pose and shape in multi-object complexes using principal geodesic analysis SO MEDICAL IMAGING AND AUGMENTED REALITY SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 3rd International Workshop on Medical Imaging and Augmented Reality (MIAR 2006) CY AUG 17-18, 2006 CL Shanghai, PEOPLES R CHINA ID SEGMENTATION; MODELS; SETS AB A main focus of statistical shape analysis is the description of variability of a population of geometric objects. In this paper, we present work in progress towards modeling the shape and pose variability of sets of multiple objects. Principal geodesic analysis (PGA) is the extension of the standard technique of principal component analysis (PCA) into the nonlinear Riemannian symmetric space of pose and our medial m-rep shape description, a space in which use of PCA would be incorrect. In this paper, we discuss the decoupling of pose and shape in multi-object sets using different normalization settings. Further, we introduce new methods of describing the statistics of object pose using a novel extension of PGA, which previously has been used for global shape statistics. These new pose statistics are then combined with shape statistics to form a more complete description of multi-object complexes. We demonstrate our methods in an application to a longitudinal pediatric autism study with object sets of 10 subcortical structures in a population of 20 subjects. The results show that global scale accounts for most of the major mode of variation across time. Furthermore, the PGA components and the corresponding distribution of different subject groups vary significantly depending on the choice of normalization, which illustrates the importance of global and local pose alignment in multi-object shape analysis. C1 Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. RP Styner, M (reprint author), Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. 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An alternative approach is the analysis of cytogenetic abnormalities associated with autism. We present a review of all studies to date that relate patients with cytogenetic abnormalities to the autism phenotype. A literature survey of the Medline and Pubmed databases was performed, using multiple keyword searches. Additional searches through cited references and abstracts from the major genetic conferences from 2000 onwards completed the search. The quality of the phenotype (i.e. of the autism spectrum diagnosis) was rated for each included case. Available specific probe and marker information was used to define optimally the boundaries of the cytogenetic abnormalities. In case of recurrent deletions or duplications on chromosome 15 and 22, the positions of the low copy repeats that are thought to mediate these rearrangements were used to define the most likely boundaries of the implicated 'Cytogenetic Regions Of Interest' (CROIs). If no molecular data were available, the sequence position of the relevant chromosome bands was used to obtain the approximate molecular boundaries of the CROI. The findings of the current review indicate: ( 1) several regions of overlap between CROIs and known loci of significant linkage and/or association findings, and ( 2) additional regions of overlap among multiple CROIs at the same locus. Whereas the first finding confirms previous linkage/association findings, the latter may represent novel, not previously identified regions containing genes that contribute to autism. This analysis not only has confirmed the presence of several known autism risk regions but has also revealed additional previously unidentified loci, including 2q37, 5p15, 11q25, 16q22.3, 17p11.2, 18q21.1, 18q23, 22q11.2, 22q13.3 and Xp22.2 - p22.3. C1 Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, NL-3584 CX Utrecht, Netherlands. Rudolf Magnus Inst Neurosci, NL-3508 TA Utrecht, Netherlands. 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Psychiatr. PD JAN PY 2006 VL 11 IS 1 BP 18 EP 28 DI 10.1038/sj.mp.4001757 PG 11 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 993QZ UT WOS:000233971300006 ER PT J AU Trikalinos, TA Karvouni, A Zintzaras, E Ylisaukko-oja, T Peltonen, L Jarvela, I Ioannidis, JPA AF Trikalinos, TA Karvouni, A Zintzaras, E Ylisaukko-oja, T Peltonen, L Jarvela, I Ioannidis, JPA TI A heterogeneity-based genome search meta-analysis for autism-spectrum disorders SO MOLECULAR PSYCHIATRY LA English DT Article DE autistic disorders; Asperger syndrome; genetics; linkage; meta-analysis; genome search ID REELIN GENE ALLELES; SEROTONIN TRANSPORTER; SUSCEPTIBILITY GENE; SCAN METAANALYSIS; INFANTILE-AUTISM; WIDE SCAN; SCREEN; LINKAGE; ASSOCIATION; REGION AB Autism and autism-spectrum disorders exhibit high heritability, although specific susceptibility genes still remain largely elusive. We performed a heterogeneity-based genome search meta-analysis (HEGESMA) of nine genome scans on autism or autism-spectrum disorders. Each genome scan was separated in 30 cM bins and the maximum linkage statistic from each bin was ranked. Significance for each bin's average rank and for between-scan heterogeneity (dis-similarity in the average ranks) was obtained through Monte Carlo tests. For autism, data from 771 affected sibpairs were synthesized across six separate genome scans. Region 7q22 - q32 reached genome-wide significance both in weighted and unweighted analyses, with evidence for significantly low between-scan heterogeneity. The flanking chromosomal region 7q32-qter reached the less stringent threshold of suggestive significance, with no evidence for low between-scan heterogeneity. For autism-spectrum disorders ( 634 affected sibpairs from five separate scans), no chromosomal region reached genome-wide significance. 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Fdn Res & Technol Hellas, Inst Biomed Res, Ioannina, Greece. RP Ioannidis, JPA (reprint author), Univ Ioannina, Sch Med, Dept Hyg & Epidemiol, Clin & Mol Epidemiol Unit, GR-45110 Ioannina, Greece. 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PD JAN PY 2006 VL 11 IS 1 BP 29 EP 36 DI 10.1038/sj.mp.4001750 PG 8 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 993QZ UT WOS:000233971300007 PM 16189507 ER PT J AU Lauritsen, MB Als, TD Dahl, HA Flint, TJ Wang, AG Vang, M Kruse, TA Ewald, H Mors, O AF Lauritsen, MB Als, TD Dahl, HA Flint, TJ Wang, AG Vang, M Kruse, TA Ewald, H Mors, O TI A genome-wide search for alleles and haplotypes associated with autism and related pervasive developmental disorders on the Faroe Islands SO MOLECULAR PSYCHIATRY LA English DT Article DE genome-wide scan; association mapping; population isolate; haplotype sharing; susceptibility locus, autism ID MULTILOCUS GENOTYPE DATA; LINKAGE DISEQUILIBRIUM; ISOLATED POPULATIONS; DIAGNOSTIC INTERVIEW; SUSCEPTIBILITY LOCUS; FOUNDER POPULATIONS; SPECTRUM DISORDERS; MOLECULAR-GENETICS; FAMILY HISTORY; COMPLEX TRAITS AB The involvement of genetic factors in the etiology of autism has been clearly established. We undertook a genome-wide search for regions containing susceptibility genes for autism in 12 subjects with childhood autism and related pervasive developmental disorders (PDDs) and 44 controls from the relatively isolated population of the Faroe Islands. In total, 601 microsatellite markers distributed throughout the human genome with an average distance of 5.80 cM were genotyped, including 502 markers in the initial scan. The Faroese population structure and genetic relatedness of cases and controls were also evaluated. Based on a combined approach, including an assumption-free test as implemented in CLUMP, Fisher's exact test for specific alleles and haplotypes, and IBD0 probability calculations, we found association between autism and microsatellite markers in regions on 2q, 3p, 6q, 15q, 16p, and 18q. The most significant finding was on 3p25.3 (P-T1 = 0.00003 and P-T4 = 0.00007), which was also supported by other genetic studies. Furthermore, no evidence of population substructure was found, and a higher degree of relatedness among cases could not be detected, decreasing the risk of inflated P-values. Our data suggest that markers in these regions are in linkage disequilibrium with genes involved in the etiology of autism, and we hypothesize susceptibility genes for autism and related PDDs to be localized within these regions. C1 Aarhus Univ Hosp, Ctr Basic Psychiat Res, Hosp Psychiat, DK-8240 Risskov, Denmark. Odense Univ Hosp, Dept Clin Biochem & Genet, DK-5000 Odense, Denmark. Copenhagen Univ Hosp, Dept Psychiat, Amager Hosp, Copenhagen S, Denmark. RP Lauritsen, MB (reprint author), Aarhus Univ Hosp, Ctr Basic Psychiat Res, Hosp Psychiat, Skovagervej 2, DK-8240 Risskov, Denmark. 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Peter Chidambi, Gayathri Lee, Anthony Meyer, Jessica TI Foundations for self-awareness: An exploration through autism SO MONOGRAPHS OF THE SOCIETY FOR RESEARCH IN CHILD DEVELOPMENT LA English DT Review ID HIGH-FUNCTIONING CHILDREN; COGNITIVE NEUROSCIENCE VIEW; MIRROR NEURON DYSFUNCTION; YOUNG-CHILDREN; SPECTRUM DISORDERS; JOINT ATTENTION; FACIAL EXPRESSIONS; CHILDHOOD AUTISM; DEVELOPMENTAL DISORDERS; EMOTION-RECOGNITION AB Developmental psychopathology holds promise for elucidating the structure of self-awareness. Here we studied social emotions in matched groups of children and adolescents with and without autism. Our aims were to determine whether there are potentially dissociable aspects of self-awareness, and to reconsider how the qualities of young children's engagement with other persons influences the development of their sense of self. Parent interviews yielded evidence that children with autism are limited in social-relational and emotional domains of self-awareness; for example, few were reported to show guilt, embarrassment, or shame. Yet according to parent report, most were affected by the moods of others, showed some degree of pity and concern, and manifested jealousy. When presented with videotaped scenes, participants with autism were similar to those without autism in identifying pride, guilt, and shame, and they were able to describe their own experiences of pride and, more rarely, guilt. In situations designed to elicit emotions, participants with autism were rated as showing pride, but they manifested lesser degrees and atypical qualities of guilt and coyness. Relatively few showed personal forms of self-consciousness when asked to pose for a photograph. We argue that in order for children to achieve depth in self-awareness, and to relate to themselves as occupying a distinctive stance within a framework of mutual self-other relatedness, they need to identify with the attitudes of other people. We interpret the present studies in terms of dissociations among three forms of social emotion: "Person-centered" qualities of relational self-awareness that require identification and are specifically limited among children with autism, more diffuse modes of relational self-consciousness, and a third group of social emotions, epitomized by jealousy, situated in a separate developmental line. We propose a rebalancing of emotion theory that gives greater prominence to children's developing forms of interpersonal and intra-psychic relatedness. C1 Tavistock Clin, London NW3 5BA, England. UCL, London WC1E 6BT, England. RP Hobson, RP (reprint author), Tavistock Clin, London NW3 5BA, England. 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PY 2006 VL 71 IS 2 BP 167 EP 179 PG 13 WC Psychology, Developmental SC Psychology GA 119GA UT WOS:000242999600002 PM 17177924 ER PT J AU Dapretto, M Davies, MS Pfeifer, JH Scott, AA Sigman, M Bookheimer, SY Iacoboni, M AF Dapretto, M Davies, MS Pfeifer, JH Scott, AA Sigman, M Bookheimer, SY Iacoboni, M TI Understanding emotions in others: mirror neuron dysfunction in children with autism spectrum disorders SO NATURE NEUROSCIENCE LA English DT Article ID IMITATION; INDIVIDUALS; ACTIVATION; MECHANISMS; EMPATHY; FACES AB To examine mirror neuron abnormalities in autism, high-functioning children with autism and matched controls underwent fMRI while imitating and observing emotional expressions. Although both groups performed the tasks equally well, children with autism showed no mirror neuron activity in the inferior frontal gyrus (pars opercularis). Notably, activity in this area was inversely related to symptom severity in the social domain, suggesting that a dysfunctional 'mirror neuron system' may underlie the social deficits observed in autism. C1 Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Ahmanson Lovelace Brain Mapping Ctr, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, David Geffen Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. RP Dapretto, M (reprint author), Univ Calif Los Angeles, Semel Inst Neurosci & Human Behav, Ahmanson Lovelace Brain Mapping Ctr, Los Angeles, CA 90095 USA. 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Neurosci. PD JAN PY 2006 VL 9 IS 1 BP 28 EP 30 DI 10.1038/nn1611 PG 3 WC Neurosciences SC Neurosciences & Neurology GA 997ZQ UT WOS:000234288000014 PM 16327784 ER PT J AU Zelazo, PD AF Zelazo, Philip David TI The Dimensional Change Card Sort (DCCS): a method of assessing executive function in children SO NATURE PROTOCOLS LA English DT Article ID RULE USE; INDIVIDUAL-DIFFERENCES; MIND; CHILDHOOD; KNOWLEDGE; AUTISM; TASK AB The dimensional change card sort ( DCCS) is an easily administered and widely used measure of executive function that is suitable for use with participants across a wide range of ages. In the standard version, children are required to sort a series of bivalent test cards, first according to one dimension ( e. g., color), and then according to the other ( e. g., shape). Most 3- year- olds perseverate during the post- switch phase, exhibiting a pattern of inflexibility similar to that seen in patients with prefrontal cortical damage. By 5 years of age, most children switch when instructed to do so. Performance on the DCCS provides an index of the development of executive function, and it is impaired in children with disorders such as attention- deficit/ hyperactivity disorder ( ADHD) and autism. We describe the protocol for the standard version ( duration = 5 min) and the more challenging border version ( duration = 5 min), which may be used with children as old as 7 years. C1 Univ Toronto, Dept Psychol, Toronto, ON M5S 3G3, Canada. RP Zelazo, PD (reprint author), Univ Toronto, Dept Psychol, 100 St George St, Toronto, ON M5S 3G3, Canada. 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Protoc. PY 2006 VL 1 IS 1 BP 297 EP 301 DI 10.1038/nprot.2006.46 PG 5 WC Biochemical Research Methods SC Biochemistry & Molecular Biology GA 232EX UT WOS:000251002200045 PM 17406248 ER PT J AU Qiu, SF Korwek, KM Weeber, EJ AF Qiu, SF Korwek, KM Weeber, EJ TI A fresh look at an ancient receptor family: Emerging roles for low density lipoprotein receptors in synaptic plasticity and memory formation SO NEUROBIOLOGY OF LEARNING AND MEMORY LA English DT Review DE reelin; apoE; Alzheimer's disease; low density lipoprotein receptors; synaptic plasticity ID HUMAN APOLIPOPROTEIN-E; LONG-TERM POTENTIATION; D-ASPARTATE RECEPTOR; PROTEIN-KINASE-C; GLYCOGEN-SYNTHASE KINASE-3-BETA; HETEROZYGOUS REELER MOUSE; CENTRAL-NERVOUS-SYSTEM; RADIAL GLIAL SCAFFOLD; ALZHEIMERS-DISEASE; AMPA RECEPTOR AB The well-known family of low-density lipoprotein receptors represents a collection of ancient membrane receptors that have been remarkably conserved throughout evolution. These multifunctional receptors, known to regulate cholesterol transport, are becoming increasingly interesting to the neuroscience community due to their ability to transduce a diversity of extracellular signals across the membrane in the adult CNS. Their roles in modulating synaptic plasticity and necessity in hippocampus-specific learning and memory have recently come to light. In addition, genetic, biochemical and behavioral studies have implicated these signaling systems in a number of human neurodegenerative and neuropsychiatric disorders involving loss of cognitive ability, such as Alzheimer's disease, schizophrenia and autism. This review describes the known functions of these receptors and discusses their potential role in processes of synaptic regulation and memory formation. (c) 2005 Elsevier Inc. All rights reserved. C1 Vanderbilt Univ, Med Ctr, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. Vanderbilt Univ, Med Ctr, Grad Program Neurosci, Nashville, TN 37232 USA. Vanderbilt Univ, Med Ctr, Kennedy Ctr Human Dev, Nashville, TN 37232 USA. RP Weeber, EJ (reprint author), Vanderbilt Univ, Med Ctr, Dept Mol Physiol & Biophys, 221 Kirkland Hall, Nashville, TN 37232 USA. 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Learn. Mem. PD JAN PY 2006 VL 85 IS 1 BP 16 EP 29 DI 10.1016/j.nlm.2005.08.009 PG 14 WC Behavioral Sciences; Neurosciences; Psychology; Psychology, Multidisciplinary SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 001JF UT WOS:000234528700002 PM 16198608 ER PT J AU Vollm, BA Taylor, ANW Richardson, P Corcoran, R Stirling, J McKie, S Deakin, JFW Elliott, R AF Vollm, BA Taylor, ANW Richardson, P Corcoran, R Stirling, J McKie, S Deakin, JFW Elliott, R TI Neuronal correlates of theory of mind and empathy: A functional magnetic resonance imaging study in a nonverbal task SO NEUROIMAGE LA English DT Article ID NEURAL MECHANISMS; BIOLOGICAL BASIS; ACQUIRED THEORY; BRAIN; PERCEPTION; CORTEX; FMRI; SELF; RECOGNITION; ATTRIBUTION AB Theory of Mind (ToM), the ability to attribute mental states to others, and empathy, the ability to infer emotional experiences, are important processes in social cognition. Brain imaging studies in healthy subjects have described a brain system involving medial prefrontal cortex, superior temporal sulcus and temporal pole in ToM processing. Studies investigating networks associated with empathic responding also suggest involvement of temporal and frontal lobe regions. In this fMRI study, we used a cartoon task derived from Sarfati et al. (1997) [Sarfati, Y., Hardy-Bayle, M.C., Besche, C., Widlocher, D. 1997. Attribution of intentions to others in people with schizophrenia: a non-verbal exploration with comic strips. Schizophrenia Research 25, 199-209] with both ToM and empathy stimuli in order to allow comparison of brain activations in these two processes. Results of 13 right-handed, healthy, male volunteers were included. Functional images were acquired using a 1.5 T Phillips Gyroscan. Our results confirmed that ToM and empathy stimuli are associated with overlapping but distinct neuronal networks. Common areas of activation included the medial prefrontal cortex, temporoparietal junction and temporal poles. Compared to the empathy condition, ToM stimuli revealed increased activations in lateral orbitofrontal cortex, middle frontal gyros, cuneus and superior temporal gyrus. Empathy, on the other hand, was associated with enhanced activations of paracingulate, anterior and posterior cingulate and amygdala. We therefore suggest that ToM and empathy both rely on networks associated with making inferences about mental states of others. However, empathic responding requires the additional recruitment of networks involved in emotional processing. These results have implications for our understanding of disorders characterized by impairments of social cognition, such as autism and psychopathy. (c) 2005 Elsevier Inc. All rights reserved. C1 Univ Manchester, Neurosci & Psychiat Unit, Manchester M13 9PT, Lancs, England. Univ Manchester, Dept Psychol, Manchester M13 9PT, Lancs, England. 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Med. PY 2006 VL 8 IS 4 BP 451 EP 460 DI 10.1385/NMM:8:4:451 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 110RW UT WOS:000242397700003 PM 17028369 ER PT J AU Marcotte, L Crino, PB AF Marcotte, Leah Crino, Peter B. TI The neurobiology of the tuberous sclerosis complex SO NEUROMOLECULAR MEDICINE LA English DT Review DE cortex; dysplasia; epilepsy; mTOR; tuberous sclerosis ID GIANT-CELL ASTROCYTOMAS; EKER RAT MODEL; TUMOR-SUPPRESSOR PROTEINS; GENE-PRODUCT; INFANTILE SPASMS; CEREBRAL-LESIONS; CORTICAL TUBERS; TSC1 GENE; 3-KINASE/AKT PATHWAY; MUTATIONAL ANALYSIS AB Tuberous sclerosis complex (TSC) is a multisystem disorder that affects numerous organ systems. Brain lesions that form during development, known as tubers, are highly associated with epilepsy, cognitive disability, and autism. 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Med. PY 2006 VL 8 IS 4 BP 531 EP 546 DI 10.1385/NMM:8:4:531 PG 16 WC Neurosciences SC Neurosciences & Neurology GA 110RW UT WOS:000242397700008 PM 17028374 ER PT J AU Melin, M Carlsson, B Anckarsater, H Rastam, M Betancur, C Isaksson, A Gillberg, C Dahl, N AF Melin, M. Carlsson, B. Anckarsater, H. Rastam, M. Betancur, C. Isaksson, A. Gillberg, C. Dahl, N. TI Constitutional downregulation of SEMA5A expression in autism SO NEUROPSYCHOBIOLOGY LA English DT Article DE autistic disorder; cDNA microarrays; gene expression; chromosome 7q31; SEMA5A ID PERVASIVE DEVELOPMENTAL DISORDERS; GENOME-WIDE; CYCLIN D2; GENE; TWIN; LINKAGE; SCREEN; BRAIN; IDENTIFICATION; FAMILY AB There is strong evidence for the importance of genetic factors in idiopathic autism. The results from independent twin and family studies suggest that the disorder is caused by the action of several genes, possibly acting epistatically. We have used cDNA microarray technology for the identification of constitutional changes in the gene expression profile associated with idiopathic autism. Samples were obtained and analyzed from 6 affected subjects belonging to multiplex autism families and from 6 healthy controls. We assessed the expression levels for approximately 7,700 genes by cDNA microarrays using mRNA derived from Epstein-Barr virus-transformed B lymphocytes. The microarray data were analyzed in order to identify up- or downregulation of specific genes. A common pattern with nine downregulated genes was identified among samples derived from individuals with autism when compared to controls. Four of these nine genes encode proteins involved in biological processes associated with brain function or the immune system, and are consequently considered as candidates for genes associated with autism. Quantitative real-time PCR confirms the downregulation of the gene encoding SEMA5A, a protein involved in axonal guidance. Epstein-Barr virus should be considered as a possible source for altered expression, but our consistent results make us suggest SEMA5A as a candidate gene in the etiology of idiopathic autism. Copyright (c) 2006 S. Karger AG, Basel. C1 Uppsala Univ, Rudbeck Lab, Dept Genet & Pathol, SE-75185 Uppsala, Sweden. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. Univ Paris 12, INSERM, U513, Creteil, France. RP Dahl, N (reprint author), Uppsala Univ, Rudbeck Lab, Dept Genet & Pathol, SE-75185 Uppsala, Sweden. 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The association and linkage study for the gamma-aminobutyric acid type A receptor beta 3 subunit gene (GABRB3), located within the chromosome 15q11-q13 autism candidate region, and ASD have been evaluated. The aim of this study was to investigate the association between GABRB3 and ASD in the Korean population. Methods: The present study was conducted with the detection of four single-nucleotide polymorphisms (rs1426217, rs2081648, rs890317, rs981778) in GABRB3 and association analysis in 104 Korean ASD trios using the transmission disequilibrium test. Results: The transmission disequilibrium test demonstrated that an allele at rs2081648 showed preferential transmission ( p = 0.027). One haplotype, including all examined markers in GABRB3, demonstrated significant association ( p = 0.043), but the global chi(2) test for haplotype transmission did not reveal an association between GABRB3 and ASD (chi(2) = 15.516, d.f. = 15). Conclusion: Our finding suggested that single-nucleotide polymorphisms in GABRB3 may play a significant role in the genetic predisposition to ASD in the Korean population. Copyright (c) 2006 S. Karger AG, Basel. C1 Eulji Univ, Sch Med, Dept Pharmacol, Taejon, South Korea. Eulji Univ, Sch Med, Div Biostat, Taejon, South Korea. Gachon Med Sch, Dept Neuropsychiat, Inchon, South Korea. Seoul Natl Univ, Bundang Hosp, Dept Psychiat, Songnam, South Korea. RP Yoo, HJ (reprint author), Eulji Univ, Sch Med, Dept Pharmacol, Taejon, South Korea. 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Whether autistic individuals differ from neurotypical individuals in these domains is debatable and, moreover, the relationship between the behaviors in these two domains remains unclear. We first compared the face processing ability of 14 adult individuals with autism with that of neurotypical controls and showed that the autistic individuals were slowed in their speed of face discrimination. We then showed that the two groups differed in their ability to derive the global whole in two different tasks, one using hierarchical compound letters and the other using a microgenetic primed matching task with geometric shapes, with the autistic group showing a bias in favor of local information. A significant correlation was also observed between performance on the face task and the configural tasks. We then confirmed the prediction that the ability to derive the global whole is not only critical for faces but also for other objects as well, as the autistic individuals performed more slowly than the control group in discriminating between objects. Taken together, the results suggest that the bias for local processing seen in autistic individuals might have an adverse impact on their ability to process faces and objects. (c) 2005 Elsevier Ltd. All rights reserved. C1 Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. Univ Haifa, Dept Psychol, IL-31999 Haifa, Israel. Univ Pittsburgh, Dept Psychiat, Pittsburgh, PA USA. Univ Pittsburgh, Dept Psychol, Pittsburgh, PA USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA. Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA USA. RP Behrmann, M (reprint author), Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. 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Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 004FJ UT WOS:000234737100009 PM 15907952 ER PT J AU Amador, SC Hood, AJ Schiess, MC Izor, R Sereno, AB AF Amador, SC Hood, AJ Schiess, MC Izor, R Sereno, AB TI Dissociating cognitive deficits involved in voluntary eye movement dysfunctions in Parkinson's disease patients SO NEUROPSYCHOLOGIA LA English DT Article DE endogenous; antisaccade; saccade inhibition; working memory; cognitive ID REFLEXIVE SACCADES; BASAL GANGLIA; FIXATION; SCHIZOPHRENIA; ANTISACCADES; INHIBITION; ACTIVATION; ATTENTION; AUTISM AB In an attempt to distinguish and define the altered cognitive processes associated with Parkinson's disease (PD), we examine and try to dissociate the components of an effective voluntary saccade: (1) the planning and execution of a voluntary saccade; (2) the suppression of reflexive eye movements: and (3) the working memory processes required. We tested 14 PD patients (off their medications) and 11 control subjects on antisaccade (AS), delayed antisaccade (DAS), and remembered antisaccade (RAS) paradigms. The three tasks required identical responses, each task only differing in a single manipulation for direct comparison-a delay period was added in the DAS, and the target was removed during the delay period of the RAS-allowing us to study the specific cognitive processes involved in the execution of a voluntary saccade. voluntary saccade response times were longer in the PD group compared to controls on all three tasks, suggesting difficulties in voluntary saccade execution. Furthermore, PD patients showed difficulty suppressing reflexive saccades (increased number of errors in the AS task and increased number of disinhibitions in the DAS task). Finally, our study did not show significant differences in either response time or error rate between the RAS and the DAS tasks for either control subjects or PD patients. In sum, we report evidence for voluntary saccade execution deficits together with problems inhibiting reflexive saccades in Parkinson's disease patients. These findings were correlated with each other and disease severity, suggesting that eye movement measurement may be a useful tool for studying higher cognitive function. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Texas, Sch Med, Dept Neurobiol & Anat, Houston, TX 77030 USA. Univ Texas, Sch Med, Dept Neurol, Houston, TX USA. RP Sereno, AB (reprint author), Univ Texas, Sch Med, Dept Neurobiol & Anat, 6431 Fannin St,MSB 7-160A, Houston, TX 77030 USA. 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An untested idea is whether this dysfunction is confined to mental states having a propositional content, such as beliefs and desire or extends to motor intentional states which allow one to make inferences about the actions of others. This study used kinematics to examine the ability to use gaze to inform one about the motor states of another in normal and autistic children. In each trial two participants, a model and an observer, were seated facing each other at a table. In three experimental blocks the model was requested to grasp a stimulus, to gaze towards the same stimulus, and to gaze away from the stimulus without performing any action. The task for the observer was to grasp the stimulus after having watched the model perform her task. We observed that normal children showed facilitation effects in terms of movement speed following the observation of the model grasping or simply gazing at the object. In contrast, autistic children did not show any evidence of facilitation in these conditions. Neither normal nor autistic children showed evidence of facilitation when the model's gaze was not directed towards the stimulus. These findings demonstrate that, in contrast to normal children, children with autism fail to use information from the model's action or gaze to plan their subsequent action, and that in autism the inability to use of another person's gaze produces a lack of understanding of the motor intention of others. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Padua, Dipartimento Psicol Gen, I-35131 Padua, Italy. Univ London, Dept Psychol, Egham TW20 0EX, Surrey, England. RP Castiello, U (reprint author), Univ Padua, Dipartimento Psicol Gen, Via Venezia 8, I-35131 Padua, Italy. 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Ietswaart, Magdalena Summers, Fiona TI Theory of mind following traumatic brain injury: The role of emotion recognition and executive dysfunction SO NEUROPSYCHOLOGIA LA English DT Article DE head injury; social cognition; executive functioning ID VERBAL FLUENCY PERFORMANCE; BLUNT HEAD-INJURY; SOCIAL COGNITION; FRONTOTEMPORAL DEMENTIA; ASPERGER-SYNDROME; BIOLOGICAL BASIS; FRONTAL-LOBE; BEHAVIOR; SCHIZOPHRENIA; AUTISM AB A number of studies have now documented that traumatic brain injury (TBI) is associated with deficits in the recognition of basic emotions, the capacity to infer mental states of others (theory of mind), as well as executive functioning. However, no study to date has investigated the relationship between these three constructs in the context of TBI. In the current study TBI participants (N = 16) were compared with demographically matched healthy controls (N = 17). It was found that TBI participants' recognition of basic emotions, as well as their capacity for mental state attribution, was significantly reduced relative to controls. Performance on both of these measures was strongly correlated in the healthy control, but not in the TBI sample. In contrast, in the TBI (but not the control) sample, theory of mind was substantially correlated with performance on phonemic fluency, a measure of executive functioning considered to impose particular demands upon cognitive flexibility and self-regulation. These results are consistent with other evidence indicating that deficits in some aspects of executive functioning may at least partially underlie deficits in social cognition following TBI, and thus help explain the prevalence of social dysfunction in TBI. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ New S Wales, Sch Psychol, Sydney, NSW 2052, Australia. Univ Aberdeen, Sch Psychol, Aberdeen AB9 1FX, Scotland. 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In a recent report, we have presented a case, M.J., with a well-circumscribed lesion to the right superior temporal gyrus (STG), who demonstrated impaired discrimination of gaze direction. In the aim to make distinct whether this impairment is unique to gaze, we have applied a spatial cueing paradigm established by Kingstone and Colleagues. In our experiment, pictorial gaze and symmetrical arrows were centrally presented as non-predictive, spatial cues in detecting peripheral targets. Fifteen normal subjects and M.J. participated in the experiment. In concordance with previous reports, controls demonstrated a significant facilitation of reaction times in detecting targets cued by congruent gaze/arrows, compared with incongruent cues. In striking contrast, M.J. showed no such congruency advantage for gaze, in the face of a normal congruency advantage for arrows. We have demonstrated that a circumscribed lesion to the right STG impairs the ability to utilize biological directional information such as gaze, but leaves the non-biological counterpart (arrows) intact. This dissociation implies that indeed, the STS specializes in processing gaze. (c) 2006 Elsevier Ltd. All rights reserved. C1 Komagino Hosp, Dept Psychiat, Hachioji, Tokyo 1938505, Japan. Keio Univ, Sch Med, Dept Neuropsychiat, Shinjuku Ku, Tokyo 1608582, Japan. Keio Univ, Dept Psychol, Tokyo 1608582, Japan. RP Akiyama, T (reprint author), Komagino Hosp, Dept Psychiat, 273 Uratakao Cho, Hachioji, Tokyo 1938505, Japan. 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Convit, Antonio TI The 'amygdala theory of autism' revisited: Linking structure to behavior SO NEUROPSYCHOLOGIA LA English DT Article DE Asperger syndrome; MRI; social cognition; theory of mind ID OBSESSIVE-COMPULSIVE DISORDER; ASPERGER-SYNDROME; RHESUS-MONKEYS; SOCIAL-BEHAVIOR; DIAGNOSTIC INTERVIEW; FUNCTIONING AUTISM; SPECTRUM DISORDER; BRAIN RESPONSES; BASAL GANGLIA; CHILDREN AB The 'amygdala theory of autism' suggests a crucial role for the amygdala in the neurobiological basis of autism spectrum disorders. However, to date evidence is lacking of a direct relationship between amygdaia measures and behavioral manifestations of autism in affected individuals. In 17 adult individuals with Asperger syndrome (AS) and 17 well-matched controls we therefore assessed associations between MRI-derived amygdala volume and behavioral variables of emotion recognition and social cognition, as well as with core AS symptomatology. Results revealed that individuals with AS exhibited impairments in emotion recognition and social cognition compared to controls and also showed atypical relationships between amygdala volumes and overall head size. We found positive associations between emotional and social understanding and amygdala volume in the control group, but not in the AS group. In the AS group however, amygdala size was negatively related to diagnostic parameters, with smaller amygdala volumes involving higher levels of restricted-repetitive behavior domains. Our data seem to indicate that in AS the amygdala is not crucially involved in social and emotional understanding. It may, however, be a mediator for narrow interest patterns and the imposition of routines and rituals. Our data, in conjunction with current literature, seem to argue for a modification of the 'amygdala theory of autism'. (c) 2006 Elsevier Ltd. All rights reserved. C1 NYU, Sch Med, Ctr Brain Hlth, New York, NY 10016 USA. Univ Bielefeld, Dept Psychol, D-4800 Bielefeld, Germany. Univ Cologne, Dept Neurosci & Rehabil, Cologne, Germany. Nathan S Kline Inst Psychiat Res, Orangeburg, NY 10962 USA. RP Convit, A (reprint author), NYU, Sch Med, Ctr Brain Hlth, HN-400,550 1st Ave, New York, NY 10016 USA. 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Bird, Chris A. TI Executive processes in Asperger syndrome: Patterns of performance in a multiple case series SO NEUROPSYCHOLOGIA LA English DT Article DE executive functions; autism spectrum disorder; problem solving; multitasking; prefrontal cortex ID AUTISM-SPECTRUM QUOTIENT; FRONTAL-LOBE; ECOLOGICAL VALIDITY; INDIVIDUALS; DISORDER; CHILDREN; NEUROPSYCHOLOGY; COMMUNICATION; MULTITASKING; DYSFUNCTION AB Mixed evidence exists for executive dysfunction in autism spectrum disorders (ASD). This may be because of the nature of the tasks used, the heterogeneity of participants, and difficulties with recruiting appropriate control groups. A comprehensive battery of 'executive' tests was administered to 22 individuals with Asperger syndrome and 22 well-matched controls. Performance was analysed both between groups and on an individual basis to identify outliers in both the ASD and control groups. There were no differences between the groups on all 'classical' tests of executive function. However, differences were found on newer tests of executive function. Specifically, deficits in planning, abstract problem solving and especially multitasking. On the tests that discriminated the groups, all of the ASD individuals except one were identified as significantly impaired (i.e. below the 5th percentile of the control mean) on at least one executive measure. This study provides evidence for significant executive dysfunction in Asperger syndrome. Greatest dysfunction appeared in response initiation and intentionality at the highest level-the ability to engage and disengage actions in the service of overarching goals. These deficits are best observed through using more recent, ecologically valid tests of executive dysfunction. Moreover, performance on these measures correlated with autistic symptomatology. (c) 2006 Elsevier Ltd. All rights reserved. C1 Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. UCL, Inst Cognit Neurosci, London, England. 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The resulting profile of memory abilities in the children with autism was characterized by relatively poor memory for complex visual and verbal information and spatial working memory with relatively intact associative learning ability, verbal working memory, and recognition memory. A stepwise discriminant function analysis of the subtests found that the Finger Windows subtest, a measure of spatial working memory, discriminated most accurately between the autism and normal control groups. A principal components analysis indicated that the factor structure of the subtests differed substantially between the children with autism and controls, suggesting differing organizations of memory ability. C1 Univ Pittsburgh, Sch Med, Dept Psychiat, Autism Res Program, Pittsburgh, PA 15213 USA. Vet Affairs Pittsburgh Healthcare Syst, Res Serv, Pittsburgh, PA USA. Univ Pittsburgh, Sch Med, Dept Psychol, Pittsburgh, PA 15260 USA. Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15260 USA. RP Minshew, NJ (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, Autism Res Program, Webster Hall,Suite 300,3811 OHara St, Pittsburgh, PA 15213 USA. EM minshewnj@upmc.edu CR Baddeley A, 2003, J COMMUN DISORD, V36, P189, DOI 10.1016/S0021-9924(03)00019-4 Baddeley A. 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A normal inversion effect was observed in the participants with autism, suggesting intact configural face processing. A priming paradigm using partial or complete faces served in Experiment 2 to assess both local and configural face processing. Overall, normal priming effects were found in participants with autism, irrespective of whether the partial face primes were intuitive face parts (i.e., eyes, nose, etc.) or arbitrary segments. An exception, however, was that participants with autism showed magnified priming with single face parts relative to typically developing control participants. The present findings argue for intact configural processing in autism along with an enhanced processing for individual face parts. The face-processing peculiarities known to characterize autism are discussed on the basis of these results and past congruent results with nonsocial stimuli. C1 Hop Riviere des Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. 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The purpose of the present experiments was to determine the effect of an enriched environment on behavioral aberrations observed in male rats exposed to valproic acid on day 12.5 of gestation (VPA rats), and proposed on the basis of etiological, anatomical, and behavioral data as an animal model of autism. Environmental enrichment reversed almost all behavioral alterations observed in the model. VPA rats after environmental enrichment (VPA-E) compared to VPA rats reared in standard conditions have higher sensitivity to pain and lower sensitivity to nonpainful stimuli; stronger acoustic prepulse inhibition; lower locomotor, repetitive/stereotypic-like activity, and enhanced exploratory activity; decreased anxiety; increased number of social behaviors; and shorter latency to social explorations. In comparison with control animals (Con), VPA-E rats exhibited increased number of pinnings in adolescence and social explorations in adulthood, and were less anxious in the elevated plus maze. 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Therefore, a model of the brain in autism must encompass not only those brain systems that subserve social-cognitive and emotional functioning, but also those that subserve the self-regulation of behavior in response to a changing social environment. We present evidence to support the hypothesis that developmental dysfunction of the orbitofrontal-amygdala circuit of the brain is a critical factor in the development of autism and that some of the characteristic deficits of persons with autism in socio-emotional cognition and behavioral self-regulation are related to early dysfunction of different components of this circuit. A secondary hypothesis posits that the degree of intellectual impairment present in individuals with autism is directly related to the integrity of the dorsolateral prefrontal-hippocampal circuit of the brain. Together, these hypotheses have the potential to help explain the neurodevelopmental basis of some of the primary manifestations of autism as well as the heterogeneity of outcomes. (c) 2005 Elsevier Ltd. All rights reserved. C1 Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA. Univ Texas, Hlth Sci Ctr, Sch Med, Dept Psychiat & Behav Sci, Houston, TX USA. RP Bachevalier, J (reprint author), Emory Univ, Yerkes Natl Primate Res Ctr, Atlanta, GA 30322 USA. 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Biobehav. Rev. PY 2006 VL 30 IS 1 BP 97 EP 117 DI 10.1016/j.neubiorev.2005.07.002 PG 21 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 004LT UT WOS:000234755000006 PM 16157377 ER PT J AU Brune, M Brune-Cohrs, U AF Brune, M Brune-Cohrs, U TI Theory of mind - evolution, ontogeny, brain mechanisms and psychopathology SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE theory of mind; human evolution; child development; brain mechanisms of theory of mind; psychopathology ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; SOCIAL COGNITION; FRONTOTEMPORAL DEMENTIA; EMOTION-RECOGNITION; EXECUTIVE FUNCTIONS; SELF-PERSPECTIVE; BIOLOGICAL BASIS; NORMAL-CHILDREN; MIRROR NEURONS AB The ability to infer other persons' mental states and emotions has been termed 'theory of mind'. It represents an evolved psychological capacity most highly developed in humans. The evolutionary origins of theory of mind can be traced back in extant non-human primates; theory of mind probably emerged as an adaptive response to increasingly complex primate social interaction. This sophisticated 'metacognitive' ability comes, however, at an evolutionary cost, reflected in a broad spectrum of psychopathological conditions. Extensive research into autistic spectrum disorders has revealed that theory of mind may be selectively impaired, leaving other cognitive faculties intact. Recent studies have shown that observed deficits in theory of mind task performance are part of a broad range of symptoms in schizophrenia, bipolar affective disorder, some forms of dementia, 'psychopathy' and in other psychiatric disorders. This article reviews the evolutionary psychology of theory of mind including its ontogeny and representation in the central nervous system, and studies of theory of mind in psychopathological conditions. (c) 2005 Elsevier Ltd. All rights reserved. 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PY 2006 VL 30 IS 4 BP 437 EP 455 DI 10.1016/j.neubiorev.2005.08.001 PG 19 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 055QD UT WOS:000238464500001 PM 16239031 ER PT J AU Gunji, A Koyama, S Senju, A Sekiguchi, T Tojo, Y Kaga, M AF Gunji, Atsuko Koyama, Sachiko Senju, Atsushi Sekiguchi, Takahiro Tojo, Yoshikuni Kaga, Makiko TI Auditory feedback in children with autism: A reduced Lombard effect SO NEUROSCIENCE RESEARCH LA English DT Meeting Abstract C1 NCNP, Natl Inst Mental Hlth, Kodaira, Tokyo, Japan. Hokkaido Univ, Res Inst Elect Sci, Sapporo, Hokkaido 060, Japan. Univ London Birkbeck Coll, London WC1E 7HX, England. Tokyo Gakugei Univ, Koganei, Tokyo 184, Japan. Ibaraki Univ, Mito, Ibaraki, Japan. RI Gunji, Atsuko/O-6323-2014 OI Gunji, Atsuko/0000-0001-8908-8739 NR 0 TC 1 Z9 1 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 2006 VL 55 SU 1 BP S134 EP S134 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 057QG UT WOS:000238609701262 ER PT J AU Al-Ayadhi, LY AF Al-Ayadhi, Laila Y. TI Gluten sensitivity in autistic children in Central Saudi Arabia SO NEUROSCIENCES LA English DT Article ID INFANTILE-AUTISM; CELIAC-DISEASE; DIETARY INTERVENTION; CONSTIPATION; SPECTRUM AB Objectives: To examine gluten sensitivity through the measurement of anti-gliadin antibody (IgA and IgG), anti-endomysial antibody (endo-IgA), anti-reticulin antibody (IgG) and anti-transglutamase antibody (IgG) levels in blood samples of autistic in the Riyadh area. Methods: The study took place in the Department of Physiology, Faculty of Medicine, King Saud University, Riyadh between September 2003 and April 2004. Thirty-three autistic children, from the Riyadh area participated in the study, all with confirmed diagnosis according to E-2 diagnostic criteria for autistic spectrum disorders. Anti-gliadin antibody (IgA and IgG), anti-endomysial antibody (endo-IgA), anti-reticulin antibody (IgG) and anti-transglutamase antibody (IgG), were measured by the enzyme linked immunosorbent assay method. Results: Thirty-three autistic children with confirmed diagnosis (30 males and 3 females) participated in the study. A significant percentage of autistic children complained of constipation as compared to control. None of the autistic examined were positive for any of the antibodies tested, including anti-gliadin antibody (IgA and IgG), anti-endomysial antibody (endo-IgA), anti-reticulin antibody (IgG) and anti-transglutamase antibody (IgG). The same results were reached with the control group. Conclusions: The present study demonstrated that gluten sensitivity is not a major cause in those autistic children examined. C1 King Saud Univ, Fac Med, Dept Physiol, Riyadh 11461, Saudi Arabia. RP Al-Ayadhi, LY (reprint author), King Saud Univ, Fac Med, Dept Physiol, POB 2925, Riyadh 11461, Saudi Arabia. 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RP Hyman, SL (reprint author), Univ Rochester, Sch Med & Dent, Dept Pediat, Golisano Childrens Hosp Strong, 601 Elmwood Ave, Rochester, NY 14642 USA. NR 0 TC 4 Z9 4 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7750 BN 0-12-366230-3 J9 INT REV RES MENT RET JI Int. Rev. Res. Ment. Retard. PY 2006 VL 30 BP 171 EP 194 PG 24 WC Education, Special; Clinical Neurology; Neurosciences; Psychology, Multidisciplinary; Rehabilitation; Toxicology SC Education & Educational Research; Neurosciences & Neurology; Psychology; Rehabilitation; Toxicology GA BDN20 UT WOS:000234420900005 ER PT J AU Brussel, W van Kuilenburg, ABP Janssens, PMW AF Brussel, W. van Kuilenburg, A. B. P. Janssens, P. M. W. TI A neonate with recurrent vomiting and generalized hypotonia diagnosed with a deficiency of dihydropyrimidine dehydrogenase SO NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS LA English DT Article; Proceedings Paper CT 10th Symposium of the European-Society-for-the-Study-of-Purine-and-Pyrimidine-Metabolism-in-Ma n (ESSPPMM) CY JUN 08-11, 2005 CL Prague, CZECH REPUBLIC SP European Soc Study Purine & Pyrimidine Metabolism Man DE neonate; vomiting; hypotonia; DPD deficiency AB Deficiency of dihydropyrimidine dehydrogenase (DPD) is a rare inborn error of pyrimidine metabolism. To date, only about 50 patients are known worldwide. The clinical picture is varied and is not yet fully described. Most patients are diagnosed at the age of 1-3 years. We present a patient diagnosed 8 weeks postpartum. The female patient presented in the first 3 days after birth with agitation, choking, and vomiting. Six weeks later, the patient presented again with vomiting and insufficient weight gain. Metabolic screening of urine showed a strongly increased excretion of uracil and thymine, with no other abnormalities. This suggested a deficiency of DPD which was confirmed by enzyme analysis in peripheral blood mononucleair (PBM) cells (patient: activity < 0.01 nmol/mg/h; controls: 9.9 +/- 2.8 nmol/mg/h). The patient was homozygous for the IVS14 + 1G > A mutation. MRI of the brain showed some cerebral atrophy; myelinization appeared normal. Many patients with DPD-deficiency suffer from convulsions and mental retardation, some show microcephaly, feeding difficulties, autism, and hypertonia. Our patient showed feeding difficulties and in the second half-year she developed slight motor retardation and generalized hypotonia. Further observation of the development of the patient may shed more light on the relationship between clinical symptoms and DPD deficiency. DPD deficiency may present in newborns with vomiting and hypotonia as the main symptoms. 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EM WBrussel@alysis.nl CR Christensen E, 1998, J INHERIT METAB DIS, V21, P272, DOI 10.1023/A:1005328424310 Enns GM, 2004, J INHERIT METAB DIS, V27, P513, DOI 10.1023/B:BOLI.0000037350.24142.d5 Van Kuilenburg ABP, 1999, HUM GENET, V104, P1, DOI 10.1007/PL00008711 Van Kuilenburg ABP, 2000, CLIN CHEM, V46, P9 van Kuilenburg ABP, 2004, BIOCHEM J, V379, P119, DOI 10.1042/BJ20031463 van Kuilenburg ABP, 2000, CLIN CANCER RES, V6, P4705 van Lenthe H, 2000, CLIN CHEM, V46, P1916 NR 7 TC 1 Z9 1 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1525-7770 J9 NUCLEOS NUCLEOT NUCL JI Nucleosides Nucleotides Nucleic Acids PY 2006 VL 25 IS 9-11 BP 1099 EP 1102 DI 10.1080/15257770600894063 PG 4 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 105GS UT WOS:000242019000024 PM 17065071 ER PT J AU Polizzi, A Pavone, P Iannetti, P Manfre, L Ruggieri, M AF Polizzi, A Pavone, P Iannetti, P Manfre, L Ruggieri, M TI Septo-optic dysplasia complex: A heterogeneous malformation syndrome SO PEDIATRIC NEUROLOGY LA English DT Article ID DIGITAL ANOMALIES; HYPOPLASIA; MUTATIONS; AGENESIS AB Septo-optic dysplasia is defined by a variable combination of dysgenesis of midline brain structures including optic nerve hypoplasia and hypothalamic-pituitary dysfunction often associated with a wide variety of brain malformations of cortical development. Multiple congenital anomalies have been reported only sporadically. Despite recent demonstration of the possible pathogenic role of HESX1/Hesx1 gene (a homeobox gene important for development of prosencephalon), the etiology of most cases of septo-optic dysplasia still remains unclear. This report describes eight children (4 males, 4 females; age 2 to 17 years) with septo-optic dysplasia who manifested dysmorphic features (involving not only the midline facial structures) and a spectrum of additional clinical and imaging features including autism, facial hemangioma, and holoprosencephaly. Full mutational screening for the HESX1 gene in seven of eight children was negative. Based on the extreme variability of the clinical and imaging phenotypes hereby observed, on literature review, and on septo-optic dysplasia animal models, this study confirmed that the phenotypic heterogeneity in septo-optic dysplasia is high. We suggest that: (1) dysmorphic features are more frequent than previously thought-they may represent a relevant part of the phenotype; (2) septo-optic dysplasia should he recategorized as an heterogeneous malformation syndrome (septo-optic dysplasia complex) (encompassing multiple brain, endocrine, and systemic anomalies) rather than a single precisely defined entity. (c) 2006 by Elsevier Inc. All rights reserved. C1 CNR, ISN, I-95125 Catania, Italy. Univ Catania, Dept Paediat, Catania, Italy. Univ Roma La Sapienza, Dept Paediat, Div Child Neurol, Rome, Italy. Cannizzaro Hosp, Neuroradiol Unit, Catania, Italy. RP Ruggieri, M (reprint author), CNR, ISN, Viale Regina Margherita,6, I-95125 Catania, Italy. 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Neurol. PD JAN PY 2006 VL 34 IS 1 BP 66 EP 71 DI 10.1016/j.pediatrneurol.2005.07.004 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 003DA UT WOS:000234660600015 PM 16376284 ER PT J AU Baldassi, S Pei, F Procida, G Igliozzi, R Muratori, F Tancredi, R Cioni, G AF Baldassi, S. Pei, F. Procida, G. Igliozzi, R. Muratori, F. Tancredi, R. Cioni, G. TI Neural correlates of global form perception in autism SO PERCEPTION LA English DT Meeting Abstract C1 Univ Florence, Dept Psychol, Florence, Italy. Univ Pisa, IRCCS Stella Maris, Dept Dev Neurosci, Pisa, Italy. EM stefano@in.cnr.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 2006 VL 35 SU S BP 72 EP 73 PG 2 WC Psychology; Psychology, Experimental SC Psychology GA 127PR UT WOS:000243599300232 ER PT J AU Pelphrey, KA AF Pelphrey, K. A. TI Brain mechanisms for visually perceiving the actions and intentions of others: Lessons from autism and typical development SO PERCEPTION LA English DT Meeting Abstract C1 Duke Univ, Dept Psychol & Brain Sci, Durham, NC 27708 USA. EM kevin.pelphrey@duke.edu 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 2006 VL 35 SU S BP 119 EP 120 PG 2 WC Psychology; Psychology, Experimental SC Psychology GA 127PR UT WOS:000243599300378 ER PT J AU Snyder, A Bahramali, H Hawker, T Mitchell, DJ AF Snyder, Allan Bahramali, Homayoun Hawker, Tobias Mitchell, D. John TI Savant-like numerosity skills revealed in normal people by magnetic pulses SO PERCEPTION LA English DT Article ID PARADOXICAL FUNCTIONAL FACILITATION; FRONTOTEMPORAL DEMENTIA; VIRTUAL LESIONS; STIMULATION; BRAIN; NUMBER; AUTISM; TASK AB Oliver Sacks observed autistic twins who instantly guessed the exact number of matchsticks that had just fallen on the floor, saying in unison "111". To test the suggestion that normal individuals have the capacity for savant numerosity, we temporarily simulated the savant condition in normal people by inhibiting the left anterior temporal lobe of twelve participants with repetitive transcranial magnetic stimulation (rTMS). This site has been implicated in the savant condition. Ten participants improved their ability to accurately guess the number of discrete items immediately following rTMS and, of these, eight became worse at guessing as the effects of the pulses receded. 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TI Visual form-processing deficits in autism SO PERCEPTION LA English DT Article ID HIGH-FUNCTIONING AUTISM; DORSAL STREAM FUNCTION; ASPERGER-SYNDROME; DEVELOPMENTAL DYSLEXIA; SPATIAL-FREQUENCY; CHILDREN; MOTION; COHERENCE; ATTENTION; BRAIN AB People with autism have a number of reported deficits in object recognition and global processing. Is there a low-level spatial integration deficit associated with this? We measured spatial-form-coherence detection thresholds using a Glass stimulus in a field of random dots, and compared performance to a similar motion-coherence task. A coherent visual patch was depicted by dots separated by a rotational transformation in space (form) or space-time (motion). To measure parallel visual integration, stimuli were presented for only 250 ms. We compared detection thresholds for children with autism, children with Asperger syndrome, and a matched control group. 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SO PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE LA German DT Book Review CR HAEUSSLER A, 2005, TEACCH ANSATZ FORDER NR 1 TC 0 Z9 0 PU VANDENHOECK & RUPRECHT PI GOTTINGEN PA THEATERSTRASSE 13,, D-37073 GOTTINGEN, GERMANY SN 0032-7034 J9 PRAX KINDERPSYCHOL K JI Prax. Kinderpsychol. Kinderpsychiatr. PY 2006 VL 55 IS 5 BP 411 EP 412 PG 2 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 061LU UT WOS:000238874700009 ER PT J AU Sarimski, K AF Sarimski, Klaus TI Children with autism-spectrum disorders (ASS). A practice-handbook for therapists, parents and teachers. SO PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE LA German DT Book Review CR BERNARDOPITZ V, 2005, KINDER AUTISMUS SPEK NR 1 TC 0 Z9 0 PU VANDENHOECK & RUPRECHT PI GOTTINGEN PA THEATERSTRASSE 13,, D-37073 GOTTINGEN, GERMANY SN 0032-7034 J9 PRAX KINDERPSYCHOL K JI Prax. Kinderpsychol. Kinderpsychiatr. PY 2006 VL 55 IS 5 BP 411 EP 412 PG 2 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 061LU UT WOS:000238874700008 ER PT J AU Sarimski, K AF Sarimski, Klaus TI Autistic spectrum disorders in very young children: Issues in the diagnostic process SO PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE LA English DT Article DE autistic spectrum disorder; early identification; intellectual disability ID PERVASIVE DEVELOPMENTAL DISORDERS; SCREENING INSTRUMENT; EARLY RECOGNITION; ASPERGER-SYNDROME; AGE; COMMUNICATION AB Autistic spectrum disorders in very young children: Issues in the diagnostic process The diagnosis of very young children with autistic spectrum disorders and differentiating the disorder from mental retardation are difficult in the early years. Some efforts to improve diagnostic practice are reviewed. The usefulness of standardized behavioural rating scales, observation of core deficits in communication and play and parental reports are discussed in view of the author's experience with 13 children (2-4 years of age). Even in the case of diagnostic uncertainty, focussing early intervention on core symptoms of autism and supporting responsive parent-child interactions is recommended in order to prevent further social isolation of children with autistic features. C1 Kinderzentrum, D-81377 Munich, Germany. RP Sarimski, K (reprint author), Kinderzentrum, Heiglhofstr 63, D-81377 Munich, Germany. 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Kinderpsychol. Kinderpsychiatr. PY 2006 VL 55 IS 6 BP 475 EP 490 PG 16 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 080WN UT WOS:000240279300004 PM 16967644 ER PT S AU Gauthier, I AF Gauthier, I BE Munakata, Y Johnson, MH TI Constraints on the acquisition of specialization for face processing SO PROCESSES OF CHANGE IN BRAIN AND COGNITIVE DEVELOPMENT: ATTENTION AND PERFORMANCE XXI SE ATTENTION AND PERFORMANCE LA English DT Article; Proceedings Paper CT 21st Meeting of the International-Association-for-the-Study-of-Attention-and-Performance CY JUL 27-31, 2004 CL Winter Pk, CO SP Int Assoc Study Attent & Performance ID EXPERT OBJECT RECOGNITION; AREA; NEWBORNS; PERCEPTION; MECHANISMS; AUTISM; BIRTH; DISCRIMINATION; STIMULI; INFANCY AB The domain-specificity of the mechanisms supporting face perception is debated both for early preferences observed in the newborn and later skills found in adults. However, an even more complex question is that of the relationship between newborns' face preference and adult face expertise. Here, I review the evidence addressing the question of the necessity of early constraints for the development of expertise with objects or faces. These results suggest little reason to postulate that newborn's face preferences constrain the acquisition of face recognition in adults, beyond conjectures of an evolutionary benefit. However, more work is needed to uncover other roles for an early face bias, as well as to understand how general biases constrain the visual system so that expertise in individuating similar objects tends to recruit the same neural regions across individuals. C1 Vanderbilt Univ, Dept Psychol, Nashville, TN 37203 USA. 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SO PROCESSES OF CHANGE IN BRAIN AND COGNITIVE DEVELOPMENT: ATTENTION AND PERFORMANCE XXI SE ATTENTION AND PERFORMANCE LA English DT Article; Proceedings Paper CT 21st Meeting of the International-Association-for-the-Study-of-Attention-and-Performance CY JUL 27-31, 2004 CL Winter Pk, CO SP Int Assoc Study Attent & Performance ID RECEPTIVE LANGUAGE DISORDER; EARLY ADULT LIFE; WILLIAMS-SYNDROME; INHERITED SPEECH; COGNITIVE-DEVELOPMENT; YOUNG-CHILDREN; FOLLOW-UP; IMPAIRMENT; PHENOTYPE; AUTISM AB If the atypical brain presented with a neat juxtaposition of parts intact and parts impaired, then atypical development might be a direct window on normal developmental change, with clear-cut single and double dissociations. Such a view emanates from the model of adult neuropsychological patients whose brains were fully and normally developed until their brain insult. The developing brain is very different. it is neither localized nor specialized at birth, and many months and years are required for the progressive modularization of the adult brain to occur. Because development plays such a crucial role in normal and atypical development and, early on, brain regions are highly interconnected, a tiny impairment in the initial state of the brain of a child with a genetic disorder may affect several brain regions and have cascading effects over time on the phenotypic outcome. This chapter considers what we have learned from atypical development about modules, genes, and evolution. Each section first looks at the Nativist claims found in the literature, and then re-evaluates them within a neuroconstructivist perspective. The final section considers what remains to be learned from developmental disorders. C1 Inst Child Hlth, Neurocognit Dev Unit, London WC1N 1EH, England. 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We propose that a collaboration between autism research and affective computing could lead to several mutually beneficial outcomes - from developing new tools to assist people with autism in understanding and operating in the socioemotional world around them, to developing new computational models and theories that will enable technology to be modified to provide an overall better socioemotional experience to all people who use it. This article describes work toward this convergence at the MIT Media Lab, and anticipates new research that might arise from the interaction between research into autism, technology, and human socioemotional intelligence. C1 MIT, Media Lab, Cambridge, MA 02142 USA. Univ Cambridge, Cambridge CB3 0FD, England. RP Picard, R (reprint author), MIT, Media Lab, E15-448,20 Ames St, Cambridge, MA 02142 USA. 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PY 2006 VL 1093 BP 228 EP 248 DI 10.1196/annals.1382.016 PG 21 WC Nanoscience & Nanotechnology; Multidisciplinary Sciences SC Science & Technology - Other Topics GA BFZ48 UT WOS:000245626300014 PM 17312261 ER PT J AU Corbett, BA Mendoza, S Abdullah, M Wegelin, JA Levine, S AF Corbett, BA Mendoza, S Abdullah, M Wegelin, JA Levine, S TI Cortisol circadian rhythms and response to stress in children with autism SO PSYCHONEUROENDOCRINOLOGY LA English DT Article DE autism; cortisol; circadian variations; stress; LHPA ID COMPLEX DEVELOPMENTAL DISORDER; DEXAMETHASONE SUPPRESSION TEST; EARLY INFANTILE-AUTISM; PSYCHOSOCIAL STRESS; SALIVARY CORTISOL; BRAIN; ABNORMALITIES; AMYGDALA; HORMONE AB Background: Autism is a severe neurodevelopmental disorder characterized by impairment in communication, social interaction, repetitive behaviors and difficulty adapting to novel experiences. The Hypothaiamic-Pituitary-Adreno-cortical (HPA) system responds consistently to perceived novel or unfamiliar situations and can serve as an important biomarker of the response to a variety of different stimuli. Previous research has suggested that children with autism may exhibit dysfunction of the HPA system, but it is not clear whether altered neuroendrocrine regulation or altered responsiveness underlies the differences between children with and without autism. In order to provide preliminary data concerning HPA regulation and responsiveness, we compared circadian rhythms and Methods: Circadian rhythms of cortisol were estimated in children with (N = 12) and without (N = 10) autism via analysis of salivary samples collected in the morning, afternoon and evening on 2 consecutive days. HPA responsiveness was assessed by examining the time course of changes in salivary cortisol in response to a mock MRI. Results: Both groups showed expected circadian variation with higher cortisol concentration in morning than in the evening samples. The children with autism, but not typical children, showed a more variable circadian rhythm as welt as statistically significant elevations in cortisol, following exposure to a novel, nonsocial stimulus. Conclusions: The results suggest that children with autism process and respond idiosyncratically to novel and threatening events resulting in an exaggerated cortisol response. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Calif Davis, MIND Inst, Dept Psychiat & Behav Sci, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Psychol, Sacramento, CA 95817 USA. Univ Calif Davis, Div Biostat, Sacramento, CA 95817 USA. RP Corbett, BA (reprint author), Univ Calif Davis, MIND Inst, Dept Psychiat & Behav Sci, 2825 50th St, Sacramento, CA 95817 USA. 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As these disorders have their origin in childhood, instruments for retrospective evaluation of childhood behavior are needed. Sampling and Methods: In this preliminary study, 20 adults with Asperger syndrome filled in the Wender-Utah Rating Scale for ADHD to describe retrospectively their childhood behavior. Results: Fourteen out of 20 adults with Asperger syndrome self-rated above the cut-off limit for ADHD. The median total score was also higher than that reported in normal populations in previous studies. When compared with 10 controls, patients with Asperger syndrome scored higher in almost all individual items. Conclusions: A high score on the Wender-Utah rating Scale for ADHD in this patient group might be a sign of true comorbidity with ADHD, an indication of overlapping features typical of both disorders, or a result of other psychiatric comorbidity originating already in childhood. Moreover, there are no data about the proper cut-off limit for ADHD in these subjects. 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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 2006 VL 43 SU 1 BP S74 EP S74 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 076NQ UT WOS:000239965400340 ER PT J AU Schaaf, RC Benevides, T Miller, LJANE Shoen, S Brett-Green, B Parham, LD May-Benson, T AF Schaaf, Roseann C. Benevides, Teal Miller, Lucy J. a. n. e. Shoen, Sarah Brett-Green, Barbara Parham, L. Diane May-Benson, Teresa TI Sensory processing, physiological reactivity and adaptive behavior in autism SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 46th Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 24-29, 2006 CL Vancouver, CANADA SP Soc Psychophysiol Res DE autism; vagal tone; adaptive behavior C1 Thomas Jefferson Univ, Philadelphia, PA 19107 USA. Univ So Calif, Los Angeles, CA 90089 USA. 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 2006 VL 43 SU 1 BP S87 EP S87 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 076NQ UT WOS:000239965400398 ER PT J AU Stroganova, TA Orekhova, EV Nygren, G Tcetlin, MM Posikera, IN Gillberg, C Elam, M AF Stroganova, Tatiana A. Orekhova, Elena V. Nygren, Gudrun Tcetlin, Marina M. Posikera, Irina N. Gillberg, Christopher Elam, Mikael TI Atypical lateralization of spontaneous EEG in young children with autism: A two sample study SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 46th Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 24-29, 2006 CL Vancouver, CANADA SP Soc Psychophysiol Res DE autism; gamma oscillations; development C1 Moscow Psychol & Pedag Univ, Moscow, Russia. Gothenburg Univ, S-41124 Gothenburg, Sweden. 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 2006 VL 43 SU 1 BP S95 EP S95 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 076NQ UT WOS:000239965400438 ER PT J AU Webb, SJ Quinn, A AF Webb, Sara Jane Quinn, Audrey TI Perception of Mooney faces by teens with and without autism SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 46th Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 24-29, 2006 CL Vancouver, CANADA SP Soc Psychophysiol Res DE autism; face processing; development C1 Univ Washington, Seattle, WA 98195 USA. NR 0 TC 1 Z9 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PY 2006 VL 43 SU 1 BP S105 EP S105 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 076NQ UT WOS:000239965400483 ER PT J AU Webb, SJ Groen, R Dawson, G Dager, S Weiss, A Phillips, J AF Webb, Sara Jane Groen, Rebecca Dawson, Geraldine Dager, Steve Weiss, Avery Phillips, James TI Eye movements, attention, and the cerebellum in autism SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 46th Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 24-29, 2006 CL Vancouver, CANADA SP Soc Psychophysiol Res DE autism; eye tracking; attention C1 Univ Washington, Seattle, WA 98195 USA. Seattle Childrens Hosp & Reg Med Ctr, Seattle, WA USA. NR 0 TC 1 Z9 1 PU BLACKWELL PUBLISHING PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DQ, OXON, ENGLAND SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PY 2006 VL 43 SU 1 BP S105 EP S105 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 076NQ UT WOS:000239965400482 ER PT J AU Wong, TKW Fung, PCW McAlonan, GM Chua, SE AF Wong, Teresa K. W. Fung, Peter C. W. McAlonan, Grainne M. Chua, Siew E. TI Event-related potentials to emotional facial expressions in children with autism SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract CT 46th Annual Meeting of the Society-for-Psychophysiological-Research CY OCT 24-29, 2006 CL Vancouver, CANADA SP Soc Psychophysiol Res DE autism; ERP; source analysis C1 Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China. 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 2006 VL 43 SU 1 BP S109 EP S109 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 076NQ UT WOS:000239965400500 ER PT J AU Bott, L Brock, J Brockdorff, N Boucher, J Lamberts, K AF Bott, Lewis Brock, Jon Brockdorff, Noellie Boucher, Jill Lamberts, Koen TI Perceptual similarity in autism SO QUARTERLY JOURNAL OF EXPERIMENTAL PSYCHOLOGY LA English DT Article ID VISUAL-SEARCH; ENHANCED DISCRIMINATION; CATEGORIZATION; INDIVIDUALS; PERFORMANCE; PROTOTYPE; CHILDREN; STIMULI; CLASSIFICATION; IDENTIFICATION AB People with autism have consistently been found to outperform controls on visuo-spatial tasks such as block design, embedded figures, and visual search tasks. Plaisted, O'Riordan, and others (Bonnel et al., 2003; O'Riordan & Plaisted, 2001; O'Riordan, Plaisted, Driver, & Baron-Cohen, 2001; Plaisted, O'Riordan, & Baron-Cohen, 1998a, 1998b) have suggested that these findings might be explained in terms of reduced perceptual similarity in autism, and that reduced perceptual similarity could also account for the difficulties that people with autism have in making generalizations to novel situations. In this study, high-functioning adults with autism and ability-matched controls performed a low-level categorization task designed to examine perceptual similarity. Results were analysed using standard statistical techniques and modelled using a quantitative model of categorization. This analysis revealed that participants with autism required reliably longer to learn the category structure than did the control group but, contrary to the predictions of the reduced perceptual similarity hypothesis, no evidence was found of more accurate performance by the participants with autism during the generalization stage. Our results suggest that when all participants are attending to the same attributes of an object in the visual domain, people with autism will not display signs of enhanced perceptual similarity. C1 Univ Warwick, Coventry CV4 7AL, W Midlands, England. RP Bott, L (reprint author), NYU, Dept Psychol, 6 Washington Pl, New York, NY 10003 USA. 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J. Exp. Psychol. PY 2006 VL 59 IS 7 BP 1237 EP 1254 DI 10.1080/02724980543000196 PG 18 WC Psychology, Biological; Physiology; Psychology; Psychology, Experimental SC Psychology; Physiology GA 057TF UT WOS:000238617400008 PM 16769623 ER PT J AU Symes, MD Remington, B Brown, T Hastings, RP AF Symes, MD Remington, B Brown, T Hastings, RP TI Early intensive behavioral intervention for children with autism: Therapists' perspectives on achieving procedural fidelity SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE behavioral intervention; autism; therapists ID CHALLENGING BEHAVIORS; YOUNG-CHILDREN; STAFF RESPONSES; ADULTS AB The variability in outcomes observed in home-based early intensive behavioral intervention for children with autism is likely in part to be the result of the quality of therapist performance. Therapist behavior in this context, however, is poorly understood. To achieve such an understanding, it will be necessary to specify how factors such as therapist, child and intervention program characteristics, as well as supervision and training provision, influence therapists' interactions with children. This study identified facilitating factors and barriers that therapists considered to influence their capacity to deliver early intensive behavioral intervention to young children with autism. Nineteen therapists associated with various service providers in the South of England were interviewed. In general, responses represented opposite poles of the same construct. For example, child factors such as compliance and competence were considered to facilitate instruction, whereas challenging behavior and lack of progress were perceived to hinder it. These issues are considered in the light of previous research on staff behavior in related contexts. The factors identified suggest specific avenues for questionnaire and experimental research to validate these findings, have implications for routine service provision and may help improve the outcomes of children receiving early intensive behavioral intervention. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Southampton, Sch Psychol, Ctr Behav Res Anal & Intervent Dev Disabilities, Southampton SO17 1BJ, Hants, England. Univ Wales, Sch Psychol, Bangor, Gwynedd, Wales. RP Symes, MD (reprint author), Univ Southampton, Sch Psychol, Ctr Behav Res Anal & Intervent Dev Disabilities, Southampton SO17 1BJ, Hants, England. EM mds4@soton.ac.uk RI Hastings, Richard/D-9657-2013 OI Hastings, Richard/0000-0002-0495-8270 CR Allen KD, 2000, J APPL BEHAV ANAL, V33, P373, DOI 10.1901/jaba.2000.33-373 Anderson S. 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PD JAN-FEB PY 2006 VL 27 IS 1 BP 30 EP 42 DI 10.1016/j.ridd.2004.07.007 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 000LL UT WOS:000234463400002 PM 15935615 ER PT J AU Green, VA Pituch, KA Itchon, J Choi, A O'Reilly, M Sigafoos, J AF Green, VA Pituch, KA Itchon, J Choi, A O'Reilly, M Sigafoos, J TI Internet survey of treatments used by parents of children with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE treatments for autism; Internet survey; parent reports ID YOUNG-CHILDREN; INTERVENTIONS AB We developed an Internet survey to identify treatments used by parents of children with autism. The survey listed I I I treatments and was distributed via colleagues and through chapters of the Autism Society of America and Autism Organizations Worldwide. A total of 552 parents submitted usable returns during the 3-month survey period. On average the parents reported using seven different treatments. The number of treatments used varied as a function of the child's age and type/severity of disability within the autism spectrum. Speech therapy was the most commonly reported intervention, followed by visual schedules, sensory integration, and applied behavior analysis. In addition, 52% of parents were currently using at least one medication to treat their child, 27% were implementing special diets, and 43% were using vitamin supplements. Because parents were using a large number of treatments, many of which lack empirical support, future research should focus on understanding the decision-making processes that underlie treatment selection by parents of children with autism. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Texas, Dept Educ Psychol, Austin, TX 78712 USA. RP Green, VA (reprint author), Univ Texas, Dept Educ Psychol, 1 Univ Stn,D5300, Austin, TX 78712 USA. 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PD JAN-FEB PY 2006 VL 27 IS 1 BP 70 EP 84 DI 10.1016/j.ridd.2004.12.002 PG 15 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 000LL UT WOS:000234463400005 PM 15919178 ER PT J AU Haworth, K AF Haworth, Karen TI Upper Paleolithic art, autism, and cognitive style: Implications for the evolution of language SO SEMIOTICA LA English DT Article DE language evolution; Paleolithic art; autism; savant syndrome; cognition; sign categories AB The exquisite quality of the Upper Paleolithic paintings is brought into relation with the artistic talents of the autistic savant. The linguistic limitations of the autistic individual suggest a congruent status of mind with the archaic people of the Upper Paleolithic, which could indicate language in its infancy. This notion is examined in terms of archaeological, paleontological, art historical, neurological, semiotic, and cognitive views on language evolution. 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A., 1989, EXTRAORDINARY PEOPLE Ucko P., 1967, PALEOLITHIC CAVE ART Williams D., 1992, NOBODY NOWHERE NR 38 TC 3 Z9 3 PU WALTER DE GRUYTER & CO PI BERLIN PA GENTHINER STRASSE 13, D-10785 BERLIN, GERMANY SN 0037-1998 J9 SEMIOTICA JI Semiotica PY 2006 VL 162 IS 1-4 BP 127 EP 174 DI 10.1515/SEM.2006.075 PG 48 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 109VI UT WOS:000242336700004 ER PT J AU Andersen, IM McGrew, SG Kaczmarska, J Malow, BA AF Andersen, I. M. McGrew, S. G. Kaczmarska, J. Malow, B. A. TI Therapeutic use of melatonin in autism spectrum disorder SO SLEEP LA English DT Meeting Abstract CT 20th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 17-22, 2006 CL Salt Lake City, UT SP Associated Process Sleep Soc C1 Vanderbilt Univ, Childrens Hosp, Nashville, TN USA. Vanderbilt Univ, Sch Med, Kennedy Ctr, 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 2006 VL 29 SU S MA 871 BP A297 EP A297 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 047ZH UT WOS:000237916701248 ER PT J AU Cuevas, R Marzec, M Howard, P Crowe, C Reed, H Malow, B AF Cuevas, R. Marzec, M. Howard, P. Crowe, C. Reed, H. Malow, B. TI Does actigraphy provide a valid measure of overnight sleep in children with autism spectrum disorders?t SO SLEEP LA English DT Meeting Abstract CT 20th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 17-22, 2006 CL Salt Lake City, UT SP Associated Process Sleep Soc C1 Vanderbilt Univ, Sch Med, Dept Neurol, Nashville, TN USA. Univ Michigan, Dept Neurol, Ann Arbor, MI 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 2006 VL 29 SU S MA 881 BP A300 EP A300 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 047ZH UT WOS:000237916701258 ER PT J AU Malow, BA Marzec, ML McGrew, SG Cuevas, RF Stone, WL AF Malow, B. A. Marzec, M. L. McGrew, S. G. Cuevas, R. F. Stone, W. L. TI Sleep in children with autism: Relation of parental sleep concerns to polysomnography and behavioral measures SO SLEEP LA English DT Meeting Abstract CT 20th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 17-22, 2006 CL Salt Lake City, UT SP Associated Process Sleep Soc C1 Vanderbilt Univ, Nashville, TN USA. Vanderbilt Univ, Childrens Hosp, Nashville, TN USA. Univ Michigan, Ann Arbor, MI USA. Vanderbilt Univ, Div Pediat Neurol, Nashville, TN USA. NR 0 TC 1 Z9 1 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 2006 VL 29 SU S MA 875 BP A298 EP A298 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 047ZH UT WOS:000237916701252 ER PT J AU Malow, BA McGrew, SG Henderson, LM Stone, WL AF Malow, B. A. McGrew, S. G. Henderson, L. M. Stone, W. L. TI Family inventory of sleep habits: Reliability and application to children with autism spectrum disorders SO SLEEP LA English DT Meeting Abstract CT 20th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 17-22, 2006 CL Salt Lake City, UT SP Associated Process Sleep Soc C1 Vanderbilt Univ, Vanderbilt Childrens Hosp, Nashville, TN 37232 USA. NR 0 TC 4 Z9 4 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 2006 VL 29 SU S MA 253 BP A85 EP A85 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 047ZH UT WOS:000237916700253 ER PT J AU Wren-Adkins, K Henderson, L Harvey, M Howard, PA Howard, PL Beth, MA AF Wren-Adkins, K. Henderson, L. Harvey, M. Howard, P. A. Howard, P. L. Beth, M. A. TI Practical tips for conducting successful polysomnograms in children with autism spectrum disorders SO SLEEP LA English DT Meeting Abstract CT 20th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 17-22, 2006 CL Salt Lake City, UT SP Associated Process Sleep Soc C1 Vanderbilt Univ, Med Ctr, Neurol Sleep Div, Nashville, TN USA. Vanderbilt Univ, Kennedy Ctr, Ctr Child Dev, 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 2006 VL 29 SU S MA 865 BP A295 EP A295 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 047ZH UT WOS:000237916701242 ER PT J AU Conty, L Tijus, C Hugueville, L Coelho, E George, N AF Conty, Laurence Tijus, Charles Hugueville, Laurent Coelho, Emmanuelle George, Nathalie TI Searching for asymmetries in the detection of gaze contact versus averted gaze under different head views: a behavioural study SO SPATIAL VISION LA English DT Article DE gaze contact; visual search; gaze direction; head orientation; social attention ID EYE CONTACT; SOCIAL ATTENTION; FACE RECOGNITION; DIRECTION; PERCEPTION; CHILDREN; LOOKING; AUTISM; ADULTS; ORIENTATION AB Eye contact is a crucial social cue constituting a frequent preliminary to interaction. Thus, the perception of others' gaze may be associated with specific processes beginning with asymmetries in the detection of direct versus averted gaze. We tested this hypothesis in two behavioural experiments using realistic eye stimuli in a visual search task. We manipulated the head orientation (frontal or deviated) and the visual field (right or left) in which the target appeared at display onset. We found that direct gaze targets presented among averted gaze distractors were detected faster and better than averted gaze targets among direct gaze distractors, but only when the head was deviated. Moreover, direct gaze targets were detected very quickly and efficiently regardless of head orientation and visual field, whereas the detection of averted gaze was strongly modulated by these factors. These results suggest that gaze contact has precedence over contextual information such as head orientation and visual field. C1 Univ Paris 06, Hop La Pitie Salpetriere, LENA, CNRS,UPR640,Lab Neurosci Cognit & Imagerie Cerebr, F-75651 Paris 13, France. Univ Paris 08, Lab Cognit & Usages, F-93526 St Denis, France. RP Conty, L (reprint author), Univ Paris 06, Hop La Pitie Salpetriere, LENA, CNRS,UPR640,Lab Neurosci Cognit & Imagerie Cerebr, 47 Blvd Hop, F-75651 Paris 13, France. 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PD JAN PY 2006 VL 10 IS 1 BP 3 EP 4 DI 10.1016/j.tics.2005.11.010 PG 2 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 006PW UT WOS:000234910400002 PM 16318924 ER PT S AU Chakrabarti, B Baron-Cohen, S AF Chakrabarti, Bhismadev Baron-Cohen, Simon BE Anders, S Ende, G Junghoffer, M Kissler, J Wildgruber, D TI Empathizing: neurocognitive developmental mechanisms and individual differences SO UNDERSTANDING EMOTIONS SE PROGRESS IN BRAIN RESEARCH LA English DT Article; Proceedings Paper CT Symposium on Understanding Emotions CY SEP, 2004 CL Constance, GERMANY SP Heidelberg Acad Sci & Humanities, Unit Konstanz, Ctr Junior Researchers HO Freudental Castle DE empathy; theory of mind; mindreading; neuroimaging; sex differences; psychopathology; individual differences; basic emotions ID HIGH-FUNCTIONING AUTISM; NORMAL SEX-DIFFERENCES; ASPERGER-SYNDROME; FACIAL EXPRESSIONS; GENDER-DIFFERENCES; SOCIAL COGNITION; NEURAL RESPONSES; NORMAL ADULTS; HAPPY FACES; MIND AB This chapter reviews the Mindreading System model encompassing four neurocognitive mechanisms (ID, EDD, SAM, and ToMM) before reviewing the revised empathizing model encompassing two new neurocognitive mechanisms (TED and TESS). 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TI Teaching an amaurotic to see - Behavior therapy of a 17-year-old patient with Somatoform disorder and childhood autism SO VERHALTENSTHERAPIE LA German DT Article DE autism; somatoform disorder; photosensitivity; behavior therapy ID ADOLESCENTS; CHILDREN AB Diagnosis: This case history describes the inpatient behavior therapy of a 17-year-old male patient of average intelligence with a pronounced photosensitivity in the sense of a somatoform disorder and underlying childhood autism. Therapy: Following detailed psychoeducation and careful reattribution of the patient's somatic illness concept, step-by-step exposure exercises for reducing photosensitivity were carried out. Independence and social competence training in order to support the development of autonomy and to improve social competencies were initiated. In addition, during the inpatient stay, the patient regularly took part in group therapy sessions in order to foster social skills. Moreover, in order to promote the perception and recognition of emotions, verbal and nonverbal expressions of feelings and the ability to address emotions, an emotional regulation training took place. Results: The goals formulated at the beginning of the therapy were extensively reached: The pronounced photosensitivity, which had caused the patient to wear sunglasses day and night for 22 weeks and constantly keep his eyes closed, was no longer discernible after only the third week of treatment. The patient increasingly learned to express his desires and needs. He increasingly managed to endure and adequately cope with situations he found difficult or stressful. In social situations, he was able to assert himself with ever-greater frequency and to voice his own opinion. His tendencies to withdraw reduced steadily and he sought out contact in the group to an increased extent. Both on the ward and during the weekends at home he showed himself to be increasingly more autonomous and active. The patient learned to put forward his own opinion more strongly to his parents and to assert his desires and interests. Conclusion: Altogether, this case history shows a successful behavior therapy treatment of a somatoform disorder with underlying childhood autism. C1 Zent Inst Seel Gesundheit, Klin Psychiat & Psychotherapie Kindes & Jugendalt, D-68072 Mannheim, Germany. RP Pelz, R (reprint author), Zent Inst Seel Gesundheit, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Postfach 12 21 20, D-68072 Mannheim, Germany. EM reta.pelz@zi-mannheim.de CR Bleichhardt G, 2004, J PSYCHOSOM RES, V56, P449, DOI 10.1016/S0022-3999(03)00630-5 CAMPO JV, 1994, J AM ACAD CHILD PSY, V33, P1223, DOI 10.1097/00004583-199411000-00003 Cohen J., 1977, STAT POWER ANAL BEHA *DGKJP, 2003, SOM STOR F45 LEITL D, P109 Fritz GK, 1997, J AM ACAD CHILD PSY, V36, P1329, DOI 10.1097/00004583-199710000-00014 Looper KJ, 2002, J CONSULT CLIN PSYCH, V70, P810, DOI 10.1037//0022-006X.70.3.810 OSTER J, 1972, PEDIATRICS, V50, P429 POUSTKA F, 2004, AUTISTISCHE STORUNGE Remschmidt H., 2001, MULTIAXIALES KLASSIF, V4 RIEF W, 1998, SOMATISIERUNGSSTORUN, P548 SPIERINGS C, 1990, DEV MED CHILD NEUROL, V32, P865 STEINHAUSEN HC, 2002, PSYCHISCHE STORUNGEN, P162 Sulz S. K. D., 2000, KOGNITION EMOTION PS NR 13 TC 1 Z9 1 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1016-6262 J9 VERHALTENSTHERAPIE JI Verhaltenstherapie PY 2006 VL 16 IS 4 BP 293 EP 299 DI 10.1159/000095800 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 120DD UT WOS:000243063000008 ER PT J AU Herguner, S Mukaddes, NM AF Herguner, Sabri Mukaddes, Naht Motavalli TI Autism and Williams syndrome: A case report SO WORLD JOURNAL OF BIOLOGICAL PSYCHIATRY LA English DT Article DE autistic disorder; Williams syndrome; 7q11.23 ID BEUREN-SYNDROME; BEHAVIOR; DISORDER; CHILDREN; REGION AB Williams syndrome (WS) is a neurodevelopmental disorder caused by a deletion in the 7q11.23 region which includes at least 17 genes. The presence of autistic features in WS is a controversial issue. While some authors describe WS as the opposite phenotype of autism, recent studies indicate that both share many common characteristics. We report a 12-year-old boy diagnosed as autistic disorder and WS with hemizygosity at the elastin locus and a karyotype of 46,XY,del(7)(q11.21q11.23). Molecular genetic studies have shown that deletion at the elastin gene may account for the cardiovascular abnormalities seen in WS, but autistic features are likely caused by other genes flanking elastin. C1 Istanbul Univ, Istanbul Fac Med, Dept Child & Adolescent Psychiat, TR-34393 Istanbul, Turkey. RP Herguner, S (reprint author), Istanbul Univ, Istanbul Fac Med, Dept Child & Adolescent Psychiat, TR-34393 Istanbul, Turkey. EM cocukergen@yahoo.com CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bellugi U, 1999, TRENDS NEUROSCI, V22, P197, DOI 10.1016/S0166-2236(99)01397-1 CURRAN ME, 1993, CELL, V73, P159, DOI 10.1016/0092-8674(93)90168-P Donnai D, 2000, AM J MED GENET, V97, P164, DOI 10.1002/1096-8628(200022)97:2<164::AID-AJMG8>3.0.CO;2-F Gillberg C., 2000, BIOL AUTISTIC SYNDRO GILLBERG C, 1994, J AUTISM DEV DISORD, V24, P381, DOI 10.1007/BF02172235 GOSCH A, 1994, AM J MED GENET, V53, P83, DOI 10.1002/ajmg.1320530118 Jones W, 2000, J COGNITIVE NEUROSCI, V12, P30, DOI 10.1162/089892900561968 Kielinen M, 2004, AUTISM, V8, P49, DOI 10.1177/1362361304040638 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x Laws G, 2004, INT J LANG COMM DIS, V39, P45, DOI 10.1080/13682820310001615797 Meng X, 1998, HUM GENET, V103, P590, DOI 10.1007/s004390050874 Muhle R., 2004, PEDIATRICS, V113, P472 Osborne LR, 1999, MOL GENET METAB, V67, P1, DOI 10.1006/mgme.1999.2844 Peterson BS, 2004, TXB BIOL PSYCHIAT, P393 Pober BR, 1996, CHILD ADOL PSYCH CL, V5, P929 REISS AL, 1985, J PEDIATR-US, V106, P247, DOI 10.1016/S0022-3476(85)80296-1 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Wu YQ, 1998, AM J MED GENET, V78, P82, DOI 10.1002/(SICI)1096-8628(19980616)78:1<82::AID-AJMG17>3.0.CO;2-K NR 19 TC 9 Z9 9 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 2006 VL 7 IS 3 BP 186 EP 188 DI 10.1080/15622970600584221 PG 3 WC Psychiatry SC Psychiatry GA 072YK UT WOS:000239708900009 PM 16861145 ER PT J AU Karlov, VA AF Karlov, V. A. TI Epileptic encephalopathy SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE epilepsy; encephalopathy ID DISORDER; AUTISM; ABNORMALITIES; SEIZURES; CHILDREN AB It is suggested to distinguish two types of epileptic encephalopathy - with and without epileptic seizures. Basing on clinical and literature data, electrographic criteria of epileptic encephalopathy were developed. They are diffuse high amplitude dysrhythmia and burst-suppression patter abnormal for age. CR Berney TP, 2000, BRIT J PSYCHIAT, V176, P20, DOI 10.1192/bjp.176.1.20 CHEZ N, 1999, EPILEPSIA, V38, P50 Engel J, 2001, EPILEPSIA, V42, P796, DOI 10.1046/j.1528-1157.2001.10401.x GILEBERG C, 1983, NEUROPEDIATRICS, V14, P206 Hilty DM, 2000, J NEUROPSYCH CLIN N, V12, P283, DOI 10.1176/appi.neuropsych.12.2.283-a Kutschke G, 1999, EPILEPSIA, V40, P20 Lewine JD, 1999, PEDIATRICS, V104, P405, DOI 10.1542/peds.104.3.405 PEREZ ER, 1993, DEV MED CHILD NEUROL, V35, P601 PLESNER AM, 1987, ACTA NEUROL SCAND, V76, P215 PLIOPLYS AV, 1994, ARCH PEDIAT ADOL MED, V148, P220 SHEVELCHINSKII SI, 2002, 4 VOST EVR K EP KLIN, P32 SHEVELCHINSKY SI, 2004, 12 MEZHD SEM MED 21, P8 State RC, 2002, AM J PSYCHIAT, V159, P918, DOI 10.1176/appi.ajp.159.6.918 STONE JL, 1986, BIOL PSYCHIAT, V21, P208, DOI 10.1016/0006-3223(86)90148-4 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 YUHASZ C, 2001, EPILEPSIA, V42, P991 Zenkov LR, 2004, ZH NEVROPATOL PSIKH, V104, P30 ZENKOV LR, 2003, FARMAKOREZISTENTNYE ZENKOV LR, 2001, 3 VOST YEVR KONF EP, P92 NR 19 TC 0 Z9 0 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 2006 VL 106 IS 2 BP 4 EP 12 PG 9 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 063QT UT WOS:000239035400001 PM 16548367 ER PT J AU Simashkova, NV Yakupova, LP Bashina, VM AF Simashkova, N. V. Yakupova, L. P. Bashina, V. M. TI Clinical and neurophysiological aspects of severe forms of autism in children SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE childhood autism; endogenous autism; Rett's syndrome; universality of autism phenomenon; EEG; theta-rhythm ID RETT SYNDROME; CHILDHOOD AB The aim of the study was to elucidate fundamentals for the phenomenon of universality of childhood autism by comparison of clinical and neurophysiological features of its severest forms - children endogenous autism (CEA) and Rett's syndrome (RS). Each group included 20 patients. Both groups were similar by age-at-disease-on set, clinical appearances during the disease course and dynamics of psychopathological syndromes. The theta-rhythm is common for CEA and RS at the disease stage with marked signs of disease acuity, autism, regress and, therefore, may be regarded as a marker of severity and development delay. The universality of autism phenomenon in its severe forms was confirmed both at the clinical and neurophysiological levels. C1 Sci Ctr Mental Hlth, Moscow, Russia. RP Simashkova, NV (reprint author), Sci Ctr Mental Hlth, Moscow, Russia. CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th BASHINA VM, 1999, AUTIZM DETSTVE Bashina V M, 2001, Zh Nevrol Psikhiatr Im S S Korsakova, V101, P20 BASHINA VM, 1994, ZH NEVROPATOL PSIKH, V94, P68 BASHINA VM, 1993, ZH NEVROPATOL PSIKH, V93, P52 Gillberg C., 1995, CLIN CHILD NEUROPSYC Gorbachevskaya N. L., 1996, Fiziologiya Cheloveka, V22, P49 HAGBERG BA, 1989, PEDIATR NEUROL, V5, P75, DOI 10.1016/0887-8994(89)90031-3 IZNAK AF, 2004, AKTUALNYE VOPROSY NA, P447 Niedermeyer E, 1997, INT J PSYCHOPHYSIOL, V26, P31, DOI 10.1016/S0167-8760(97)00754-X SCHOPLER E, 1988, CHILDHOOD AUTISM RAT, P1 SIMASHKOVA NV, 2005, 14 SYEZD PSIKH MOSCO Tiganov AS, 2005, Z NEVROL PSIKHIATRII, V105, P4 TREVATHAN E, 1988, ANN NEUROL, V23, P425 VORSANOVA SG, 2003, PSIKHIATRIYA, V1, P62 YAKUPOVA LP, 2005, 14 SYEZD PSIKH ROSS, P502 YURYEVA OP, 1970, ZH NEVROPATOL PSIKH, V70, P1229 1994, MEZHDUNARODNAYA KLAS NR 18 TC 1 Z9 1 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 2006 VL 106 IS 7 BP 12 EP 19 PG 8 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 142HI UT WOS:000244639700002 PM 16921713 ER PT J AU Simashkova, NV AF Simashkova, N. V. TI Psychotic forms of atypical autism in children SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article ID NEUROPHYSIOLOGICAL ASPECTS; RETT-SYNDROME AB The aim of the study was to determine clinical borders of psychotic forms of atypical autism in children, its psychopathological and age-specific manifestations as well as nosological peculiarities and to specify its pathogenetic features. Eighty patients with childhood endogenous autism, Rett syndrome, fragile X syndrome, Down syndrome have been studied during 14 years. The study showed that psychoses similar by symptoms and course, which are characterized by attacks and regressive-catatonic disorders, may develop in the course of atypical autism. These psychoses develop on the background of dysontogenesis with consequent replacement of the following stages: autistic, regressive, catatonic, with returning to the autistic stage between attacks. Psychopathological similarity of these psychoses in different disorders correlated with EEG changes of the same type (appearance of the marked u-rhythm at the regressive stage of psychosis). C1 Sci Ctr Mental Hlth, Moscow, Russia. RP Simashkova, NV (reprint author), Sci Ctr Mental Hlth, Moscow, Russia. CR BASHINA VM, 1999, AUTIZM DETSTVE Bashina V M, 2001, Zh Nevrol Psikhiatr Im S S Korsakova, V101, P20 BASHINA VM, 1993, ZH NEVROPATOL PSIKH, V93, P52 DAVYDOVSKY IV, 1964, VESTN AKAD MED NAUK, V9, P81 DENISOVA LV, 1986, THESIS MOSCOW Gillberg C., 2004, 16 WORLD C INT ASS C, P3 Gillberg C., 1995, CLIN CHILD NEUROPSYC GILLBERG C, 1992, CLIN DEV MED, P126 GILLBERG K, 2004, PSIKHIATRIYA DETSKOG GORBACHEVSKAYA NL, 1999, AUTIZM DETSTVE, P131 HAGBERG BA, 1989, PEDIATR NEUROL, V5, P75, DOI 10.1016/0887-8994(89)90031-3 JACKSON JH, 1931, SELECTED WRITINGS J, P1 Kanner L, 1943, NERV CHILD, V2, P217 KUPRIYANOVA TA, 1991, THESIS MOSCOW LICHKO AY, 1979, PODROSTKOVAYA PSIKHI MARINCHEVA GS, 1988, UMSTVENNAYA OTSTALOS NULLER YL, 1994, MKB10 MEZHDUNARODNAY Schopler E., 1988, CHILDHOOD AUTISM RAT SIMASHKOVA NV, 2004, PSIKHIATRIYA, V1, P7 SIMASHKOVA NV, 2005, 14 SYEZD PSIKHIATROV Simashkova NV, 2006, ZH NEVROL PSIKHIATR, V106, P12 SKVORTSOV IA, 2003, RAZVITIYE NERVNOY SI SNEZHNEVSKII AV, 1974, NOZOLOGIYA PSIKHOZOV, P156 Tiganov AS, 2005, Z NEVROL PSIKHIATRII, V105, P4 VOLKMAR FR, 2000, COMP TXB PSYCHIAT, V2, P2659 VORSANOVA SG, 2005, 15 SYEZD PSIKH MOSCO, P188 Vorsanova SG, 2002, ZH NEVROPATOL PSIKH, V102, P23 VORSANOVA SG, 2003, PSIKHIATRIYA, V1, P62 YAKUPOVA LP, 2005, 14 SYEZD PSIKH MOSCO YUROV IY, 2004, ZH NEVROL I PSIKHIAT, V104, P73 YURYEVA OP, 1970, ZH NEVROPATOL PSIKH, V70, P1229 NR 31 TC 1 Z9 1 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 2006 VL 106 IS 10 BP 17 EP 26 PG 12 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 142HR UT WOS:000244640600003 PM 17117670 ER PT J AU Proselkova, ME Kozlovskaya, GV Platonova, NV AF Proselkova, M. E. Kozlovskaya, G. V. Platonova, N. V. TI Mental disorders in children after the sexual abuse SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE children psychiatry; child sexual abuse; mental disorders; age-specific features of PTSD AB Consequences of intrafamily noncontact abuse (40 children aged from 3 to 13 years) and out-of-family contact abuse (15 children aged from 7 to 15 years) have been studied. The intrafamily abuse was long-term and demanded from a child the immersion into situation of "secrecy". The out-of-family abuse had a character of the extreme influence upon a victim. Independently of the abuse character, border-line mental disorders were found in all children. A character of these disorders was determined by the specifics of psychogenic factor, its duration and child's age. A decreased mood, different levels of autism and disturbances of cognitive function were common features of border-line disorders. In cases of intrafamily abuse, uncontrolled drives, sexual character of games and fantasies, elements of depersonalization and age-specific transformation of affective disorders from depressiveness to clysphoric aggressive reactions were observed. In the out-of-family contact abuse, especially in teenagers, the main appearances approached to posttraumatic stress syndrome. In all cases, there was a trend to stronger differentiation of affective disorders, intensification of drives and formation of characteristic pathologic changes as children get older. C1 Sci Ctr Mental Hlth, Moscow, Russia. RP Proselkova, ME (reprint author), Sci Ctr Mental Hlth, Moscow, Russia. CR ANTONIN YM, 1991, PONYATIYE PRESTUPNOG, P3 Asanova N.K., 1997, RUKOVODSTVO PREDUPRE ASHURST P, 1991, PHYS SIGS CHILD ABUS BAGLEY K, 1969, SCALES INFANT DEV BEBCHUK MA, 1993, THESIS MOSCOW BENAMU E, 1996, DETI NASILIS, P74 DANILOVA LY, 1998, 4 KONGR PED ROSS MOS, P124 DOGADINA MA, 1998, THESIS MOSCOW FINKELHOR D, 1984, CHILD SEXUAL ABUSE N, P95 GURYEVA VA, 1996, PODROSTKOVAYA SUDEBN, P27 KEMPE CH, 1962, JAMA-J AM MED ASSOC, V181, P17 KHORN AM, 1994, KONF NAS DETI MOSCOW KONYSHEVA LP, 1988, THESIS MOSCOW KOVALEV VV, 1981, SOTSIALNO PSIKHICHES, P11 KUDRYAVTSEV IA, 1988, SUDEBNAYA PSIKHOLOGO LICHKO AE, 1985, PODROSTKOVAYA PSIKHI MARGOLINA IA, 2003, ZH NEVROPATOL PSIKH, V103, P5 MOROZOVA MV, 1994, THESIS MOSCOW MOROZOVA NB, 1996, DETI NASILIYE, P78 POPOV YV, 1998, 4 KONGR PED ROSS MOS, P112 ROUZ M, 1996, DETI NASILIYE, P92 SAFONOVA TY, 1997, REABILITATSIYA DETEY, P280 SHAKHOVA BZ, 1993, THESIS MOSCOW SHOSTAKOVICH BV, 1994, POLOVYE PRESTUPLENIY Siegel J A, 2000, Violence Vict, V15, P235 SIMSON TP, 1958, NEVROZY DETEY PREDUP SUKHAREVA GY, 1955, KLINICHESKIYE LEKTSI, V1, P458 USHAKOV GK, 1973, DETSKAYA PSIHIATRIYA ZUBOVA YA, 1997, POSTTRAVMATICHESKIYE NR 29 TC 0 Z9 0 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 2006 VL 106 IS 12 BP 20 EP 23 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 142HV UT WOS:000244641000003 PM 17274391 ER PT J AU Bobylova, MY Petrukhin, AS Dunaevskaya, GN Piliya, SV Ilina, ES AF Bobylova, M. Yu. Petrukhin, A. S. Dunaevskaya, G. N. Piliya, S. V. Ilina, E. S. TI Clinical and psychological features of children with agenesis of the vermis cerebelli SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE agenesis or hypoplasia of the vermis; cerebelli; autism; development delay; mutism; dysarthrias; hyperactivity; MRI ID DOWN-SYNDROME; WILLIAMS-SYNDROME; TRANSGENIC MICE; SYSTEM; BRAIN; LANGUAGE; AUTISM; MEMORY; MOUSE; PLAY AB The article considers behavioral disturbances in children with anomalies of the cerebellum found by MRI studies. Presented are literature data on the relations between pathology of the cerebellum and early autism in children. The cerebellum is involved not only in movement coordination but also in social adaptation and speech communication. Cerebellum-specific genes expressed in early age are similar to those of hippocampus. Our own study of children with agenesis of the vermis cerebelli detected by MRI and behavioral disturbances included 20 children aged 3-15 years (mean age 7,05 years, 12 male, 8 female). Some autistic features have been found. C1 Russian State Med Univ, Moscow 117437, Russia. RP Bobylova, MY (reprint author), Russian State Med Univ, Moscow 117437, Russia. CR Baxter LL, 2000, HUM MOL GENET, V9, P195, DOI 10.1093/hmg/9.2.195 Chang Y C, 1998, Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi, V39, P285 CONDON WS, 1985, DYSLEXIA NEUROSCIENT de Lagran MM, 2004, NEUROBIOL DIS, V15, P132, DOI 10.1016/j.nbd.2003.10.002 Eckert M, 2004, NEUROSCIENTIST, V10, P362, DOI 10.1177/1073858404263596 Ellison-Wright Z, 2004, EUR J NEUROSCI, V19, P1505, DOI 10.1111/j.1460-9568.2004.03236.x Fabbro F, 2000, J NEUROLINGUIST, V13, P173, DOI 10.1016/S0911-6044(00)00010-5 Fletcher Jack M, 2002, Semin Pediatr Neurol, V9, P201, DOI 10.1053/spen.2002.35500 GOLANI J, 1976, PERSPECTIVES ETHOLOG HOLROYD S, 1991, BIOL PSYCHIAT, V29, P287, DOI 10.1016/0006-3223(91)91291-X Kang PS, 2002, CLIN NUCL MED, V27, P827, DOI 10.1097/01.RLU.0000031619.06055.65 Lenhoff HM, 1997, SCI AM, V277, P68 Lincoln A, 2002, NEUROCASE, V8, P226, DOI 10.1093/neucas/8.3.226 Lopes C, 2003, BIOCHEM BIOPH RES CO, V305, P915, DOI 10.1016/S0006-291X(03)00867-2 Martin LA, 2004, GENES BRAIN BEHAV, V3, P158, DOI 10.1111/j.1601-183x.2004.00067.x Pierce K, 2001, BIOL PSYCHIAT, V49, P655, DOI 10.1016/S0006-3223(00)01008-8 Prats-Vinas JM, 2000, REV NEUROLOGIA, V31, P357 REISS AL, 1988, AM J MED GENET, V31, P407, DOI 10.1002/ajmg.1320310220 SALLOWAY S, 1997, NEUROPSYCHIATRY LIMB, P3 Schmitt JE, 2001, J PSYCHIAT RES, V35, P225, DOI 10.1016/S0022-3956(01)00024-3 Silveri MC, 2000, J NEUROLINGUIST, V13, P129, DOI 10.1016/S0911-6044(00)00008-7 Tendler Y, 1999, MOL BRAIN RES, V72, P40, DOI 10.1016/S0169-328X(99)00202-8 Vandeinse D, 1997, Pediatr Rehabil, V1, P41 WILLIAMS CA, 1982, AM J MED GENET, V11, P453, DOI 10.1002/ajmg.1320110411 NR 24 TC 0 Z9 0 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 2006 VL 106 IS 8 BP 21 EP 25 PG 5 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 142HM UT WOS:000244640100003 PM 16972592 ER PT J AU Radzivil, MG Bashina, VM AF Radzivil, M. G. Bashina, V. M. TI An effect of long-term cerebrolysin therapy in combination with neuroleptics on behavioral and cognitive disturbances in endogenous childhood autism SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE childhood autism; therapy; cerebrolysin; neuroleptics AB An open prospective clinical study included 25 patients with childhood autism aged from 3 to 8 years (mean age 5 years 11 months). Patients received 2 therapeutic courses (15 intramuscular Cerebrolysin injections of 1,0 ml every other day per course) with 2 months interval and basic antipsychotic therapy using typical neuroleptics in age-adjusted dosages. The duration of the study was 180 days. Significant or very significant improvement was achieved after the 1(st) Cerebrolysin course in 38% patients, after the 2(nd) course in more than 50% and to the end of the follow-up (180(th) day) in 71% of patients. There were no cases of deterioration during the trial. The autism severity as measured by the CARS scale consistently decreased from the day 0 to the day 180 - from 37,7 to 32,6 scores, respectively (p < 0,001) in all assessments as compared with the baseline. To the end of the study, the patients demonstrated a significant decrease in mental retardation by 0,2 years. A statistically significant improvement was achieved in cognitive activity, attention during task performing as well as in self-service (by 0,3 years), receptive and expressive speech, cognitive performance and perception (by 0,2 years), fine motor function (by 0,1 years). The combined therapy comprising neuroleptics and Cerebrolysin double course can be recommended for correction of behavioral disorders and cognitive dysfunction in patients with mild moderate and moderate/severe autism. C1 Sci Ctr Mental Hlth, Moscow, Russia. RP Radzivil, MG (reprint author), Sci Ctr Mental Hlth, Moscow, Russia. CR BASHINA VM, 1999, AUTIZM DETSTVE BASHINA VM, 2002, SOTS KLIN PSIKHIAT, V4, P39 BASHINA VM, 2003, PSIKHIATRIYA, V3, P7 BASHINA VM, 2004, PSYCHOPHARMACOL BIOL, V2, P674 BASHINA VM, 2004, PSIKHIATRIYA, V3, P35 GORBACHEVSKAYA N, 2001, BRAIN DEV S1, V23, P90 KRASNOPEROVA MG, 2004, EUR NEUROPSYCHOPHARM, V14, P55 Krasnoperova MG, 2004, ZH NEVROPATOL PSIKH, V104, P5 PITERS T, 2001, DETSKY AUTIZM KHREST, P336 SCHOPLER E, 1988, CHILDHOOD AUTISM RAT, P1 Skvortsov IA, 1998, ZH NEVROPATOL PSIKH, V98, P17 Tiganov AS, 2005, Z NEVROL PSIKHIATRII, V105, P4 VINDISH M, 2003, PSIKHIATRIYA, V4, P17 NR 13 TC 3 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 2006 VL 106 IS 2 BP 21 EP 25 PG 7 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 063QT UT WOS:000239035400004 PM 16548370 ER PT J AU Vorsanova, SG Jourov, IY Demidova, IA Voinova-Ulas, VY Kravets, VS Soloviev, IV Gorbachevskaya, NL Yurov, YB AF Vorsanova, S. G. Jourov, I. Yu. Demidova, I. A. Voinova-Ulas, V. Yu. Kravets, V. S. Soloviev, I. V. Gorbachevskaya, N. L. Yurov, Yu. B. TI Variations of heterochromatic chromosomal regions and chromosome abnormalities in children with autism: identification of genetic markers in autistic spectrum disorders SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE autism; variations of heterochromatic regions; cytogenetic and molecular cytogenetic analysis; chromosome abnormalities AB In the present study, the cytogenetic and molecular cytogenetic analysis of 90 children with autism and their mothers (18 subjects) was carried out. Chromosome fragility and abnormalities were found in four cases: mos 47,XXX[98]/ 46,XX[2]; 46,XY,r(22)(p11q13); 46,XY,inv(2)(p11.2q13),16qh-; 46Y,fra(X)(q27.3)16qh-. Using C-banding and quantitative fluorescent in situ hybridization (FISH), the significantly increased incidence of heterochromatic region variation was shown in autism as compared to the controls (48 and 16%, respectively). Pericentric 9phqh inversion was not characteristic of the patients with autism whereas heterochromatic variations 1phqh, 9qh(+) and 16qh- were more frequent in autism (p < 0,05). Basing on the data obtained, a possible role of position effect in autism pathogenesis as well as a potential of heterochromatic region variation analysis for the search of biological markers of autistic spectrum disorders are discussed. C1 Moscow Sci Res Inst Pediat & Pediat Surg, Moscow, Russia. RP Vorsanova, SG (reprint author), Moscow Sci Res Inst Pediat & Pediat Surg, Moscow, Russia. 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Psikhiatrii Im S S Korsakova PY 2006 VL 106 IS 6 BP 52 EP 57 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 119LG UT WOS:000243013200009 PM 16841485 ER PT J AU Strata, F delpolyi, AR Bonham, BH Chang, EF Liu, RC Nakahara, H Merzenich, MM AF Strata, F delpolyi, AR Bonham, BH Chang, EF Liu, RC Nakahara, H Merzenich, MM TI Perinatal anoxia degrades auditory system function in rats SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article; Proceedings Paper CT 34th Annual Meeting of the Society-for-Neuroscience CY OCT 23-27, 2004 CL San Diego, CA SP Soc Neurosci DE auditory behavior; auditory brainstem responses; auditory cortex; autism; language learning impairment ID BRAIN-STEM RESPONSES; CENTRAL NERVOUS-SYSTEM; HEARING-LOSS; INFERIOR COLLICULUS; HYPOXIA; AUTISM; CORTEX; MONKEYS; IMPAIRMENT; CHILDREN AB Little is known about the neural bases of the reduced auditory and cortical processing speeds that have been recorded in language-impaired, autistic, schizophrenic, and other disabled human populations. Although there is strong evidence for genetic contributions to etiologies, epigenetic factors such as perinatal anoxia (PA) have been argued to be contributors, or causal, in a significant proportion of cases. In this article, we explored the consequences of PA on this elementary aspect of auditory behavior and on auditory system function in rats that were briefly perinatally anoxic. PA rats had increased acoustic thresholds and reduced processing efficiencies recorded in an auditory behavioral task. These rats had modestly increased interpeak intervals in their auditory brainstem responses, and substantially longer latencies in poststimulus time histogram responses recorded in the primary auditory cortex. The latter were associated with degraded primary auditory cortex receptive fields and a disrupted tonotopy. These processing deficits are consistent with the parallel behavioral and physiological deficits recorded in children and adults with a history of language-learning impairment and autism. C1 Univ Calif San Francisco, WM Keck Ctr Integrat Neurosci, Coleman Lab, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Otolaryngol Head & Neck Surg, San Francisco, CA 94143 USA. RP Strata, F (reprint author), Univ Calif San Francisco, WM Keck Ctr Integrat Neurosci, Coleman Lab, San Francisco, CA 94143 USA. 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Natl. Acad. Sci. U. S. A. PD DEC 27 PY 2005 VL 102 IS 52 BP 19156 EP 19161 DI 10.1073/pnas.0509520102 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 998WG UT WOS:000234350000067 PM 16365292 ER PT J AU Lepisto, T Kujala, T Vanhala, R Alku, P Huotilainen, M Naatanen, R AF Lepisto, T Kujala, T Vanhala, R Alku, P Huotilainen, M Naatanen, R TI The discrimination of and orienting to speech and non-speech sounds in children with autism SO BRAIN RESEARCH LA English DT Article DE autism; sound discrimination; orienting; event-related potential; mismatch negativity (MMN); P3a ID EVENT-RELATED POTENTIALS; BRAIN POTENTIALS; INVOLUNTARY ATTENTION; ELECTROPHYSIOLOGICAL EVIDENCE; MINICOLUMNAR PATHOLOGY; MISMATCH NEGATIVITY; SPECTRUM DISORDER; JOINT ATTENTION; COMPLEX SOUNDS; PERCEPTION AB The present study aimed to find out how different stages of cortical auditory processing (sound encoding, discrimination, and orienting) are affected in children with autism. To this end, auditory event-related potentials (ERP) were studied in 15 children with autism and their controls. Their responses were recorded for pitch, duration, and vowel changes in speech stimuli, and for corresponding changes in the nonspeech counterparts of the stimuli, while the children watched silent videos and ignored the stimuli. The responses to sound repetition were diminished in amplitude in the children with autism, reflecting impaired sound encoding. The mismatch negativity (MMN), an ERP indexing sound discrimination, was enhanced in the children with autism as far as pitch changes were concerned. This is consistent with earlier studies reporting auditory hypersensitivity and good pitch-processing abilities, as well as with theories proposing enhanced perception of local stimulus features in individuals with autism. The discrimination of duration changes was impaired in these children, however. Finally, involuntary orienting to sound changes, as reflected by the P3a ERP, was more impaired for speech than non-speech sounds in the children with autism, suggesting deficits particularly in social orienting. This has been proposed to be one of the earliest symptoms to emerge, with pervasive effects on later development. (c) 2005 Elsevier B.V. All rights reserved. C1 Univ Helsinki, Dept Psychol, Cognit Brain Res Unit, FIN-00014 Helsinki, Finland. Univ Helsinki, Helsinki Brain Res Ctr, Helsinki, Finland. Univ Helsinki, Helsinki Collegium Adv Studies, Helsinki, Finland. Univ Helsinki, Hosp Children & Adolescents, Dept Child Neurol, Helsinki, Finland. Helsinki Univ Technol, Lab Acoust & Audio Signal Proc, 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 DEC 15 PY 2005 VL 157 SI SI MA 12 BP 371 EP 372 DI 10.1016/j.cbi.2005.10.057 PG 2 WC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology SC Biochemistry & Molecular Biology; Pharmacology & Pharmacy; Toxicology GA 998RN UT WOS:000234337000062 PM 16429495 ER PT J AU [Anonymous] AF [Anonymous] TI Neuroscience - Reflecting badly SO NATURE LA English DT News Item AB Mirella Dapretto and her team at the University of California, Los Angeles, studied mirror neurons in normal children and in those with mild autism. The mirror neurons in the autistic children were far less active than normal, and were least active in the children whose social skills were worst affected. 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Recently, oxytocin administration in humans was shown to increase trust, suggesting involvement of the amygdala, a central component of the neurocircuitry of fear and social cognition that has been linked to trust and highly expresses oxytocin receptors in many mammals. However, no human data on the effects of this peptide on brain function were available. Here, we show that human amygdala function is strongly modulated by oxytocin. We used functional magnetic resonance imaging to image amygdala activation by fear-inducing visual stimuli in 15 healthy males after double-blind crossover intranasal application of placebo or oxytocin. Compared with placebo, oxytocin potently reduced activation of the amygdala and reduced coupling of the amygdala to brainstem regions implicated in autonomic and behavioral manifestations of fear. 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RTT is caused by mutations in the X-linked gene encoding methyl-CpG binding protein 2 (MeCP2). Mutations in MECP2 cause a variety of neurodevelopmental disorders including X-linked mental retardation, psychiatric disorders, and some cases of autism. Although MeCP2 was identified as a methylation-dependent transcriptional repressor, transcriptional profiling of RNAs from mice lacking MeCP2 did not reveal significant gene expression changes, suggesting that MeCP2 does not simply function as a global repressor. Changes in expression of a few genes have been observed, but these alterations do not explain the full spectrum of Rett-like phenotypes, raising the possibility that additional MeCP2 functions play a role in pathogenesis. In this study, we show that MeCP2 interacts with the RNA-binding protein Y box-binding protein 1 and regulates splicing of reporter minigenes. Importantly, we found aberrant alternative splicing patterns in a mouse model of RTT. 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EM tcaruso@vt.edu CR Heyman K, 2005, SCIENTIST, V19, P17 NR 1 TC 0 Z9 0 PU SCIENTIST INC PI PHILADELPHIA PA 3535 MARKET ST, SUITE 200, PHILADELPHIA, PA 19104-3385 USA SN 0890-3670 J9 SCIENTIST JI Scientist PD DEC 5 PY 2005 VL 19 IS 23 BP 8 EP 8 PG 1 WC Information Science & Library Science; Multidisciplinary Sciences SC Information Science & Library Science; Science & Technology - Other Topics GA 989DS UT WOS:000233653700002 ER PT J AU Easterbrooks, SR Handley, CM AF Easterbrooks, SR Handley, CM TI Behavior change in a student with a dual diagnosis of deafness and pervasive developmental disorder: A case study SO AMERICAN ANNALS OF THE DEAF LA English DT Article AB THE BROAD TERM pervasive developmental disorder (PPD) describes a set of symptoms that occur along a continuum of severity; these symptoms are often referred to as autism spectrum disorders (ASDs). Little is known about the incidence and prevalence of ASDs among students who are deaf or hard of hearing (DHH). Teachers of DHH students, who must work with individuals with dual diagnoses, are at a loss for guidance from the literature. The authors review the literature on ASDs (also referred to as PDD) within the DHH population, provide results of a single-subject study to reduce PDD-type behaviors in a child with hearing loss, and argue that teachers of students who are DHH must learn about practices associated with applied behavior analysis as an tool for intervening therapeutically with children with dual diagnoses of hearing loss plus an ASD. C1 Georgia State Univ, Dept Educ Psychol & Special Educ, Atlanta, GA 30303 USA. Univ No Colorado, Sch Educ, Greeley, CO 80639 USA. RP Easterbrooks, SR (reprint author), Georgia State Univ, Dept Educ Psychol & Special Educ, Atlanta, GA 30303 USA. CR Alberto P. 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Deaf PD WIN PY 2005 VL 150 IS 5 BP 401 EP 407 DI 10.1353/aad.2006.0001 PG 7 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 025FQ UT WOS:000236251100002 PM 16610472 ER PT J AU Sahoo, T Shaw, CA Young, AS Whitehouse, NL Schroer, RJ Stevenson, RE Beaudet, AL AF Sahoo, T Shaw, CA Young, AS Whitehouse, NL Schroer, RJ Stevenson, RE Beaudet, AL TI Array-based comparative genomic hybridization analysis of recurrent chromosome 15q rearrangements SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE Angelman syndrome; autism; chromosome 15; comparative genomic hybridization; isodicentric 15; Prader-Willi syndrome ID PRADER-WILLI-SYNDROME; ANGELMAN-SYNDROME; INTERSTITIAL DUPLICATIONS; LINKAGE-DISEQUILIBRIUM; PROXIMAL 15Q; MOLECULAR CHARACTERIZATION; 15Q11-Q13 REARRANGEMENTS; PERICENTROMERIC REGION; AUTISM; DISORDERS AB Genomic rearrangements of chromosome 15q11-q13 cause diverse phenotypes including autism, Prader-Willi syndrome (PWS), and Angelman syndrome (AS). This region is subject to genomic imprinting and characterized by complex combinations of low copy repeat elements. Prader-Willi and Angelman syndrome are caused primarily by 15q11-13 deletions of paternal and maternal origin, respectively. Autism is seen with maternal, but not paternal, interstitial duplications. Isodicentric 15q most often of maternal origin, is associated with a complex phenotype often including autistic features. Limitations of conventional cytogenctic tests preclude a detailed analysis in most patients with 15q rearrangements. We have developed a microarray for comparative genomic hybridization utilizing 106 genomic clones from chromosome 15q to characterize this region. The array accurately localized all breakpoints associated with gains or losses on 15q. The results confirmed the location of the common breakpoints associated with interstitial deletions and duplications. The majority of idic(15q) chromosomes are comprised of symmetrical arms with four copies of the breakpoint 1 to breakpoint 5 region. Patients with less common breakpoints that are not distinguished by routine cytogenetic methods were more accurately characterized by array analysis. This microarray provides a detailed characterization for chromosomal abnormalities involving 15q11-q14 and is useful for more precise genotype-phenotype correlations for autism, PWS, AS, and idic(15) syndrome. (c) 2005 Wiley-Liss, Inc. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Greenwood Genet Ctr, JC Self Res Inst Human Genet, Greenwood, SC 29646 USA. RP Sahoo, T (reprint author), Baylor Coll Med, Dept Mol & Human Genet, 1 Baylor Plaza,Rm T619, Houston, TX 77030 USA. 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J. Med. Genet. A PD DEC 1 PY 2005 VL 139A IS 2 BP 106 EP 113 DI 10.1002/ajmg.a.31000 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 989TJ UT WOS:000233696500007 PM 16284940 ER PT J AU Stern, L Francoeur, MJ Primeau, MN Sommerville, W Fombonne, E Mazer, BD AF Stern, L Francoeur, MJ Primeau, MN Sommerville, W Fombonne, E Mazer, BD TI Immune function in autistic children SO ANNALS OF ALLERGY ASTHMA & IMMUNOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; INFLAMMATORY-BOWEL-DISEASE; RUBELLA VACCINATION; INTRAVENOUS IMMUNOGLOBULIN; CAUSAL ASSOCIATION; CHILDHOOD AUTISM; MEASLES-VIRUS; NO EVIDENCE; MUMPS; MMR AB Background: There have been reports that some children with autistic spectrum disorders have abnormal immune function. However, data in this area remain scarce and conflicting. Objective: To evaluate the immune function of a series of autistic children in the context of this proposed association. Methods: We prospectively collected data on 24 autistic children who, between January 1, 1996, and September 30, 1998, were referred unsolicited to an immunology clinic. We examined the clinical history and evaluated immunoglobulin levels; specific antibody titers to diphtheria, tetanus, and Haemophilus influenzae; T- + B-cell numbers; T-cell proliferation; and complement studies. Results: Seven of the 24 children had a history of recurrent infections. Only 2 patients had immunoglobulin levels that were outside the age-adjusted reference ranges, I of whom was subsequently diagnosed as having common variable immune deficiency. All the patients had normal in vitro T-cell function and complement study results, and only 2 of 24 patients had subtle derangements in T-cell numbers. Elevated levels of IgE were found in 5 patients, which correlated with a clinical history of atopy. Low diphtheria or tetanus antibody levels were found in 12 patients, but in 11 of these, vaccination status was not up-to-date. Conclusions: Most of the autistic children studied had normal immune function, suggesting that routine immunologic investigation is unlikely to be of benefit in most autistic children and should be considered only when there is a history suggestive of recurrent infections. C1 McGill Univ, Montreal Childrens Hosp, Ctr Hlth, Dept Psychiat, Montreal, PQ H3H 1P3, Canada. McGill Univ, Montreal Childrens Hosp, Ctr Hlth, Div Allergy & Immunol, Montreal, PQ H3H 1P3, Canada. RP Mazer, BD (reprint author), McGill Univ, Montreal Childrens Hosp, Ctr Hlth, Dept Psychiat, 2300 Tupper St, Montreal, PQ H3H 1P3, Canada. 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Allergy Asthma Immunol. PD DEC PY 2005 VL 95 IS 6 BP 558 EP 565 PG 8 WC Allergy; Immunology SC Allergy; Immunology GA 996KV UT WOS:000234173700014 PM 16400896 ER PT J AU Lindgren, KA Folstein, SE Tomblin, JB Tager-Flusberg, H AF Lindgren, KA Folstein, SE Tomblin, JB Tager-Flusberg, H TI Investigation of language impairment in first-degree relatives of children with autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 130th Annual Meeting of the American-Neurological-Association CY SEP 25-28, 2005 CL San Diego, CA SP Amer Neurol Assoc, AstraZeneca C1 Boston Univ, Sch Med, Lab Dev Cognit Neurosci, Boston, MA 02118 USA. Univ Iowa, Iowa City, IA USA. RI Tager-Flusberg, Helen/D-5265-2009 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 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD DEC PY 2005 VL 58 IS 6 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 989WE UT WOS:000233703900045 ER PT J AU Beaumont, A Montgomery, D AF Beaumont, A Montgomery, D TI The effects of neurofeedback on a child with autism SO APPLIED PSYCHOPHYSIOLOGY AND BIOFEEDBACK LA English DT Meeting Abstract DE autism; neurofeedback; EEG C1 Nova SE Univ, Plantation, FL 33324 USA. NR 0 TC 0 Z9 0 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1090-0586 J9 APPL PSYCHOPHYS BIOF JI Appl. Psychophysiol. Biofeedback PD DEC PY 2005 VL 30 IS 4 BP 407 EP 407 PG 1 WC Psychology, Clinical SC Psychology GA 998DW UT WOS:000234299800022 ER PT J AU Cuisset, JM Joriot, S Auvin, S Goze, O Medjkane, F Salloum, A Delion, P Vallee, L AF Cuisset, JM Joriot, S Auvin, S Goze, O Medjkane, F Salloum, A Delion, P Vallee, L TI Neuropediatric approach to autism SO ARCHIVES DE PEDIATRIE LA French DT Review DE autistic disorders; brain pathology; child development disorders, pervasive ID LINKED MENTAL-RETARDATION; INFANTILE-AUTISM; MECP2 MUTATIONS; IDENTIFICATION; ABNORMALITY; CHILDREN AB Autism is defined by 3 main criteria: disturbance of reciprocal social interaction, disturbance of communication (including language comprehension and spoken language) and disturbance of normal variation in behaviour and imaginative activities; an onset before age 36 months is also required. The neuropediatric contribution to autism is dominated by the search for an underlying organic etiology, especially if there are arguments for an associated encephalopathy: ante- or perinatal medical history, dysmorphic signs, skin spots, neurological abnomalities, somatic abnomalities compatible with a neurometabolic disorder. The main associated conditions with autism are: chromosome anomalies, monogenic syndrome (including fragile X syndrome), neurocutaneous syndromes, epileptic encephalopathies, neurometabolic diseases, and dystrophinopathies. The identification of an associated medical condition to autism is primordial in prospect of genetic counselling, and by the change induced in familial perception of autism. (c) 2005 Elsevier SAS. Tous droits reserves. C1 CHRU, Hop Roger Salengro, Serv Neuropediat, F-59037 Lille, France. CHRU, Hop Fontan, Serv Psychiat Infantojuvenile, F-59037 Lille, France. RP Cuisset, JM (reprint author), CHRU, Hop Roger Salengro, Serv Neuropediat, F-59037 Lille, France. EM jm-cuisset@chru-lille.fr CR *AM PSYCH ASS, 1996, MINI DSM, V4, P58 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Belmonte Matthew K, 2003, Brain Res Cogn Brain Res, V17, P651 Boddaert N, 2002, PEDIATR RADIOL, V32, P1 Carney RM, 2003, PEDIATR NEUROL, V28, P205, DOI 10.1016/S0887-8994(02)00624-0 CIESIELSKI KT, 1994, ACTA NEUROBIOL EXP, V54, P151 COURCHESNE E, 1994, AM J ROENTGENOL, V162, P123 DARDENNE P, 1975, REV NEUROPSYCH INFAN, V23, P139 DRAVET C, 2002, SYNDROMES EPILEPTIQU, P81 Elger CE, 1998, DRUG-RESISTANT SEVERE PARTIAL EPILEPSY IN CHILDREN: DIAGNOSTIC STRATEGIES AND SURGICAL TREATMENTS, P173 Gervais H, 2004, NAT NEUROSCI, V7, P801, DOI 10.1038/nn1291 Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 GOLDSON E, 1992, DEV MED CHILD NEUROL, V34, P826 GUERRINI R, 2002, SYNDROMES EPILEPTIQU, P105 Kanner L, 1943, NERV CHILD, V2, P217 Kerr AM, 2001, BRAIN DEV-JPN, V23, P208, DOI 10.1016/S0387-7604(01)00193-0 Kieffer-Renaux V, 1997, ANAE, V42, P84 KOMOTO J, 1984, J AUTISM DEV DISORD, V14, P191, DOI 10.1007/BF02409661 Laumonnier F, 2004, AM J HUM GENET, V74, P552, DOI 10.1086/382137 LELORD G, 1991, AUTISME ENFANT, P37 LIVET MO, 1998, NEUROLOGIE PEDIAT, P953 LYON G, 1996, NEUROLOGY HEREDITARY, P292 MESSERSCHMITT P, 1994, REVISIONS ACCELEREES, P269 MISES R, 1988, PSYCHIAT ENFANT, V31, P67 Muhle R, 2004, PEDIATRICS, V113, pE472, DOI 10.1542/peds.113.5.e472 Partington MW, 2004, CLIN GENET, V66, P39, DOI 10.1111/j.1399-0004.2004.00268.x SMALLEY SL, 1992, J AUTISM DEV DISORD, V22, P339, DOI 10.1007/BF01048239 STEFFENBURG S, 1991, DEV MED CHILD NEUROL, V33, P495 Steffenburg S, 1996, PEDIATR NEUROL, V14, P131, DOI 10.1016/0887-8994(96)00011-2 TREVATHAN E, 1988, ANN NEUROL, V23, P425 Valik D, 1997, PEDIATR NEUROL, V16, P252, DOI 10.1016/S0887-8994(97)89979-1 Viani F, 1991, EPILEPSIES, V3, P179 NR 32 TC 0 Z9 0 PU ELSEVIER FRANCE-EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0929-693X J9 ARCH PEDIATRIE JI Arch. Pediatr. PD DEC PY 2005 VL 12 IS 12 BP 1734 EP 1741 DI 10.1016/j.arcped.2005.09.016 PG 8 WC Pediatrics SC Pediatrics GA 996RC UT WOS:000234191000011 PM 16219450 ER PT J AU Williams, K Leonard, H d'Espaignet, ET Colvin, L Slack-Smith, L Stanley, F AF Williams, K Leonard, H d'Espaignet, ET Colvin, L Slack-Smith, L Stanley, F TI Hospitalisations from birth to 5 years in a population cohort of Western Australian children with intellectual disability SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article AB Aims: To describe the hospitalisation history in the first five years of life for all children born in Western Australia (WA) between 1983 and 1992 and diagnosed with intellectual disability ( ID). Methods: Unit record linkage of the WA Midwives Collection, WA Intellectual Disability Database, and the WA Hospital Morbidity Dataset provided the population database of WA born children with and without ID. Affected children were divided into those co-affected with autism spectrum disorders (ASD), and those whose ID had or had no known biomedical cause. Those without a biomedical cause were further subdivided into mild-moderate and severe categories. Results: On average, ID affected children were more likely than non-affected children to be admitted to hospital (RR: 1.64; 95% CI 1.6 to 1.7), on more occasions (5.3 versus 2.2 admissions), for longer (29.6 versus 8.3 days), and for a larger range of clinical diagnoses. The only exception was the group of children co-diagnosed with ASD whose hospitalisation profile resembled more that of non-affected children. Conclusions: This total population study is unique because of the availability of the system of linkable population registers and administrative health databases in WA. The results indicated that this vulnerable population of children with ID has substantial medical needs. This paper points to the need for authorities to develop supportive programmes for this population especially in the current climate of de-medicalisation of ID. More research is not only needed on the welfare of the affected children but also on the impact of the substantial medical and other needs of affected children on the rest of their immediate and extended families. C1 Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, Perth, WA 6872, Australia. Univ Western Australia, Ctr Child Hlth Res, Nedlands, WA 6009, Australia. Univ Western Australia, Sch Populat Hlth, Nedlands, WA 6009, Australia. Univ Western Australia, Sch Dent, Nedlands, WA 6009, Australia. RP Leonard, H (reprint author), Univ Western Australia, Telethon Inst Child Hlth Res, Ctr Child Hlth Res, POB 855, Perth, WA 6872, Australia. EM hleonard@ichr.uwa.edu.au RI Colvin, Lyn/F-6886-2012; Slack-Smith, Linda/H-5846-2014; Leonard, Helen/A-1010-2013 OI Colvin, Lyn/0000-0002-8492-9954; Slack-Smith, Linda/0000-0001-5859-7055; Leonard, Helen/0000-0001-6405-5834 CR Australian Institute of Health and Welfare, 2002, AUSTR HLTH 2002 Beange HP, 1996, MED J AUSTRALIA, V164, P159 Blair C, 2002, J SPEC EDUC, V36, P14, DOI 10.1177/00224669020360010201 Bower C., 1995, PERSPECT HUM BIOL, V1, P29 Chapman DA, 2002, AM J MENT RETARD, V107, P46, DOI 10.1352/0895-8017(2002)107<0046:ERFFMR>2.0.CO;2 COLVIN L, 2000, CHILDHOOD HOSP MORBI COREN LA, 2001, PEDIATRICS, V107, pE86 *ED DEP W AUSTR, 1995, SOC JUST ED POL GUID HEBER R, 1961, AM J MENT DEFIC, V64 Hilton JM, 1999, J PAEDIATR CHILD H, V35, P383, DOI 10.1046/j.1440-1754.1999.00386.x Jansen DEMC, 2004, J INTELL DISABIL RES, V48, P93, DOI 10.1111/j.1365-2788.2004.00483.x Leonard H, 2003, PAEDIATR PERINAT EP, V17, P58, DOI 10.1046/j.1365-3016.2003.00469.x *NATL COD CTR, 1996, AUSTR VERS INT CLASS Sherrard J, 2001, Inj Prev, V7, P56, DOI 10.1136/ip.7.1.56 Silva D, 1999, CHILD ADOLESCENT HLT Stanley FJ, 1997, SEMIN NEONATOL, V2, P195, DOI 10.1016/S1084-2756(97)80015-2 StataCorp, 2003, STAT STAT SOFTW REL *US PHS, 2001, CLOS GAP NAT BLUEPR Van Schrojenstein Lantman-De Valk HM, 2000, FAM PRACT, V17, P405 WATSON L, 1999, REPOORT W AUSTR CERE NR 20 TC 16 Z9 16 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD DEC PY 2005 VL 90 IS 12 BP 1243 EP 1248 DI 10.1136/adc.2004.062422 PG 6 WC Pediatrics SC Pediatrics GA 986BX UT WOS:000233425000010 PM 16301550 ER PT J AU Hazlett, HC Poe, M Gerig, G Smith, RG Provenzale, J Ross, A Gilmore, J Piven, J AF Hazlett, HC Poe, M Gerig, G Smith, RG Provenzale, J Ross, A Gilmore, J Piven, J TI Magnetic resonance Imaging and head circumference study of brain size in autism - Birth through age 2 years SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; MR-IMAGES; TISSUE CLASSIFICATION; SEGMENTATION; LIFE; CHILDHOOD; CHILDREN; VOLUMES; ADULTS AB Context: While the neuroanatomical basis of autism is not yet known, evidence. suggests that brain enlargement may be characteristic of this disorder. inferences about the timing of brain enlargement have recently come from studies of head circumference (HC). Objectives: To examine brain volume and HC in individuals with autism as compared with control individuals. Design: A cross-sectional study of brain volume was conducted at the first time point in an ongoing longitudinal magnetic resonance imaging study of brain development in autism. Retrospective longitudinal HC measurements were gathered from medical records on a larger sample of individuals with autism and local control individuals. Setting: Clinical research center. Participants: The magnetic resonance imaging study included 51 children with autism and 25 control children between 18 and 35 months of age (the latter included both developmentally delayed and typically developing children). Retrospective, longitudinal HC data were examined from birth to age 3 years in 113 children with autism and 189 local control children. Main Outcome Measures: Cerebral cortical (including cortical lobes) and cerebellar gray and white matter magnetic resonance imaging brain volumes as well as retrospective HC data from medical records were studied. Results: Significant enlargement was detected in cerebral cortical volumes but not cerebellar volumes in individuals with autism. Enlargement was present in both white and gray matter, and it was generalized throughout the cerebral cortex. Head circumference appears normal at birth, with a significantly increased rate of HC growth appearing to begin around 12 months of age. Conclusions: Generalized enlargement of gray and white matter cerebral volumes, but not cerebellar volumes, are present at 2 years of age in autism. Indirect evidence suggests that this increased rate of brain growth in autism may have its onset postnatally in the latter part of the first year of life. C1 Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC 27599 USA. Duke Univ, Med Ctr, Dept Anesthesiol, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Radiol, Durham, NC 27710 USA. RP Hazlett, HC (reprint author), Univ N Carolina, Neurodev Disorders Res Ctr, Campus Box 3367, Chapel Hill, NC 27599 USA. 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Gen. Psychiatry PD DEC PY 2005 VL 62 IS 12 BP 1366 EP 1376 DI 10.1001/archpsyc.62.12.1366 PG 11 WC Psychiatry SC Psychiatry GA 990FA UT WOS:000233727400010 PM 16330725 ER PT J AU Schlosser, RW Wendt, O Angermeier, KL Shetty, M AF Schlosser, RW Wendt, O Angermeier, KL Shetty, M TI Searching for evidence in augmentative and alternative communication: Navigating a scattered literature SO AUGMENTATIVE AND ALTERNATIVE COMMUNICATION LA English DT Article DE augmentative and alternative communication; evidence-based practice; literature searching ID SYSTEMATIC REVIEWS; FIND EVIDENCE; CLINICIAN GUIDE; SIGN LANGUAGE; CHILDREN; AUTISM; MEDLINE; SPEECH; STRATEGIES; NEED AB With increasing emphasis on evidence-based practice (EBP) as the preferred approach to practice in augmentative and alternative communication (AAC), knowledge of and skills in the EBP process have become critical to practitioners. The efficient searching of best and current research evidence to aid with clinical or educational practice is one of the core skills in the EBP process. Because of its interdisciplinary nature, evidence pertaining to AAC is scattered across numerous sources in a variety of larger fields. In this article, we aim to (a) establish assumptions and underpinnings for the search of research evidence in support of EBP in AAC, (b) identify informational databases, (c) review search terminology, (d) suggest practical strategies for successful searches in support of EBP, and (e) exemplify these strategies with several search illustrations. C1 Northeastern Univ, Dept Speech Language Pathol & Audiol, Boston, MA 02115 USA. Purdue Univ, Dept Educ Studies, W Lafayette, IN USA. Purdue Univ, Dept Speech Language & Hearing Sci, W Lafayette, IN USA. RP Schlosser, RW (reprint author), Northeastern Univ, Dept Speech Language Pathol & Audiol, 151C Forsyth, Boston, MA 02115 USA. 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PD DEC PY 2005 VL 21 IS 4 BP 233 EP 255 DI 10.1080/07434610500194813 PG 23 WC Audiology & Speech-Language Pathology; Rehabilitation SC Audiology & Speech-Language Pathology; Rehabilitation GA 015DJ UT WOS:000235531800001 ER PT J AU Sutherland, DE Gillon, GG Yoder, DE AF Sutherland, DE Gillon, GG Yoder, DE TI AAC use and service provision: A survey of New Zealand speech-language therapists SO AUGMENTATIVE AND ALTERNATIVE COMMUNICATION LA English DT Article DE augmentative and alternative communication (AAC); survey; demographic; service delivery ID COMMUNICATION; AUTISM AB Augmentative and alternative communication (AAC) services for people with complex communication needs in New Zealand were investigated by surveying speech-language therapists. Two separate survey forms were developed and mailed to speech- language therapists who worked with either students or adults. In both survey forms, information was requested about (a) the provision of AAC intervention, (b) the professional needs of speech-language therapists providing AAC services, and (c) demographic information about students with complex communication needs. Low-tech communication options and sign language were the most commonly reported AAC strategies used by adults and students with complex communication needs. Students aged 5 - 10 years received the most AAC intervention. Cerebral palsy, intellectual disabilities and autism spectrum disorders were the most commonly reported etiologies of students who used AAC. A total of 86% of the respondents indicated a desire for further AAC information or training. C1 Univ Canterbury, Christchurch 1, New Zealand. RP Sutherland, DE (reprint author), Private Bag 4800, Christchurch, New Zealand. 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A., 1995, AUGMENTATIVE ALTERNA, V11, P249, DOI 10.1080/07434619512331277389 JINKS A, 1994, AUGMENTATIVE ALTERNA, V10, P184, DOI 10.1080/07434619412331276890 JOHNSON H, 1988, 5 BIENN C INT SOC AU Johnson Jr R, 1988, ADV PSYCHOPHYSIOLOGY, V3, P69 KIERNAN C, 1982, SIGNS SYMBOLS USE NO KING J, 1998, AUGMENTATIVE ALTERNA, V14, P222, DOI 10.1080/07434619812331278396 LAFONTAINE LM, 1987, AUGMENTATIVE ALTERNA, V3, P153, DOI 10.1080/07434618712331274439 Lasker JP, 2000, AUG ALTER COMMUN SER, P107 Light JC, 1998, J COMMUN DISORD, V31, P153, DOI 10.1016/S0021-9924(97)00087-7 Matas J., 1985, AUGMENTATIVE ALTERNA, V1, P17, DOI 10.1080/07434618512331273491 McCalland F., 1998, AUGMENTATIVE ALTERNA, V14, P228, DOI 10.1080/07434619812331278406 Murphy J., 1995, AUGMENTATIVE ALTERNA, V11, P26, DOI 10.1080/07434619512331277119 Russell A, 1995, AUGMENTATIVE ALTERNA, V11, P138, DOI 10.1080/07434619512331277259 Rutter M, 1999, J CHILD PSYCHOL PSYC, V40, P169, DOI 10.1017/S0021963098003461 SCHERER MJ, 2000, LIVING STATE STUCK H Simpson K., 1998, AUGMENTATIVE ALTERNA, V14, P212, DOI 10.1080/07434619812331278386 *STAT NZ, 2002, NZ CENS POP DWELL 20 Statistics New Zealand, 1998, DIS COUNTS VONTETZCHNER S, 2000, INTRO AUGMENTATIVE A Wehmeyer ML, 1998, MENT RETARD, V36, P44, DOI 10.1352/0047-6765(1998)036<0044:NSOTUO>2.0.CO;2 Phillips B, 1993, Assist Technol, V5, P36 NR 30 TC 13 Z9 13 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 0743-4618 J9 AUGMENT ALTERN COMM JI Augment. Altern. Commun. PD DEC PY 2005 VL 21 IS 4 BP 295 EP 307 DI 10.1080/07434610500103483 PG 13 WC Audiology & Speech-Language Pathology; Rehabilitation SC Audiology & Speech-Language Pathology; Rehabilitation GA 015DJ UT WOS:000235531800005 ER PT J AU Ozonoff, S Williams, BJ Landa, R AF Ozonoff, S Williams, BJ Landa, R TI Parental report of the early development of children with regressive autism - The delays-plus-regression phenotype SO AUTISM LA English DT Article DE autism; delays-plus-regression; regressive autism ID CHILDHOOD DISINTEGRATIVE DISORDER; INFANTILE-AUTISM; DIAGNOSTIC INTERVIEW; EARLY RECOGNITION; HOME VIDEOTAPES; RUBELLA VACCINATION; SPECTRUM DISORDERS; YOUNG-CHILDREN; SPEECH LOSS; POPULATION AB Most children with autism demonstrate developmental abnormalities in their first year, whereas others display regression after mostly normal development. Few studies have examined the early development of the latter group. This study developed a retrospective measure, the Early Development Questionnaire (EDQ), to collect specific, parent-reported information about development in the first 18 months. Based on their EDQ scores, 60 children with autism between the ages of 3 and 9 were divided into three groups: an early onset group (n = 29), a definite regression group (n = 23), and a heterogeneous mixed group (n = 8). Significant differences in early social development were found between the early onset and regression groups. However, over 50 percent of the children who experienced a regression demonstrated some early social deficits during the first year of life, long before regression and the apparent onset of autism. This group, tentatively labeled 'delays-plus-regression', deserves further study. C1 Univ Calif Davis, Davis, CA 95616 USA. Univ Utah, Salt Lake City, UT 84112 USA. Johns Hopkins Sch Med, Baltimore, MD USA. RP Ozonoff, S (reprint author), Univ Calif Davis, Davis, CA 95616 USA. EM sally.ozonoff@ucdmc.ucdavis.edu CR Adrien J L, 1992, Acta Paedopsychiatr, V55, P71 American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bale JF, 2002, AM J MED GENET, V113, P229, DOI 10.1002/ajmg.10935 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 Bernard S, 2001, MED HYPOTHESES, V56, P462, DOI 10.1054/mehy.2000.1281 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x BURACK JA, 1992, J CHILD PSYCHOL PSYC, V33, P607, DOI 10.1111/j.1469-7610.1992.tb00894.x BURD L, 1988, J AM ACAD CHILD PSY, V27, P252, DOI 10.1097/00004583-198803000-00021 Creak Mildred, 1961, BRIT MED J, V2, P889 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 DELONG GR, 1981, ARCH NEUROL-CHICAGO, V38, P191 DeMyer M., 1979, PARENTS CHILDREN AUT Dissanayake C, 1997, J AUTISM DEV DISORD, V27, P295, DOI 10.1023/A:1025802515241 FINNEY HC, 1981, EVALUATION REV, V5, P207, DOI 10.1177/0193841X8100500204 Fombonne E, 2002, AUTISM, V6, P149, DOI 10.1177/1362361302006002002 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 Goldberg WA, 2003, J AUTISM DEV DISORD, V33, P607, DOI 10.1023/B:JADD.0000005998.47370.ef GUPTA PC, 1984, NEUROPEDIATRICS, V15, P191, DOI 10.1055/s-2008-1052365 HARPER J, 1975, J AUTISM CHILD SCHIZ, V5, P25, DOI 10.1007/BF01537970 Henry B., 1994, PSYCHOL ASSESSMENT, V6, P92, DOI DOI 10.1037/1040-3590.6.2.92 HOSHINO Y, 1987, JPN J PSYCHIAT NEUR, V41, P237 KANNE RL, 1943, NERV CHILD, V3, P217 Kobayashi R, 1998, ACTA PSYCHIAT SCAND, V98, P296, DOI 10.1111/j.1600-0447.1998.tb10087.x KURITA H, 1992, J AUTISM DEV DISORD, V22, P175, DOI 10.1007/BF01058149 KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 Lainhart JE, 2002, AM J MED GENET, V113, P231, DOI 10.1002/ajmg.10615 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lingam R, 2003, ARCH DIS CHILD, V88, P666, DOI 10.1136/adc.88.8.666 Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 Lord C., 1997, HDB AUTISM PERVASIVE, P195 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x Lord C, 2004, J CHILD PSYCHOL PSYC, V45, P936, DOI 10.1111/j.1469-7610.2004.t01-1-00287.x 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 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Madsen KM, 2003, PEDIATRICS, V112, P604, DOI 10.1542/peds.112.3.604 Maestro S, 1999, PSYCHOPATHOLOGY, V32, P292, DOI 10.1159/000029102 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Osterling JA, 2002, DEV PSYCHOPATHOL, V14, P239 ROBBINS LC, 1963, J ABNORM PSYCHOL, V66, P261, DOI 10.1037/h0049084 ROGERS SJ, 1990, J AM ACAD CHILD PSY, V29, P863, DOI 10.1097/00004583-199011000-00004 ROGERS SJ, 1991, J AM ACAD CHILD PSY, V30, P483, DOI 10.1097/00004583-199105000-00021 Shinnar S, 2001, PEDIATR NEUROL, V24, P185, DOI 10.1016/S0887-8994(00)00266-6 SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 Siperstein R, 2004, J AUTISM DEV DISORD, V34, P731, DOI 10.1007/s10803-004-5294-y Sparrow S, 1984, VINELAND ADAPTIVE BE Stefanatos GA, 2002, CHILD NEUROPSYCHOL, V8, P195, DOI 10.1076/chin.8.3.195.13498 Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 STONE WL, 1994, ARCH PEDIAT ADOL MED, V148, P174 Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 TAYLOR V, 1999, CORRECTIONS J, V3, P3 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 VOLKMAR FR, 1995, J AM ACAD CHILD PSY, V34, P1092, DOI 10.1097/00004583-199508000-00020 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 Werner E, 2005, ARCH GEN PSYCHIAT, V62, P889, DOI 10.1001/archpsyc.62.8.889 YARROW MR, 1970, MONOGR SOC RES CHILD, V35, P1 NR 61 TC 62 Z9 63 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 DEC PY 2005 VL 9 IS 5 BP 461 EP 486 DI 10.1177/1362361305057880 PG 26 WC Psychology, Developmental SC Psychology GA 994RY UT WOS:000234050100002 PM 16287700 ER PT J AU Williams, E Kendell-Scott, L Costall, A AF Williams, E Kendell-Scott, L Costall, A TI Parents' experiences of introducing everyday object use to their children with autism SO AUTISM LA English DT Article DE autism; everyday object use; parent interviews; qualitative analysis; social influence AB A semi-structured interview study, investigating the acquisition of everyday object use in children with autism and developmentally matched controls, is presented. Parents were asked to describe how their child currently used various everyday objects during mealtime and washing routines, the process by which this came about, and any problems encountered in attempting to introduce appropriate object use. Following transcription, the interviews were treated using a method combining phenomenological and content analysis. The statements generated were condensed, using progressive categorization, into three tables of summary statements. These represented the different sources of influence on the children's object use and the problems parents experienced in attempting to guide their child's actions. Relative to comparison groups, parents of children with autism reported that they experienced more problems and used more intensive teaching methods, and that their children were less actively involved. The findings are discussed in relation to the influence of other people in shaping object use and implications for intervention programmes. C1 Univ Surrey, Guildford GU2 5XH, Surrey, England. King Alfreds Univ, Winchester, Hants, England. Univ Portsmouth, Portsmouth, Hants, England. RP Williams, E (reprint author), Univ Surrey, Guildford GU2 5XH, Surrey, England. EM e.i.williams@surrey.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Bayley N, 1993, BAYLEY SCALES INFANT Carpenter M., 2000, AUTISM SPECTRUM DISO, P31 Giorgi A., 1985, PHENOMENOLOGY PSYCHO, P8 HETU R, 1988, British Journal of Audiology, V22, P251, DOI 10.3109/03005368809076462 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Park C. C., 1983, SIEGE 1 YEARS AUTIST Sparrow S, 1984, VINELAND ADAPTIVE BE UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 Valsiner J, 1987, CULTURE DEV CHILDREN World Health Organization, 1990, INT CLASS DIS, V10th Yardley L., 1992, PSYCHOL HEALTH, V6, P85, DOI 10.1080/08870449208402025 NR 13 TC 7 Z9 8 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 DEC PY 2005 VL 9 IS 5 BP 495 EP 514 DI 10.1177/1362361305057869 PG 20 WC Psychology, Developmental SC Psychology GA 994RY UT WOS:000234050100004 PM 16287702 ER PT J AU Howlin, P Alcock, J Burkin, C AF Howlin, P Alcock, J Burkin, C TI An 8 year follow-up of a specialist supported employment service for high-ability adults with autism or Asperger syndrome SO AUTISM LA English DT Article DE adults with Asperger syndrome; adults with high-functioning; autism; supported employment ID RECEPTIVE LANGUAGE DISORDER; DIAGNOSTIC INTERVIEW; INDIVIDUALS; OUTCOMES; CHILDREN; LIFE AB Few supported employment programmes have been specifically designed for people with autism, especially those who are more able. This study examines the outcome of a supported employment service (NAS Prospects) for adults with autism or Asperger syndrome (IQ 60+) over an 8 year period. Approximately 68 percent of clients found employment. Of the 192 jobs, the majority were permanent contracts and most involved administrative, technical or computing work. Assessment of current clients indicates that IQ, language skills and educational attainments are high. However, work has also been found for those of lower abilities. Individuals supported by Prospects show a rise in salaries, contribute more tax and claim fewer benefits. Satisfaction with the scheme is high among clients, employers and support workers. Although the programme continues to incur a financial deficit, this has decreased. Moreover, there are many non-financial benefits, which are difficult to quantify. The importance of specialist employment support of this kind is discussed. C1 Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. Royal Holloway Univ London, London, England. Natl Autist Soc, London, England. RP Howlin, P (reprint author), Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. RI Howlin, Patricia/A-7622-2011 CR Alcock J., 2003, EVALUATION PROSPECTS Barnard J, 2001, IGNORED INELIGIBLE R Beyer S., 1996, BRIT J LEARN DISABIL, V24, P134 BROACH S, 2003, PEOPLE AUTISM SPECTR Brownell R, 2000, EXPRESSIVE ONE WORD, V3rd DEAN N, 2001, 82 DEP WORK PENS WOR Dunn L. 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C., 1956, STANDARD PROGR MATRI RUSCH FR, 1993, J REHABIL, V59, P31 Smith M, 1995, GUIDE SUCCESSFUL EMP Stevens P, 1999, J INTELL DISABIL RES, V43, P19, DOI 10.1046/j.1365-2788.1999.43120169.x Venter A., 1992, HIGH FUNCTIONING IND, P187 NR 24 TC 58 Z9 58 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 DEC PY 2005 VL 9 IS 5 BP 533 EP 549 DI 10.1177/1362361305057871 PG 17 WC Psychology, Developmental SC Psychology GA 994RY UT WOS:000234050100006 PM 16287704 ER PT J AU James, WH AF James, WH TI The sex ratio of the sibs of probands with autism SO AUTISM LA English DT Letter ID PARENTAL HORMONE-LEVELS; CONCEPTION; BIRTH; TIME CR Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 James WH, 2004, HUM REPROD, V19, P1250, DOI 10.1093/humrep/deh245 James WH, 1996, J THEOR BIOL, V180, P271, DOI 10.1006/jtbi.1996.0102 Manning JT, 2002, DIGIT RATIO POINTER Manning JT, 2001, DEV MED CHILD NEUROL, V43, P160, DOI 10.1017/S0012162201000317 MANNING JT, 2002, J THEOR BIOL, V2217, P93 NR 6 TC 3 Z9 3 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 DEC PY 2005 VL 9 IS 5 BP 551 EP 552 DI 10.1177/1362361305057881 PG 2 WC Psychology, Developmental SC Psychology GA 994RY UT WOS:000234050100007 PM 16287705 ER PT J AU Potter, D AF Potter, D TI MMR and autism: What parents need to know SO AUTISM LA English DT Book Review CR FITZPATRICK M, 2004, MMR AUTISM PARENTS N 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 DEC PY 2005 VL 9 IS 5 BP 553 EP 555 DI 10.1177/1362361305057882 PG 3 WC Psychology, Developmental SC Psychology GA 994RY UT WOS:000234050100008 ER PT J AU Zarkowska, E AF Zarkowska, E TI Autism with severe learning difficulties SO AUTISM LA English DT Book Review C1 Appl Psychol Serv, Surrey, England. RP Zarkowska, E (reprint author), Appl Psychol Serv, Surrey, England. CR JORDAN R, 2001, AUSTISM SEVERE LEARN 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 DEC PY 2005 VL 9 IS 5 BP 555 EP 556 DI 10.1177/136236130500900508 PG 2 WC Psychology, Developmental SC Psychology GA 994RY UT WOS:000234050100010 ER PT J AU Rapp, JT Vollmer, TR Hovanetz, AN AF Rapp, JT Vollmer, TR Hovanetz, AN TI Evaluation and treatment of swimming pool avoidance exhibited by an adolescent girl with autism SO BEHAVIOR THERAPY LA English DT Article ID MENTALLY-RETARDED ADULT; PHOBIA; DESENSITIZATION; PROGRAM; FEAR AB We evaluated and treated swimming pool avoidance that was exhibited by a 14-year-old girl diagnosed with autism. In part, treatment involved blocking for flopping (dropping to the ground) and elopement (running away from the pool) and access to food for movements toward a swimming pool. Treatment also involved reinforcement for exposure to various depths of water. Generalization of treatment outcome was demonstrated by showing sustained effects with her mother without food reinforcement and, subsequently, by replicating these effects with her mother in an untrained setting. C1 Univ Florida, Gainesville, FL 32611 USA. RP Rapp, JT (reprint author), Texana MHMR, Behav Treatment & Training Ctr, 1818 Collins Rd, Richmond, TX 77469 USA. 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