FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Yan, WL Guan, XY Green, ED Nicolson, R Yap, TK Zhang, JH Jacobsen, LK Krasnewich, DM Kumra, S Lenane, MC Gochman, P Damschroder-Williams, PJ Esterling, LE Long, RT Martin, BM Sidransky, E Rapoport, JL Ginns, EI AF Yan, WL Guan, XY Green, ED Nicolson, R Yap, TK Zhang, JH Jacobsen, LK Krasnewich, DM Kumra, S Lenane, MC Gochman, P Damschroder-Williams, PJ Esterling, LE Long, RT Martin, BM Sidransky, E Rapoport, JL Ginns, EI TI Childhood-onset schizophrenia/autistic disorder and t(1;7) reciprocal translocation: Identification of a BAC contig spanning the translocation breakpoint at 7q21 SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE psychosis; autistic disorder; translocation ID SUSCEPTIBILITY GENES; AUTOIMMUNE-DISEASES; AUTISTIC DISORDER; ASSOCIATION; CHROMOSOME-7; PEDIGREES; LINKAGE; SPEECH; STATE; SCAN AB Childhood-onset schizophrenia (COS) is defined by the development of first psychotic symptoms by age 12, While recruiting patients with COS refractory to conventional treatments for a trial of atypical antipsychotic drugs, we discovered a unique case who has a familial t(1;7)(p22;q21) reciprocal translocation and onset of psychosis at age 9, The patient also has symptoms of autistic disorder, which are usually transient before the first psychotic episode among 40-50% of the childhood schizophrenics but has persisted in him even after the remission of psychosis, Cosegregating with the translocation, among the carriers in the family available for the study, are other significant psychopathologies, including alcohol/drug abuse, severe impulsivity, and paranoid personality and language delay, This case may provide a model for understanding the genetic basis of schizophrenia or autism. Here we report the progress toward characterization of genomic organization across the translocation breakpoint at 7q21, The polymorphic markers, D7S630/D7S492 and D7S2410/D7S646, immediately flanking the breakpoint, may be useful for further confirming the genetic linkage for schizophrenia or autism in this region. Published 2000 Wiley-Liss, Inc.(dagger). C1 NIMH, Child Psychiat Branch, Bethesda, MD 20892 USA. NIMH, Clin Neurosci Branch, Bethesda, MD 20892 USA. Natl Human Genom Res Inst, Canc Genet Lab, Bethesda, MD USA. Natl Human Genom Res Inst, Genome Technol Branch, Bethesda, MD USA. NIH, Div Comp Res & Technol, Bethesda, MD 20892 USA. Natl Lib Med, Natl Ctr Biotechnol Informat, Bethesda, MD 20894 USA. Natl Inst Deafness & Other Commun Disorders, Genet Mol Lab, Bethesda, MD USA. RP Yan, WL (reprint author), NIMH, Child Psychiat Branch, Bldg 49,Rm B1EE16, Bethesda, MD 20892 USA. RI Nicolson, Robert/E-4797-2011; Guan, Xin-Yuan/A-3639-2009 OI Guan, Xin-Yuan/0000-0002-4485-6017 CR ALAGHBANDRAD J, 1995, J AM ACAD CHILD PSY, V34, P1273, DOI 10.1097/00004583-199510000-00012 Ashley-Koch A, 1999, GENOMICS, V61, P227, DOI 10.1006/geno.1999.5968 Barrett S, 1999, AM J MED GENET, V88, P609 Blouin JL, 1998, NAT GENET, V20, P70 Bouffard GG, 1997, GENOME RES, V7, P673 DeLisi LE, 1999, AM J MED GENET, V88, P215, DOI 10.1002/(SICI)1096-8628(19990618)88:3<215::AID-AJMG1>3.0.CO;2-R Faraone SV, 1998, AM J MED GENET, V81, P290, DOI 10.1002/(SICI)1096-8628(19980710)81:4<290::AID-AJMG3>3.0.CO;2-Y FINNEY GOH, 1989, LANCET, V2, P1214 Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 Frazier JA, 1996, ARCH GEN PSYCHIAT, V53, P617 FROSTER U, 1993, LANCET, V342, P178, DOI 10.1016/0140-6736(93)91385-Y Gilvarry CM, 1996, SCHIZOPHR RES, V19, P33, DOI 10.1016/0920-9964(95)00045-3 GORDON CT, 1994, J AUTISM DEV DISORD, V24, P537, DOI 10.1007/BF02172134 Bailey A, 1998, HUM MOL GENET, V7, P571 Jacobsen LK, 1996, BIOL PSYCHIAT, V40, P1222, DOI 10.1016/0006-3223(95)00625-7 Janssen PA, 1996, PAEDIATR PERINAT EP, V10, P52, DOI 10.1111/j.1365-3016.1996.tb00026.x LANDER E, 1995, NAT GENET, V11, P241, DOI 10.1038/ng1195-241 LOPREIATO JO, 1992, J DEV BEHAV PEDIATR, V13, P281 MARINONI JC, 1995, CLIN GENET, V47, P90 MOISES HW, 1995, NAT GENET, V11, P321, DOI 10.1038/ng1195-321 Moldin SO, 1997, NAT GENET, V17, P127, DOI 10.1038/ng1097-127 Nicolson R, 1999, BIOL PSYCHIAT, V46, P1418, DOI 10.1016/S0006-3223(99)00231-0 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 RODRIGUEZ ALT, 1994, J NERV MENT DIS, V182, P478 Ross RG, 1999, AM J MED GENET, V88, P188, DOI 10.1002/(SICI)1096-8628(19990416)88:2<188::AID-AJMG17>3.3.CO;2-5 RUSSELL AT, 1989, J AM ACAD CHILD PSY, V28, P399, DOI 10.1097/00004583-198905000-00017 RUSSELL CG, 1996, J NIH RES, V8, P70 SVERD J, 1993, J AUTISM DEV DISORD, V23, P407, DOI 10.1007/BF01046229 VOLKMAR FR, 1991, AM J PSYCHIAT, V148, P1705 WATKINS JM, 1988, J CHILD PSYCHOL PSYC, V29, P865, DOI 10.1111/j.1469-7610.1988.tb00759.x Wright P, 1996, SCHIZOPHR RES, V20, P261, DOI 10.1016/0920-9964(96)82950-1 NR 31 TC 29 Z9 29 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD DEC 4 PY 2000 VL 96 IS 6 BP 749 EP 753 DI 10.1002/1096-8628(20001204)96:6<749::AID-AJMG10>3.0.CO;2-K PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 380RM UT WOS:000165717300010 PM 11121174 ER PT J AU Smith, M Filipek, PA Wu, C Bocian, M Hakim, S Modahl, C Spence, MA AF Smith, M Filipek, PA Wu, C Bocian, M Hakim, S Modahl, C Spence, MA TI Analysis of a 1-megabase deletion in 15q22-q23 in an autistic patient: Identification of candidate genes for autism and of homologous DNA segments in 15q22-q23 and 15q11-q13 SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; 15q22-q23; 15q11-q13; PTPN9; SLP-1[hUNC24] ID DUPLICATION; PROTEIN; UNC-24; 15Q; PML AB We have identified a one megabase deletion in the 15q22-15q23 region in a patient with autism, developmental delay, and mild dysmorphism, Genes that map within the deletion region and genes that are interrupted or rearranged at the deletion breakpoints are candidate genes for autism. Fluroescence in situ hybridization studies in this patient revealed that part or all of the PML gene is absent from one chromosome 15 and a BAC clone containing the D15S124 gene locus hybridizes to only one chromosome 15, BAC clones containing the PTPN9, and SLP-1[hUNC24] genes showed markedly reduced hybridization in the 15q22-q23 region on one chromosome 15 in the patient, These BACs also hybridize to the 15q11-q13 region in close proximity to SNRPN and HERC2, and in this region there is equal intensity of signal on the normal and on the deleted chromosome, There are previous reports of deletions and duplications of the 15q11-q13 region in patients with autism. Our patient represents the first report of a 15q22-q23 deletion. Hybridization of the PTPN9 and Slp-1 Bac clones to the 15q11-q13 and the 15q22-q23 regions of chromosome 15 may be due to the presence of PTPN9 or SLP-I gene sequences or to the presence of other gene sequences or to non-coding homologous DNA sequences, The PTPN9 gene encodes a non-receptor protein tyrosine phosphatase, The Slp-1 [hUNC24] gene is expressed mainly in the brain. (C) 2000 Wiley-Liss, Inc. C1 Univ Calif Irvine, Dept Pediat, Irvine, CA 92697 USA. RP Smith, M (reprint author), Univ Calif Irvine, Dept Pediat, Med Sci 1,Room C214, Irvine, CA 92697 USA. 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PD DEC 4 PY 2000 VL 96 IS 6 BP 765 EP 770 DI 10.1002/1096-8628(20001204)96:6<765::AID-AJMG13>3.0.CO;2-L PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 380RM UT WOS:000165717300013 PM 11121177 ER PT J AU Persico, AM Militerni, R Bravaccio, C Schneider, C Melmed, R Trillo, S Montecchi, F Palermo, MT Pascucci, T Puglisi-Allegra, S Reichelt, KL Conciatori, M Baldi, A Keller, F AF Persico, AM Militerni, R Bravaccio, C Schneider, C Melmed, R Trillo, S Montecchi, F Palermo, MT Pascucci, T Puglisi-Allegra, S Reichelt, KL Conciatori, M Baldi, A Keller, F TI Adenosine deaminase alleles and autistic disorder: Case-control and family-based association studies SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; dipeptidyl-peptidase IV; imprinting; serotonin; transmission disequilibrium test ID MENTAL-RETARDATION; LINKAGE DISEQUILIBRIUM; PLATELET SEROTONIN; INFANTILE-AUTISM; GENE; DIAGNOSIS; MUTATION; CHILDREN; TWIN; CD26 AB Adenosine deaminase (ADA) plays a relevant role in purine metabolism, immune responses, and peptidase activity, which may be altered in some autistic patients. Codominant ADA1 and ADA2 alleles code for ADA1 and ADA2 allozymes, the most frequent protein isoforms in the general population. Individuals carrying one copy of the ADA2 allele display 15 to 20% lower catalytic activity compared to ADA1 homozygotes. Recent preliminary data suggest that ADA2 alleles may be more frequent among autistic patients than healthy controls. The present study was undertaken to replicate these findings in a new case-control study, to test for linkage/association using a family-based design, and to characterize ADA2-carrying patients by serotonin blood levels, peptiduria, and head circumference. ADA2 alleles were significantly more frequent in 91 Caucasian autistic patients of Italian descent than in 152 unaffected controls (17.6% vs. 7.9%, P = 0.018), as well as among their fathers. Family-based tests involving these 91 singleton families, as well as 44 additional Caucasian-American trios, did not support significant linkage/association. However, the observed preferential maternal transmission of ADA2 alleles, if replicated, may point toward linkage disequilibrium between the ADA2 polymorphism and an imprinted gene variant located in its vicinity. Racial and ethnic differences in ADA allelic distributions, together with the low frequency of the ADA2 allele, may pose methodological problems to future linkage/association studies. Direct assessments of ADA catalytic activity in autistic individuals and unaffected siblings carrying ADA1/ADA1 vs ADA1/ADA2 genotypes may provide stronger evidence of ADA2 contributions to autistic disorder. 2000 Wiley-Liss, Inc. C1 Neurosci Lab, Lab Physiol & Neurosci, I-00155 Rome, Italy. II Univ Naples, Dept Child Neuropsychiat, Naples, Italy. SW Autism Res Ctr, Phoenix, AZ USA. Osped Bambino Gesu, IRCCS, Div Child Neuropsychiat, Rome, Italy. Clin Autism & Dev Disabil, I-00155 Rome, Italy. Univ La Sapienza, Dept Psychol, Rome, Italy. Univ Oslo, Rikshosp, Dept Pediat Res, N-0027 Oslo, Norway. RP Keller, F (reprint author), Neurosci Lab, Lab Physiol & Neurosci, Libera Univ Campus Biomed,Via Longoni 83, I-00155 Rome, Italy. 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PD DEC 4 PY 2000 VL 96 IS 6 BP 784 EP 790 DI 10.1002/1096-8628(20001204)96:6<784::AID-AJMG18>3.0.CO;2-7 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 380RM UT WOS:000165717300018 PM 11121182 ER PT J AU Goizet, C Excoffier, E Taine, L Taupiac, E El Moneim, AA Arveiler, B Bouvard, M Lacombe, D AF Goizet, C Excoffier, E Taine, L Taupiac, E El Moneim, AA Arveiler, B Bouvard, M Lacombe, D TI Case with autistic syndrome and chromosome 22q13.3 deletion detected by FISH SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE del(22)(q13.3); developmental delay; autism; mental retardation; chromosome 22 ID MENTAL-RETARDATION; MOLECULAR CHARACTERIZATION; PARTIAL MONOSOMY; DISORDERS; 22Q; REARRANGEMENTS; CHILDREN; PATIENT AB Autism is a rare neurodevelopmental disorder with a strong genetic component, Cooccurrence of autism and chromosomal abnormalities is useful to localize candidate regions that may include gene(s) implicated in autism determinism, Several candidate chromosomal regions are known, but association of chromosome 22 abnormalities with autism is unusual. We report a child with autistic syndrome and a de novo 22q13.3 cryptic deletion detected by FISH. Previously described cases with 22q13.3 deletions shared characteristic developmental and speech delay, but autism was not specifically reported, This case emphasizes a new candidate region that may bear a gene involved in autism etiopathogenesis. (C) 2000 Wiley-Liss, Inc. C1 CHU Pellegrin Enfants, Serv Genet Med, F-33076 Bordeaux, France. CH Charles Perrens, Dept Child Psychiat, Bordeaux, France. RP Goizet, C (reprint author), CHU Pellegrin Enfants, Serv Genet Med, Pl Amelie Raba Leon, F-33076 Bordeaux, France. 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J. Med. Genet. PD DEC 4 PY 2000 VL 96 IS 6 BP 839 EP 844 DI 10.1002/1096-8628(20001204)96:6<839::AID-AJMG29>3.0.CO;2-R PG 6 WC Genetics & Heredity SC Genetics & Heredity GA 380RM UT WOS:000165717300029 PM 11121193 ER PT J AU Szatmari, P Bryson, SE Streiner, DL Wilson, F Archer, L Ryerse, C AF Szatmari, P Bryson, SE Streiner, DL Wilson, F Archer, L Ryerse, C TI Two-year outcome of preschool children with autism or Asperger's syndrome SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID BEHAVIOR CHECKLIST; FOLLOW-UP; DISORDER; VALIDITY; HISTORY AB Objective: DSM-IV specifies that Asperger's disorder is a type of pervasive developmental disorder without clinically significant cognitive or language delay. There are no data, however, on the outcome of children with Asperger's disorder or on whether their outcome differs from that of children with autism. The objectives of this study were to compare the outcome of groups of children with these disorders over a period of 2 yea rs on variables independent of the defining criteria and to identify variables that might account for these differences. Method: All children 4-6 years of age who came for assessment or were currently in treatment at a pervasive developmental disorder service of one of several centers in a large geographic region were identified. Children who received a diagnosis of autism (N=46) or Asperger's syndrome (N=20) on the basis of a diagnostic interview and had an IQ in the nonretarded range were given a battery of cognitive, language, and behavioral tests. Families were contacted roughly 2 yea rs after the date of their enrollment in the study, and many of the tests were readministered. Results: Children with Asperger's syndrome had better social skills and fewer autistic symptoms 2 years after study enrollment than the children with autism. The differences in outcome could not be explained by initial differences in IQ and language abilities. Children with autism who had developed verbal fluency at follow-up were very similar to the children with Asperger's syndrome at study enrollment. Conclusions: Although the exact mechanism for the differences in outcome remain to be determined, it appears that Asperger's disorder and autism represent parallel but potentially overlapping developmental trajectories. C1 McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8S 4L8, Canada. McMaster Univ, Dept Clin Epidemiol & Biostat, Hamilton, ON L8S 4L8, Canada. York Univ, Dept Psychol, N York, ON M3J 1P3, Canada. RP Szatmari, P (reprint author), Hamilton Hlth Sci Ctr, Dept Psychiat & Behav Neurosci, Chedoke Campus,POB 2000,Stn A, Hamilton, ON L8N 3Z5, Canada. 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J. Psychiat. PD DEC PY 2000 VL 157 IS 12 BP 1980 EP 1987 DI 10.1176/appi.ajp.157.12.1980 PG 8 WC Psychiatry SC Psychiatry GA 378NA UT WOS:000165589400014 PM 11097964 ER PT J AU Zilbovicius, M Boddaert, N Belin, P Poline, JB Remy, P Mangin, JF Thivard, L Barthelemy, C Samson, Y AF Zilbovicius, M Boddaert, N Belin, P Poline, JB Remy, P Mangin, JF Thivard, L Barthelemy, C Samson, Y TI Temporal lobe dysfunction in childhood autism: A PET study SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID POSITRON EMISSION TOMOGRAPHY; HERPES-SIMPLEX ENCEPHALITIS; CEREBRAL BLOOD-FLOW; SUMMARIZED EVALUATION; BRAIN; METABOLISM; GLUCOSE; CHILDREN; CORTEX; SCALE AB Objective: The nature of the underlying brain dysfunction of childhood autism, a life-long severe developmental disorder, is not well understood. Although researchers using functional brain imaging have attempted to contribute to this debate, previous studies have failed to report consistent localized neocortical brain dysfunction. The authors reasoned that early methods may have been insensitive to such dysfunction, which may now be detectable with improved technology. Method: To test this hypothesis, regional cerebral blood flow was measured with positron emission tomography (PET) in 21 children with primary autism and in 10 nonautistic children with idiopathic mental retardation. Autistic and comparison groups were similar in average age and developmental quotients. The authors first searched for focal brain dysfunction in the autistic group by using a voxel-based whole brain analysis and then assessed the sensitivity of the method to detect the abnormality in individual children. An extension study was then performed in an additional group of 12 autistic children. Results: The first autistic group had a highly significant hypoperfusion in both temporal lobes centered in associative auditory and adjacent multimodal cortex, which was detected in 76% of autistic children. Virtually identical results were found in the second autistic group in the extension study. Conclusions: PET and voxel-based image analysis revealed a localized dysfunction of the temporal lobes in school-aged children with idiopathic autism. Further studies will clarify the relationships between these temporal abnormalities and the perceptive, cognitive, and emotional developmental abnormalities characteristic of this disorder. C1 CEA, Serv Hosp Frederic Joliot, Direct Sci Vivant, Dept Rech Med, F-91406 Orsay, France. INSERM, Tours, France. Hop La Pitie Salpetriere, Serv Urgences Cerebrovasc, Paris, France. RP Zilbovicius, M (reprint author), CEA, Serv Hosp Frederic Joliot, Direct Sci Vivant, Dept Rech Med, 4 Pl Gen Leclerc, F-91406 Orsay, France. RI Belin, Pascal/C-6247-2009 OI Belin, Pascal/0000-0002-7578-6365 CR ADRIEN JL, 1988, NEUROPSYCHIAT ENFAN, V36, P253 BACHEVALIER J, 1994, NEUROPSYCHOLOGIA, V32, P627, DOI 10.1016/0028-3932(94)90025-6 BARTHELEMY C, 1990, J AUTISM DEV DISORD, V20, P189, DOI 10.1007/BF02284718 Barthelemy C, 1997, J AUTISM DEV DISORD, V27, P139, DOI 10.1023/A:1025887723360 DEVOLDER A, 1987, BRAIN DEV-JPN, V9, P581 Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 BRUNET O, 1976, ECHELLE DEV PSYCHOMO Chugani HT, 1996, ANN NEUROL, V39, P643, DOI 10.1002/ana.410390514 COURCHESNE E, 1988, NEW ENGL J MED, V318, P1349, DOI 10.1056/NEJM198805263182102 COURCHESNE E, 1994, NEUROLOGY, V44, P214 DANSART P, 1988, ACTUALITE PSYCHIAT, V4, P8 DELONG GR, 1981, ARCH NEUROL-CHICAGO, V38, P191 FOX PT, 1984, J CEREBR BLOOD F MET, V4, P329 Friston KJ, 1994, HUMAN BRAIN MAPPING, V2, P189, DOI DOI 10.1002/HBM.460020402 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P107, DOI 10.1007/BF01046406 Gillberg C., 1992, BIOL AUTISTIC SYNDRO GILLBERG C, 1986, J AUTISM DEV DISORD, V16, P369, DOI 10.1007/BF01531665 Gloor P., 1997, TEMPORAL LOBE LIMBIC HAMEURY L, 1995, EUR CHILD ADOLES PSY, V4, P123 HEROLD S, 1988, PSYCHOL MED, V18, P823 HORWITZ B, 1988, ARCH NEUROL-CHICAGO, V45, P749 Kanner L, 1943, NERV CHILD, V2, P217 Mangin J.-F., 1995, Journal of Mathematical Imaging and Vision, V5, DOI 10.1007/BF01250286 Pandya D.N., 1985, CEREB CORTEX, V4, P3 Piven J, 1996, J AM ACAD CHILD PSY, V35, P530, DOI 10.1097/00004583-199604000-00020 Piven J, 1997, CURR OPIN NEUROBIOL, V7, P708, DOI 10.1016/S0959-4388(97)80093-1 PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 RUMSEY JM, 1985, ARCH GEN PSYCHIAT, V42, P448 SELTZER B, 1978, BRAIN RES, V149, P1, DOI 10.1016/0006-8993(78)90584-X Talairach J., 1988, CO PLANAR STEREOTAXI ZILBOVICIUS M, 1995, AM J PSYCHIAT, V152, P248 ZILBOVICIUS M, 1992, AM J PSYCHIAT, V149, P924 NR 34 TC 137 Z9 139 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD DEC PY 2000 VL 157 IS 12 BP 1988 EP 1993 DI 10.1176/appi.ajp.157.12.1988 PG 6 WC Psychiatry SC Psychiatry GA 378NA UT WOS:000165589400015 PM 11097965 ER PT J AU Haznedar, MM Buchsbaum, MS Wei, TC Hof, PR Cartwright, C Bienstock, CA Hollander, E AF Haznedar, MM Buchsbaum, MS Wei, TC Hof, PR Cartwright, C Bienstock, CA Hollander, E TI Limbic circuitry in patients with autism spectrum disorders studied with positron emission tomography and magnetic resonance imaging SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID ANTERIOR CINGULATE CORTEX; GLUCOSE-METABOLISM; BRAIN; HIPPOCAMPUS; ATTENTION; PERFORMANCE; ADULTS; VOLUME; MRI AB Objective: Cytoarchitectonic changes in the anterior cingulate cortex, hippocampus, subiculum, entorhinal cortex, amygdala, mammillary bodies, and septum were reported in a postmortem study of autism. Previously, the authors found smaller cingulate volume and decreased metabolism of the cingulate in seven autistic patients. In this study, they measured the volume and glucose metabolism of the amygdala, hippocampus, and cingulate gyrus in an expanded group of 17 patients with autism spectrum disorders (autism [N=10] or Asperger's disorder [N=7]) and 17 age- and sex-matched healthy volunteers. Method: Subjects performed a serial verbal learning test during F-18-deoxyglucose uptake. The amygdala, hippocampus, and cingulate gyrus were outlined on magnetic resonance imaging scans, volumes of the structures were applied to matching coregistered positron emission tomography scans, and three-dimensional significance probability mapping was performed. Results: Significant metabolic reductions in both the anterior and posterior cingulate gyri were visualized in the patients with autism spectrum disorders. Both Asperger's and autism patients had relative glucose hypometabolism in the anterior and posterior cingulate as confirmed by analysis of variance; regional differences were also found with three-dimensional significance probability mapping. No group differences were found in either the metabolism or the volume of the amygdala or the hippocampus. However, patients with autism spectrum disorders showed reduced volume of the right anterior cingulate gyrus, specifically in Brodmann's area 24'. Conclusions: Compared with age- and sex-matched healthy volunteers, patients with autism spectrum disorders showed significantly decreased metabolism in both the anterior and posterior cingulate gyri. C1 Mt Sinai Sch Med, Neurosci PET Lab, Dept Psychiat, New York, NY 10029 USA. RP Haznedar, MM (reprint author), Mt Sinai Sch Med, Neurosci PET Lab, Dept Psychiat, Box 1505,1 Gustave L Levy Pl, New York, NY 10029 USA. 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E., 1993, Human Brain Mapping, V1, P3, DOI 10.1002/hbm.460010103 RUMSEY JM, 1985, ARCH GEN PSYCHIAT, V42, P448 SAITOH O, 1995, NEUROLOGY, V45, P317 SIEGEL BV, 1992, J NEUROPSYCH CLIN N, V4, P406 Talairach J., 1988, CO PLANAR STEREOTAXI Wu J, 1999, AM J PSYCHIAT, V156, P1149 Wu J, 1999, AM J PSYCHIAT, V156, P1666 NR 31 TC 220 Z9 220 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD DEC PY 2000 VL 157 IS 12 BP 1994 EP 2001 DI 10.1176/appi.ajp.157.12.1994 PG 8 WC Psychiatry SC Psychiatry GA 378NA UT WOS:000165589400016 PM 11097966 ER PT J AU Constantino, JN Todd, RD AF Constantino, JN Todd, RD TI Genetic structure of reciprocal social behavior SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 46th Annual Meeting of the American-Academy-of-Child-and-Adolescent-Psychiaty CY OCT 19-24, 1999 CL CHICAGO, ILLINOIS SP Amer Acad Child & Adolescent Psychiart ID AUTISM AB Objective: The study examined the genetic structure of deficits in reciprocal social behavior in an epidemiologic sample of male twins. Method: Pa rents of 232 pairs of 7-15-year-old male twins completed the Social Reciprocity Scale to provide data on their children's reciprocal social behavior. Scale scores were analyzed by using structural equation modeling. Results: Intraclass (twin-twin) correlations for scores on the Social Reciprocity Scale were 0.73 for monozygotic twins (N=98 pairs) and 0.37 for dizygotic twins (N=134 pairs). The best fitting model of causal influences on reciprocal social behavior incorporated additive genetic influences and unique environmental influences. Conclusions: For school-age boys in the general population, reciprocal social behavior is highly heritable, with a genetic structure similar to that reported for autism in clinical samples. Continuous measures of reciprocal social behavior may be useful for characterizing the broader autism phenotype and may enhance the statistical power of genetic studies of autism. C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Pediat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Dept Genet, St Louis, MO 63110 USA. 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PD DEC PY 2000 VL 157 IS 12 BP 2043 EP 2045 DI 10.1176/appi.ajp.157.12.2043 PG 3 WC Psychiatry SC Psychiatry GA 378NA UT WOS:000165589400025 PM 11097975 ER PT J AU Munir, F Cornish, KM Wilding, J AF Munir, F Cornish, KM Wilding, J TI Nature of the working memory deficit in Fragile-X syndrome SO BRAIN AND COGNITION LA English DT Article DE working memory; fragile-X syndrome; phonological memory; visuospatial memory; executive skills ID SWEDISH MULTICENTER; COGNITIVE PROFILES; EXECUTIVE FUNCTION; INFANTILE-AUTISM; DYSFUNCTION; PHENOTYPE; CHILDREN; FEMALES; MALES; TASK AB Working memory performance in a group of young Fragile X males with FMR-1 full mutation was compared to a learning disabled comparison group comprising Down's syndrome males and two control groups of mainstream schoolchildren. Performance was assessed on a battery of tasks tapping the three components of working memory-phonological loop, visual-spatial sketch pad, and the central executive. The results indicated that the Fragile X group displayed a general impairment on working memory tasks that cannot be attributed to a single working memory component per se. Instead, the results suggest that Fragile X males have a working memory deficit that may be attributed to how much attentional resource a specific task requires and their overall available executive capacity, irrespective of the working memory subsystem. (C) 2000 Academic Press. C1 Univ Nottingham, Sch Med, Div Psychiat, Sect Dev Psychiat, Nottingham NG7 2UH, England. Univ London, Royal Holloway & Bedford New Coll, Dept Psychol, Egham TW20 0EX, Surrey, England. RP Cornish, KM (reprint author), Univ Nottingham, Sch Med, Div Psychiat, Sect Dev Psychiat, E Floor,South Block, Nottingham NG7 2UH, England. CR Baddeley A. D., 1986, WORKING MEMORY Baddeley A. 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L, 1989, J MEM LANG, V28, P27 WAHLSTROM J, 1986, AM J MED GENET, V23, P403, DOI 10.1002/ajmg.1320230132 Wechsler D., 1992, WECHSLER INTELLIGENC WELSH MC, 1991, DEV NEUROPSYCHOL, V7, P131 WILSON BA, 1991, RIVERNEAD BEHAV MEMO NR 52 TC 58 Z9 59 PU ACADEMIC PRESS INC 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 DEC PY 2000 VL 44 IS 3 BP 387 EP 401 DI 10.1006/brcg.1999.1200 PG 15 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 383HP UT WOS:000165877300005 PM 11104532 ER PT J AU Pareek, M Pattison, HM AF Pareek, M Pattison, HM TI The two-dose measles, mumps, and rubella (MMR) immunisation schedule: factors affecting maternal intention to vaccinate SO BRITISH JOURNAL OF GENERAL PRACTICE LA English DT Article DE measles; mumps; rubella; vaccine; MMR; immunisation; mother; patient attitudes; patient beliefs; autism; Crohn's disease ID IMMUNIZATION; ASSOCIATION; AUTISM AB Background. In the light of sub-optimal uptake of the measles, mumps, and rubella (MMR) vaccination, we investigated the factors that influence the intentions of mothers to vaccinate. Method. A cross-sectional survey of 300 mothers in Birmingham with children approaching a routine MMR vaccination was conducted using a postal questionnaire to measure: intention to vaccinate, psychological variables, knowledge of the vaccine, and socioeconomic status. The vaccination status of the children was obtained from South Birmingham Child Health Surveillance Unit. Results. The response rate was 59%. Fewer mothers approaching the second MMR vaccination (Group 2) intended to fake their children for this vaccination than Group 1 (mothers approaching the first MMR vaccination) (Mann-Whitney U = 2180, P<0.0001). Group 2 expressed more negative beliefs about the outcome of having the MMR vaccine ('vaccine outcome beliefs') (Mann-Whitney U = 2155, P<0.0001), were more likely to believe it was 'unsafe' (chi (2) = 9.114, P = 0.004) and that it rarely protected (chi (2) = 6.882, P = 0.014) than Group 1. The commonest side-effect cited was general malaise, but 29.8% cited autism. The most trusted source of information was the general practitioner but the most common source of information on side-effects was television (34.6%). Multiple linear regression revealed that, in Group 1, only 'vaccine outcome beliefs' significantly predicted intention (77.1% of the variance). In Group 2 'vaccine outcome beliefs', attitude to the MMR vaccine, and prior MMR status all predicted intention (93% of the variance). Conclusion. A major reason for the low uptake of the MMR vaccination is that it is not perceived to be important for children's health, particularly the second dose. Health education from GPs is likely to have a considerable impact. C1 Univ Birmingham, Sch Med, Dept Primary Care & Gen Practice, Birmingham B15 2TT, W Midlands, England. RP Pattison, HM (reprint author), Univ Birmingham, Sch Med, Dept Primary Care & Gen Practice, Birmingham B15 2TT, W Midlands, England. RI Pattison, Helen/D-2702-2009 OI Pattison, Helen/0000-0002-9483-4342 CR AJZEN I, 1986, J EXP SOC PSYCHOL, V22, P453, DOI 10.1016/0022-1031(86)90045-4 CALLENDER C, 1996, MATERNTIY RIGHTS BEN *DEP HLTH WELSH OF, 1996, IMM INF DIS DeStefano F, 1999, LANCET, V353, P1987, DOI 10.1016/S0140-6736(99)00160-9 Evans MR, 1998, ARCH DIS CHILD, V79, P141 *MED COMM AG COMM, 1999, CURR PROBL CURR PHAR, V25, P9 NORUSIS MJ, 1997, SPSS WINDOWS BASE SY Peckham C., 1989, NATL IMMUNISATION ST PIGEON N, 1992, RISK PERCEPTION RATCLIFFE P, 1996, ETHNICITY 1991 CENSU, V3, P88 SLY F, 1996, LABOUR MARKET TR MAR, P91 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Thomas DR, 1998, LANCET, V351, P1927, DOI 10.1016/S0140-6736(98)24026-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 2000, CDR WEEKLY, V10, P109 NR 15 TC 37 Z9 37 PU ROYAL COLL GENERAL PRACTITIONERS PI LONDON PA 14 PRINCES GATE, HYDE PARK, LONDON, ENGLAND SW7 1PU SN 0960-1643 J9 BRIT J GEN PRACT JI Br. J. Gen. Pract. PD DEC PY 2000 VL 50 IS 461 BP 969 EP 971 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 381EC UT WOS:000165748500008 PM 11224968 ER PT J AU Scheuffgen, K Happe, F Anderson, M Frith, U AF Scheuffgen, K Happe, F Anderson, M Frith, U TI High "intelligence," low "IQ"? Speed of processing and measured IQ in children with autism SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID INSPECTION TIME; FOLLOW-UP; PATTERNS; LANGUAGE; ABILITY; MEMORY; ACTS AB The uneven profile of performance on standard assessments of intelligence and the high incidence of savant skills have prompted interest in the nature of intelligence in autism. The present paper reports the first group study of speed of processing in children with autism (IQ 1 SD below average) using an inspection time task. The children with autism showed inspection times as fast as an age-matched group of young normally developing children (IQ 1 SD above average). They were also significantly faster than mentally handicapped children without autism of the same age, even when these groups were pairwise matched on Wechsler IQ. To the extent that IT tasks tap individual differences in basic processing efficiency, children with autism in this study appear to have preserved information processing capacity despite poor measured IQ. These findings have implications for the role of general and specific cognitive systems in knowledge and skill acquisition: far from showing that children with autism are unimpaired, we suggest that our data may demonstrate the vital role of social insight in the development of manifest "intelligence". C1 UCL, Inst Cognit Neurosci, London WC1N 3AR, England. UCL, Dept Psychol, London WC1N 3AR, England. Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London, England. Univ Western Australia, Nedlands, WA 6009, Australia. RP Frith, U (reprint author), UCL, Inst Cognit Neurosci, Alexandra House,17 Queen Sq, London WC1N 3AR, England. EM u.frith@ucl.ac.uk RI Frith, Uta/C-1757-2008; Happe, Francesca/D-5544-2012 OI Frith, Uta/0000-0002-9063-4466; CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDERSON M, 1986, PERS INDIV DIFFER, V7, P677, DOI 10.1016/0191-8869(86)90037-1 ANDERSON M, IN PRESS INTELLIGENC Anderson M., 1992, INTELLIGENCE DEV COG ASARNOW RF, 1987, J CHILD PSYCHOL PSYC, V28, P273, DOI 10.1111/j.1469-7610.1987.tb00210.x BALDWIN DA, 1993, DEV PSYCHOL, V29, P832, DOI 10.1037/0012-1649.29.5.832 Baron-Cohen S, 1993, UNDERSTANDING OTHER BRAND C, 1980, INTELLIGENCE LEARNIN BRAND CR, 1982, MODEL INTELLIGENCE Burack J. 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V., 1995, MIND SAVANT LANGUAGE Spearman C, 1904, AM J PSYCHOL, V15, P201, DOI 10.2307/1412107 STERNBERG RJ, 1988, BRIT J PSYCHOL, V79, P527 TAYLOR MM, 1967, J ACOUST SOC AM, V41, P782, DOI 10.1121/1.1910407 TOMASELLO M, 1992, SOCIAL DEV, V1, P68 Townsend J, 1996, DEV PSYCHOPATHOL, V8, P563 VERNON PA, 1983, INTELLIGENCE, V7, P53, DOI 10.1016/0160-2896(83)90006-5 Waterhouse L, 1996, PSYCHOL REV, V103, P457, DOI 10.1037/0033-295X.103.3.457 Wechsler D., 1992, WECHSLER INTELLIGENC NR 59 TC 42 Z9 43 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 32 AVENUE OF THE AMERICAS, NEW YORK, NY 10013-2473 USA SN 0954-5794 J9 DEV PSYCHOPATHOL JI Dev. Psychopathol. PD WIN PY 2000 VL 12 IS 1 BP 83 EP 90 DI 10.1017/S095457940000105X PG 8 WC Psychology, Developmental SC Psychology GA 301AJ UT WOS:000086285700005 PM 10774597 ER PT J AU Dunn-Geier, J Ho, HH Auersperg, E Doyle, D Eaves, L Matsuba, C Orrbine, E Whiting, S AF Dunn-Geier, J Ho, HH Auersperg, E Doyle, D Eaves, L Matsuba, C Orrbine, E Whiting, S TI Effect of secretin on children with autism: a randomized controlled trial SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID TYROSINE-HYDROXYLASE ACTIVITY; BEHAVIORAL TREATMENT; RAT; BRAIN; DISORDER AB To determine the effect of intravenous porcine secretin on autistic behaviours in children aged 2 to 7 years, the effects of secretin on (1) performance on a standardized language measure, and (2) autistic behaviours, as rated by parents and child development professionals was examined. Employing a randomized, double-blind, placebo-controlled design, 95 participants were assigned to one of two groups and administered a single dose of either secretin or placebo. A follow-up assessment was conducted 3 weeks after the injection, No significant differences in language or autistic behaviour measures were observed at the 3-week follow-up between the groups. Also, there was no significant difference in the proportion of individuals who improved by greater than or equal to6 points on the language measure at follow-up. This study showed no significant effects of secretin on children with autism. Our results are consistent with a systematic review of randomized controlled trials evaluating the effect of secretin in children with autism. C1 Childrens Hosp Eastern Ontario, Child Dev Serv, Dept Pediat, Div Neurol, Ottawa, ON K1H 8L1, Canada. Univ British Columbia, Dept Pediat, Vancouver, BC V6T 1W5, Canada. Ridge Meadows Hosp, Maple Ridge, BC, Canada. RP Dunn-Geier, J (reprint author), Childrens Hosp Eastern Ontario, Child Dev Serv, Dept Pediat, Div Neurol, 401 Smyth Rd, Ottawa, ON K1H 8L1, Canada. CR Ahmad K, 1999, LANCET, V354, P2140, DOI 10.1016/S0140-6736(05)77047-1 ALTMAN DG, 1985, STATISTICIAN, V34, P125, DOI 10.2307/2987510 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th FUXE K, 1979, FED PROC, V38, P2333 BABARCZY E, 1994, PHARM BIOCH BEHAV, V51, P469 BABU GN, 1983, BRAIN RES BULL, V11, P25, DOI 10.1016/0361-9230(83)90053-9 Bayley N, 1993, BAYLEY SCALES INFANT BECK G, 1998, UNLOCKING POTENTIAL Begg C, 1996, JAMA-J AM MED ASSOC, V276, P637, DOI 10.1001/jama.276.8.637 Bryson SE, 1998, MENT RETARD DEV D R, V4, P97, DOI 10.1002/(SICI)1098-2779(1998)4:2<97::AID-MRDD6>3.0.CO;2-U Campbell M, 1996, J AM ACAD CHILD PSY, V35, P134, DOI 10.1097/00004583-199602000-00005 CHARLTON CG, 1983, PEPTIDES, V4, P739, DOI 10.1016/0196-9781(83)90029-3 CHARLTON CG, 1981, PEPTIDES, V2, P45, DOI 10.1016/0196-9781(81)90054-1 Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 Conter RL, 1996, SURGERY, V119, P208, DOI 10.1016/S0039-6060(96)80171-1 EAVES RC, 1993, J ABNORM CHILD PSYCH, V21, P481, DOI 10.1007/BF00916315 FREMEAU RT, 1986, J NEUROCHEM, V46, P1947 FREMEAU RT, 1983, J NEUROSCI, V3, P1620 GORDON CT, 1992, AM J PSYCHIAT, V149, P363 GREENSPAN S, 1999, PEDIATRICS, V135, P559 Greenspan S. I., 1992, INFANCY EARLY CHILDH Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 KARELSON E, 1995, NEUROPEPTIDES, V28, P21, DOI 10.1016/0143-4179(95)90070-5 Krug DA, 1993, AUTISM SCREENING INS Lotter V., 1978, AUTISM REAPPRAISAL C, P475 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 MCDOUGLE CJ, 1997, HDB AUTISM PERVASIVE, P707 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 MCKEON TW, 1993, BRAIN RES, V607, P345, DOI 10.1016/0006-8993(93)91529-2 National Institute of Mental Health, 1985, PSYCHOPHARMACOL BULL, V21, P839 Nickel RE, 1996, INFANT YOUNG CHILD, V8, P29 Normand SLT, 1999, STAT MED, V18, P321, DOI 10.1002/(SICI)1097-0258(19990215)18:3<321::AID-SIM28>3.0.CO;2-P Prizant Barry, 1998, Seminars in Speech and Language, V19, P329, DOI 10.1055/s-2008-1064053 REICHELT K, 1990, J APPL NUTR, V42, P2 Richman D. M., 1999, FOCUS AUTISM OTHER D, V14, P204, DOI 10.1177/108835769901400402 RIMLAND B, 1998, RES REV INT, V12, P3 Rimland B, 1996, J AUTISM DEV DISORD, V26, P237, DOI 10.1007/BF02172019 Roid G., 1997, LEITER INT PERFORMAN Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Schopler E., 1988, CHILDHOOD AUTISM RAT SCHWARZSCHILD MA, 1991, J NEUROCHEM, V56, P400, DOI 10.1111/j.1471-4159.1991.tb08165.x Thorndike RL, 1986, STANFORD BINET INTEL Trottier G, 1999, J PSYCHIATR NEUROSCI, V24, P103 TULASSAY Z, 1990, WIEN MED WOCHENSCHR, V140, P361 Volkmar FR, 1999, NEW ENGL J MED, V341, P1842, DOI 10.1056/NEJM199912093412412 WATANABE Y, 1991, GASTROENTEROL JPN, V26, P86 Wechsler D., 1989, WECHSLER PRESCHOOL P Wing L., 1987, HDB AUTISM PERVASIVE, P3 Zimmerman I.L., 1992, PRESCHOOL LANGUAGE S NR 50 TC 64 Z9 64 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD DEC PY 2000 VL 42 IS 12 BP 796 EP 802 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 384YQ UT WOS:000165975200002 PM 11132252 ER PT J AU Cunningham, E O'Neill, RE AF Cunningham, E O'Neill, RE TI Comparison of results of functional assessment and analysis methods with young children with autism SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article ID SELF-INJURIOUS-BEHAVIOR; ABERRANT BEHAVIOR; SETTINGS; INTERVENTION; ISSUES; BASE AB The comparative validity of different strategies for conducting functional assessments and analyses continues to be an issue for debate among researchers and clinicians. This study compared results from rating scale, structured interview, descriptive observation, and experimental functional analysis approaches to the assessment of the problem behaviors of three young children with autism. The results indicated good agreement across indirect and direct methods. Limitations of the study, as well as implications for research and clinical application were discussed. C1 Univ Utah, Salt Lake City, UT 84112 USA. RP O'Neill, RE (reprint author), Univ Utah, 1705 E Campus Ctr Dr,Rm 221, Salt Lake City, UT 84112 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARNDORFER RE, 1994, TOP EARLY CHILD SPEC, V14, P64 BELFIORE PJ, 1993, EDUC TRAIN MENT RET, V28, P57 COLE ML, 1999, M ASS BEH AN CHIC IL Cone JD, 1997, BEHAV RES THER, V35, P259, DOI 10.1016/S0005-7967(96)00101-5 CRAWFORD J, 1992, J ASSOC PERS SEVERE, V17, P77 DERBY KM, 1992, J APPL BEHAV ANAL, V25, P713, DOI 10.1901/jaba.1992.25-713 Durand V. M., 1992, MOTIVATION ASSESSMEN DURAND VM, 1988, J AUTISM DEV DISORD, V18, P99 Freeman KA, 2000, EDUC TRAIN MENT RET, V35, P55 GOH HL, 1996, M ASS BEH AN SAN FRA Gresham FM, 1999, BEHAV DISORDERS, V24, P180 Harding J, 1999, BEHAV MODIF, V23, P316, DOI 10.1177/0145445599232008 Iwata B. A., 1990, PERSPECTIVES USE NON, P301 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P413, DOI 10.1901/jaba.1994.27-413 IWATA BA, 1990, BEHAV ANAL TREATMENT, P101 KAHNG SW, 1999, J APPL BEHAV ANAL, V31, P593 Kazdin A. E., 1982, SINGLE CASE RES DESI KERN L, 1999, FUNCTIONAL ANAL PROB, P197 Kratochwill TR, 1996, SCHOOL PSYCHOL REV, V25, P342 LERMAN DC, 1993, J APPL BEHAV ANAL, V26, P293, DOI 10.1901/jaba.1993.26-293 Lewis T. J., 1994, DIAGNOSTIQUE, V19, P103 Lewis TJ, 1996, SCHOOL PSYCHOL QUART, V11, P1, DOI 10.1037/h0088918 MACE FC, 1991, J APPL BEHAV ANAL, V24, P553, DOI 10.1901/jaba.1991.24-553 NANGLE DW, 1992, M ASS BEH AN SAN FRA Nelson JR, 1999, BEHAV DISORDERS, V24, P169 O'Neill R. E., 1997, FUNCTIONAL ASSESSMEN, V2nd SASSO GM, 1992, J APPL BEHAV ANAL, V25, P809, DOI 10.1901/jaba.1992.25-809 SCOTTI JR, 1994, BEHAV THER, V25, P721, DOI 10.1016/S0005-7894(05)80206-0 STURMEY P, 1995, RES DEV DISABIL, V16, P269, DOI 10.1016/0891-4222(95)00014-E Vollmer TR, 1996, RES DEV DISABIL, V17, P229, DOI 10.1016/0891-4222(96)00006-6 WACKER D, 1990, PERSPECTIVES USE NON, P349 WACKER D, 1993, BEHAV ANAL TREATMENT, P297 WACKER DP, 1999, FUNCTIONAL ANAL PROB, P32 ZARCONE JR, 1991, RES DEV DISABIL, V12, P349, DOI 10.1016/0891-4222(91)90031-M NR 36 TC 11 Z9 11 PU COUNCIL EXCEPTIONAL CHILDREN PI RESTON PA 1920 ASSOCIATION DR, RESTON, VA 22091-1589 USA SN 0013-1237 J9 EDUC TRAIN MENT RET JI Educ. Train. Mental Retard. Dev. Disabil. PD DEC PY 2000 VL 35 IS 4 BP 406 EP 414 PG 9 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 432UR UT WOS:000168714500006 ER PT J AU McComas, J Hoch, H Paone, D El-Roy, D AF McComas, J Hoch, H Paone, D El-Roy, D TI Escape behavior during academic tasks: A preliminary analysis of idiosyncratic establishing operations SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE destructive behavior; establishing operations; functional analysis; academic tasks; negative reinforcement ID SELF-INJURY; FUNCTIONAL-ANALYSIS; EXTINCTION AB The presence or absence of idiosyncratic stimuli has been demonstrated to predictably alter the occurrence of problem behavior. By specifying stimuli related to negatively reinforced behavior during academic tasks, it may be possible to identify methods of instruction that decrease the occurrence of problem behavior. The current study used a four-step procedure that involved a functional analysis, descriptive assessment, establishing operations (EO) analysis, and follow-up evaluation (a) to identify the operant function of destructive behavior and (b) to evaluate the effects of idiosyncratic features of academic task demands and related methods of instruction on the occurrence of negatively reinforced destructive behavior of 3 boys with developmental disabilities and autism in a classroom setting. The data suggest that the four-step procedure was effective in identifying methods of instruction that decreased the likelihood of destructive behavior without disrupting the maintaining contingencies for destructive behavior. Results are discussed in terms of establishing operations for negatively reinforced destructive behavior during academic tasks and related methods of instruction in classroom settings. C1 Univ Minnesota, Dept Educ Psychol, Minneapolis, MN 55455 USA. CUNY, Queens Coll, New York, NY 10021 USA. CUNY, Grad Sch, New York, NY 10021 USA. CUNY, Univ Ctr, New York, NY 10021 USA. RP McComas, J (reprint author), Univ Minnesota, Dept Educ Psychol, 224 Burton Hall,178 Pillsbury Dr SE, Minneapolis, MN 55455 USA. CR Cameron M. J., 1992, BEHAV RESIDENTIAL TR, V7, P327, DOI 10.1002/bin.2360070502 Carr EG, 1997, J APPL BEHAV ANAL, V30, P673, DOI 10.1901/jaba.1997.30-673 Daly EJ, 1999, J APPL BEHAV ANAL, V32, P83, DOI 10.1901/jaba.1999.32-83 Dunlap G, 1994, J Appl Behav Anal, V27, P505, DOI 10.1901/jaba.1994.27-505 GOH HL, 1994, J APPL BEHAV ANAL, V27, P173, DOI 10.1901/jaba.1994.27-173 Halle J. W., 1993, COMMUNICATIVE ALTERN, P83 Horner RH, 1997, J APPL BEHAV ANAL, V30, P601, DOI 10.1901/jaba.1997.30-601 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Jolivette K, 1999, BEHAV DISORDERS, V24, P210 KELLER FS, 1950, PRINICPLES PSYCHOL Lerman DC, 1999, J APPL BEHAV ANAL, V32, P1, DOI 10.1901/jaba.1999.32-1 MCCOMAS JJ, 1996, J BEHAV ED, V6, P191, DOI 10.1007/BF02110232 McComas JJ, 1996, J APPL BEHAV ANAL, V29, P397, DOI 10.1901/jaba.1996.29-397 MICHAEL J, 1982, J EXP ANAL BEHAV, V37, P149, DOI 10.1901/jeab.1982.37-149 MICHAEL J, 1993, BEHAV ANALYST, V16, P191 NORTHUP J, 1994, J APPL BEHAV ANAL, V27, P33, DOI 10.1901/jaba.1994.27-33 Smith RG, 1997, J APPL BEHAV ANAL, V30, P343, DOI 10.1901/jaba.1997.30-343 Smith RG, 1995, J APPL BEHAV ANAL, V28, P515, DOI 10.1901/jaba.1995.28-515 Vaughn BJ, 1997, J APPL BEHAV ANAL, V30, P299, DOI 10.1901/jaba.1997.30-299 NR 19 TC 30 Z9 30 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2000 VL 33 IS 4 BP 479 EP 493 DI 10.1901/jaba.2000.33-479 PG 15 WC Psychology, Clinical SC Psychology GA 397KC UT WOS:000166694000007 PM 11214024 ER PT J AU Kennedy, CH Meyer, KA Knowles, T Shukla, S AF Kennedy, CH Meyer, KA Knowles, T Shukla, S TI Analyzing the multiple functions of stereotypical behavior for students with autism: Implications for assessment and treatment SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE stereotypy; autism; response-reinforcer relations ID SELF-INJURY; MENTAL-RETARDATION; EYE POKING; INTERVENTION; DISABILITIES; CHILDREN AB We studied behavioral functions associated with stereotypical responses for students with autism. In Study 1, analogue functional analyses (attention, demand, no-attention, and recreation conditions) were conducted for 5 students. Results suggested that stereotypy was multiply determined or occurred across all assessment conditions. For 2 students, stereotypy was associated with positive and negative reinforcement and the absence of environmental stimulation. For 2 other students, stereotypy occurred at high levels across all experimental conditions. For the 5th student, stereotypy was associated with negative reinforcement and the absence of environmental stimulation. In Study 2, the stereotypy of 1 student was further analyzed on a function-by-function basis. Within a concurrent-schedules procedure, alternative responses were taught to the student using functional communication training. The results of Study 2 showed that similar topographies of stereotypy, based on qualitatively different reinforcers, were reduced only when differential reinforcement contingencies for alternative forms of communication were implemented for specific response-reinforcer relations. Our results suggest that the causes of stereotypy for students with autism are complex and that the presumed association between response topography and behavioral function may be less important than previously realized. C1 Vanderbilt Univ, Peabody Coll, Dept Special Educ, Nashville, TN 37203 USA. E Carolina Univ, Greenville, NC 27858 USA. Florida Int Univ, Miami, FL 33199 USA. RP Kennedy, CH (reprint author), Vanderbilt Univ, Peabody Coll, Dept Special Educ, Box 328, Nashville, TN 37203 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baumeister A. 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PD WIN PY 2000 VL 33 IS 4 BP 559 EP 571 DI 10.1901/jaba.2000.33-559 PG 13 WC Psychology, Clinical SC Psychology GA 397KC UT WOS:000166694000014 PM 11214031 ER PT J AU DeLeon, IG Anders, BM Rodriguez-Catter, V Neidert, PL AF DeLeon, IG Anders, BM Rodriguez-Catter, V Neidert, PL TI The effects of noncontingent access to single- versus multiple-stimulus sets on self-injurious behavior SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE self-injurious behavior; noncontingent reinforcement; environmental enrichment; satiation ID DISABILITIES AB The automatically reinforced self-injury of a girl with autism was treated by providing noncontingent access to a single set of preferred toys during 30-min sessions. The reductive effects of the intervention waned as the session progressed. Rotating toy sets after 10 min or providing access to multiple toy sets resulted in reductions that lasted the entire 30 min. C1 Kennedy Krieger Inst, Neurobehav Unit, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Baltimore, MD 21218 USA. RP DeLeon, IG (reprint author), Kennedy Krieger Inst, Neurobehav Unit, 707 N Broadway, Baltimore, MD 21205 USA. CR Adelinis JD, 1999, J APPL BEHAV ANAL, V32, P519, DOI 10.1901/jaba.1999.32-519 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Green CW, 1996, J APPL BEHAV ANAL, V29, P67, DOI 10.1901/jaba.1996.29-67 Ringdahl JE, 1997, J APPL BEHAV ANAL, V30, P203, DOI 10.1901/jaba.1997.30-203 NR 4 TC 15 Z9 15 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2000 VL 33 IS 4 BP 623 EP 626 DI 10.1901/jaba.2000.33-623 PG 4 WC Psychology, Clinical SC Psychology GA 397KC UT WOS:000166694000020 PM 11214037 ER PT J AU Williams, G Donley, CR Keller, JW AF Williams, G Donley, CR Keller, JW TI Teaching children with autism to ask questions about hidden objects SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; questions; language acquisition; verbal behavior AB We taught 2 4-year-old children with autism to ask questions of an adult who held a closed box with a toy inside. The treatment package (modeling, prompting, and reinforcement) was evaluated with a multiple baseline design across the three question forms during training, generalization, and follow-up evaluations. The first question form ("What's that!") produced the name of the hidden item. The second form ("Can I see it!") produced sight of it, and the third form ("Can I have it'") produced the item itself. Both children learned to ask questions about hidden objects. C1 Appl Behav Consultant Serv, New York, NY USA. Univ Wisconsin, Oshkosh, WI 54901 USA. RP Williams, G (reprint author), 66 Regency Circle, Englewood, NJ 07631 USA. CR CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 Koegel LK, 1998, AM J MENT RETARD, V102, P346 TAYLOR BA, 1995, J APPL BEHAV ANAL, V28, P3, DOI 10.1901/jaba.1995.28-3 NR 3 TC 22 Z9 22 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2000 VL 33 IS 4 BP 627 EP 630 DI 10.1901/jaba.2000.33-627 PG 4 WC Psychology, Clinical SC Psychology GA 397KC UT WOS:000166694000021 PM 11214038 ER PT J AU Weber, AM Egelhoff, JC McKellop, JM Franz, DN AF Weber, AM Egelhoff, JC McKellop, JM Franz, DN TI Autism and the cerebellum evidence from tuberous sclerosis SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID INFANTILE-AUTISM; CHILDHOOD AUTISM; POSTERIOR-FOSSA; BEHAVIOR; SIZE; CLASSIFICATION; ASSOCIATION; HYPOPLASIA; DISORDERS; CHILDREN C1 Childrens Hosp, Med Ctr, Cincinnati, OH 45229 USA. Univ Cincinnati, Coll Med, Cincinnati, OH USA. RP Weber, AM (reprint author), Childrens Hosp, Med Ctr, 3333 Burnet Ave, Cincinnati, OH 45229 USA. 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Autism Dev. Disord. PD DEC PY 2000 VL 30 IS 6 BP 511 EP 517 DI 10.1023/A:1005679108529 PG 7 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100002 PM 11261463 ER PT J AU Goldberg, MC Landa, R Lasker, A Cooper, L Zee, DS AF Goldberg, MC Landa, R Lasker, A Cooper, L Zee, DS TI Evidence of normal cerebellar control of the vestibulo-ocular reflex (VOR) in children with high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE postrotatory vestibular nystagmus; vestibule-ocular reflex; high-functioning autism ID PERVASIVE DEVELOPMENTAL DISORDERS; BRAIN-STEM; INFANTILE-AUTISM; POSTERIOR-FOSSA; DYSFUNCTION AB The effect of "tilt-suppression" on post-rotatory vestibular nystagmus was investigated to assess the function of the caudal cerebellar vermis (lobules IX and X, or nodulus and uvula) in 13 school-age children with high-functioning autism (HFA) and 10 normal controls. Tilt-suppression of the vestibule-ocular reflex (VOR) refers to the decreasing of the duration of post-rotatory vestibular nystagmus that occurs when the head is moved out of the plane in which it was located during the previous sustained constant-velocity rotation. The participant is rotated in a vestibular chair with the head upright and then the head is tilted forward just after the chair stops rotating. Such tilt-suppression is impaired with lesions of the cerebellar nodulus and portions of the uvula. Results show that children with HFA have normal post-rotatory nystasmus with the head upright and normal attenuation of postrotatory nystagmus induced by head tilt. These behavioral findings suggest that lobules IX and X of the cerebellum are spared in high-functioning autism. C1 Johns Hopkins Univ, Sch Med, Baltimore, MD 21287 USA. RP Goldberg, MC (reprint author), Kennedy Krieger Inst, Dept Psychiat, 707 N Broadway,Suite 522, Baltimore, MD 21205 USA. 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Autism Dev. Disord. PD DEC PY 2000 VL 30 IS 6 BP 519 EP 524 DI 10.1023/A:1005631225367 PG 6 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100003 PM 11261464 ER PT J AU Wimpory, DC Hobson, RP Williams, JMG Nash, S AF Wimpory, DC Hobson, RP Williams, JMG Nash, S TI Are infants with autism socially engaged? A study of recent retrospective parental reports SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE infant sociability; intersubjectivity; autism ID EARLY RECOGNITION; HOME VIDEOTAPES; JOINT ATTENTION; YOUNG-CHILDREN; COMMUNICATION; POPULATION; BEHAVIORS; IMITATION; SYMPTOMS; DISORDER AB The purpose of this study was to identify the specific aspects of social engagement that distinguish infants with autism from infants of similar age and developmental level who do not have autism. Ten parents of preschoolers with autism and 10 parents of matched children without autism were given a semistructured interview, the Detection of Autism by Infant Sociability Interview (DAISI), which elicits reports on whether 19 aspects of social engagement characteristic of typically developing infants were present at some time during the child's first 24 months. The reports of infants with autism differed from those of the control group on 16 items. Findings suggest that infants with autism have marked limitation in both person-to-person and person person-object social engagement, in keeping with the theory that autism involves impairments in primary as well as secondary intersubjectivity (Hobson, 1993a). C1 Univ Wales, Sch Psychol, Bangor LL57 2DG, Gwynedd, Wales. Tavistock Clin, London NW3 5BA, England. UCL, London, England. RP Wimpory, DC (reprint author), Univ Wales, Sch Psychol, Bangor LL57 2DG, Gwynedd, Wales. 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PD DEC PY 2000 VL 30 IS 6 BP 525 EP 536 DI 10.1023/A:1005683209438 PG 12 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100004 PM 11261465 ER PT J AU Charlop-Christy, MH Le, L Freeman, KA AF Charlop-Christy, MH Le, L Freeman, KA TI A comparison of video modeling with in vivo modeling for teaching children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE comparison of video and in vivo modeling; autism ID ACQUISITION; PERFORMANCE; STIMULUS; SKILLS; PEER AB The present study was designed to compare the effectiveness of video modeling with in vivo modeling for teaching developmental skills to children with autism. A multiple baseline design across five children and within child across the two modeling conditions (video and in vivo) and across tasks was used. Each child was presented two similar tasks from his or her curriculum; one task was used for the video condition, while the other was used for the in vivo condition. 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Autism Dev. Disord. PD DEC PY 2000 VL 30 IS 6 BP 537 EP 552 DI 10.1023/A:1005635326276 PG 16 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100005 PM 11261466 ER PT J AU Bryan, LC Gast, DL AF Bryan, LC Gast, DL TI Teaching on-task and on-schedule behaviors to high-functioning children with autism via picture activity schedules SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; graduated guidance procedure; picture activity book ID PHOTOGRAPHIC ACTIVITY SCHEDULES; MENTALLY-RETARDED ADULTS; SKILLS; MAINTENANCE; STUDENTS; PROMPTS; INDEPENDENCE; DISABILITIES; ACQUISITION; ADOLESCENTS AB The purpose of this investigation was to evaluate the effectiveness of a two-component reaching package (graduated guidance and visual activity schedules) in teaching young students with autism to increase on-task and on-schedule behavior. Four children enrolled in a resource-based classroom in a public elementary school served as participants. An A-B-A-B withdrawal design was used to evaluate the effectiveness of a picture activity schedule on the percentage of intervals scored as on-task and on-schedule. Generalization measures were taken on the percentage of intervals scored as on-task and on-schedule with novel activities. The results of the investigation indicate that (a) student performance rose to criterion levels upon introduction of the graduated guidance procedure, (b) student performance maintained when the picture activity book was available (Book Only) and dropped when the picture activity book was not available (No Book), and (c) student performance generalized to novel activities. The implications of these findings show the importance for future development and use of visual activity schedules to promote the independent functioning of students with autism spectrum disorders in their least restrictive environments. C1 Univ Georgia, Dept Special Educ, Athens, GA 30602 USA. Gwinnett Cty Publ Sch, Lawrenceville, GA USA. RP Gast, DL (reprint author), Univ Georgia, Dept Special Educ, Athens, GA 30602 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BILLINGSLEY F, 1980, BEHAV ASSESS, V2, P229 Bondy A. S., 1994, FOCUS AUTISTIC BEHAV, V9, P1, DOI DOI 10.1177/108835769400900301 CARSON P, 1991, FABULOUS FILE FOLDER CARSON P, 1997, LETS LEARN BIG BOOK COHEN DJ, HDB AUTISM PERVASIVE CONNIS RT, 1979, J APPL BEHAV ANAL, V12, P355, DOI 10.1901/jaba.1979.12-355 *EBSCO CURR MAT, 1985, SENS PENC HANDW PROG FRANK AR, 1985, J APPL BEHAV ANAL, V18, P179, DOI 10.1901/jaba.1985.18-179 Frost L. A., 1994, PICTURE EXCHANGE COM HALL LJ, 1995, EDUC TRAIN MENT RET, V30, P208 Hodgdon L. A., 1995, VISUAL STRATEGIES IM JOHNSON BF, 1991, BEHAV MODIF, V15, P187 JOHNSON BF, 1981, BEHAV MODIF, V5, P187, DOI 10.1177/014544558152003 JOLLY AC, 1993, J ASSOC PERS SEVERE, V18, P46 Kaufman A. S., 1985, KAUFMAN TEST ED ACHI Koegel R. 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PD DEC PY 2000 VL 30 IS 6 BP 553 EP 567 DI 10.1023/A:1005687310346 PG 15 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100006 PM 11261467 ER PT J AU Chin, HY Bernard-Opitz, V AF Chin, HY Bernard-Opitz, V TI Teaching conversational skills to children with autism: Effect on the development of a theory of mind SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE conversational skills; autism; theory of mind ID BELIEF; ABILITY; COMMUNICATION; ACQUISITION; LANGUAGE AB This research examined whether children with autism could be trained to improve their conversational skills and whether this led to changes in standard tests of theory of mind (ToM). Three high-functioning children with autism participated in a multiple baseline across participants design. The children were taught how to initiate a conversation, take turns during conversation, listen attentively, maintain a conversation topic, and change a conversation topic appropriately. The children were tested for ToM using False Belief tasks before and after training sessions. Results indicate that the amount of shared interest exhibited by the children with autism during conversation with their caregivers increased during training sessions. The children also made more responses that were appropriate to the context of the conversation. Performance on the False Belief tasks remained constant throughout the study. Results are dis cussed with respect to the implications of results of performance in standard ToM tasks. C1 Natl Univ Singapore, Dept Social Work & Psychol, Singapore 117548, Singapore. RP Chin, HY (reprint author), Natl Univ Singapore, Dept Social Work & Psychol, Singapore 117548, Singapore. 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PD DEC PY 2000 VL 30 IS 6 BP 569 EP 583 DI 10.1023/A:1005639427185 PG 15 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100007 PM 11261468 ER PT J AU Jacobson, JW Mulick, JA AF Jacobson, JW Mulick, JA TI System and cost research issues in treatments for people with autistic disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; cost; service selection; early intensive behavioral intervention ID BEHAVIORAL TREATMENT; EARLY INTERVENTION; CHILDREN; PEDIATRICIANS; AGE AB Parents of children with autism and pervasive developmental disorder and educational and clinical practitioners providing services to them regularly confront a wide range of service selection and financial decisions that are not as yet effectively addressed by applied research. Relevant systems issues span a very broad range of concerns: (a) systems delivery models and issues (e.g., costs of services, implementation of intensive intervention, and teacher or therapist training), (b) how best to integrate treatments; (c) providing treatment to those with limited monetary resources: (d) cost and cost/benefit analyses; (e) how to educate adult psychiatrists (as well as other practitioners and personnel) regarding autism: and (f) gaps between research and practice. C1 New York State Off Mental Retardat & Dev Disabil, Bureau Planning & Serv Design, Albany, NY 12229 USA. Independent Living Capital Dist Inc, Schenectady, NY USA. Ohio State Univ, Dept Pediat, Columbus, OH 43210 USA. Ohio State Univ, Dept Psychol, Columbus, OH 43210 USA. RP Jacobson, JW (reprint author), New York State Off Mental Retardat & Dev Disabil, Bureau Planning & Serv Design, 44 Holland Ave, Albany, NY 12229 USA. CR Anderson S. 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Autism Dev. Disord. PD DEC PY 2000 VL 30 IS 6 BP 585 EP 593 DI 10.1023/A:1005691411255 PG 9 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100008 PM 11261469 ER PT J AU Marcus, LM Rubin, JS Rubin, MA AF Marcus, LM Rubin, JS Rubin, MA TI Benefit-cost analysis and autism services: A response to Jacobson and Mulick SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID BEHAVIORAL TREATMENT; YOUNG-CHILDREN; PROGRAMS C1 Univ N Carolina, Sch Med, Dept Psychiat, Div TEACCH, Chapel Hill, NC 27514 USA. Miami Univ, Oxford, OH 45056 USA. RP Marcus, LM (reprint author), Univ N Carolina, Sch Med, Dept Psychiat, Div TEACCH, Chapel Hill, NC 27514 USA. CR Dawson G., 1997, EFFECTIVENESS EARLY, P307 Feinberg E, 1998, INFANT YOUNG CHILD, V10, P54 Freeman BJ, 1997, J AUTISM DEV DISORD, V27, P641, DOI 10.1023/A:1025850715183 Gresham FM, 1997, BEHAV DISORDERS, V22, P185 Gresham FM, 1997, BEHAV DISORDERS, V22, P219 Hurth J, 1999, INFANT YOUNG CHILD, V12, P17 Jacobson J, 1998, BEHAV INTERVENT, V13, P201, DOI DOI 10.1002/(SICI)1099-078X Jacobson JW, 2000, J AUTISM DEV DISORD, V30, P585, DOI 10.1023/A:1005691411255 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MIKESELL JL, 1991, FISCAL ADM ANAL APPL SCHOPLER E, 1989, J CONSULT CLIN PSYCH, V57, P162 Sheinkopf SJ, 1998, J AUTISM DEV DISORD, V28, P15, DOI 10.1023/A:1026054701472 NR 12 TC 6 Z9 6 PU KLUWER ACADEMIC/PLENUM PUBL 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 DEC PY 2000 VL 30 IS 6 BP 595 EP 598 DI 10.1023/A:1005643528093 PG 4 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100009 PM 11261470 ER PT J AU Mancina, C Tankersley, M Kamps, D Kravits, T Parrett, J AF Mancina, C Tankersley, M Kamps, D Kravits, T Parrett, J TI Brief report: Reduction of inappropriate vocalizations for a child with autism using a self-management treatment program SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE self-management procedures; autism; inappropriate vocalization ID DISRUPTIVE BEHAVIOR; TREATMENT PACKAGE AB Self-management procedures that incorporate elements of self-assessment, self-recording, and self-reinforcement have reduced stereotypic (i.e., repetitive) behaviors in children with autism in clinical settings. This study examined the affects of a self-management program used to reduce high rates of inappropriate vocalizations (e.g.. humming, tongue clucking, perseverative and echolalic words/phrases) in a 12-year-old girl having autism served in a public school classroom. When self-management was applied to inappropriate vocalizations in a multiple-baseline design during leisure, prevocational, and reading tasks, the occurrence of vocalizations decreased. implications for teaching these procedures in classroom settings are discussed. C1 Univ Kansas, Kansas City, KS USA. Kent State Univ, Kent, OH 44242 USA. Kansas Publ Sch, Kansas City, KS USA. RP Kamps, D (reprint author), Juniper Gardens Childrens Project, 650 Minnesota Ave,2nd Floor, Kansas City, KS 66101 USA. 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PD DEC PY 2000 VL 30 IS 6 BP 599 EP 606 DI 10.1023/A:1005695512163 PG 8 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100010 PM 11261471 ER PT J AU Stone, WL Coonrod, EE Ousley, OY AF Stone, WL Coonrod, EE Ousley, OY TI Brief report: Screening tool for autism in two-year-olds (STAT): Development and preliminary data SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID JOINT ATTENTION; YOUNG-CHILDREN; NONVERBAL-COMMUNICATION; SOCIAL COMMUNICATION; BEHAVIORAL TREATMENT; LANGUAGE-DEVELOPMENT; PRESCHOOL-CHILDREN; FIELD TRIAL; IMITATION; DISORDERS C1 Vanderbilt Univ, Sch Med, Nashville, TN 37212 USA. Georgia State Univ, Atlanta, GA 30303 USA. RP Stone, WL (reprint author), Vanderbilt Child Dev Ctr, 426 Med Ctr S,2100 Pierce Ave, Nashville, TN 37232 USA. 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PD DEC PY 2000 VL 30 IS 6 BP 621 EP 622 DI 10.1023/A:1005655930819 PG 2 WC Psychology, Developmental SC Psychology GA 404XG UT WOS:000167127100015 PM 11261476 ER PT J AU Court, JA Martin-Ruiz, C Graham, A Perry, E AF Court, JA Martin-Ruiz, C Graham, A Perry, E TI Nicotinic receptors in human brain: topography and pathology SO JOURNAL OF CHEMICAL NEUROANATOMY LA English DT Review DE nicotinic acetylcholine receptors; Parkinson's disease; Alzheimer's disease; dementia with Lewy bodies; autism; Down's syndrome; schizophrenia ID ALPHA-BUNGAROTOXIN BINDING; MESSENGER-RNA EXPRESSION; HUMAN CEREBRAL-CORTEX; HUMAN FRONTAL-CORTEX; LEWY BODY DEMENTIA; NIGROSTRIATAL DOPAMINERGIC-NEURONS; EXPOSURE DIFFERENTIALLY AFFECTS; POSITRON EMISSION TOMOGRAPHY; RAT STRIATAL SYNAPTOSOMES; AGE-RELATED-CHANGES AB Brain nicotinic acetylcholine receptors (nAChR) are a class of ligand-gated channels composed of alpha and beta subunits with specific structural, functional and pharmacological properties. They participate in the physiological and behavioural effects of acetyl choline and mediate responses to nicotine. They are associated with numerous transmitter systems and their expression is altered during development and ageing as well as in diseases such as autism, schizophrenia, Alzheimer's disease, Parkinson's disease and Lewy body dementia. Nicotinic receptors containing a number of different subunits are highly expressed during early human development. Disorders believed to be associated with abnormal brain maturation involve deficits in both alpha4 beta2, in the case of autism, and alpha7 possibly in addition to alpha4 beta2 nAChRs in the case of schizophrenia. In ageing and age-related neurodegenerative disorders nAChR deficits are predominantly associated with alpha4-containing receptors, although some studies also indicate the involvement of alpha3 and alpha7 subunits. Whilst ageing appears to be associated with reductions in subunit mRNA as well as protein expression, in Alzheimers disease only protein loss is apparent. Nicotinic therapy may be of benefit in a number of neurological conditions, however studies evaluating further both the distribution of specific subunit involvement and the correlation of nAChR deficits with clinical symptoms are required to inform therapeutic strategy. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Joint MRC New Castle Univ, Newcastle Gen Hosp, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England. RP Court, JA (reprint author), Joint MRC New Castle Univ, Newcastle Gen Hosp, MRC Bldg,Westgate Rd, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England. 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Chem. Neuroanat. PD DEC PY 2000 VL 20 IS 3-4 BP 281 EP 298 DI 10.1016/S0891-0618(00)00110-1 PG 18 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 404TP UT WOS:000167117200009 PM 11207426 ER PT J AU Klinger, LG Renner, P AF Klinger, LG Renner, P TI Performance-based measures in autism: Implications for diagnosis, early detection, and identification of cognitive profiles SO JOURNAL OF CLINICAL CHILD PSYCHOLOGY LA English DT Article ID EXECUTIVE FUNCTION; CHILDHOOD AUTISM; RATING-SCALE; MENTAL-RETARDATION; ASPERGER-SYNDROME; CENTRAL COHERENCE; INFANTILE-AUTISM; MIND ABILITIES; CHILDREN; INDIVIDUALS AB Provides a critical review of performance-based assessment measures in autism. Currently, performance-based measures of autism are being explored in two domains: structured play sessions and cognitive-neuropsychological assessments. Structured play sessions are designed to elicit the behavioral symptoms associated with autism to provide a consistent and valid means of early detection and diagnosis of autism across different evaluators and settings. These structured play sessions provide a supplement to diagnostic instruments based on parental report. Cognitive-neuropsychological tasks have been used to identify possible underlying cognitive impairments in autism including executive function, theory of mind, selective attention, and abstraction. Currently, cognitive tasks ave useful in treatment planning but are inappropriate for diagnostic purposes. Important goals for the future will be to integrate parent-report diagnostic interviews and structured play observations and to identify aprofile of cognitive impairments that are specific to pervasive developmental disorders that can be incorporated into diagnostic protocols. C1 Univ Alabama, Dept Psychol, University, AL 35486 USA. RP Klinger, LG (reprint author), Univ Alabama, Dept Psychol, Box 970348, University, AL 35486 USA. 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Clin. Child Psychol. PD DEC PY 2000 VL 29 IS 4 BP 479 EP 492 DI 10.1207/S15374424JCCP2904_3 PG 14 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 373FQ UT WOS:000165278000002 PM 11126628 ER PT J AU Bosacki, SL AF Bosacki, SL TI Theory of mind and self-concept in preadolescents: Links with gender and language SO JOURNAL OF EDUCATIONAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT Biennial Meeting of the Society-for-Research-in-Child-Development CY APR 16, 1999 CL ALBUQUERQUE, NEW MEXICO SP Soc Res Child Dev ID INDIVIDUAL-DIFFERENCES; CHILDREN; ADOLESCENCE; BEHAVIOR; BELIEFS; ADULTS; AUTISM; MODEL AB The investigation of the ability to attribute mental states to others and to see them as the basis for people's actions has been referred to as "theory of mind" (ToM) research. This study assessed ToM, or social understanding, in preadolescents and examined individual differences in the relations among social understanding, self-concept, and language competence. One hundred twenty-eight preadolescents (64 girls, 64 boys; mean age = 11 years, 9 months) completed tasks concerning self-concept and vocabulary and participated in a story-telling interview that assessed social and self-understanding. There were positive associations between children's social understanding and (a) self-understanding, (b) self-perceptions of behavioral conduct, and (c) general vocabulary ability. Independent of vocabulary ability, girls scored higher than boys on both social and self-understanding tasks. C1 Brock Univ, Fac Educ, St Catharines, ON L2S 3A1, Canada. RP Bosacki, SL (reprint author), Brock Univ, Fac Educ, St Catharines, ON L2S 3A1, Canada. CR Astington J. 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PD DEC PY 2000 VL 92 IS 4 BP 709 EP 717 DI 10.1037//0022-0663.92.4.709 PG 9 WC Psychology, Educational SC Psychology GA 381XL UT WOS:000165789300010 ER PT J AU Rowe, D Rudkin, A Crawford, L AF Rowe, D Rudkin, A Crawford, L TI Cerebral dominance and schizophrenia-spectrum disorders in adults with intellectual disability SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE cerebral dominance; handedness; laterality; neurodevelopmental hypothesis; schizophrenia ID LEARNING-DISABILITY; LEFT-HANDEDNESS; PEOPLE; AUTISM AB Studies of the general population without intellectual disability have suggested an association between atypical handedness and schizophrenia-spectrum disorders (SSDs). Mixed handedness is taken as an index of diminished cerebral dominance or laterality The present study addressed the clues tion of whether such findings extend to the neurodevelopmentally 'at risk' population of adults with intellectual disability and SSDs compared with. appropriate controls. Fourteen patients with a dual diagnosis of intellectual disability and SSD were compared with 14 controls with. intellectual disability alone. Assessments of self-reported hand preference and relative hand skill were completed. Self-report of hand preference revealed highly significantly greater mixed-handedness in the SSD group. Furthermore, relative hand skill performance was significantly diminished for the dominant hand. The discrepancy between dominant and nondominant hand functioning was lower in the SSD group and this association was highly significant. The results of the present study support the usefulness of such detailed laterality assessment in this population. Mixed laterality, over and above that of the population with general intellectual disability and developmental disorder, was associated with SSD. These results are consistent with the neurodevelopmental hypothesis of schizophrenia and its cognitive neuropsychiatric/neuropsychological sequelae. C1 Littlemore Mental Hlth Ctr, Oxford Clin, Reg Secure Unit, Oxford, England. RP Rowe, D (reprint author), Littlemore Mental Hlth Ctr, Oxford Clin, Reg Secure Unit, Oxford, England. 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Intell. Disabil. Res. PD DEC PY 2000 VL 44 BP 638 EP 643 DI 10.1046/j.1365-2788.2000.00304.x PN 6 PG 6 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 383VR UT WOS:000165905400002 PM 11115018 ER PT J AU Hurley, RA Lewine, JD Jones, GM Orrison, WW Taber, KH AF Hurley, RA Lewine, JD Jones, GM Orrison, WW Taber, KH TI Application of magnetoencephalography to the study of autism SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID CHILDREN; DISORDERS; LANGUAGE C1 Baylor Coll Med, Dept Psychiat & Behav Sci, Houston, TX 77030 USA. Baylor Coll Med, Dept Radiol, Houston, TX 77030 USA. Baylor Coll Med, Herbert J Frensley Ctr Imaging Res, Houston, TX 77030 USA. Vet Affairs Med Ctr, Psychiat Serv, Houston, TX 77030 USA. Univ Utah, Dept Radiol, Ctr Adv Med Technol, Salt Lake City, UT 84132 USA. RP Hurley, RA (reprint author), Baylor Coll Med, Dept Psychiat & Behav Sci, 1 Baylor Plaza, Houston, TX 77030 USA. 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Neuropsychiatr. Clin. Neurosci. PD WIN PY 2000 VL 12 IS 1 BP 1 EP 3 PG 3 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 280JY UT WOS:000085100700001 PM 10678505 ER PT J AU Yell, ML Drasgow, E AF Yell, ML Drasgow, E TI Litigating a free appropriate public education: The Lovaas hearings and cases SO JOURNAL OF SPECIAL EDUCATION LA English DT Article ID BEHAVIORAL TREATMENT; AUTISTIC-CHILDREN AB Between 1993 and 1998 there were 45 published due process hearings and court cases in which parents of children with autism challenged the appropriateness of a school district's educational program for their child. These hearings and cases involved parental requests for school districts to provide, fund, or reimburse them for the Lovaas treatment program for their young children. The purpose of this article is to examine how these hearings and cases affect the definition of "appropriate" special education programs. First, we review previous legislative and litigative definitions of a free appropriate public education (FAPE). Next, we analyze the Lovaas treatment hearings and cases to identify factors associated with winning and losing decisions. Finally, we discuss the implications of these decisions to provide guidance to schools in adhering to the procedural and substantive requirements of a FAPE. C1 Univ S Carolina, Columbia, SC 29208 USA. RP Yell, ML (reprint author), Univ S Carolina, 235-G Wardlaw, Columbia, SC 29208 USA. CR Alberto P. A., 1999, APPL BEHAV ANAL TEAC BAER DM, 1968, J APPL BEHAV ANAL, V1, P91, DOI 10.1901/jaba.1968.1-91 Baird M. M., 1999, P 20 NAT I LEG ISS E Deno S. L., 1992, PREVENTING SCH FAILU, V36, P5 FUCHS D, 1990, EXCEPT CHILDREN, V57, P102 GORN D, 1996, WHAT DO I DO ANSWER Heflin L. J., 1998, FOCUS AUTISM OTHER D, V13, P212 HUEFNER DS, 1991, HARVARD J LAW PUBL P, V14, P483 Lovaas O. 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PD WIN PY 2000 VL 33 IS 4 BP 205 EP 214 DI 10.1177/002246690003300403 PG 10 WC Education, Special SC Education & Educational Research GA 279UC UT WOS:000085062700003 ER PT J AU Ingram, JL Stodgell, CJ Hyman, SL Figlewicz, DA Weitkamp, LR Rodier, PM AF Ingram, JL Stodgell, CJ Hyman, SL Figlewicz, DA Weitkamp, LR Rodier, PM TI Discovery of allelic variants of HOXA1 and HOXB1: Genetic susceptibility to autism spectrum disorders SO TERATOLOGY LA English DT Article AB Background: Family studies have demonstrated that the autism spectrum disorders (ASDs) have a major genetic etiologic component, but expression and penetrance of the phenotype are variable. Mice with null mutations of Hoxa1 or Hoxb1, two genes critical to hindbrain development, have phenotypic features frequently observed in autism, but no naturally occurring variants of either gene have been identified in mammals. Methods: By sequencing regions of genomic DNA of patients with autism spectrum disorders, we detected a substitution variant at HOXA1 and an insertion variant at HOXB1, both in coding regions of the genes. Fifty-seven individuals ascertained for a diagnosis of an ASD, along with 166 of their relatives, were typed for these variants. Two non-ASD populations were typed, and the frequency of the newly identified alleles was determined in all groups. The genotypes of the ASD families were tested for conformation to Hardy-Weinberg proportions and Mendelian expectations for gene transmission. Results: The frequency of the variants was 10-25% in persons of European or African origin. In the ASD families, there was a significant deviation from the HOXA1 genotype ratios expected from Hardy-Weinberg proportions (P = 0.005). Among affected offspring, a significant deviation from Mendelian expectation in gene transmission (P = 0.011) was observed. No statistically significant effects were detected when the same analyses were applied to the HOXB1 locus, but there was evidence of an interaction between HOXA1, HOXB1, and gender in susceptibility to ASDs. Conclusions: The results support a role for HOXA1 in susceptibility to autism, and add to the existing body of evidence implicating early brain stem injury in the etiology of ASDs. (C) 2000 Wiley-Liss, Inc. C1 Univ Rochester, Sch Med & Dent, Dept Obstet & Gynecol, Rochester, NY 14642 USA. Univ Rochester, Sch Med & Dent, Dept Environm Med, Rochester, NY 14642 USA. Univ Rochester, Sch Med & Dent, Dept Pediat, Rochester, NY 14642 USA. Univ Rochester, Sch Med & Dent, Dept Neurol, Rochester, NY 14642 USA. Univ Rochester, Sch Med & Dent, Dept Psychiat, Div Genet, Rochester, NY 14642 USA. RP Rodier, PM (reprint author), Univ Rochester, Sch Med & Dent, Dept Obstet & Gynecol, 601 Elmwood Ave, Rochester, NY 14642 USA. 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RP Kissoon, N (reprint author), Univ Florida, Hlth Sci Ctr Jacksonville, 820 Prudential Dr,Suite 203,Howard Bldg, Jacksonville, FL 32207 USA. CR *CINN DUS SYRV CTR, 1999, COMMUN DIS REP CDR W, P9 ODENT MR, 1994, JAMA-J AM MED ASSOC, V272, P592 WAKEFIELD AJ, 1998, LANCET, V351, P1327 NR 3 TC 1 Z9 1 PU UNIV WEST INDIES FACULTY MEDICAL SCIENCES PI KINGSTON PA MONA CAMPUS, KINGSTON 7, JAMAICA SN 0043-3144 J9 W INDIAN MED J JI West Ind. Med. J. PD DEC PY 2000 VL 49 IS 4 BP 257 EP 258 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 474MX UT WOS:000171112000001 PM 11211528 ER PT J AU Christie, CDC AF Christie, CDC TI Causal link between MMR vaccination and autism: Fact or fiction? SO WEST INDIAN MEDICAL JOURNAL LA English DT Editorial Material C1 Univ W Indies, Fac Med Sci, Dept Obstet Gynaecol & Child Hlth, Child Hlth Sect, Kingston 7, Jamaica. RP Christie, CDC (reprint author), Univ W Indies, Fac Med Sci, Dept Obstet Gynaecol & Child Hlth, Child Hlth Sect, Kingston 7, Jamaica. CR Bauer S, 1995, Pediatr Rev, V16, P168, DOI 10.1542/pir.16-5-168 Bauer S, 1995, Pediatr Rev, V16, P130, DOI 10.1542/pir.16-4-130 Beale AJ, 1998, LANCET, V351, P906, DOI 10.1016/S0140-6736(05)70317-2 Chen RT, 1998, LANCET, V351, P611, DOI 10.1016/S0140-6736(05)78423-3 COWLEY G, 2000, NEWSWEEK 0731, P53 Gangarosa EJ, 1998, LANCET, V351, P356, DOI 10.1016/S0140-6736(97)04334-1 HOWSON CP, 1991, I MED ADVERSE EVENTS Lee JW, 1998, LANCET, V351, P905, DOI 10.1016/S0140-6736(98)26012-0 *RED BOOK, 2000, REP COMM INF DIS Rodier PM, 1998, MENT RETARD DEV D R, V4, P121, DOI 10.1002/(SICI)1098-2779(1998)4:2<121::AID-MRDD9>3.0.CO;2-S Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 12 TC 2 Z9 2 PU UNIV WEST INDIES FACULTY MEDICAL SCIENCES PI KINGSTON PA MONA CAMPUS, KINGSTON 7, JAMAICA SN 0043-3144 J9 W INDIAN MED J JI West Ind. Med. J. PD DEC PY 2000 VL 49 IS 4 BP 266 EP 267 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 474MX UT WOS:000171112000004 PM 11211531 ER PT J AU O'Riordan, M AF O'Riordan, M TI Superior modulation of activation levels of stimulus representations does not underlie superior discrimination in autism SO COGNITION LA English DT Article DE discrimination; priming; autism ID KANIZSA SUBJECTIVE FIGURES; VISUAL-SEARCH; SELECTIVE ATTENTION; CONJUNCTION SEARCH; GUIDED SEARCH; CENTRAL LOCUS; INHIBITION; OBJECTS; CHILDREN; TASK AB The performance of children with and without autism was compared in object-based positive and negative priming tasks within a visual search procedure. Object-based positive and negative priming effects were found in both groups of children. This result provides the first evidence for the activation of object-based representations during visual search task performance and further supports the notion that both excitatory and inhibitory guidance mechanisms are involved in target location in visual search. The children with autism were overall better than the typically developing children at visual search, thus replicating demonstrations of superior discrimination in autism. Furthermore, there was no difference between the magnitude of the positive nor the negative priming effects of the groups. This finding suggests that excitatory and inhibitory control operate comparably in autism and normal development. These results are discussed in the light of the superior ability of individuals with autism to discriminate between items. More specifically, it is argued that superior discrimination in autism does not result from enhanced top-down excitatory and inhibitory control. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP O'Riordan, M (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. 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Method: Selective review of the literature detailing data pertaining to symptoms and disorders sometimes encountered in connection with autism or Asperger syndrome. Results: A large number of medical conditions, psychiatric disorders and behavioural and motor dyscontrol symptoms are associated with autism and Asperger syndrome. Conclusion: Comorbidity is to be expected in autism spectrum disorders - directly or indirectly. Comorbid conditions may be markers for underlying pathophysiology and suggest a more varied treatment approach. There is a great need for in-depth research into this area, meaning that the exclusion criteria of current diagnostic manuals, i.e. those that rule out a diagnosis of autism in some disorders, and a diagnosis of certain other disorders in autism may have to be revised. C1 Gothenburg Univ, Dept Child & Adolescent Psychiat, Annedals Clin, S-41345 Gothenburg, Sweden. RP Gillberg, C (reprint author), Gothenburg Univ, Dept Child & Adolescent Psychiat, Annedals Clin, S-41345 Gothenburg, Sweden. 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Scand. PD NOV PY 2000 VL 102 IS 5 BP 321 EP 330 DI 10.1034/j.1600-0447.2000.102005321.x PG 10 WC Psychiatry SC Psychiatry GA 371CJ UT WOS:000165160000002 PM 11098802 ER PT J AU Pertejo, MA Guerra, MP Gilaberte, I AF Pertejo, MA Guerra, MP Gilaberte, I TI An open study of fluoxetine in children with autism SO ACTAS ESPANOLAS DE PSIQUIATRIA LA Spanish DT Article DE pervasive developmental disorder; fluoxetine.; children ID OBSESSIVE-COMPULSIVE DISORDER; YOUNG-CHILDREN; DOUBLE-BLIND; ADOLESCENTS; PLACEBO; ADULTS; TRIAL AB Introduction: Serotonergic dysfunction have been implicated in the pathophysiology of the autism. SRIs have shown efficacy in improving some symptoms in children with Autism. Objectives: To Evaluate, in a pilot study the efficacy, and safety of fluoxetine in very young children with autism. Method: I year open-label trial tons made with fluoxetine on 12 patients (3 to 13 years old) with Pervasive Developmental Disorder CGI-severity was used to assess the severity and the improvement of symptoms. Individual symptoms improvement was assessed by both parents and therapists Fluoxetine dose was titrated in all patients from 1.2 ml/day to reach a final doses of 3,6 or 5 ml/day in four weeks. Tolerance tons assessed by collecting spontaneous adverse events Results: II children completed the study Children experienced a moderate or marked improvement (final score in CGI 3 to 5). Communication and attention skills were improved There were also a decrease of-rituals, stereotypies and repetitive behaviours. Most common adverse Events were increase of impulsivity and restlessness, other events were sleep disturbances and lost of appetite. children needed concomitant medication with carbamacepine and I with levopromacine along tbe study. Conclusions: These results support that Fluoxetine at doses of 5 ml/day (20 mg/day) could help to improve some symptoms in Pervasive Developmental Disorders and allow to increase the effectiveness of therapies in these patients. Move studies are needed to confirm these results. C1 Hosp Nino Jesus, Serv Psiquiatria, Hosp Dia Psiquiatr Infantil, Madrid 28009, Spain. Serv Salud Mental Vallecas, Madrid, Spain. Lilly, Dept Clin Invest, Madrid, Spain. RP Guerra, MP (reprint author), Hosp Nino Jesus, Serv Psiquiatria, Hosp Dia Psiquiatr Infantil, Avda Menendez Pelayo 65, Madrid 28009, Spain. 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Psiquiatri. PD NOV-DEC PY 2000 VL 28 IS 6 BP 353 EP 356 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 407JU UT WOS:000167269100002 ER PT J AU Edelson, SB AF Edelson, SB TI A proposed cause and treatment for autism SO ARCHIVES OF CLINICAL NEUROPSYCHOLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0887-6177 J9 ARCH CLIN NEUROPSYCH JI Arch. Clin. Neuropsychol. PD NOV PY 2000 VL 15 IS 8 BP 802 EP 802 PG 1 WC Psychology, Clinical; Psychology SC Psychology GA 388AF UT WOS:000166154700277 ER PT J AU Maziade, M Merette, C Cayer, M Roy, MA Szatmari, P Cote, R Thivierge, J AF Maziade, M Merette, C Cayer, M Roy, MA Szatmari, P Cote, R Thivierge, J TI Prolongation of brainstem auditory-evoked responses in autistic probands and their unaffected relatives SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; WHOLE-BLOOD SEROTONIN; INFANTILE-AUTISM; 1ST-DEGREE RELATIVES; DIAGNOSTIC INTERVIEW; CHROMOSOME-15 LOCUS; STEM RESPONSES; CHILDREN; CEREBELLAR; SCHIZOPHRENIA AB Background: Brain function, as indexed by brain electrical activity, is heritable in humans, and it may be impaired in autism. Autism also has strong genetic determinants, and like all major psychiatric disorders, its complex clinical phenotype renders genetic studies difficult. Innovative strategies focused on alternative biological phenotypes are needed. Methods: The early brain auditory-evoked response was assessed in 73 autistic probands and 251 relatives who were compared with 521 normal controls. Results: We first confirmed in the autistic probands the presence of a slowing in nerve conduction in the auditory system as expressed by the prolongation of early brain auditory-evoked response under the form of I-III interpeak latencies (IPLs). Furthermore, we observed the same I-III IPL prolongation in the unaffected first degree relatives of the autistic probands compared with controls. Despite clear evidence of a coaggregation of autism and I-III IPL prolongation in families, the IPLs did not seem to be the sole liability factor for autism as suggested by the observation of 52% of families in which the autistic proband and relatives showed normal IPLs. 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Psychiatry PD NOV PY 2000 VL 57 IS 11 BP 1077 EP 1083 DI 10.1001/archpsyc.57.11.1077 PG 7 WC Psychiatry SC Psychiatry GA 369FR UT WOS:000165055700008 PM 11074874 ER PT J AU Critchley, HD Daly, EM Bullmore, ET Williams, SCR Van Amelsvoort, T Robertson, DM Rowe, A Phillips, M McAlonan, G Howlin, P Murphy, DGM AF Critchley, HD Daly, EM Bullmore, ET Williams, SCR Van Amelsvoort, T Robertson, DM Rowe, A Phillips, M McAlonan, G Howlin, P Murphy, DGM TI The functional neuroanatomy of social behaviour - Changes in cerebral blood flow when people with autistic disorder process facial expressions SO BRAIN LA English DT Article DE Asperger syndrome; attention; autism; facial expression; fMRI ID INFANTILE-AUTISM; ASPERGER-SYNDROME; CHILDHOOD AUTISM; BRAIN; INDIVIDUALS; MIND; ABNORMALITIES; DYSFUNCTION; ACTIVATION; PATHWAY AB Although high-functioning individuals with autistic disorder (i.e. autism and Asperger syndrome) are of normal intelligence,they have life-long abnormalities in social communication and emotional behaviour. However, the biological basis of social difficulties in autism is poorly understood. Facial expressions help shape behaviour, and we investigated if high-functioning people with autistic disorder show neurobiological differences from controls when processing emotional facial expressions. We used functional MRI to investigate brain activity in nine adults with autistic disorder (mean age +/- standard deviation 37 +/- 7 years; IQ 102 +/- 15) and nine controls (27 +/- 7 years; IQ 116 +/- 10) when explicitly (consciously) and implicitly (unconsciously) processing emotional facial expressions, Subjects with autistic disorder differed significantly from controls in the activity of cerebellar, mesolimbic and temporal lobe cortical regions of the brain when processing facial expressions. Notably, they did not activate a cortical 'face area' when explicitly appraising expressions, or the left amygdala region and left cerebellum when implicitly processing emotional facial expressions, High-functioning people with autistic disorder have biological differences from controls when consciously and unconsciously processing facial emotions, and these differences are most likely to be neurodevelopmental in origin. This may account for some of the abnormalities in social behaviour associated with autism. C1 Univ London Kings Coll, Dept Med Psychol, Inst Psychiat, London SE5 8AF, England. Univ London Kings Coll, Dept Neuroimaging, Inst Psychiat, London SE5 8AF, England. St George Hosp, Sch Med, Dept Psychiat, London, England. Univ Cambridge, Addenbrookes Hosp, Dept Psychiat, Cambridge CB2 2QQ, England. RP Murphy, DGM (reprint author), Univ London Kings Coll, Dept Med Psychol, Inst Psychiat, De Crespigny Pk, London SE5 8AF, England. RI Howlin, Patricia/A-7622-2011; Williams, Steve/D-6979-2011; turton, miranda/F-4682-2011; McAlonan, Grainne/G-1541-2011; daly, eileen/B-6716-2011; critchley, hugo/G-9267-2011; Bullmore, Edward/C-1706-2012 OI McAlonan, Grainne/0000-0002-4466-2343; Bullmore, Edward/0000-0002-8955-8283 CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 BACHEVALIER J, 1994, NEUROPSYCHOLOGIA, V32, P627, DOI 10.1016/0028-3932(94)90025-6 Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 BARONCOHEN S, 1994, BRIT J PSYCHIAT, V165, P640, DOI 10.1192/bjp.165.5.640 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x BAUMAN M, 1985, NEUROLOGY, V35, P866 Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x Brammer MJ, 1997, MAGN RESON IMAGING, V15, P763, DOI 10.1016/S0730-725X(97)00135-5 BRYSON SE, 1990, DEV ATTENTION RES TH, P405 Chugani DC, 1997, ANN NEUROL, V42, P666, DOI 10.1002/ana.410420420 CIESIELSKI KT, 1994, ACTA NEUROBIOL EXP, V54, P151 COURCHESNE E, 1988, NEW ENGL J MED, V318, P1349, DOI 10.1056/NEJM198805263182102 COURCHESNE E, 1993, AM J ROENTGENOL, V160, P387 Critchley H, 2000, HUM BRAIN MAPP, V9, P93, DOI 10.1002/(SICI)1097-0193(200002)9:2<93::AID-HBM4>3.0.CO;2-Z DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Ekman P., 1975, PICTURES FACIAL AFFE Ekman Paul, 1998, EXPRESSION EMOTIONS Friston KJ, 1996, MAGNET RESON MED, V35, P346, DOI 10.1002/mrm.1910350312 GAFFAN D, 1992, P471 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 Haas RH, 1996, J CHILD NEUROL, V11, P84 Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 HASHIMOTO T, 1995, J AUTISM DEV DISORD, V25, P1, DOI 10.1007/BF02178163 Haznedar MM, 1997, AM J PSYCHIAT, V154, P1047 HORWITZ B, 1988, ARCH NEUROL-CHICAGO, V45, P749 HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 Kanwisher N, 1999, NEUROREPORT, V10, P183, DOI 10.1097/00001756-199901180-00035 KLEIMAN MD, 1992, NEUROLOGY, V42, P753 Ledoux J., 1998, EMOTIONAL BRAIN MYST LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Minshew NJ, 1999, NEUROLOGY, V52, P917 Morris JS, 1999, P NATL ACAD SCI USA, V96, P1680, DOI 10.1073/pnas.96.4.1680 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x PHILLIPS ML, 1997, NATURE, V389, P496 PIVEN J, 1990, AM J PSYCHIAT, V147, P734 Piven J, 1997, AM J PSYCHIAT, V154, P1051 Piven J, 1998, J AUTISM DEV DISORD, V28, P105, DOI 10.1023/A:1026084430649 PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Puce A, 1998, J NEUROSCI, V18, P2188 Schmahmann JD, 1998, BRAIN, V121, P561, DOI 10.1093/brain/121.4.561 SEIGEL BV, 1995, SCHIZOPHREN RES, V17, P85 Sprengelmeyer R, 1996, BRAIN, V119, P1647, DOI 10.1093/brain/119.5.1647 Talairach J., 1988, COPLANAR STEREOTAXIC Warrington E., 1984, RECOGNITION MEMORY T Wechsler D, 1981, ADULT INTELLIGENCE S WHO, 1993, ICD 10 INT CLASS DIS Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 ZILBOVICIUS M, 1995, AM J PSYCHIAT, V152, P248 NR 49 TC 429 Z9 438 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD NOV PY 2000 VL 123 BP 2203 EP 2212 DI 10.1093/brain/123.11.2203 PN 11 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 375QR UT WOS:000165413200003 PM 11050021 ER PT J AU Rajendran, G Mitchell, P AF Rajendran, G Mitchell, P TI Computer mediated interaction in Asperger's syndrome: the Bubble Dialogue program SO COMPUTERS & EDUCATION LA English DT Article DE adult learning; cooperative/collaborative learning; computer-mediated communication; human-computer interface ID CARD SORTING TEST; DYSEXECUTIVE SYNDROME; VISUAL ILLUSIONS; AUTISM; CHILDREN; MIND; INDIVIDUALS; BELIEF; ABNORMALITIES AB This paper reports the use of a computer application, Bubble Dialogue, with two primary aims: (1) to assess the experience of computer-mediated role-taking on the interpersonal understanding, executive abilities and verbal abilities of two young male adults with Asperger's syndrome (a diagnosis given to higher functioning individuals with autism); (2) to investigate whether blind raters judged differently between Bubble Dialogue scripts produced by individuals with Asperger's syndrome and scripts produced by individuals with emotional and behavioural difficulties. The results show that there was no detectable improvement in the interpersonal understanding of the participants with Asperger's syndrome, but there was an improvement in their executive function scores. Additionally, the blind ratings revealed that only one of the 'Asperger' Bubble Dialogue scripts was different from the scripts generated by individuals with emotional and behavioural difficulties. Conceivably, Bubble Dialogue helps to regulate interaction, such that the social impairments characteristics of Asperger's syndrome are less conspicuous. (C) 2000 Published by Elsevier Science Ltd. C1 Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Rajendran, G (reprint author), Univ Nottingham, Sch Psychol, Univ Pk, Nottingham NG7 2RD, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BADDELEY A, 1988, BRAIN COGNITION, V7, P212, DOI 10.1016/0278-2626(88)90031-0 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Dunn L M., 1982, BRIT PICTURE VOCABUL Evans JJ, 1997, PSYCHOL MED, V27, P635, DOI 10.1017/S0033291797004790 Ferland MB, 1998, J CLIN EXP NEUROPSYC, V20, P473, DOI 10.1076/jcen.20.4.473.1475 Frith U., 1994, SOCIAL DEV, V3, P108, DOI DOI 10.1111/J.1467-9507.1994.TB00031.X Frith U., 1989, AUTISM EXPLAINING EN Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 GRANT DA, 1948, J EXP PSYCHOL, V38, P404, DOI 10.1037/h0059831 GRAY B, 1991, GETTING STARTED BUBB Hadwin J, 1997, J AUTISM DEV DISORD, V27, P519, DOI 10.1023/A:1025826009731 Hadwin J, 1996, DEV PSYCHOPATHOL, V8, P345 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x HAPPE FGE, 1993, COGNITION, V48, P101, DOI 10.1016/0010-0277(93)90026-R HOBSON RP, 1990, PSYCHOL REV, V97, P114, DOI 10.1037/0033-295X.97.1.114 JONES A, 1997, J COMPUTING CHILDHOO, V8, P119 Kanner L, 1943, NERV CHILD, V2, P217 Mitchell P., 1996, ACQUIRING CONCEPTION Mitchell P, 1997, INTRO THEORY MIND CH MOORE DJ, 2000, IN PRESS INNOVATIONS, V37 Norman D., 1986, CONSCIOUSNESS SELF R, V4, P1 ONeill M, 1997, J AUTISM DEV DISORD, V27, P283, DOI 10.1023/A:1025850431170 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x OZONOFF S, 1995, NEUROPSYCHOLOGY, V9, P491, DOI 10.1037//0894-4105.9.4.491 PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x Ropar D, 1999, J CHILD PSYCHOL PSYC, V40, P1283, DOI 10.1017/S0021963099004667 RUTTER M, 1987, J AUTISM DEV DISORD, V17, P159, DOI 10.1007/BF01495054 SHALLICE T, 1988, NERUOPSYCHOLOGY MENT Swettenham J, 1996, J CHILD PSYCHOL PSYC, V37, P157, DOI 10.1111/j.1469-7610.1996.tb01387.x WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 32 TC 14 Z9 14 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0360-1315 J9 COMPUT EDUC JI Comput. Educ. PD NOV PY 2000 VL 35 IS 3 BP 189 EP 207 DI 10.1016/S0360-1315(00)00031-2 PG 19 WC Computer Science, Interdisciplinary Applications; Education & Educational Research SC Computer Science; Education & Educational Research GA 359LQ UT WOS:000089612700002 ER PT J AU Fidler, DJ Bailey, JN Smalley, SL AF Fidler, DJ Bailey, JN Smalley, SL TI Macrocephaly in autism and other pervasive developmental disorders SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID HEAD CIRCUMFERENCE; DIAGNOSTIC INTERVIEW; BIRTH; SIZE; MRI AB To assess the prevalence of macrocephaly (head circumference greater than or equal to1.88 standart deviations above normative data for age and sex or >97th centile) in autism and other pervasive developmental disorders, 41 children with autism, and a comparison group of 21 children with tuberous sclerosis complex (TSC) or an unspecified seizure disorder were studied. Familiality of head circumference was also assessed from measurements of 133 first-degree relatives. Significantly higher rates of macrocephaly were found in probands with autism (12.2%) and their first-degree relatives (15.5%) when compared against a published normative sample. The incidence of macrocephaly in the comparison group of probands with TSC and seizure disorder (9.5%) and their first-degree relatives (8.3%) was higher than normative data as well, although the relation between macrocephaly and autism was more pronounced. Bead circumference and extreme scores reflecting macrocephaly were moderately heritable in the present sample (H-2 = 0.47). The increased prevalence of macrocephaly in relatives of children with autism compared with control children suggests that this characteristic may be a familial risk factor in the pathogenesis of autism. C1 Univ Calif Los Angeles, Sch Med, Dept Psychiat & Biobehav Sci, Inst Neuropsychiat, Los Angeles, CA 90069 USA. RP Fidler, DJ (reprint author), Univ Calif Los Angeles, Sch Med, Dept Psychiat & Biobehav Sci, Inst Neuropsychiat, 760 Westwood Plaza, Los Angeles, CA 90069 USA. 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Med. Child Neurol. PD NOV PY 2000 VL 42 IS 11 BP 737 EP 740 DI 10.1017/S0012162200001365 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 376PL UT WOS:000165465900004 PM 11104344 ER PT J AU Sheldon, L Turk, J AF Sheldon, L Turk, J TI Monozygotic boys with fragile X syndrome SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID IDENTICAL-TWINS; POSTERIOR-FOSSA; FULL MUTATION; FOLIC-ACID; AUTISM; NEUROANATOMY; CHILDREN; FEMALES; INDIVIDUALS; RECOGNITION AB Monozygotic twin boys with fragile X syndrome underwent thorough genetic, psychiatric, neurological, and language evaluations at 10 years of age. They both demonstrated physical features, speech and language difficulties, social problems, and attentional deficits that characterize the behavioural phenotype of fragile X syndrome. Despite identical genetic constitutions, there were important developmental and behavioural heterogeneities. 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Med. Child Neurol. PD NOV PY 2000 VL 42 IS 11 BP 768 EP 774 DI 10.1017/S0012162200001420 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 376PL UT WOS:000165465900010 PM 11104350 ER PT J AU O'Neill, DK Happe, FGE AF O'Neill, Daniela K. Happe, Francesca G. E. TI Noticing and commenting on what's new: differences and similarities among 22-month-old typically developing children, children with Down syndrome and children with autism SO DEVELOPMENTAL SCIENCE LA English DT Article AB Twenty 22-month-old typically developing children (TD), 11 children with Down syndrome (DS) and 10 children with autism (A), all functioning at a one- or two-word linguistic level, were given eight series of four toys to explore. In each series, the first three toys (i.e. Trials 1-3) were identical, but the fourth toy (i.e. Trial 4) differed on a property or in identity. The children sat beside their mother and the experimenter while exploring the toys. Of interest was whether (1) the TD children would show more exploratory and communicative behavior related to the toys on Trials I and 4 than 2 and 3, and (2) how the response patterns of nontypically developing children would compare. The DS group showed a pattern of responding similar to that of the TD group with respect to their attention and interest in the toys, although a much lower rate of communicating with their mother. In contrast, the A group differed significantly from both other groups with respect to both the toys they found of interest and the timing of their topic initiations. Implications for observing declarative communication among children with Down syndrome and children with autism are discussed. C1 [O'Neill, Daniela K.] Univ Waterloo, Dept Psychol, Waterloo, ON N2L 3G1, Canada. RP O'Neill, DK (reprint author), Univ Waterloo, Dept Psychol, Waterloo, ON N2L 3G1, Canada. 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Psychiatr. Clin. Biol. Ther. PD NOV PY 2000 VL 27 SI 3 BP 22 EP 29 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 401YW UT WOS:000166957800006 ER PT J AU Bowler, DM Gardiner, JM Grice, S Saavalainen, P AF Bowler, DM Gardiner, JM Grice, S Saavalainen, P TI Memory illusions: False recall and recognition in adults with Asperger's syndrome SO JOURNAL OF ABNORMAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT 6th Annual Meeting of the Cognitive-Neuroscience-Society CY APR, 1999 CL WASHINGTON, D.C. SP Cognit Neurosci Soc ID REMEMBERING WORDS; AUTISM; YOUNGER; LISTS; OLDER AB As persons on the autistic spectrum are known not to use semantic features of word Lists to aid recall. they might show diminished susceptibility to illusory memories that typically occur with lists of associated items. Alternatively, since such individuals also have poor source monitoring, they might show greater susceptibility. The authors found that adults with Asperger's syndrome (n = 10) recalled similar proportions of a nonpresented strong associate of the study list items, compared with controls (n = 15). In Experiment 2, rates of true and false recognition of study list associates did not differ significantly between Asperger (n = 10) and control (n = 10) participants. Moreover, the Asperger participants made fewer remember and more know judgments than controls for veridical but not for false recognitions. Thus, deficits found in some aspects of memory in people with Asperger's syndrome do not affect their susceptibility to memory illusions. C1 City Univ London, Dept Psychol, London EC1V 0HB, England. Inst Child Hlth, Neurocognit Dev Unit, London, England. Univ Joensuu, Dept Psychol, FIN-80101 Joensuu, Finland. RP Bowler, DM (reprint author), City Univ London, Dept Psychol, Northampton Sq, London EC1V 0HB, England. 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Abnorm. Psychol. PD NOV PY 2000 VL 109 IS 4 BP 663 EP 672 DI 10.1037//0021-843X.109.4.663 PG 10 WC Psychology, Clinical; Psychology, Multidisciplinary SC Psychology GA 390QA UT WOS:000166306800011 PM 11195990 ER PT J AU Burd, L Stenehjem, A Franceschini, LA Kerbeshian, J AF Burd, L Stenehjem, A Franceschini, LA Kerbeshian, J TI A 15-year follow-up of a boy with pyridoxine (vitamin B-6)-dependent seizures with autism, breath holding, and severe mental retardation SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID DEPENDENT SEIZURES; VITAMIN-B6; MAGNESIUM; CHILDREN; EPILEPSY AB Pyridoxine (vitamin B-6 (2q31) dependency is a rare autosomal-recessive disorder that causes a severe seizure disorder of prenatal or neonatal onset. The abnormality appears to inhibit the binding of vitamin B-6 to the enzyme glutamic acid decarboxylase-1, which is needed for the biosynthesis of gamma -aminobutyric acid (GABA). Most patients with pyridoxine-dependent seizures require lifelong treatment with pyridoxine. The full range of associated symptomatology is unknown since fewer than 100 cases have been reported. A majority of cases are mentally retarded. We report a 15-year-old boy with pyridoxine-dependent seizures, nonpyridoxine-dependent seizures, severe mental retardation, autistic disorder, aerophagia, breath holding, and self-injury. This complex outcome should alert clinicians to the wide range of neuropsychiatric outcomes associated with this disorder. C1 Univ N Dakota, Sch Med & Hlth Sci, Dept Pediat, Grand Forks, ND 58201 USA. Univ N Dakota, Sch Med & Hlth Sci, Dept Neurosci, Grand Forks, ND 58201 USA. RP Burd, L (reprint author), Child Evaluat & Treatment Program, 1300 S Columbia Rd, Grand Forks, ND 58202 USA. 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PD NOV PY 2000 VL 15 IS 11 BP 763 EP 765 DI 10.1177/088307380001501111 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 473DP UT WOS:000171025000011 PM 11108513 ER PT J AU Mottron, L Peretz, I Menard, E AF Mottron, L Peretz, I Menard, E TI Local and global processing of music in high-functioning persons with autism: Beyond central coherence? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; cognition; development; idiot savants; memory; music; neuropsychology; perception ID BRAIN-DAMAGED PATIENTS; EXECUTIVE FUNCTION; NEURAL MECHANISMS; CHILDREN; INDIVIDUALS; MEMORY; MIND; TASK; ABILITIES; MELODIES AB A multi-modal abnormality in the integration of parts and whole has been proposed to account for a bias toward local stimuli in individuals with autism (Frith, 1989; Mottron & Belleville, 1993). In the current experiment, we examined the utility of hierarchical models in characterising musical information processing in autistic individuals. Participants were 13 high-functioning individuals with autism and 13 individuals of normal intelligence matched on chronological age, nonverbal IQ, and laterality, and without musical experience. The task consisted of same-different judgements of pairs of melodies. Differential local and global processing was assessed by manipulating the level, local or global, at which modifications occurred. No deficit was found in the two measures of global processing. In contrast, the clinical group performed better than the comparison group in the detection of change in nontransposed, contour-preserved melodies that tap local processing. These findings confirm the existence of a "local bias" in music perception in individuals with autism, but challenge the notion that it is accounted for by a deficit in global music processing. The present study suggests that enhanced processing of elementary physical properties of incoming stimuli, as found previously in the visual modality, may also exist in the auditory modality. C1 Hop Riviere des Prairies, Clin Specialisee Autisme, Montreal, PQ, Canada. Univ Montreal, Montreal, PQ H3C 3J7, Canada. RP Mottron, L (reprint author), Hop Riviere des Prairies, Clin Specialisee Autisme, 7070 Blvd Perras, Montreal, PQ, Canada. 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Child Psychol. Psychiatry Allied Discip. PD NOV PY 2000 VL 41 IS 8 BP 1057 EP 1065 DI 10.1017/S0021963099006253 PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 374GU UT WOS:000165338100011 PM 11099122 ER PT J AU Volkmar, F AF Volkmar, F TI Teaching children with autism to mind read: A practical guide. SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Book Review CR Howlin P., 1999, TEACHING CHILDREN AU NR 1 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD NOV PY 2000 VL 41 IS 8 BP 1082 EP 1082 PG 1 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 374GU UT WOS:000165338100026 ER PT J AU Bugge, M Bruun-Petersen, G Brondum-Nielsen, K Friedrich, U Hansen, J Jensen, G Jensen, PKA Kristofferson, U Lundsteen, C Niebuhr, E Rasmussen, KR Rasmussen, K Tommerup, N AF Bugge, M Bruun-Petersen, G Brondum-Nielsen, K Friedrich, U Hansen, J Jensen, G Jensen, PKA Kristofferson, U Lundsteen, C Niebuhr, E Rasmussen, KR Rasmussen, K Tommerup, N TI Disease associated balanced chromosome rearrangements: a resource for large scale genotype-phenotype delineation in man SO JOURNAL OF MEDICAL GENETICS LA English DT Article DE translocations; inversions; abnormal phenotypes; frequency ID PRADER-WILLI-SYNDROME; LINKED MENTAL-RETARDATION; NAIL-PATELLA SYNDROME; PRENATAL-DIAGNOSIS; CANDIDATE GENE; TRANSLOCATION; CHILDREN; SNRPN; BREAKPOINTS; DELETIONS AB Disease associated balanced chromosomal rearrangements (DBCRs), which truncate, delete, or otherwise inactivate specific genes, have been instrumental for positional cloning of many disease genes. A network of cytogenetic laboratories, Mendelian Cytogenetics Network (MCN), has been established to facilitate the identification and mapping of DBCRs. To get an estimate of the potential of this approach, we surveyed all cytogenetic archives in Denmark and southern Sweden, with a population of similar to6.6 million. The nine laboratories have performed 71 739 postnatal cytogenetic tests. Excluding Robertsonian translocations and chromosome 9 inversions, we identified 216 DBCRs (similar to0.3%),including a minimum estimate of 114 de novo reciprocal translocations (0.16%) and eight de novo inversions (0.01%). Altogether, this is six times more frequent than in the general population, suggesting a causal relationship with the traits involved in most of these cases. Of the identified cases, only 25 (12%) have been published, including 12 cases with known syndromes and 13 cases with unspecified mental retardation/congenital malformations. The remaining DBCRs were associated with a plethora of traits including mental retardation, dysmorphic features, major congenital malformations, autism, and male and female infertility. Several of the unpublished DBCRs defined candidate breakpoints for nail-patella, Prader-Willi, and Schmidt syndromes, ataxia, and ulna aplasia. The implication of the survey is apparent when compared with MCN; altogether, the 292 participating laboratories have performed >2.5 million postnatal analyses, with an estimated similar to 7500 DBCRs stored in their archives, of which more than half might be causative mutations. In addition, an estimated 450-500 novel cases should be detected each year. Our data illustrate that DBCRs and MCN are resources for large scale establishment of phenotype-genotype relationships in man. C1 Univ Copenhagen, IMBG, Dept Med Genet, DK-2200 Copenhagen, Denmark. Vejle Hosp, Dept Clin Genet, Vejle, Denmark. John F Kennedy Inst, DK-2600 Glostrup, Denmark. Univ Aarhus, Inst Human Genet, DK-8000 Aarhus, Denmark. Univ Hosp, Dept Clin Genet, Cytogenet Registry, Aarhus, Denmark. Frederiksberg Hosp, Inst Pathol, Chromosome Lab, Frederiksberg, Denmark. Univ Hosp, Dept Clin Genet, Lund, Sweden. Rigshosp, Dept Clin Genet, DK-2100 Copenhagen, Denmark. Odense Univ Hosp, Dept Clin Genet, Odense, Denmark. RP Tommerup, N (reprint author), Univ Copenhagen, IMBG, Dept Med Genet, Blegdamsvej 3, DK-2200 Copenhagen, Denmark. 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PD NOV PY 2000 VL 37 IS 11 BP 858 EP 865 DI 10.1136/jmg.37.11.858 PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 374LD UT WOS:000165345900007 PM 11073540 ER PT J AU Blum, K Braverman, ER Holder, JM Lubar, JF Monastra, VJ Miller, D Lubar, JO Chen, TJH Comings, DE AF Blum, K Braverman, ER Holder, JM Lubar, JF Monastra, VJ Miller, D Lubar, JO Chen, TJH Comings, DE TI Reward deficiency syndrome: A biogenetic model for the diagnosis and treatment of impulsive, addictive, and compulsive behaviors SO JOURNAL OF PSYCHOACTIVE DRUGS LA English DT Review DE dopamine D; gene; genetics; impulsive; addictive and compulsive behaviors; neurotransmitters; reward deficiency syndrome ID DOPAMINE-RECEPTOR GENE; GAMMA-VINYL GABA; POSITRON EMISSION TOMOGRAPHY; EVENT-RELATED POTENTIALS; SUBSTANCE USE DISORDER; ALCOHOL-PREFERRING AA; SCANDINAVIAN CHRONIC-ALCOHOLICS; INDUCED MORPHINE WITHDRAWAL; TYROSINE-HYDROXYLASE GENE; BRAIN ELECTRICAL-ACTIVITY AB The dopaminergic system, and in particular the dopamine D-2 receptor, has been implicated in reward mechanisms. The net effect of neurotransmitter interaction at the mesolimbic brain region induces "reward" when dopamine (DA) is released from the neuron at the nucleus accumbens and interacts with a dopamine D-2 receptor. "The reward cascade" involves the release of serotonin, which in turn at the hypothalmus stimulates enkephalin, which in turn inhibits GABA at the substania nigra, which in turn fine tunes the amount of DA released at the nucleus accumbens or "reward site." It is well known that under normal conditions in the reward site DA works to maintain our normal drives. In fact, DA has become to be known as the "pleasure molecule" and/or the "antistress molecule." When DA is released into the synapse, it stimulates a number a DA receptors (D1-D5) which results in increased feelings of well-being and stress reduction. A consensus of the literature suggests that when there is a dysfunction in the brain reward cascade, which could be caused by certain genetic variants (polygenic), especially in the DA system causing a hypodopaminergic trait, the brain of that person requires a DA fix to feel good. This trait leads to multiple drug-seeking behavior. This is so because alcohol, cocaine, heroin, marijuana, nicotine, and glucose all cause activation and neuronal release of brain DA, which could heal the abnormal cravings. Certainly after ten years of study we could say with confidence that carriers of the DAD2 receptor A1 allele have compromised D-2 receptors. Therefore lack of D2 receptors causes individuals to have a high risk for multiple addictive, impulsive and compulsive behavioral propensities, such as severe alcoholism, cocaine, heroin, marijuana and nicotine use, glucose bingeing, pathological gambling, sex addiction, ADHD, Tourette's Syndrome, autism, chronic violence, posttraumatic stress disorder, schizoid/avoidant cluster, conduct disorder and antisocial behavior. In order to explain the breakdown of the reward cascade due to both multiple genes and environmental stimuli (pleiotropism) and resultant aberrant behaviors, Blum united this hypodopaminergic trait under the rubric of a reward deficiency syndrome. C1 Univ N Texas, Dept Sci Biol, Denton, TX 76203 USA. PharmcoGenomics, San Antonio, TX USA. PATH Med Fdn, New York, NY USA. Amer Coll Addictionol & Compuls Disorders, Miami Beach, FL USA. New York Sch Med, Dept Psychiat, New York, NY USA. Graceland Univ, Dept Addict Studies, Independence, MO USA. 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Results indicated that the group with autism demonstrated significant impairments in procedural learning compared with the group of controls. No significant difference in judgment of explicit time intervals was found. The data suggest that deficits in procedural learning may contribute to the cognitive and behavioral phenotype of autism; these deficits may be secondary to abnormalities in cerebellar-frontal circuitry. C1 Kennedy Krieger Inst, Dept Dev Cognit Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA. RP Mostofsky, SH (reprint author), Kennedy Krieger Inst, Dept Dev Cognit Neurol, 707 N Broadway, Baltimore, MD 21205 USA. 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In the autistic group, the regional cerebral blood flow was significantly higher in the right temporal and right parietal lobes than that in the left ones. Inversely, the regional cerebral blood flow in the frontal and occipital lobes was significantly higher on the left side than on the right side. In the nonautistic group, except for in the dorso-medio-lateral frontal lobes (left > right), there was no difference in the regional cerebral blood flow in either cerebrum or cerebellum. A positive correlationship between regional cerebral flow and development quotient (intelligence quotient) was observed in the left laterotemporal and both dorso-medio-lateral frontal areas, and a negative one was observed in the cerebellar vermis area. These results suggest that the regional cerebral blood flow decrease in the temporal and frontal areas relates to not only the brain mechanism of autism reported previously but also intelligence levels. (C) 2000 by Elsevier Science Inc. All rights reserved. C1 Naruto Univ Educ, Dept Educ Handicapped Children, Naruto, Tokushima, Japan. NCNP, Natl Ctr Nervous Mental & Muscular Disorder, Natl Ctr Hosp, Dept Child Neurol, Kodaira, Tokyo, Japan. NCNP, Natl Ctr Nervous Mental & Muscular Disorder, Natl Ctr Hosp, Dept Roentgenol, Kodaira, Tokyo, Japan. RP Hashimoto, T (reprint author), Naruto Univ Educ, Dept Educ Handicapped Children, 748 Nakashima, Naruto, Tokushima, Japan. 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Inq. PD NOV-DEC PY 2000 VL 20 IS 5 BP 637 EP 647 DI 10.1080/07351692009348913 PG 11 WC Psychology, Psychoanalysis SC Psychology GA 386ZX UT WOS:000166096600002 ER PT J AU Shapiro, T AF Shapiro, T TI Autism and the psychoanalyst SO PSYCHOANALYTIC INQUIRY LA English DT Article ID CHILDREN; EMOTION C1 Cornell Univ, Weill Med Coll, Ithaca, NY 14853 USA. New York Psychoanalyt Inst, New York, NY USA. RP Shapiro, T (reprint author), Cornell Univ, Weill Med Coll, Ithaca, NY 14853 USA. 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Inq. PD NOV-DEC PY 2000 VL 20 IS 5 BP 648 EP 659 DI 10.1080/07351692009348914 PG 12 WC Psychology, Psychoanalysis SC Psychology GA 386ZX UT WOS:000166096600003 ER PT J AU Volkmar, FR AF Volkmar, FR TI Understanding autism: Implications for psychoanalysis SO PSYCHOANALYTIC INQUIRY LA English DT Article ID INFANTILE-AUTISM; SELF-RECOGNITION; CHILDREN AB Several lines of evidence inform current psychoanalytic thinking about infantile autism. Although early psychoanalytic interest in autism centered around the notion that experience might play a role in pathogenesis a large body of data suggest this is not the case; rather the condition appears to be the result of genetic and other neurobiological factors. Studies of children with autism do, however, suggest basic problems in capacities for object relations and other aspects of ego development which must be understood in the context of autistic social dysfunction. The study of normally developing infants raises considerable questions about the validity of notions such as a normal autistic phase; rather than for the normally developing child interest in the social world appears to be an innate capacity and one which has considerable importance for our understanding of the nature of early ego development and capacities for self-object differentiation. C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Volkmar, FR (reprint author), Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. CR American Psychiatric Association, 1980, DIAGN STAT MAN, V3rd BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BENDER L, 1947, AM J ORTHOPSYCHIAT, V17, P40 Bettelheim B., 1967, EMPTY FORTRESS BRODY S, 1982, PSYCHOANAL QUART, V51, P526 BROTHERS L, 1989, AM J PSYCHIAT, V146, P10 Bruner J. S., 1974, INTEGRATION CHILD SO, P167 Cairns R. 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PD NOV-DEC PY 2000 VL 20 IS 5 BP 660 EP 674 DI 10.1080/07351692009348915 PG 15 WC Psychology, Psychoanalysis SC Psychology GA 386ZX UT WOS:000166096600004 ER PT J AU Murphy, M Bolton, PF Pickles, A Fombonne, E Piven, J Rutter, M AF Murphy, M Bolton, PF Pickles, A Fombonne, E Piven, J Rutter, M TI Personality traits of the relatives of autistic probands SO PSYCHOLOGICAL MEDICINE LA English DT Article ID FAMILY HISTORY; PSYCHIATRIC-DISORDERS; PARENTS; RELIABILITY; INDIVIDUALS; STRESS; PATTERNS; CHILDREN; SCHEDULE; BEHAVIOR AB Background. There is substantial evidence that the genetic liability to autism confers a risk for a range of more subtle social and communication impairments, as well as stereotyped and repetitive behaviours. Recent research suggests that increased expression of particular personality traits may be a manifestation of the liability to autism. Methods. To investigate this we examined the personality traits of the adult relatives of 99 autistic and 36 Down's syndrome probands, using the informant version of the Modified Personality Assessment Schedule. Results. There was significantly increased expression of the traits anxious, impulsive, aloof, shy, over-sensitive, irritable and eccentric among the autism relatives with evidence of different profiles for male and female relatives and for parents and adult children. Factor analysis revealed three broad groups of traits, two of which ('withdrawn' and 'difficult') appeared to reflect impairments in social functioning and a third group of anxiety related traits ('tense'). Each of these factors differed in their pattern of associations with the factor we termed 'withdrawn' showing a similar pattern of association to that found for other autism related conditions. The 'tense' factor appeared in part to be related to the burden of caring for an autistic child. Conclusions. 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SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN 37232 USA. New England Med Ctr, Boston, MA 02111 USA. Univ Iowa, Iowa City, IA USA. Univ N Carolina, Chapel Hill, NC USA. NR 0 TC 2 Z9 2 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 178 BP 46 EP 46 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700181 ER PT J AU Wang, CH Miller, MB Ichikawa, S Hillman, R Miles, JH AF Wang, CH Miller, MB Ichikawa, S Hillman, R Miles, JH TI Identification of a novel transcript in linkage disequilibrium with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Missouri, Dept Neurol, Columbia, MO USA. Univ Missouri, Dept Biochem, Columbia, MO USA. Univ Missouri, Dept Child Hlth, Columbia, MO 65201 USA. Univ Missouri, Dept Psychol, Columbia, MO USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 179 BP 46 EP 46 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700179 ER PT J AU Buxbaum, JD Silveman, D Smith, CJ Kilifarski, MA Reichert, JG Lawlor, BA Fizgerald, M Greenberg, DA Davis, KL AF Buxbaum, JD Silveman, D Smith, CJ Kilifarski, MA Reichert, JG Lawlor, BA Fizgerald, M Greenberg, DA Davis, KL TI A genome-wide linkage study in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 199 BP 49 EP 49 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700198 ER PT J AU Santangelo, SL Buxbaum, J Silverman, J Pericak-Vance, M Ashley-Koch, A AF Santangelo, SL Buxbaum, J Silverman, J Pericak-Vance, M Ashley-Koch, A CA Collaborat Linkage Study Autism TI Confirmatory evidence of linkage for autism to 7q based on combined analysis of three independent data sets. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Tufts Univ, Sch Med, Boston, MA 02111 USA. Univ Iowa, CLSA, Iowa City, IA 52242 USA. Univ N Carolina, CLSA, Chapel Hill, NC 27515 USA. Vanderbilt Univ, CLSA, Nashville, TN 37240 USA. Tufts Univ, CLSA, Medford, MA 02155 USA. Harvard Univ, Sch Publ Hlth, Boston, MA 02115 USA. Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. Duke Univ, Durham, NC 27706 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 200 BP 49 EP 49 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700201 ER PT J AU Browne, CE Dennis, NR Bolton, P Thomas, NS Jacobs, PA AF Browne, CE Dennis, NR Bolton, P Thomas, NS Jacobs, PA TI Duplications of the Prader-Willi/Angelman critical region: An association with autism? SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Salisbury District Hosp, Wessex Reg Genet Lab, Salisbury, Wilts, England. Princess Anne Hosp, Wessex Clin Genet Serv, Southampton, Hants, England. Sect Dev Psychiat, Cambridge, England. RI Bolton, Patrick/E-8501-2010 OI Bolton, Patrick/0000-0002-5270-6262 NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 261 BP 61 EP 61 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700262 ER PT J AU Nurmi, EL Han, MK Kesterson, RA Sutcliffe, JS AF Nurmi, EL Han, MK Kesterson, RA Sutcliffe, JS TI Partial duplications of the APBA2Gene in a chromosome 15q autism region corresponds with 15q duplicon structures. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN 37232 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 262 BP 61 EP 61 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700264 ER PT J AU Mehta, L Yenamandra, A Perrone, R Koduru, P AF Mehta, L Yenamandra, A Perrone, R Koduru, P TI De novo chromosomal insertion in a child with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 N Shore Univ Hosp, Div Med Genet, Manhasset, NY USA. N Shore Univ Hosp, Dept Labs, Manhasset, NY USA. NYU, Sch Med, Manhasset, NY USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 554 BP 111 EP 111 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700556 ER PT J AU Miles, JH Takahashi, N Mudrick, JD AF Miles, JH Takahashi, N Mudrick, JD TI Repetitive behaviors differentiate autism subgroups. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Missouri, Columbia, MO USA. NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 588 BP 117 EP 117 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700591 ER PT J AU Telvi, L Ion, A Sevin, C Lallou, R Roger, M Patton, MA Chaussain, JL AF Telvi, L Ion, A Sevin, C Lallou, R Roger, M Patton, MA Chaussain, JL TI Abnormal sex development and autism in a 46,XX female with 9p24.1-pter chromosomal rearrangement. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Hop St Vincent de Paul, F-75674 Paris, France. St George Hosp, Sch Med, London, England. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 796 BP 152 EP 152 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700795 ER PT J AU Borg, I Stout, K Sargan, DR Morgan, D Willatt, L Kalscheuer, V Tommerup, N Ropers, HH Ferguson-Smith, MA AF Borg, I Stout, K Sargan, DR Morgan, D Willatt, L Kalscheuer, V Tommerup, N Ropers, HH Ferguson-Smith, MA TI Breakpoint mapping of an apparently balanced 2;8 translocation reveals a cryptic deletion on 2q in a child with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Cambridge, Dept Clin Vet Med, Cambridge CB3 0ES, England. Addenbrookes NHS Trust, Dept Med Genet, Cambridge, England. Max Planck Inst Mol Genet, Berlin, Germany. Addenbrookes NHS Trust, Cytogenetics Lab, Cambridge CB2 2QQ, England. IMBG, Dept Med Genet, Copenhagen, Denmark. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 836 BP 159 EP 159 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700836 ER PT J AU Wolff, DJ Clifton, K Charles, J AF Wolff, DJ Clifton, K Charles, J TI Assessment of subtelomeric regions of children with autism: Detection of a 2q deletion. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Med Univ S Carolina, Dept Pathol & Lab Med, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Med Lab Sci, Charleston, SC 29425 USA. Med Univ S Carolina, Dept Pediat, Charleston, SC 29425 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 857 BP 162 EP 162 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700858 ER PT J AU Kesterson, RA Nurmi, EL Johnson, DK Sutcliffe, JS AF Kesterson, RA Nurmi, EL Johnson, DK Sutcliffe, JS TI An in situ hybridization-based strategy to detect neuronal patterns of genomic imprinting in the autism candidate region of chromosome 15q11-q13. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. Oak Ridge Natl Lab, Mammalian Genet & Dev Sect, Oak Ridge, TN USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 873 BP 165 EP 165 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700875 ER PT J AU Asano, E Kuivaniemi, H Huq, M Tromp, G Behen, M Rothermel, R Herron, J Chugani, DC AF Asano, E Kuivaniemi, H Huq, M Tromp, G Behen, M Rothermel, R Herron, J Chugani, DC TI Novel polymorphisms in the upstream region of VIPR2 gene suggest a possible role in gastrointestinal problems and stereotypical behaviors in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Wayne State Univ, Childrens Hosp Michigan, Detroit, MI USA. Wayne State Univ, Ctr Mol Med & Genet, Detroit, MI USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 889 BP 169 EP 169 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700890 ER PT J AU Han, MK Chen, YH Nurmi, EL Sutcliffe, JS AF Han, MK Chen, YH Nurmi, EL Sutcliffe, JS TI Gene structure, expression and organization at the GABRG3 locus in the human 15q11-q13 autism candidate region. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN 37232 USA. NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 996 BP 187 EP 187 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400700998 ER PT J AU Zwaigenbaum, L Szatmari, P Goldberg, J Bryson, S Mahoney, W Bartolucci, G AF Zwaigenbaum, L Szatmari, P Goldberg, J Bryson, S Mahoney, W Bartolucci, G TI The broader autism phenotype: Defining genetically informative dimensions. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 McMaster Univ, Hamilton, ON L8S 4L8, Canada. NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 1149 BP 213 EP 213 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400701148 ER PT J AU Vicente, AM Coutinho, A Mota-Vieira, L Marques, C Oliveira, G AF Vicente, AM Coutinho, A Mota-Vieira, L Marques, C Oliveira, G TI Genetic variation of serotonin system genes in a sample of autism families from Portugal. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Inst Gulbenkian Ciencia, Oeiras, Portugal. Hosp Pediat Coimbra, Coimbra, Portugal. Hosp Divino Espirito Santo, Ponta Delgada, Azores, Portugal. RI Mota-Vieira, Luisa/I-5909-2013 OI Mota-Vieira, Luisa/0000-0003-1451-6705 NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 1671 BP 303 EP 303 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400701674 ER PT J AU Smith, M Wu, C Escamilla, J Filipek, PA Bocian, ME Spence, MA AF Smith, M Wu, C Escamilla, J Filipek, PA Bocian, ME Spence, MA TI Identification of functionally homologous genes in two regions on chromosome 15 associated with cytogenetic abnormalities in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 1904 BP 342 EP 342 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400701904 ER PT J AU Folstein, SE AF Folstein, SE CA CLSA TI Autism LOD on chromosome 7q was increased subsetting the sample on language acquisition. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 New England Med Ctr, Dept Psychiat, Boston, MA USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. Vanderbilt Univ, Dept Genet, Nashville, TN USA. Univ Iowa, Dept Human Genet, Iowa City, IA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 1944 BP 349 EP 349 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400701945 ER PT J AU Crawford, LR Bailey, J Merriman, BL Kustanovich, I Smalley, S Nelson, S AF Crawford, LR Bailey, J Merriman, BL Kustanovich, I Smalley, S Nelson, S TI The characterization and genotyping of single nucleotide polymorphisms in coding regions of brain-expressed Autism candidate genes. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 1956 BP 351 EP 351 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400701957 ER PT J AU Holden, JJA Schutz, CK Robinson, PD Polley, D Macciardi, F White, BN AF Holden, JJA Schutz, CK Robinson, PD Polley, D Macciardi, F White, BN TI A model for the genetic etiology of autism spectrum disorders involving alleles at maternal and fetal susceptibility loci. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Queens Univ & Ongwanada, Kingston, ON, Canada. McMaster Univ, Hamilton, ON L8S 4L8, Canada. Ctr Addict & Mental Hlth, Toronto, ON, Canada. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 2000 BP 358 EP 358 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400702000 ER PT J AU Szatmari, P Jones, MB Zwaigenbaum, L Palmour, RM Mejia, J AF Szatmari, P Jones, MB Zwaigenbaum, L Palmour, RM Mejia, J TI Testing for maternal and fetal effects in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 McMaster Univ, Dept Psychiat, Hamilton, ON L8S 4L8, Canada. Penn State Univ, Milton S Hershey Med Ctr, Coll Med, Hershey, PA 17033 USA. McGill Univ, Dept Psychiat, Montreal, PQ H3A 2T5, Canada. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 2001 BP 358 EP 358 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400702003 ER PT J AU Zhang, H Zhang, C Robitaille, S Grayson, DR Guidotti, AR Macciardi, F Leggo, J Holden, JJA AF Zhang, H Zhang, C Robitaille, S Grayson, DR Guidotti, AR Macciardi, F Leggo, J Holden, JJA TI The Rein gene as a candidate locus for autism spectrum disorders. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Queens Univ & Ongwanada, Kingston, ON, Canada. Univ Illinois, Chicago, IL USA. Ctr Addict & Mental Hlth, Toronto, ON, Canada. NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 2007 BP 359 EP 359 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400702009 ER PT J AU Abuya, P Ashley-Koch, A Wolpert, CM Menold, MM Matsumoto, N Basu, S Greenblatt, DM Powell, CM Cuccaro, ML Ledbetter, DH Green, ED Vance, JM Pericak-Vance, MA Gilbert, JR AF Abuya, P Ashley-Koch, A Wolpert, CM Menold, MM Matsumoto, N Basu, S Greenblatt, DM Powell, CM Cuccaro, ML Ledbetter, DH Green, ED Vance, JM Pericak-Vance, MA Gilbert, JR TI Isolation and analysis of Autism candidate genes on 7q. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ N Carolina, Dept Pediat, Chapel Hill, NC USA. Univ S Carolina, W S Hall Psychiat Inst, Columbia, SC 29208 USA. NIH, NHGRI, Bethesda, MD USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 2025 BP 362 EP 362 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400702027 ER PT J AU Wassink, TH Piven, J Sheffield, VC AF Wassink, TH Piven, J Sheffield, VC TI Screening of autism candidate disease genes. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract C1 Univ Iowa, Coll Med, Dept Psychiat, Iowa City, IA 52242 USA. Univ N Carolina, Coll Med, TEACCH, Chapel Hill, NC USA. Univ Iowa, Coll Med, Dept Pediat, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Howard Hughes Med Inst, Iowa City, IA 52242 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 5720 SOUTH WOODLAWN AVE, CHICAGO, IL 60637-1603 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD OCT PY 2000 VL 67 IS 4 SU 2 MA 2027 BP 362 EP 362 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 355TA UT WOS:000089400702028 ER PT J AU Desbordes, EB Le Roy, F AF Desbordes, EB Le Roy, F TI Psychological assessment of autistic child SO ANNALES MEDICO-PSYCHOLOGIQUES LA French DT Article DE autism; psychological assessment; adaptive scales; line of development; heterogeneity AB The question of knowing whether there are any really untestable autistic children is attempting the impossible. Because of their pathology, these children do not follow the usual required norms, the established IQ's and in fact, do not match the finality of the tools at the clinician's disposal. Moreover, the global nature of the scales sometimes hides the autistic child's specificity, the heterogeneity of his profile and his abilities, which is subsequently not conducive to therapeutic or educational care. For us, psychological assessment must be adaptive to each child, repeated and constantly evolving and each interpretation must be finely tuned and above all, complementary to other methods. In the face of clinical practice, research and care, it is up to each clinician to choose the most relevant and adapted instruments or scales according to the child in front of him in order to achieve the set objectives. C1 Univ Rennes 2, Hop Bohars Brest, Sect Psychiat Infantojuvenile, F-35043 Rennes, France. Hop Bohars, Sect Psychiat Infantojuvenile, F-29820 Bohars, France. Univ Bretagne Occidentale, F-29269 Brest, France. RP Le Roy, F (reprint author), 4 Rue Languedoc, F-29200 Brest, France. CR ADRIEN JL, 1996, AUTISME JEUNE ENFANT, P38 ADRIEN JL, 1988, NEUROPSYCHIAT ENFAN, V36, P9 Bruner J. S, 1996, DEV ENFANT SAVOIR FA FISCHER KW, 1980, PSYCHOL REV, V87, P477, DOI 10.1037//0033-295X.87.6.477 Gesell AL, 1934, ATLAS INFANT BEHAV GUIDETTI M, 1982, REV EUROPEENNE PSYCH, V42, P185 JOSSE D, 1997, MANUEL BLR C, P167 LURIA AR, FONCTIONS CORTICALES, P978 MISES R, 1994, RETARDS TROUBLES INT, P191 Nadel J., 1998, ENFANCE, V1, P111 PEETERS T, 1996, AUTISME COMPREHENSIO PRY R, 1996, CAHIERS CERFEE, V13 SANDBERG AD, 1993, BRIT J PSYCHOL, V84, P365 WECHSLER D, 1956, MESURE INTELLIGENCE, P13 NR 14 TC 0 Z9 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0003-4487 J9 ANN MED-PSYCHOL JI Ann. Med.-Psychol. PD OCT PY 2000 VL 158 IS 8 BP 605 EP 619 PG 15 WC Pharmacology & Pharmacy; Psychiatry; Psychology; Psychology, Multidisciplinary SC Pharmacology & Pharmacy; Psychiatry; Psychology GA 374LY UT WOS:000165347700001 ER PT J AU Schreck, KA AF Schreck, KA TI It can be done: An example of a behavioral Individualized Education Program (IEP) for a child with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article AB With state agencies and scientists recommending Early Intensive Behavioral Intervention (EIBI) for children with autism, the demand for qualified behavior consultants exceeds the supply. Consequently, children with autism are either receiving alternative, ineffective, and unsubstantiated treatments or are receiving EIBI programming from unqualified personnel. Additionally, when school districts are approached to provide services, the resulting Individualized Education Programs (IEPs) are typically not behavioral and lack the detailed and specific objectives required for children with autism. This article was written to provide parents and educators with an objective and quantifiable IEP, which has been used! as a guideline for treatment for a 4-year;old boy with autism. Copyright (C) 2000 John Wiley & Sons, Ltd. C1 Penn State Univ Harrisburg, Harrisburg Psychol Program, Middletown, PA 17057 USA. RP Schreck, KA (reprint author), Penn State Univ Harrisburg, Harrisburg Psychol Program, 777 W Harrisburg Pike, Middletown, PA 17057 USA. CR BRUNININKS RH, 1996, SCALES INDEPENDENT B *CENTR OH FAM EARL, 1998, PAR PACK GUID FAM FA DUNN LM, 1997, PEAB PICT VOC TEST GARDNER MF, 1990, EXPRESSIVE ONE WORD Jacobson J, 1998, BEHAV INTERVENT, V13, P201, DOI DOI 10.1002/(SICI)1099-078X MULLEN EM, 1995, MANUAL SCALES EARLY *NEW YORK STAT DEP, 1999, CLIN PRACT GUID TECH Shook G. L., 1996, BEHAV INTERVENTION Y, P221 NR 8 TC 5 Z9 5 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD OCT-DEC PY 2000 VL 15 IS 4 BP 279 EP 300 DI 10.1002/1099-078X(200010/12)15:4<279::AID-BIN68>3.0.CO;2-B PG 22 WC Psychology, Clinical SC Psychology GA 379HN UT WOS:000165636700001 ER PT J AU Schreck, KA AF Schreck, KA TI When everybody cares: Case studies of ABA with people with autism SO BEHAVIORAL INTERVENTIONS LA English DT Book Review ID BEHAVIORAL TREATMENT; CHILDREN C1 Penn State Univ Harrisburg, Middletown, PA 17057 USA. RP Schreck, KA (reprint author), Penn State Univ Harrisburg, 777 W Harrisburg Pike, Middletown, PA 17057 USA. CR Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 Foxx RM, 1996, BEHAV ANALYST, V19, P147 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 NEWMAN AB, 1999, EVERYBODY CARES CASE *NY STAT DEP HLTH, 1999, CLIN PRACT GUID AUT PERRY R, 1995, J AM ACAD CHILD ADOL, V87, P751 NR 7 TC 0 Z9 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD OCT-DEC PY 2000 VL 15 IS 4 BP 359 EP 360 DI 10.1002/1099-078X(200010/12)15:4<359::AID-BIN62>3.0.CO;2-Y PG 2 WC Psychology, Clinical SC Psychology GA 379HN UT WOS:000165636700007 ER PT J AU Szatmari, P AF Szatmari, P TI The classification of autism, Asperger's syndrome, and pervasive developmental disorder SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Review DE autism; Asperger's syndrome; pervasive developmental disorder; DSM classification ID ADAPTIVE-BEHAVIOR SCALES; SPECTRUM DISORDERS; CHILDREN; CHILDHOOD; INDIVIDUALS; CRITERIA AB Objective: The current classification of the pervasive developmental disorders (PDDs) as conceptualized in both the DSM-IV and ICD-10 is deeply unsatisfying to many parents, front-line clinicians, and academic researchers. Is the diagnostic validity of the various disorders simply lacking empirical data for full substantiation, or does the overall conceptualization of the category have more fundamental problems, not reflecting the "true" nature of the phenomena? This paper argues the latter hypothesis. I review the historical development of the classification of PDD, summarize recent empirical data on issues of reliability and validity, and suggest a new approach to classification and understanding. C1 McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. RP Szatmari, P (reprint author), Hamilton Hlth Sci Corp, Chedoke Campus,Patterson Bldg,Room 207, Hamilton, ON L8N 3Z5, Canada. 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J. Psychiat.-Rev. Can. Psychiat. PD OCT PY 2000 VL 45 IS 8 BP 731 EP 738 PG 8 WC Psychiatry SC Psychiatry GA 373YJ UT WOS:000165317400006 PM 11086556 ER PT J AU Patterson, JL AF Patterson, JL TI Development of constructed phrases in a child with language impairment SO CLINICAL LINGUISTICS & PHONETICS LA English DT Article DE word combinations; formulae; language acquisition; language impairment ID INDIVIDUAL-DIFFERENCES; AUTISTIC-CHILDREN; EARLY VOCABULARY; ACQUISITION; ECHOLALIA AB The emerging use of constructed utterances by a pre-school boy who initially used single words and routine phrases is described during a 7-month period, from 4;8-5;3. Emerging constructed phrases were consistent with a mixture of gestalt and analytic acquisition strategies. Some constructed phrases were variations on earlier routine phrases, and others were combinations of words that did not appear in earlier routines. Discussion of the child's course of language development is related to the literature on typical language acquisition and a model of language development in individuals with autism. C1 Univ New Mexico, Dept Speech & Hearing Sci, Speech Language Hearing Ctr, Albuquerque, NM 87131 USA. RP Patterson, JL (reprint author), Univ New Mexico, Dept Speech & Hearing Sci, Speech Language Hearing Ctr, 901 Vassar NE, Albuquerque, NM 87131 USA. RI Patterson, Janet/C-5925-2009 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARTHUR G, 1952, ARTHUR ADAPTATION LE BATES E, 1994, J CHILD LANG, V21, P85 Bates E., 1988, 1 WORDS GRAMMAR BRAINE MDS, 1976, MONOGR SOC RES CHILD, V41, P1, DOI 10.2307/1165959 DUCHAN J, 1994, PRAGMATICS THEORY PR, P149 Fillmore L.W., 1979, INDIVIDUAL DIFFERENC, P203 GALLAGHER TM, 1984, J SPEECH HEAR DISORD, V49, P368 GOLDFIELD B, 1993, DEV LANGUAGE, P299 HICKEY T, 1993, J CHILD LANG, V20, P27 LEONARD LB, 1983, J SPEECH HEAR DISORD, V48, P25 LIEVEN EVM, 1992, J CHILD LANG, V19, P287 Nelson K., 1973, MONOGRAPHS SOC R 149, V38, P1, DOI 10.2307/1165788 Nelson K, 1985, MAKING SENSE ACQUISI PEREZPEREIRA M, 1994, J CHILD LANG, V21, P317 PETERS AM, 1993, LANGUAGE, V69, P742, DOI 10.2307/416885 PINE JM, 1993, J CHILD LANG, V20, P551 PLUNKETT K, 1993, J CHILD LANG, V20, P43 PRIZANT BM, 1981, J SPEECH HEAR DISORD, V46, P241 PRIZANT BM, 1983, J SPEECH HEAR DISORD, V48, P296 PRIZANT BM, 1984, J SPEECH HEAR RES, V27, P183 Scharfkenaker S K, 1990, ASHA, V32, P45 SCHOPMEYER BB, 1992, FRAGILE X CHILD SNYDERMCLEAN L, 1984, SEMINARS SPEECH LANG, V5, P213, DOI 10.1055/s-0028-1085179 SONNEMEIER R, 1994, PRAGMATICS THEORY PR, P134 TOMASELLO M, 1999, DEV LANGUAGE WEISS AL, 1983, J SPEECH HEAR DISORD, V48, P154 NR 27 TC 0 Z9 0 PU TAYLOR & FRANCIS LTD PI LONDON PA 11 NEW FETTER LANE, LONDON EC4P 4EE, ENGLAND SN 0269-9206 J9 CLIN LINGUIST PHONET JI Clin. Linguist. Phon. PD OCT PY 2000 VL 14 IS 7 BP 545 EP 556 DI 10.1080/026992000750020369 PG 12 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 369QP UT WOS:000165078700005 ER PT J AU Jung, TP Makeig, S Westerfield, M Townsend, J Courchesne, E Sejnowski, TJ AF Jung, TP Makeig, S Westerfield, M Townsend, J Courchesne, E Sejnowski, TJ TI Removal of eye activity artifacts from visual event-related potentials in normal and clinical subjects SO CLINICAL NEUROPHYSIOLOGY LA English DT Article DE artifact removal; electrooculographic; independent component analysis; single-trial event-related potentials; event-related potential ID INDEPENDENT COMPONENT ANALYSIS; SPATIAL ATTENTION; ELECTROENCEPHALOGRAPHIC RECORDINGS; BLIND SEPARATION; FREQUENCY-DOMAIN; EEG; RESPONSES; AUTISM AB Objectives: Electrical potentials produced by blinks and eye movements present serious problems for electroencephalographic (EEG) and event-related potential (ERP) data interpretation and analysis, particularly for analysis of data from some clinical populations. Often, all epochs contaminated by large eye artifacts are rejected as unusable, though this may prove unacceptable when blinks and eye movements occur frequently. Methods: Frontal channels are often used as reference signals to regress out eye artifacts, but inevitably portions of relevant EEG signals also appearing in EOG channels are thereby eliminated or mixed into other scalp channels. A generally applicable adaptive method for removing artifacts from EEG records based on blind source separation by independent component analysis (ICA) (Neural Computation 7 (1995) 1129; Neural Computation 10(8) (1998) 2103; Neural Computation 11(2) (1999) 606) overcomes these limitations. Results: Results on EEG data collected from 28 normal controls and 22 clinical subjects performing a visual selective attention task show that ICA can be used to effectively detect, separate and remove ocular artifacts from even strongly contaminated EEG recordings. The results compare favorably to those obtained using rejection or regression methods. Conclusions: The ICA method can preserve ERP contributions from all of the recorded trials and all the recorded data channels, even when none of the single trials are artifact-free. (C) 2000 Elsevier Science ireland Ltd. All rights reserved. C1 Univ Calif San Diego, Inst Neural Computat, Dept 0523, La Jolla, CA 92093 USA. Salk Inst, Howard Hughes Med Inst, San Diego, CA 92186 USA. Salk Inst, Computat Neurobiol Lab, San Diego, CA 92186 USA. USN, Hlth Res Ctr, San Diego, CA 92186 USA. Childrens Hosp Res Ctr, La Jolla, CA 92037 USA. RP Jung, TP (reprint author), Univ Calif San Diego, Inst Neural Computat, Dept 0523, La Jolla, CA 92093 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT BELL AJ, 1995, NEURAL COMPUT, V7, P1129, DOI 10.1162/neco.1995.7.6.1129 BERG P, 1991, CLIN PHYS PHYSIOL M, V12, P49, DOI 10.1088/0143-0815/12/A/010 BERG P, 1994, ELECTROEN CLIN NEURO, V90, P229, DOI 10.1016/0013-4694(94)90094-9 COMON P, 1994, SIGNAL PROCESS, V36, P287, DOI 10.1016/0165-1684(94)90029-9 Friston KJ, 1998, NEUROIMAGE, V7, P30, DOI 10.1006/nimg.1997.0306 Girolami M, 1998, NEURAL COMPUT, V10, P2103, DOI 10.1162/089976698300016981 Hecaen H., 1962, INTERHEMISPHERIC REL HILLYARD SA, 1970, ELECTROEN CLIN NEURO, V28, P173, DOI 10.1016/0013-4694(70)90185-9 Jung TP, 1998, NEURAL NETW SIGNAL P, VVIII, P63, DOI 10.1109/NNSP.1998.710633 Jung TP, 2000, PSYCHOPHYSIOLOGY, V37, P163, DOI 10.1017/S0048577200980259 Jung TP, 1998, ADV NEUR IN, V10, P894 Jung TP, 1999, ADV NEUR IN, V11, P118 KENEMANS JL, 1991, PSYCHOPHYSIOLOGY, V28, P114, DOI 10.1111/j.1469-8986.1991.tb03397.x KENEMANS JL, 1989, BIOL PSYCHOL, V28, P199, DOI 10.1016/0301-0511(89)90001-X Ladavas E, 1997, J COGNITIVE NEUROSCI, V9, P67, DOI 10.1162/jocn.1997.9.1.67 Lagerlund TD, 1997, J CLIN NEUROPHYSIOL, V14, P73, DOI 10.1097/00004691-199701000-00007 Lee T. 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Neurophysiol. PD OCT PY 2000 VL 111 IS 10 BP 1745 EP 1758 DI 10.1016/S1388-2457(00)00386-2 PG 14 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 365KU UT WOS:000089951100005 PM 11018488 ER PT J AU Peterson, CC AF Peterson, CC TI Kindred spirits - Influences of siblings' perspectives on theory of mind SO COGNITIVE DEVELOPMENT LA English DT Article DE siblings; mental state; theory-of-mind; family communication ID INDIVIDUAL-DIFFERENCES; CHILDRENS KNOWLEDGE; BELIEF; EMOTIONS; DEAFNESS; STATES; AUTISM; TALK AB Two experiments were conducted to examine the development of a theory of mind in 265 children aged 3 to 5 years from families of varied size. Even after verbal mental age was controlled, those who had a sibling aged 12 months to 12 years outperformed only-children in both experiments. However, the presence of a very young infant, or of siblings who were teenagers or young adults, exerted no benefit. Also, in contrast to some previous studies, younger child siblings and twins were just as helpful as older child siblings. The presence of multiple child siblings of varied ages above and below that of the participant predicted advanced theory of mind development over and above the effects of own age and verbal ability, despite the fact that neither overall family size nor birth order were significant predictors. These findings were reconciled with those of previous sibling constellation research around a model of family social influences in which the opportunity to play, converse, and disagree in distinctively childish ways with brothers and sisters provides unique insights into the workings of the human mind. (C) 2001 Elsevier Science Inc. All rights reserved. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Peterson, CC (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. 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PD OCT-DEC PY 2000 VL 15 IS 4 BP 435 EP 455 DI 10.1016/S0885-2014(01)00040-5 PG 21 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 442XP UT WOS:000169310500003 ER PT J AU Charman, T Baron-Cohen, S Swettenham, J Baird, G Cox, A Drew, A AF Charman, T Baron-Cohen, S Swettenham, J Baird, G Cox, A Drew, A TI Testing joint attention, imitation, and play as infancy precursors to language and theory of mind SO COGNITIVE DEVELOPMENT LA English DT Article DE theory of mind; language; joint attention; play; imitation; precursors ID AUTISM SPECTRUM DISORDERS; YOUNG-CHILDREN; PRETEND PLAY; 2ND YEAR; INDIVIDUAL-DIFFERENCES; ABILITIES; REPRESENTATION; PERFORMANCE; UNDERSTAND; BELIEFS AB Various theoretical accounts propose that an important developmental relation existsbetween joint attention, play, and imitation abilities, and later theory of mind ability. However, very little direct empirical evidence supports these claims for putative "precursor" theory of mind status. A small sample (N=13) of infants, for whom measures of play, joint attention, and imitation had been collected at 20 months of age, was followed-up longitudinally at 44 months and a battery of theory of mind measures was conducted. Language and IQ were measured at both timepoints. Imitation ability at 20 months was longitudinally associated with expressive, but not receptive, language ability at 44 months. In contrast, only the joint attention behaviours of gaze switches between an adult and an active toy and looking to an adult during an ambiguous goal detection task at 20 months were longitudinally associated with theory of mind ability at 44 months. It is argued that joint attention, play, and imitation, and language and theory of mind, might form part of st shared social-communicative representational system in infancy that becomes increasingly specialised and differentiated as development progresses. (C) 2001 Elsevier Science Inc. All rights reserved. C1 UCL, Inst Child Hlth, Behav Sci Unit, London WC1N 1EH, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 1TN, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 1TN, England. UCL, Dept Human Commun Sci, London WC1N 1EH, England. Guys St Thomas & Kings Coll, Sch Med, Bloomfield Clin, London, England. Guys St Thomas & Kings Coll, Sch Med, Newcomen Ctr, London, England. RP Charman, T (reprint author), UCL, Inst Child Hlth, Behav Sci Unit, 30 Guilford St, London WC1N 1EH, England. 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PD OCT-DEC PY 2000 VL 15 IS 4 BP 481 EP 498 DI 10.1016/S0885-2014(01)00037-5 PG 18 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 442XP UT WOS:000169310500005 ER PT J AU Gerardin-Collet, V AF Gerardin-Collet, V TI Autism and the theory of the mind: a 'natural' version of the puppet paradigm. SO EVOLUTION PSYCHIATRIQUE LA French DT Article DE autism; pragmatism; role play; theory of the mind ID REPRESENTATION AB Some of the findings in the literature on autism and the theory of the mind have been considered and commented on, and the problem of intentionality has been examined. The study consists of a pragmatic analysis of an autistic conversation. A transcribed version of a recording made of an autistic child during role-play with puppets has been included and helps to Focus attention on child's activity, i.e., his interaction with the puppets and his role of actor in a story. This spontaneous situation has: been compared to the experimental tests of Baron-Cohen. The story that was enacted is interesting, as it has double imposture as its main theme. This could well be the reason why it causes problems to autistic subjects. Throughout the role-playing interaction, the child reacted in a particular manner. In reply to the question 'who are you?'. the child answered with an 'either..or' ('I'm either the wolf or little red riding hood'), and combined this with an objective and deductive reasoning ('as I have the wolf puppet, I'm the wolf'; or 'as I have the little red riding hood puppet. I'm little red riding hood'). This reasoning was based on reality, and not on the role in the story. Also, aspects such as belief, the content of that belief, and more explicitly the wolf's treacherous intention and his strategy were not grasped by the child. 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PD OCT PY 2000 VL 30 IS 5 BP 369 EP 371 DI 10.1023/A:1005595303185 PG 3 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100001 ER PT J AU Schreibman, L AF Schreibman, L TI Intensive behavioral/psychoeducational treatments for autism: Research needs and future directions SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE intensive behavioral treatment; autism ID SCHIZOPHRENIC CHILDREN; BEHAVIORAL TREATMENT; PARADIGM; PARENTS; SPEECH AB It is widely acknowledged that, to date, the forms of treatment enjoying the broadest empirical validation for effectiveness with individuals with autism are those treatments based upon a behavioral model and that such treatments are best implemented intensively and early in the child's development. This paper describes several features important in the success of this model and presents remaining issues to be addressed for improving treatment effectiveness. 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PD OCT PY 2000 VL 30 IS 5 BP 373 EP 378 DI 10.1023/A:1005535120023 PG 6 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100002 PM 11098871 ER PT J AU Wolery, M AF Wolery, M TI Commentary: The environment as a source of variability: Implications for research with individuals who have autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID DISABILITIES; STUDENTS C1 Univ N Carolina, Frank Porter Graham Child Dev Ctr, Chapel Hill, NC 27599 USA. RP Wolery, M (reprint author), Univ N Carolina, Frank Porter Graham Child Dev Ctr, CB 8180, Chapel Hill, NC 27599 USA. CR Ammerman R., 1997, HDB PREVENTION TREAT, P157 Dawson G., 1997, EFFECTIVENESS EARLY, P307 HARING TG, 1990, J APPL BEHAV ANAL, V23, P235, DOI 10.1901/jaba.1990.23-235 HARRIS SL, 1994, PRESCHOOL ED PROGRAM Koegel R. L., 1995, TEACHING CHILDREN AU Sameroff AJ, 1975, REV CHILD DEV RES, P187 Sidman M., 1960, TACTICS SCI RES EVAL Wolery M, 1997, J SPEC EDUC, V31, P61 NR 8 TC 6 Z9 6 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 379 EP 381 DI 10.1023/A:1005587104093 PG 3 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100003 PM 11098872 ER PT J AU Koegel, LK AF Koegel, LK TI Interventions to facilitate communication in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; communicative intervention ID FOLLOW-UP; BEHAVIORAL TREATMENT; SEVERE DISABILITIES; PRESCHOOL-CHILDREN; SIGN LANGUAGE; ACQUISITION; STUDENTS; PROFILES; PARENTS; SPEECH AB The purpose of this article is to discuss research opportunities arising from the current literature in the area of communication. Six general themes are discussed, including (a) increasing spontaneity, initiations, and the variety of functions of language verbal and nonverbal children with autism exhibit; (b) assessing and teaching precursors relating to positive outcome; (c) the importance of family involvement in intervention programs; (d) best practices for implementation of communicative interventions; (e) the interrelationship between language and other behavioral symptoms of autism; and (f) the social and pragmatic use of language. These areas are discussed in terms of improving assessment and intervention practices to produce greater long-term communicative outcomes for individuals with autism. C1 Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. RP Koegel, LK (reprint author), Univ Calif Santa Barbara, Santa Barbara, CA 93106 USA. 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Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 393 EP 398 DI 10.1023/A:1005591205002 PG 6 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100005 PM 11098874 ER PT J AU Rogers, SJ AF Rogers, SJ TI Interventions that facilitate socialization in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE social dysfunction; autism; social interventions ID SOCIAL-INTERACTION SKILLS; SCRIPT-FADING PROCEDURE; YOUNG-CHILDREN; PEER INTERACTIONS; SEVERE DISABILITIES; PRESCHOOL-CHILDREN; BEHAVIOR-CHANGE; PLAY SKILLS; INITIATIONS; STUDENTS AB Social dysfunction is perhaps the most defining and handicapping feature of autism. Improved social functioning has long been considered one of the most important intervention outcomes. A variety of social interventions have been designed, empirically examined, and published in the autism literature. Children with autism have been found to be responsive to a wide variety of interventions aimed at increasing their social engagement with others, both adults and peers. Successful strategies employing peer-mediated approaches and peer tutoring have involved typically developing peers. Furthermore, several studies have demonstrated that social engagement directly affects other important behaviors like language, even when these behaviors are not. specifically targeted by the teaching program. Thus, while an area of severe involvement, social behavior is also responsive to intervention. C1 Univ Colorado, Hlth Sci Ctr, JFK Partners, Denver, CO 80262 USA. RP Rogers, SJ (reprint author), Univ Colorado, Hlth Sci Ctr, JFK Partners, 4200 E 9th Ave,Campus Box C-234, Denver, CO 80262 USA. 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Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 399 EP 409 DI 10.1023/A:1005543321840 PG 11 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100006 PM 11098875 ER PT J AU Dawson, G Watling, R AF Dawson, G Watling, R TI Interventions to facilitate auditory, visual, and motor integration in autism: A review of the evidence SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; sensory integration therapy; occupational therapy; auditory integration training ID ASPERGER-SYNDROME; OCCUPATIONAL-THERAPY; LEARNING-DISABILITIES; CHILDREN; CLUMSINESS; SYMPTOMS; INFANCY; AGE; DEFENSIVENESS; BEHAVIORS AB Evidence is reviewed on the prevalence of sensory and motor abnormalities in autism and the effectiveness of three interventions designed to address such abnormalities-sensory integration therapy, traditional occupational therapy, and auditory integration training. Although sensory processing and motor abnormalities are neither universal nor specific to autism, the prevalence of such abnormalities in autism is relatively high. There is, however, little controlled research on the effectiveness of interventions designed to address these abnormalities. Four objective outcome studies of sensory integration therapy were identified. These were of such small scale that no firm conclusions regarding efficacy could be made. No empirical studies of traditional occupational therapy in autism were found. Five studies of auditory integration training were found. Results of these studies provided no, or at best equivocal, support for the use of auditory integration training in autism. C1 Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. RP Dawson, G (reprint author), Univ Washington, Ctr Human Dev & Disabil, Box 357920, Seattle, WA 98195 USA. CR American Academy of Pediatrics, 1998, PEDIATRICS, V102, P431 Ayres A. 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Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 415 EP 421 DI 10.1023/A:1005547422749 PG 7 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100008 PM 11098877 ER PT J AU Goldstein, H AF Goldstein, H TI Commentary: Interventions to facilitate auditory, visual, and motor integration: "Show me the data" SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID OCCUPATIONAL-THERAPY; CHILDREN; AUTISM C1 Florida State Univ, Dept Commun Disorders, Tallahassee, FL 32306 USA. RP Goldstein, H (reprint author), Florida State Univ, Dept Commun Disorders, Tallahassee, FL 32306 USA. CR Bettison S, 1996, J AUTISM DEV DISORD, V26, P361, DOI 10.1007/BF02172480 Case-Smith J, 1999, AM J OCCUP THER, V53, P489 Case-Smith J, 1999, AM J OCCUP THER, V53, P506 Edelson SM, 1999, AM J OCCUP THER, V53, P145 Edelson SM, 1999, FOCUS AUTISM OTHER D, V14, P73, DOI 10.1177/108835769901400202 Gravel J, 1994, AM J SPEECH-LANG PAT, V3, P25 Nickel RE, 1996, INFANT YOUNG CHILD, V8, P29 Rimland B., 1994, AM J SPEECH-LANG PAT, V3, P16 RIMLAND B, 1995, J AUTISM DEV DISORD, V25, P61, DOI 10.1007/BF02178168 Tharpe AM, 1999, LANG SPEECH HEAR SER, V30, P378 Watling R, 1999, AM J OCCUP THER, V53, P498 NR 11 TC 13 Z9 13 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 423 EP 425 DI 10.1023/A:1005599406819 PG 3 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100009 PM 11098878 ER PT J AU McDougle, CJ Kresch, LE Posey, DJ AF McDougle, CJ Kresch, LE Posey, DJ TI Repetitive thoughts and behavior in pervasive developmental disorders: Treatment with serotonin reuptake inhibitors SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; serotonin reuptake inhibitors; obsessive-compulsive disorder ID OBSESSIVE-COMPULSIVE DISORDER; AUTISTIC DISORDER; MENTAL-RETARDATION; DOUBLE-BLIND; FLUOXETINE TREATMENT; SELF-INJURY; CHILDREN; CLOMIPRAMINE; ADULTS; SERTRALINE AB Repetitive thoughts and behavior are considered integral and core components of autistic disorder. Results from recent studies suggest that the types of repetitive thoughts and behavior of adults with autism and those with obsessive-compulsive disorder (OCD) may be different. Serotonin reuptake inhibitors (SRIs), the primary drug treatment for patients with OCD, may reduce the repetitive phenomena of some autistic patients. Two controlled studies of the nonselective SRI clomipramine have shown the drug to be more efficacious than the relatively selective norepinephrine reuptake inhibitor desipramine and placebo in children with autism. One controlled study of the selective SRI fluvoxamine found it to be significantly better than placebo for reducing repetitive phenomena and aggression in adults with autistic disorder. Additional research is needed. C1 Indiana Univ, Sch Med, Dept Psychiat, Sect Child & Adolescent Psychiat, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), Indiana Univ, James Whitcomb Riley Hosp Children, 702 Barnhill Dr,Room 3701, Indianapolis, IN 46202 USA. 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Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 427 EP 435 DI 10.1023/A:1005551523657 PG 9 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100010 PM 11098879 ER PT J AU King, BH AF King, BH TI Pharmacological treatment of mood disturbances, aggression, and self-injury in persons with pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; dopamine; serotonin; drug ID PROFOUND MENTAL-RETARDATION; DOUBLE-BLIND; AUTISTIC DISORDER; CLOMIPRAMINE TREATMENT; RETARDED PATIENTS; BASE-LINE; BEHAVIOR; PLACEBO; CHILDREN; EFFICACY AB Aggression, self-injury, and mood disturbances in persons with autistic disorders, while not uncommon, do not constitute core features of autism. Moreover, these problems can occur for a variety of reasons, which need to be assessed in order to plan appropriate and frequently combined (behavioral-pharmacological) treatments. Drugs acting primarily in the dopaminergic, serotonergic, adrenergic, opioidergic, and glutamatergic systems all have been explored in the treatment of aggression and self-injury. While no single drug or class of medication has yet emerged as consistently effective, a number of drugs appear promising. Advances in the assessment of aggressive behaviors, the identification of predictors of drug response, and additional controlled clinical drug trials specifically aimed at these target behaviors are essential in improving the approach to these problematic behaviors in the context of autistic disorder. C1 Dartmouth Med Sch, Lebanon, NH 03756 USA. RP King, BH (reprint author), Dartmouth Med Sch, 1 Med Ctr Dr, Lebanon, NH 03756 USA. 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Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 439 EP 445 DI 10.1023/A:1005555624566 PG 7 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100012 PM 11098881 ER PT J AU Aman, MG Langworthy, KS AF Aman, MG Langworthy, KS TI Pharmacotherapy for hyperactivity in children with autism and other pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; hyperactivity; PDDNOS; overactivity; pharmacotherapy; inattention ID BEHAVIORAL SYMPTOMS; SCHIZOPHRENIC CHILDREN; INFANTILE-AUTISM; STIMULANT-DRUGS; OPEN TRIAL; NALTREXONE; HALOPERIDOL; RISPERIDONE; PLACEBO; DEXTROAMPHETAMINE AB We reviewed pharmacological treatments used in children with autism and PDD-NOS who present with hyperactive symptoms. Some 41 studies were identified from the following drug categories: antipsychotics (n = 13), serotonin reuptake inhibitors (n = 3), antianxiety drugs (n = 4), psychostimulants (n = 10), alpha adrenergic agonists (n = 2), opiate blockers (n = 7), and other drugs (n = 2). Empirical evidence for significant reductions in hyperactive symptoms was strongest for the antipsychotics, psychostimulants, and naltrexone. Most studies have focused on the reduction of overactivity, and more emphasis needs to be placed on distractibility and attentional variables. A theoretical model was proposed in which participants' attentional performance may be used to predict clinical response to psychostimulants. More carefully controlled and comprehensive studies of hyperactivity are badly needed in these children. C1 Ohio State Univ, Nisonger Ctr Mental Retardat & Dev Disabil, Columbus, OH 43210 USA. RP Aman, MG (reprint author), Ohio State Univ, Nisonger Ctr Mental Retardat & Dev Disabil, Columbus, OH 43210 USA. 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When the metabolic consequences of an enzyme defect are well defined (e.g., phenylketonuria, 5'-nucleotidase superactivity), treatment with diet, drugs, or nutritional supplements may bring about a dramatic reduction in autistic symptoms. This review evaluates evidence for metabolic etiologies in autism spectrum disorders, as well as for the efficacy of dietary and vitamin treatments. The relationship between gastrointestinal abnormalities and autism spectrum disorders is also considered. C1 Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. RP Page, T (reprint author), Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. 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Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 481 EP 484 DI 10.1023/A:1005520111362 PG 4 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100019 PM 11098888 ER PT J AU Tuchman, R AF Tuchman, R TI Treatment of seizure disorders and EEG abnormalities in children with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; seizure disorders; EEG abnormalities ID LANDAU-KLEFFNER SYNDROME; PERVASIVE DEVELOPMENTAL DISORDER; FOCAL INTERICTAL SPIKES; MAGNETOENCEPHALOGRAPHIC PATTERNS; EPILEPTIFORM ACTIVITY; CHILDHOOD EPILEPSY; REACTION-TIME; REGRESSION; PERCEPTION AB The treatment of seizure disorders EEG epileptiform abnormalities without epilepsy in children with autism spectrum disorders (ASD) is considered within the context of the relationship of epilepsy and epileptiform disorders to language; behavior, and cognition. 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Autism Dev. Disord. PD OCT PY 2000 VL 30 IS 5 BP 485 EP 489 DI 10.1023/A:1005572128200 PG 5 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100020 PM 11098889 ER PT J AU McClelland, JL AF McClelland, JL TI The basis of hyperspecificity in autism: A preliminary suggestion based on properties of neural nets SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; neural networks; hyperspecificity AB This article reviews a few key ideas about the representation of information in neural networks and uses these ideas to address one aspect of autism, namely, the apparent hyperspecificity that is often seen in autistic children's application of previously acquired information. Hyper specificity is seen as reflecting a possible feature of the neural codes used to represent concepts in the autistic brain. C1 Carnegie Mellon Univ, Dept Psychol, Pittsburgh, PA 15213 USA. Ctr Neural Basis Cognit, Pittsburgh, PA USA. 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PD OCT PY 2000 VL 30 IS 5 BP 503 EP 508 DI 10.1023/A:1005528313179 PG 6 WC Psychology, Developmental SC Psychology GA 373EU UT WOS:000165276100023 PM 11098892 ER PT J AU Searcy, E Burd, L Kerbeshian, J Stenehjem, A Franceschini, LA AF Searcy, E Burd, L Kerbeshian, J Stenehjem, A Franceschini, LA TI Asperger's syndrome, X-linked mental retardation (MRX23), and chronic vocal tic disorder SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM; PREVALENCE; TWIN AB Pervasive developmental disorders are severe disorders of development with no consistent neurobiologic etiology and most often an idiopathic etiology. We report a 12-year-old male who met criteria for a pervasive developmental disorder (Asperger's syndrome) and a chronic tic disorder. The child also has an X-Linked cognitive impairment ((MRX23). The presence of tic symptomatology, pervasive developmental disorder, and fragile X syndrome has previously been reported. 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PD OCT PY 2000 VL 15 IS 10 BP 699 EP 702 DI 10.1177/088307380001501013 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 364MA UT WOS:000089895100012 PM 11063087 ER PT J AU Klin, A AF Klin, A TI Attributing social meaning to ambiguous visual stimuli in higher-functioning autism and Asperger syndrome: The social attribution task SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Asperger syndrome; autistic disorder; social attribution; social cognition; theory of mind ID MENTAL-RETARDATION; ADAPTIVE-BEHAVIOR; MIND ABILITIES; TEACHING THEORY; CHILDREN; INDIVIDUALS; RELIABILITY; DEFICITS; REPRESENTATION; CONVERSATION AB More able individuals with autism and Asperger syndrome (AS) have been shown to pass relatively high level theory of mind (ToM) tasks without displaying commensurate levels of social adaptation in naturalistic settings. This paper presents a social cognitive procedure-the Social Attribution Task (SAT)-that reduces factors thought to facilitate ToM task performance without facilitating real-life social functioning. Sixty participants with autism (N = 20), AS (N = 20), and normally developing adolescents and adults (N = 20) with normative IQs were asked to provide narratives describing Heider and Simmel's (1944) silent cartoon animation in which geometric shapes enact a social plot. These narratives were coded in terms of the participants' abilities to attribute social meaning to the geometric cartoon. The SAT provides reliable and quantified scores on seven indices of social cognition. Results revealed marked deficits in both clinical groups across all indices. These deficits were not related to verbal IQ or level of metalinguistic skills. Individuals with autism and AS identified about a quarter of the social elements in the story, a third of their attributions were irrelevant to the social plot, and they used pertinent ToM terms very infrequently. They were also unable to derive psychologically based personality features From the shapes' movements. When provided with more explicit verbal information on the nature of the cartoon, individuals with AS improved their performance slightly more than those with autism, but not significantly so. C1 Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT 06520 USA. RP Klin, A (reprint author), Yale Univ, Sch Med, Yale Child Study Ctr, 230 S Frontage Rd, New Haven, CT 06520 USA. 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PD OCT PY 2000 VL 41 IS 7 BP 831 EP 846 DI 10.1017/S0021963099006101 PG 16 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 372KT UT WOS:000165233400003 PM 11079426 ER PT J AU Boucher, J Lewis, V Collis, GM AF Boucher, J Lewis, V Collis, GM TI Voice processing abilities in children with autism, children with specific language impairments, and young typically developing children SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; emotional expression; facial perception; specific language impairment; voice processing ID PERVASIVE DEVELOPMENTAL DISORDERS; FACE RECOGNITION; PERCEPTION; EMOTION; SPEECH; CUES AB It is well established that people with autism have impaired face processing, but much less is known about voice processing in autism. Four experiments were therefore carried out to assess (1) familiar voice-face and sound-object matching; (2) familiar voice recognition; (3) unfamiliar voice discrimination; and (4) vocal affect naming and vocal-facial affect matching. in Experiments 1 and 2 language-matched children with specific language impairment (SLI) were the controls. In Experiments 3 and 4 language-matched children with SLI and young mainstream children were the controls. The results were unexpected: the children with autism were not impaired relative to controls on Experiments 1, 2 and 3, and were superior to the children with SLI on both parts of Experiment 4, although impaired on affect matching relative to the mainstream children. These results are interpreted in terms of an unexpected impairment of voice processing in the children with SLI associated partly, but not wholly, with an impairment of cross-modal processing. Performance on the experimental tasks was not associated with verbal or nonverbal ability in either of the clinical groups. The implications of these findings for understanding autism and SLI are discussed. C1 Univ Warwick, Dept Psychol, Coventry CV7 4L, W Midlands, England. RP Boucher, J (reprint author), Univ Warwick, Dept Psychol, Coventry CV7 4L, W Midlands, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BALTAXE CAM, 1987, J AUTISM DEV DISORD, V17, P255, DOI 10.1007/BF01495060 Beitchman JH, 1996, J CHILD PSYCHOL PSYC, V37, P961, DOI 10.1111/j.1469-7610.1996.tb01493.x Bishop D. V. 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PD OCT PY 2000 VL 41 IS 7 BP 847 EP 857 DI 10.1017/S0021963099006149 PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 372KT UT WOS:000165233400004 PM 11079427 ER PT J AU Kamio, Y Toichi, M AF Kamio, Y Toichi, M TI Dual access to semantics in autism: Is pictorial access superior to verbal access SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; semantic priming; pictorial semantic processing; verbal semantic processing; pictorial superiority ID HIGH-FUNCTIONING AUTISM; NORMAL-CHILDREN; INFANTILE-AUTISM; SEX-DIFFERENCES; WORD FLUENCY; IDIOT SAVANT; MEMORY; PICTURES; LANGUAGE; PEOPLE AB The main aim of the present study was to compare pictures and words with respect to access to semantic systems in autism using a semantic priming paradigm. A word completion task was conducted using both within-modality (word-word, WW) and cross-modality (picture-word, PW) conditions on a group of high-functioning adolescents and adults with autism (N = 20) and a control group (N = 20) matched on chronological age, mental age, Verbal IQ and Performance IQ. Both groups showed semantic priming effects in both modality conditions, generating significantly more responses for related prime-target pairs than for unrelated pairs. Although the control group performed similarly on both priming tasks, the autistic group performed significantly better on a PW task than on a WW task. These findings suggest the possible advantage of pictures over words in access to semantics in autism. The theoretical implications are discussed in terms of functional asymmetry between verbal and pictorial semantic operations that may be specific to autism. C1 Kyoto Univ, Fac Med, Dept Neuropsychiat, Kyoto 6068397, Japan. 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Child Psychol. Psychiatry Allied Discip. PD OCT PY 2000 VL 41 IS 7 BP 859 EP 867 DI 10.1017/S0021963099006137 PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 372KT UT WOS:000165233400005 PM 11079428 ER PT J AU Sandler, AD Bodfish, JW AF Sandler, AD Bodfish, JW TI Placebo effects in autism: Lessons from secretin SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Editorial Material ID DOUBLE-BLIND; DISORDER; HEALTH; ADULTS C1 Thoms Rehabil Hosp, Olson Huff Ctr Child Dev, Asheville, NC 28813 USA. Western Carolina Ctr, Human Dev Res & Training Inst, Morganton, NC USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. RP Sandler, AD (reprint author), Thoms Rehabil Hosp, Olson Huff Ctr Child Dev, 68 Sweeten Creek Rd, Asheville, NC 28813 USA. 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Dev. Behav. Pediatr. PD OCT PY 2000 VL 21 IS 5 BP 347 EP 350 PG 4 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 363VG UT WOS:000089857900005 PM 11064962 ER PT J AU Ghaziuddin, M AF Ghaziuddin, M TI Autism in Down's syndrome: a family history study SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autism; Down's syndrome; family history study ID CHILDREN; POPULATION; PHENOTYPE; DISORDERS; SPECTRUM AB Several recent reports have described the occurrence of autism in subjects with Down's syndrome (DS). However, relatively little is known about the family history of these subjects, especially with reference to autism. In order to address this issue, the present author examined 11 subjects with DS and autism (DSM-III-R; nine males), and compared them with seven controls with DS but without autism (DSM-III-R; three males). Details about family psychiatric history were obtained from both groups with an emphasis on autism and related disorders. Subjects with both DS and autism had an excess of first-degree relatives who met the description of the broader phenotype of autism. Seven (64%) of the subjects with autism had an affected parent as against one (14%) of the control group. Similarly, four out of Ir siblings (36%) in the DS with autism group showed features suggestive of the broader autistic phenotype compared to none in the control group. These findings suggest that, at least in some cases, autism-specific genetic factors may be important even when autism occurs in the presence of known medical conditions. Further studies of the mechanism of comorbidity of autism with medical conditions may help clarify the aetiology of the disorder. C1 Univ Michigan, Med Ctr, Tauman Ctr 0390, Ann Arbor, MI 48109 USA. RP Ghaziuddin, M (reprint author), Univ Michigan, Med Ctr, Tauman Ctr 0390, 1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. 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Intell. Disabil. Res. PD OCT PY 2000 VL 44 BP 562 EP 566 DI 10.1046/j.1365-2788.2000.00271.x PN 5 PG 5 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 368TK UT WOS:000090133500004 PM 11079353 ER PT J AU Olney, MF AF Olney, MF TI Working with autism and other social-communication disorders SO JOURNAL OF REHABILITATION LA English DT Article ID FACILITATED COMMUNICATION; LEARNING-DISABILITIES; IMPAIRMENT; ATTENTION AB Individuals with autism and related developmental disabilities such as Asperger's Syndrome and Pervasive Developmental Disorder present special challenges to rehabilitation counselors. Although their experiences have been described clinically, seldom have the perceptions of individuals with autism and their parents been actively sought. This article reviews the literature on autism from a variety of perspectives: medical, behavioral, social, and personal. An analysis of 18 first hand accounts, interviews, and autobiographical works by people with autism and their parents contribute insights into the experience of autism and related disabilities. The article concludes with specific suggestions to help rehabilitation counselors maximize the success of individuals with autism and related disabilities. C1 Univ Illinois, Rehabil Program, Champaign, IL 61820 USA. RP Olney, MF (reprint author), Univ Illinois, Rehabil Program, 120 Huff Hall,MC 588,1206 S 4th, Champaign, IL 61820 USA. 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A hypotonic-hyporesponsive episode (HHE) is the sudden onset of hypotonia, hyporesponsiveness, and pallor or cyanosis that occurs within 48 hours after childhood immunizations. This syndrome has been primarily associated with pertussis-containing vaccines administered to children <2 years of age, and has been estimated to occur once every 1750 diphtheria-tetanus-pertussis (DTwP) vaccinations. Previous studies of HHE were limited by small numbers of cases and, sometimes, by limited details of the event. Objectives. To characterize a large number of HHE cases reported to the Vaccine Adverse Event Reporting System (VAERS), to assist clinicians in identifying HHE, and to assist researchers in investigating the risk factors, cause, and pathogenesis of this syndrome. Methods. More than 40 000 VAERS reports received between 1996 and 1998 were screened for HHE by a computer algorithm and reviewed, and a telephone follow-up questionnaire was administered to the witness of HHE. Results. There were 215 HHE cases, all nonfatal. The median age of onset of HHE was 4.0 months (range: 1.1-107 months). Over half of the reports (53%) concerned females. The median birth weight was 3.36 kg (range: 1.27-4.96 kg); 4.7% had a birth weight <2500 g. The median interval between vaccination and HHE was 210 minutes (range: 1 minute-2 days). Among children with HHE who were <24 months of age, the episode occurred within 5 minutes in only 8.5%, compared with 66.7% of children with HHE >24 months of age. There were no relevant findings regarding family medical history or the mothers' gestational history. Nearly all of the children (98.6%) returned to their prevaccination state according to the telephone questionnaire; median time to return was 6 hours (range: 1 minute-4 months). The 3 children reported as not returning to their prevaccination state all had VAERS reports submitted after they developed conditions (autism, complex partial epilepsy, and developmental delays with infantile spasms) that are not known to be causally associated with immunization. The vast majority of children (93%) with HHE received a pertussis-containing vaccine, either diphtheria-tetanus-acellular pertussis (DTaP, 28%), DTwP (11%), or diphtheria-tetanus-pertussis-Haemophilus influenzae type b (DTwP-HIB, 61%). During the HHE episode, 90.1% of the children had pallor and 49% had cyanosis. Because of the HHE event, 6.8% of children had had all vaccines withheld as of the date of the interview. Of the remainder, 66.5% of children have had 1 or more subsequent vaccinations or vaccine components withheld, and 26.7% have not had any subsequent vaccinations withheld. Only 1 child was reported to have had a repeat episode of HHE, occurring after hepatitis B vaccination. From 1996 to 1998, the number of HHE reports decreased from 99 to 38, when the predominant pertussis vaccine administered to infants changed from whole-cell to acellular. Conclusion. This study represents the largest published case series of children with HHE and supports the generally benign, self-limited, nonrecurrent nature of this syndrome. Although HHE has been less frequently reported to VAERS after increased use of DTaP, HHE does occur after the administration of DTaP and other nonpertussis-containing vaccines. Although most parents and pediatricians withheld the pertussis component of subsequent vaccinations, many did not, with no reported adverse events occurring in the children after the subsequent immunizations. Restricting the definition of HHE to a more narrow age range (eg, <2 years of age) is also proposed because most of the older children probably experienced vasovagal syncope rather than HHE within 5 minutes of immunization. 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PD SEP 29 PY 2000 VL 405 IS 1-3 BP 89 EP 101 DI 10.1016/S0014-2999(00)00544-6 PG 13 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 360PQ UT WOS:000089676800010 PM 11033317 ER PT J AU Naqvi, S Cole, T Graham, JM AF Naqvi, S Cole, T Graham, JM TI Cole-Hughes macrocephaly syndrome and associated autistic manifestations SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE Cole-Hughes syndrome; macrocephaly; autism; mental retardation; attention deficit hyperactivity disorder; obesity AB Based on cases that had been excluded from a previous clinical study of Sotos syndrome, Cole and Hughes [1991: Am J Med Genet 41: 115-124] reported a new syndrome associated with marked obesity, occasional delayed bone age, distinctive facial anomalies, mental retardation, and progressive postnatal macrocephaly in the context of autosomal dominant familial macrocephaly, Subsequently, Stevenson et al, [1997: Lancet 349:1744-1745] emphasized the association of progressive postnatal macrocephaly with autism, and they suggested that this might comprise a recognizable autism syndrome, We report two additional patients with Cole-Hughes syndrome and associated autistic characteristics with attention deficit hyperactivity disorder. These patients seem to manifest a distinctive behavioral phenotype associated with Cole-Hughes syndrome and they manifest a distinct subgroup of persons with autism that may ultimately shed light on the pathogenesis of this disorder. (C) 2000 Wiley-Liss, Inc. C1 Univ Calif Los Angeles, Sch Med,Int Skeletal Dysplasia Registry, Cedars Sinai Med Ctr,SHAREs Child Disabil Ctr, Steven Spielberg Pediat Res Ctr,Ahmanson Dept Ped, Los Angeles, CA 90048 USA. Birmingham Womens Hosp, Clin Genet Unit, Birmingham, W Midlands, England. Thalians Community Mental Hlth Ctr, Cedars Sinai Med Ctr, Dept Psychiat, Los Angeles, CA USA. RP Graham, JM (reprint author), Univ Calif Los Angeles, Sch Med,Int Skeletal Dysplasia Registry, Cedars Sinai Med Ctr,SHAREs Child Disabil Ctr, Steven Spielberg Pediat Res Ctr,Ahmanson Dept Ped, 444 S San Vicente Blvd,1001, Los Angeles, CA 90048 USA. CR Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Bristol MM, 1996, J AUTISM DEV DISORD, V26, P121, DOI 10.1007/BF02172002 COLE TRP, 1991, AM J MED GENET, V41, P115, DOI 10.1002/ajmg.1320410128 Cook EH, 1998, AM J HUM GENET, V62, P1077, DOI 10.1086/301832 Davidovitch M, 1996, J CHILD NEUROL, V11, P389 GHAZIUDDIN M, 1998, 1998 CHILD PSYCH M L GILLBERG C, 1991, J AM ACAD CHILD PSY, V30, P489, DOI 10.1097/00004583-199105000-00022 Insel TR, 1997, AM J PSYCHIAT, V154, P726 Lainhart JE, 1997, J AM ACAD CHILD PSY, V36, P282, DOI 10.1097/00004583-199702000-00019 MILES JH, 1998, AM J HUM GENET, V63, pA49 Piven J, 1997, AM J PSYCHIAT, V154, P1051 PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 SMALLEY SL, 1995, AM J MED GENET, V60, P19, DOI 10.1002/ajmg.1320600105 Stevenson RE, 1997, LANCET, V349, P1744, DOI 10.1016/S0140-6736(05)62956-X Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 NR 16 TC 15 Z9 15 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD SEP 11 PY 2000 VL 94 IS 2 BP 149 EP 152 DI 10.1002/1096-8628(20000911)94:2<149::AID-AJMG7>3.0.CO;2-# PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 345TN UT WOS:000088831400007 PM 10982971 ER PT J AU Howard, MA Cowell, PE Boucher, J Broks, P Mayes, A Farrant, A Roberts, N AF Howard, MA Cowell, PE Boucher, J Broks, P Mayes, A Farrant, A Roberts, N TI Convergent neuroanatomical and behavioural evidence of an amygdala hypothesis of autism SO NEUROREPORT LA English DT Article DE amygdala; MRI; neuropsychology; social perception; stereology ID FACE PROCESSING IMPAIRMENTS; FACIAL EXPRESSIONS; RECOGNITION; EMOTION; DAMAGE; DISORDER; VOLUME; BRAIN; FEAR; MRI AB In this study we report a convergence of behavioural and neuroanatomical evidence in support of an amygdala hypothesis of autism. We find that people with high-functioning autism (HFA) show neuropsychological profiles characteristic of the effects of amygdala damage, in particular selective impairment in the recognition of facial expressions of fear, perception of eye-gaze direction, and recognition memory for faces. Using quantitative magnetic resonance (MR) image analysis techniques, we find that the same individuals also show abnormalities of medial temporal lobe (MTL) brain structure, notably bilaterally enlarged amygdala volumes. These results combine to suggest that developmental malformation of the amygdala may underlie the social-cognitive impairments characteristic of HFA. This malformation may reflect incomplete neuronal pruning in early development. NeuroReport 11:2931-2935 (C) 2000 Lippincott Williams & Wilkins. C1 Univ Liverpool, Magnet Resonance & Image Anal Res Ctr, Liverpool L69 3BX, Merseyside, England. Univ Sheffield, Dept Human Commun Sci, Sheffield S10 2TA, S Yorkshire, England. Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. St Lukes Hosp, Dept Clin Hlth Psychol, Bradford BD5 0NA, W Yorkshire, England. Univ Sheffield, Dept Psychol, Sheffield S10 2TF, S Yorkshire, England. Univ Liverpool, Dept Psychol, Liverpool L69 7ZA, Merseyside, England. Univ Nottingham, Div Psychiat, Nottingham NG3 6AA, England. RP Howard, MA (reprint author), Univ Liverpool, Magnet Resonance & Image Anal Res Ctr, POB 147, Liverpool L69 3BX, Merseyside, England. 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RP Bookheimer, S (reprint author), Univ Calif Los Angeles, Sch Med, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90095 USA. CR Bettelheim B., 1967, EMPTY FORTRESS INFAN COURCHESNE E, 1988, NEW ENGL J MED, V318, P1349, DOI 10.1056/NEJM198805263182102 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 DAMASIO H, 1980, ARCH NEUROL-CHICAGO, V37, P504 FILIPEK PA, 1995, CURR OPIN NEUROL, V8, P134, DOI 10.1097/00019052-199504000-00009 Howard MA, 2000, NEUROREPORT, V11, P2931, DOI 10.1097/00001756-200009110-00020 LEINER HC, 1993, TRENDS NEUROSCI, V16, P444, DOI 10.1016/0166-2236(93)90072-T Whalen PJ, 1998, J NEUROSCI, V18, P411 NR 8 TC 1 Z9 1 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD SEP 11 PY 2000 VL 11 IS 13 BP F13 EP F13 DI 10.1097/00001756-200009110-00001 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 354ZC UT WOS:000089360300001 ER PT J AU Quigley, EMM Hurley, D AF Quigley, EMM Hurley, D TI Autism and the gastrointestinal tract SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Editorial Material ID CHILDREN; DISORDER; DISEASE; COLITIS; MEASLES C1 Natl Univ Ireland Univ Coll Cork, Dept Med, Cork, Ireland. RP Quigley, EMM (reprint author), Natl Univ Ireland Univ Coll Cork, Cork Univ Hosp, Cork, Ireland. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x EDWARDS LL, 1991, MOVEMENT DISORD, V6, P151, DOI 10.1002/mds.870060211 Fernandez-Banares F, 1999, AM J GASTROENTEROL, V94, P418 Frith U, 1991, AUTISM ASPERGER SYND Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Lightdale JR, 2000, GASTROENTEROLOGY, V118, pA66 MCCASHLAND TJ, 1992, J CLIN GASTROENTEROL, V15, P52 *MED RES COUNC, 1999, REP STRAT DEV GROUP Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P1389 PFEIFFER RF, 1996, SEMIN NEUROL, V16 REICHELT K-L, 1990, Journal of Applied Nutrition, V42, P1 Rodier PM, 1996, J COMP NEUROL, V370, P247, DOI 10.1002/(SICI)1096-9861(19960624)370:2<247::AID-CNE8>3.0.CO;2-2 RODIER PM, 2000, SCI AM, V282, P38 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 1999, ITAL J GASTROENTEROL, V31, P247 Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 2000, LANCET, V355, P1379 NR 19 TC 13 Z9 13 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0002-9270 J9 AM J GASTROENTEROL JI Am. J. Gastroenterol. PD SEP PY 2000 VL 95 IS 9 BP 2154 EP 2156 PG 3 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 354BR UT WOS:000089310400002 PM 11007210 ER PT J AU Wakefield, AJ Anthony, A Murch, SH Thomson, M Montgomery, SM Davies, S O'Leary, JJ Berelowitz, M Walker-Smith, JA AF Wakefield, AJ Anthony, A Murch, SH Thomson, M Montgomery, SM Davies, S O'Leary, JJ Berelowitz, M Walker-Smith, JA TI Enterocolitis in children with developmental disorders (Retracted article. See vol. 105, pg. 1214, 2010) SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID NODULAR LYMPHOID HYPERPLASIA; COMMON VARIABLE IMMUNODEFICIENCY; NONSPECIFIC COLITIS; LYMPHONODULAR HYPERPLASIA; SMALL-INTESTINE; MEASLES-VIRUS; T-CELLS; AUTISM; HYPOGAMMAGLOBULINEMIA; INFECTION AB OBJECTIVE: Intestinal pathology, i.e., ileocolonic lymphoid nodular hyperplasia (LNH) and mucosal inflammation, has been described in children with developmental disorders. This study describes some of the endoscopic and pathological characteristics in a group of children with developmental disorders (affected children) that are associated with behavioral regression and bowel symptoms, and compares them with pediatric controls. METHODS: Ileocolonoscopy and biopsy were performed on 60 affected children (median age 6 yr, range 3-16; 53 male). Developmental diagnoses were autism (50 patients), Asperger's syndrome (five), disintegrative disorder (two), attention deficit hyperactivity disorder (ADHD) (one), schizophrenia (one), and dyslexia (one). Severity of ileal LNH was graded (0-3) in both affected children and 37 developmentally normal controls (median age 11 yr, range 2-13 yr) who were investigated for possible inflammatory bowel disease (IBD). Tissue sections were reviewed by three pathologists and scored on a standard proforma. Data were compared with ileocolonic biopsies from 22 histologically normal children (controls) and 20 children with ulcerative colitis (UC), scored in an identical manner. Gut pathogens were sought routinely. RESULTS: Ileal LNH was present in 54 of 58 (93%) affected children and in five of 35 (14.3%) controls (p < 0.001). Colonic LNH was present in 18 of 60 (30%) affected children and in two of 37 (5.4%) controls (p < 0.01). Histologically, reactive follicular hyperplasia was present in 46 of 52 (88.5%) ileal biopsies from affected children and in four of 14 (29%) with UC, but not in non-IBD controls (p < 0.01). Active ileitis was present in four of 51 (8%) affected children but not in controls. Chronic colitis was identified in 53 of 60 (88%) affected children compared with one of 22 (4.5%) controls and in 20 of 20 (100%) with UC. Scores of frequency and severity of inflammation were significantly greater in both affected children and those with UC, compared with controls (p < 0.001). CONCLUSIONS: A new variant of inflammatory bowel disease is present in this group of children with developmental disorders. (Am J Gastroenterol 2000;95:2285-2295. (C) 2000 by Am. Cell. of Gastroenterology). C1 Univ London, Royal Free & Univ Coll, Sch Med, Dept Med,Inflammatory Bowel Dis Study Grp, London NW3 2QG, England. Univ London, Royal Free & Univ Coll, Sch Med, Dept Histopathol, London NW3 2QG, England. Univ London, Royal Free & Univ Coll, Sch Med, Dept Paediat Gastroenterol, London NW3 2QG, England. Univ London, Royal Free & Univ Coll, Sch Med, Dept Paediat Psychiat, London NW3 2QG, England. Coombe Womens Hosp, Univ Dept Pathol, Dublin, Ireland. Trinity Coll Dublin, Dublin, Ireland. RP Wakefield, AJ (reprint author), Univ London, Royal Free & Univ Coll, Sch Med, Dept Med,Inflammatory Bowel Dis Study Grp, Royal Free Campus, London NW3 2QG, England. 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J. Gastroenterol. PD SEP PY 2000 VL 95 IS 9 BP 2285 EP 2295 PG 11 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 354BR UT WOS:000089310400022 PM 11007230 ER PT J AU Tassone, F Hagerman, RJ Chamberlain, WD Hagerman, PJ AF Tassone, F Hagerman, RJ Chamberlain, WD Hagerman, PJ TI Transcription of the FMR1 gene in individuals with fragile X syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE mental retardation; autism; gene silencing; transcription; RT-PCR ID PREMATURE OVARIAN FAILURE; RAPID ANTIBODY-TEST; CARRIER FEMALES; CGG REPEAT; FULL MUTATION; PREMUTATION; PCR; INSTABILITY; EXPRESSION; EXPANSION AB Fragile X syndrome generally arises as a consequence of a large expansion of a CGG trinucleotide repeat element that is located in the GC-rich promoter region of the fragile X mental retardation gene (FMR1). In the conventional model for fragile X, clinical involvement arises as a consequence of silencing of the FMR1 gene, with the attendant loss of FMR1 protein (FMRP). However, it has recently been demonstrated that most males with large premutation alleles (100-200 repeats), or with unmethylated full mutation alleles, have FMR1 mRNA levels that are higher than normal, despite reduced levels of FMRP. In the current work, we extend and confirm these observations using quantitative (fluorescent) reverse transcription polymerase chain reaction on larger sample populations, establishing that even for smaller premutation alleles (55-100 repeats) the mRNA levels are significantly elevated (mean 2.1-fold elevation; P = 3.9 x 10(-3)), relative to normal controls. Thus, an abnormal molecular phenotype is established close to the upper end of the normal range. We also demonstrate that the levels of FMR1 mRNA are elevated in females with premutation alleles; however, the mRNA levels are more varied than in the males, and are attenuated in a manner that is consistent with the fraction of normal alleles that are active in any given individual. Finally, we demonstrate that in lymphoblastoid cells derived from a patient with a severe form of fragile X caused by a point mutation in the second KH domain of the gene, but with a normal CGG element (25 repeats), the FMR1 mRNA level is normal. Thus, although models in which FMRP level (or level of function) modulates transcriptional activity remain viable, other explanations for the elevated message levels, including direct (cis) effects of the CGG element on transcription, must also be considered. Am. J. Med. Genet. (Semin. Med. Genet.) 97:195-203, 2000. (C) 2000 Wiley-Liss, Inc. C1 Univ Colorado, Hlth Sci Ctr, Sch Med, Dept Biochem & Mol Genet B121, Denver, CO 80262 USA. 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J. Med. Genet. PD FAL PY 2000 VL 97 IS 3 BP 195 EP 203 DI 10.1002/1096-8628(200023)97:3<195::AID-AJMG1037>3.0.CO;2-R PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 389WC UT WOS:000166260800005 PM 11449488 ER PT J AU Roginski, RS Raj, BKM Finkernagel, SW Sciorra, LJ AF Roginski, RS Raj, BKM Finkernagel, SW Sciorra, LJ TI Chromosome mapping of the human homologue of a new glutamate receptor gene suggests roles in neuroprotection and autism SO ANESTHESIOLOGY LA English DT Meeting Abstract C1 UMDNJ, Robert Wood Johnson Med Sch, New Brunswick, NJ USA. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0003-3022 J9 ANESTHESIOLOGY JI Anesthesiology PD SEP PY 2000 VL 93 IS 3A SU S MA A739 BP U188 EP U188 PG 1 WC Anesthesiology SC Anesthesiology GA 351BU UT WOS:000089136800700 ER PT J AU Wang, CH Miller, MB Hillman, RE Miles, JH AF Wang, CH Miller, MB Hillman, RE Miles, JH TI Identification of a novel transcript in linkage disequilibrium with autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 TC 9 Z9 9 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2000 VL 48 IS 3 MA 8 BP 512 EP 513 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 349BU UT WOS:000089024600360 ER PT J AU Roseman, B Schneider, E Crimmins, D Bostwick, H Visintainer, P Dong, S Accardo, P AF Roseman, B Schneider, E Crimmins, D Bostwick, H Visintainer, P Dong, S Accardo, P TI The use of secretin to treat autism: A pilot study SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2000 VL 48 IS 3 MA P86 BP 541 EP 542 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 349BU UT WOS:000089024600466 ER PT J AU Jacobson, JW AF Jacobson, JW TI Early intensive behavioral intervention: Emergence of a consumer-driven service model SO BEHAVIOR ANALYST LA English DT Article; Proceedings Paper CT Annual Conference of the New-York-State-Association-for-Behavior-Analysis CY SEP, 1997 CL TARRYTOWN, NEW YORK SP New York State Assoc Behav Anal DE parents; advocacy; early intervention; certification; public policy ID DEVELOPMENTAL-DISABILITIES; AUTISTIC-CHILDREN; PERSPECTIVE; EDUCATION; PROGRAM; ISSUES; REFORM; LEGAL; AGE AB Parents are becoming influential stimulators and shapers of public policy in regard to educational services for their children. Increasingly, this advocacy has created a controversy about the role of applied behavior analysis as a foundation for early intensive behavioral intervention in autism. Uncertainties exist in policy regarding the role of behavior analysis in early intervention and the capacity of behavior analysis to field a trained work force. Based on contacts with parents of children with autism and information available in a variety of forms on the Internet, there is a rising demand for fundamentally better early intervention services that are available and accessible, provide active intervention, and are based on principles of behavior analysis. Contemporary movements in special and early education, however, appear to be nonconducive to scientifically based treatments, and school districts seem hostile to an increasing role for behavior analysis and to the establishment of services that are responsive to changing parental priorities for the education of their children with autism and related disorders. C1 Independent Living Capital Dist Inc, Schenectady, NY USA. RP Jacobson, JW (reprint author), 627 Plymouth Ave, Schenectady, NY 12308 USA. 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PD FAL PY 2000 VL 23 IS 2 BP 149 EP 171 PG 23 WC Psychology, Clinical SC Psychology GA 373RT UT WOS:000165303200002 PM 22478344 ER PT J AU Ohnishi, T Matsuda, H Hashimoto, T Kunihiro, T Nishikawa, M Uema, T Sasaki, M AF Ohnishi, T Matsuda, H Hashimoto, T Kunihiro, T Nishikawa, M Uema, T Sasaki, M TI Abnormal regional cerebral blood flow in childhood autism SO BRAIN LA English DT Article DE autism; theory of mind; regional cerebral blood flow (rCBF); single photon emission computed tomography ID INFANTILE-AUTISM; BRAIN; MIND; CHILDREN; DISORDER; DEFICITS; ADULTS; STATE; SPECT AB Neuroimaging studies of autism have shown abnormalities in the limbic system and cerebellar circuits and additional sites. These findings are not, however, specific or consistent enough to build up a coherent theory of the origin and nature of the brain abnormality in autistic patients. Twenty-three children,vith infantile autism and 26 nonautistic controls matched for IQ and age were examined using brain-perfusion single photon emission computed tomography with technetium-99m ethyl cysteinate dimer, In autistic subjects, we assessed the relationship between regional cerebral blood flow (rCBF) and symptom profiles. Images were anatomically normalized, and voxel-by-voxel analyses were performed. Decreases in rCBF in autistic patients compared with the control group were identified in the bilateral insula, superior temporal gyri and left prefrontal cortices, Analysis of the correlations between syndrome scores and rCBF revealed that each syndrome was associated with a specific pattern of perfusion in the limbic system and the medial prefrontal cortex, The results confirmed the associations of (i) impairments in communication and social interaction that are thought to be related to deficits in the theory of mind (ToM) with altered perfusion in the medial prefrontal cortex and anterior cingulate gyrus, and (ii) the obsessive desire for sameness with altered perfusion in the right medial temporal lobe, The perfusion abnormalities seem to be related to the cognitive dysfunction observed in autism, such as deficits in ToM, abnormal responses to sensory stimuli, and the obsessive desire for sameness. 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PD SEP PY 2000 VL 18 BP 319 EP 333 DI 10.1348/026151000165715 PN 3 PG 15 WC Psychology, Developmental SC Psychology GA 353EW UT WOS:000089262700001 ER PT J AU Lewis, V Norgate, S Collis, G Reynolds, R AF Lewis, V Norgate, S Collis, G Reynolds, R TI The consequences of visual impairment for children's symbolic and functional play SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID BLIND-CHILDREN; AUTISM; PRESCHOOLERS AB Children with visual impairments are reported to be delayed in producing pretend play in naturalistic settings. This study examined the play of 18 children with visual impairments aged between 21 and 86 months on two structured tests of play. Appropriate functional play with miniature versions of everyday objects was distinguished from symbolic play involving substituting one object for another, pretending something has a property it does not have, or referring to something as if it were present. As a group, the children showed impaired functional and symbolic play. However, four children met the diagnostic criteria for autism and engaged in little or no play. When these children were excluded, the remaining children had lower functional play test scores than expected for their chronological age, but symbolic play test scores which were at the appropriate level for their chronological age. The functional and symbolic play of children with no vision or only light perception did nor differ significantly from children with some vision. The production of symbolic play was strongly related to language ability, although functional play was not related to language ability. It is argued that children with visual impairment, but no behaviours characteristic of autism, can develop the ability to play both functionally and symbolically, but that lack of visual access to play materials may limit their ability to demonstrate these skills. C1 Open Univ, Sch Educ, Ctr Human Dev & Learning, Milton Keynes MK4 6AA, Bucks, England. Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. RP Lewis, V (reprint author), Open Univ, Sch Educ, Ctr Human Dev & Learning, Milton Keynes MK4 6AA, Bucks, England. 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PD SEP PY 2000 VL 70 BP 464 EP 464 PN 3 PG 1 WC Psychology, Educational SC Psychology GA 356YP UT WOS:000089472000015 ER PT J AU Ben Shalom, D AF Ben Shalom, D TI Developmental depersonalization: The prefrontal cortex and self-functions in autism SO CONSCIOUSNESS AND COGNITION LA English DT Editorial Material DE self model; limbic system; prefrontal cortex; autism ID ATTENTION; CHILDREN; MODEL; MIND AB The human self model suggests that the construct of self involves functions such as agency, body-centered spatial perspectivity, and long-term unity. Vogeley, Kurthen, Falkai. and Maieret (1999) suggest that agency is subserved by the prefrontal cortex and other association areas of the cortex, spatial perspectivity by the prefrontal cortex and the parietal lobes, and long-term unity by the prefrontal cortex and the temporal lobes and that all of these functions are impaired in schizophrenia. Exploring the connections between the prefrontal cortex and the construct of self, the present article extends the application of the self model to autism. It suggests that in contrast to schizophrenia, agency and spatial perspectivity are probably preserved in autism, but that, similarly to schizophrenia, long-term unity is probably impaired. This hypothesis is compatible with a model of neuropsychological dysfunction in autism in a neural network including parts of the prefrontal cortex, the temporal lobes, and the cerebellum. (C) 2000 Academic Press. C1 Ben Gurion Univ Negev, Zlotowski Ctr Neurosci, IL-84105 Beer Sheva, Israel. RP Ben Shalom, D (reprint author), Ben Gurion Univ Negev, Dept Foreign Literatures & Linguist, IL-84105 Beer Sheva, Israel. 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Opin. Psychiatr. PD SEP PY 2000 VL 13 IS 5 BP 481 EP 484 DI 10.1097/00001504-200009000-00003 PG 4 WC Psychiatry SC Psychiatry GA 351EB UT WOS:000089143900003 ER PT J AU Dawson, G Ashman, SB Carver, LJ AF Dawson, G Ashman, SB Carver, LJ TI The role of early experience in shaping behavioral and brain development and its implications for social policy SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Review ID CORTICOTROPIN-RELEASING-FACTOR; LONG-TERM POTENTIATION; QUANTITATIVE DENDRITIC ANALYSIS; MATERNAL DEPRESSIVE SYMPTOMS; MOTHER INFANT INTERACTIONS; PITUITARY-ADRENAL AXIS; RHESUS-MONKEY INFANTS; PRENATAL STRESS; NONDEPRESSED MOTHERS; FOLLOW-UP AB This article provides a targeted review of the scientific literature on the effects of experience on early brain and behavioral development and later outcome as it pertains to risk for some forms of child psychopathology. It is argued that ample evidence exists indicating that the prenatal and early postnatal years likely represent a sensitive period with respect to the effects of stress on the developing nervous system and behavioral outcome, and with respect to the long-term beneficial effects of early interventions on brain and behavioral development for some genetically based disorders, such as phenylketonuria and autism. Moreover, evidence suggests that parental mental health during the first years of life has a significant influence on early brain activity and behavior, and long-term behavioral outcome. It is concluded that, although prevention and early intervention efforts should not exclusively focus on the earliest years of development, such efforts should begin during this period. 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PD FAL PY 2000 VL 12 IS 4 BP 695 EP 712 DI 10.1017/S0954579400004089 PG 18 WC Psychology, Developmental SC Psychology GA 390PA UT WOS:000166304500008 PM 11202040 ER PT J AU Powell, JE Edwards, A Edwards, M Pandit, BS Sungum-Paliwal, SR Whitehouse, W AF Powell, JE Edwards, A Edwards, M Pandit, BS Sungum-Paliwal, SR Whitehouse, W TI Changes in the incidence of childhood autism and other autistic spectrum disorders in preschool children from two areas of the West Midlands, UK SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PREVALENCE; JAPAN AB The incidence of childhood autism and other autistic spectrum disorders (ASDs) in preschool children was determined for two areas of the West Midlands between 1991 and 1996. children diagnosed before the age of 5 sears and residing within the study areas at diagnosis were detected from the records of four child development centres. The incidence rate per 10000 children per year for the combined areas was 8.3 for all children with ASDs, 3.5 for classical childhood autism (CA), and 4.8 for of her ASDs. Rates were similar in both areas, despite differences in social deprivation and proportions of ethnic minorities. While rates for classical CA increased by 18% per year, a much larger increase (55% per year) was seen for 'other ASDs', suggesting that clinicians are becoming increasingly able and/or willing to diagnose ASDs in preschool children. C1 Univ Birmingham, Dept Publ Hlth & Epidemiol, Birmingham B15 2TT, W Midlands, England. Stonydelph Hlth Ctr, Tamworth, NSW, Australia. Birmingham Childrens Hosp NHS Trust, Birmingham, W Midlands, England. Parkview Clin, Birmingham, W Midlands, England. Birmingham Childrens Hosp NHS Trust, Birmingham, W Midlands, England. RP Powell, JE (reprint author), Univ Birmingham, Dept Publ Hlth & Epidemiol, Birmingham B15 2TT, W Midlands, England. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Fombonne E, 1996, J AUTISM DEV DISORD, V26, P673, DOI 10.1007/BF02172357 FOMBONNE E, 1992, SOC PSYCH PSYCH EPID, V27, P203, DOI 10.1007/BF00789007 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Hennekens CH, 1987, EPIDEMIOLOGY MED Honda H, 1996, BRIT J PSYCHIAT, V169, P228, DOI 10.1192/bjp.169.2.228 Kanner L, 1943, NERV CHILD, V2, P217 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 *OFF POP CENS SURV, 1993, 1991 CENS STAFF *OFF POP CENS SURV, 1992, 1991 CENS W MIDL RITVO ER, 1989, AM J PSYCHIAT, V146, P194 Takei N, 1996, BRIT J PSYCHIAT, V169, P671 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, 1996, BRIT MED J, V312, P327 Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 WING L, 1980, BRIT J PSYCHIAT, V137, P410, DOI 10.1192/bjp.137.5.410 Wing L, 1993, Eur Child Adolesc Psychiatry, V2, P61, DOI 10.1007/BF02098832 World Health Organization, 1993, ICD10 CLASS MENT BEH NR 22 TC 64 Z9 67 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD SEP PY 2000 VL 42 IS 9 BP 624 EP 628 DI 10.1017/S001216220000116X PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 360AP UT WOS:000089644500008 PM 11034456 ER PT J AU Massey, NG Wheeler, JJ AF Massey, NG Wheeler, JJ TI Acquisition and generalization of activity schedules and their effects on task engagement in a young child with autism in an inclusive pre-school classroom SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article ID PHOTOGRAPHIC ACTIVITY SCHEDULES; PROMPTS AB Efficacy of individualized activity schedules with a 4-year old child diagnosed with autism who attended an integrated public pre-school classroom was examined. Graduated physical guidance and a system of most-to-least prompts were used during skill acquisition stages with teacher proximity and level of prompts being eventually faded. A multiple baseline across activities (work and leisure) assessed performance across baseline, treatment, and maintenance conditions with stimulus generalization being assessed during a third activity (lunch). Results support the findings from MacDuff: Krantz, and McClannahan (1993) in that a child with autism can successfully acquire the skills necessary to independently follow activity schedules and generalize these skills to other settings with minimal training. The study represents an advance in applied research in the use of visual cues with children who experience autism in school settings; most notably an integrated pre-school classroom serving children with disabilities and typical same-aged peers. C1 Tennessee Technol Univ, Cookeville, TN 38505 USA. Vanderbilt Univ, Peabody Coll, Nashville, TN 37203 USA. RP Wheeler, JJ (reprint author), Tennessee Technol Univ, Box 5074, Cookeville, TN 38505 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th HALL LJ, 1995, EDUC TRAIN MENT RET, V30, P208 Hodgdon L. A., 1995, VISUAL STRATEGIES IM KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P137, DOI 10.1901/jaba.1993.26-137 MACDUFF GS, 1993, J APPL BEHAV ANAL, V26, P89, DOI 10.1901/jaba.1993.26-89 MESIBOV GB, 1994, CURR I AUT, P195 PIERCE KL, 1994, J APPL BEHAV ANAL, V27, P471, DOI 10.1901/jaba.1994.27-471 Quill K. A., 1995, FOCUS AUTISTIC BEHAV, V10, P10, DOI DOI 10.1177/108835769501000302 SYMONS F, 1994, J BEHAV THER EXP PSY, V25, P317, DOI 10.1016/0005-7916(94)90040-X NR 9 TC 38 Z9 38 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 0013-1237 J9 EDUC TRAIN MENT RET JI Educ. Train. Mental Retard. Dev. Disabil. PD SEP PY 2000 VL 35 IS 3 BP 326 EP 335 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 432UN UT WOS:000168714200009 ER PT J AU Kielinen, M Linna, SL Moilanen, I AF Kielinen, M Linna, SL Moilanen, I TI Autism in Northern Finland SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE Autism; autistic spectrum; cumulative incidence; CARS; prevalence ID INFANTILE-AUTISM; CHILDHOOD AUTISM; TOTAL POPULATION; PREVALENCE; EPIDEMIOLOGY; JAPAN; DISORDERS; CHILDREN; FRENCH AB Resent research reports show that autistic spectrum disorders may actually be more common than previously believed. General awareness and clinical knowledge of these disorders have increased, and the criteria in the ICD-10 and the DSM-IV are also now more detailed. The diagnostic criteria and the methods of ascertainment influence the prevalence. The age specific incidence obtained in this study showed the cumulative incidence to be lowest, 6.1 per 10 000, in the oldest age group of 15- to 18-year-old children, and highest, 20.7 per 10 000, in the age group of 5-7 year-olds, when the criteria of the ICD-10 and the DSM-IV were used. In this study, almost 50% of the autistic cases had a tested IQ above 70. The degree of autism, as assessed by the Childhood Autism Rating Scale (CARS), varied from mild autistic features in 8.5% through moderate in 58.5% to severe in 33.0%. C1 Univ Oulu, Dept Pediat, Clin Child Psychiat, FIN-90220 Oulu, Finland. RP Kielinen, M (reprint author), Univ Oulu, Dept Pediat, Clin Child Psychiat, Kajaanintie 52, FIN-90220 Oulu, Finland. 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Child Adolesc. Psych. PD SEP PY 2000 VL 9 IS 3 BP 162 EP 167 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 366NP UT WOS:000090011700002 PM 11095038 ER PT J AU Luteijn, EF Serra, M Jackson, S Steenhuis, MP Althaus, M Volkmar, F Minderaa, R AF Luteijn, EF Serra, M Jackson, S Steenhuis, MP Althaus, M Volkmar, F Minderaa, R TI How unspecified are disorders of children with a pervasive developmental disorder not otherwise specified? A study of social problems in children with PDD-NOS and ADHD SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE social problems; PDD-NOS-ADHD-autism; parent questionnaires ID DEFICIT HYPERACTIVITY DISORDER; DSM-III-R; VISUAL-ATTENTION; DIAGNOSIS; AUTISM; ABILITIES; IV AB This study examines possible differences and similarities between social behaviour problems in children with problems classified as pervasive developmental disorder not otherwise specified (PDD-NOS) and a group of children with problems classified as ADHD, as measured by parent questionnaires. The instruments involved were the CBCL (Child Behaviour Checklist), the ABC (Autism Behaviour Checklist) and a new instrument: the CSBQ (Children's Social Behaviour Questionnaire). In comparing the PDD-NOS group and the ADHD group, the results show that, according to parent reports, both groups have severe problems in executing appropriate social behaviour, but the PDD-NOS group can be distinguished from the ADHD group by the nature and the extent of these problems. The PDD-NOS group had significantly more social problems las measured by the CBCL Social scale), withdrawn problems las measured by the CBCL Withdrawn scale) and PDD-specific problems las measured on the ABC Relating scale, the ABC Language scale, the CSBQ total score, the CSBQ Social Interaction scale and CBSQ Communication scale). In addition, although the descriptions of the social problems are global, i.e. on scale level, the results also show that the social problems of PDD-NOS children can be positively formulated and described as at least including severe social interaction problems, withdrawn behaviours and communication problems. C1 Univ Groningen, Ctr Child & Adolescent Psychiat, Groningen, Netherlands. Univ Groningen, Dept Dev Psychol, Groningen, Netherlands. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Luteijn, EF (reprint author), Hanzeplein 1, NL-9713 GZ Groningen, Netherlands. CR Achenbach TM, 1991, MANUAL CHILD BEHAV C Althaus M, 1996, CHILD NEUROPSYCHOL, V2, P17, DOI 10.1080/09297049608401347 Althaus M, 1996, CHILD NEUROPSYCHOL, V2, P30, DOI 10.1080/09297049608401348 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Barkley R. A., 1997, ADHD NATURE SELFCONT Barkley R. A., 1997, ADHD NATURE SELF CON Barkley RA, 1990, ATTENTION DEFICIT HY, V2nd Barkley R.A., 1997, ATTENTION DEFICIT HY BARTKO JJ, 1976, PSYCHOL BULL, V83, P762, DOI 10.1037//0033-2909.83.5.762 Buitelaar JK, 1998, J CHILD PSYCHOL PSYC, V39, P911, DOI 10.1017/S0021963098002820 Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 Clark T., 1999, EUROPEAN CHILD ADOLE, V8, P850 Cohen D. 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Child Adolesc. Psych. PD SEP PY 2000 VL 9 IS 3 BP 168 EP 179 PG 12 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 366NP UT WOS:000090011700003 PM 11095039 ER PT J AU Nyden, A Hjelmquist, E Gillberg, C AF Nyden, A Hjelmquist, E Gillberg, C TI Autism spectrum and attention - deficit disorders in girls. Some neuropsychological aspects SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE attention-deficit hyperactivity; PDDNOS neuropsychology girls ID HYPERACTIVITY DISORDER; SEX-DIFFERENCES; CHILDREN; ADHD; IMPAIRMENTS; CHILDHOOD; BOYS AB This study compared the neuropsychological test profiles of non-mentally retarded girls and boys consecutively referred to a neuropsychiatric clinic and those of contrast cases of girls from mainstream classrooms of one Goteborg school district. To avoid overreliance on the male prototype with regard to diagnostic criteria the clinical group comprised a mixed sample of girls and boys without diagnostic subgrouping. Clinic girls had a lower IQ than comparison girls. Girls were more impaired than the boys with respect to executive functions and scored less well on theory of mind tasks. Previous studies have shown girls with autism and mental retardation to be more severely affected than boys both with regard to level of intellectual functioning and overall measures of brain dysfunction. The present study indicates that clinic girls with a variety of neuropsychiatric disorders at higher levels of intellectual functioning (some of which met diagnostic criteria for autism spectrum disorder) may also be more severely affected than boys with corresponding types of "surface" problems. C1 Gothenburg Univ, Dept Child & Adolescent Psychiat, S-41124 Gothenburg, Sweden. Univ Gothenburg, Dept Psychol, SE-40530 Gothenburg, Sweden. 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PD SEP PY 2000 VL 9 IS 3 BP 180 EP 185 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 366NP UT WOS:000090011700004 PM 11095040 ER PT J AU Demeter, K AF Demeter, K TI Assessing the developmental level in Rett syndrome: an alternative approach? SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE Rett syndrome; developmental level; learning; assessment strategies ID PRESERVED SPEECH VARIANT; COMMUNICATION ABILITIES; DIFFERENTIAL-DIAGNOSIS; COMPLEX; AUTISM; WORKSHOP; MEMORY; GIRLS; XQ28 AB Reviewing the literature concerning the developmental level of Rett Syndrome (RS) girls, one is confronted with important difficulties in interpreting the meaning of the results of these studies. Anecdotal evidence from parents suggests that RS girls might understand more than these studies indicate. Analyses of these examples suggests that there are other learning mechanisms than those assessed in classical developmental tests, which are important for RS girls in order to learn to know and understand their world. Studies on learning and memory in early infancy have demonstrated a variety of such mechanisms and particularly classical conditions provide a theoretical framework to understand the learning processes of these girls. Based on this theoretical background, an assessment strategy can be developed, with the possibility to differentiate even very low functioning RS girls. C1 Univ Hosp St Rafael, Ctr Dev Disabil, B-3000 Louvain, Belgium. RP Demeter, K (reprint author), Univ Hosp St Rafael, Ctr Dev Disabil, Kapucijnenvoer 33, B-3000 Louvain, Belgium. 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Y., 1992, HIGH FUNCTIONING IND, P11 TUPPER L, 1999, WORKSH ANN STAT C AU VANBOURGONDIEN ME, 1987, J AUTISM DEV DISORD, V17, P417 Wing L., 1992, HIGH FUNCTIONING IND, P129 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wing L, 1991, AUTISM ASPERGER SYND, P93, DOI DOI 10.1017/CB09780511526770.003 WING L, 1981, PSYCHOL MED, V11, P115 NR 50 TC 10 Z9 11 PU NATL ASSOC GIFTED CHILDREN PI WASHINGTON PA 1707 L ST, NW, STE 550, WASHINGTON, DC 20006 USA SN 0016-9862 J9 GIFTED CHILD QUART JI Gifted Child Q. PD FAL PY 2000 VL 44 IS 4 BP 222 EP 230 DI 10.1177/001698620004400403 PG 9 WC Education, Special SC Education & Educational Research GA 368YJ UT WOS:000090144800003 ER PT J AU Charman, T AF Charman, T TI Asperger syndrome or high-functioning autism? SO INFANT AND CHILD DEVELOPMENT LA English DT Book Review C1 Inst Child Hlth, London, England. RP Charman, T (reprint author), Inst Child Hlth, 30 Guilford St, London, England. RI Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR SCHOPLER E, 1998, ASPERGER SYNDROME HI NR 1 TC 0 Z9 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1522-7227 J9 INFANT CHILD DEV JI Infant Child Dev. PD SEP PY 2000 VL 9 IS 3 BP 173 EP 175 PG 3 WC Psychology, Developmental SC Psychology GA 359TN UT WOS:000089628300006 ER PT J AU Schopler, E AF Schopler, E TI Asperger syndrome or high-functioning autism? Reply from Editor, Eric Schopler, University of North Carolina SO INFANT AND CHILD DEVELOPMENT LA English DT Editorial Material C1 Univ N Carolina, Chapel Hill, NC 27515 USA. RP Schopler, E (reprint author), Univ N Carolina, Chapel Hill, NC 27515 USA. NR 0 TC 0 Z9 0 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1522-7227 J9 INFANT CHILD DEV JI Infant Child Dev. PD SEP PY 2000 VL 9 IS 3 BP 175 EP 175 PG 1 WC Psychology, Developmental SC Psychology GA 359TN UT WOS:000089628300007 ER PT J AU Houzel, D Marin-Friley, I Moussaoui, E AF Houzel, D Marin-Friley, I Moussaoui, E TI Autism clinic moving SO INFANT MENTAL HEALTH JOURNAL LA English DT Meeting Abstract C1 CHR Clemenceau, Clemenceau, France. NR 0 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD SEP-OCT PY 2000 VL 21 IS 4-5 MA 258 BP 315 EP 315 PG 1 WC Psychology, Developmental SC Psychology GA 357DG UT WOS:000089482800255 ER PT J AU Marin-Friley, I Moussaoui, E Houzel, D AF Marin-Friley, I Moussaoui, E Houzel, D TI Early signs in infant autism SO INFANT MENTAL HEALTH JOURNAL LA English DT Meeting Abstract C1 CHR Clemenceau, Caen, France. NR 0 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD SEP-OCT PY 2000 VL 21 IS 4-5 MA 308 BP 332 EP 332 PG 1 WC Psychology, Developmental SC Psychology GA 357DG UT WOS:000089482800305 ER PT J AU De Kimpe, V Tremblay, PH Doehring, PJ AF De Kimpe, V Tremblay, PH Doehring, PJ TI Training professionals in the use of the CHAT (Checklist for Autism in Toddlers) SO INFANT MENTAL HEALTH JOURNAL LA English DT Meeting Abstract C1 Douglas Hosp, Montreal, PQ, Canada. Riviere Des Prairies Hosp, Montreal, PQ, Canada. NR 0 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD SEP-OCT PY 2000 VL 21 IS 4-5 MA 414 BP 367 EP 367 PG 1 WC Psychology, Developmental SC Psychology GA 357DG UT WOS:000089482800409 ER PT J AU Marin-Friley, I Moussaoui, E Houzel, D AF Marin-Friley, I Moussaoui, E Houzel, D TI Early signs in infant autism SO INFANT MENTAL HEALTH JOURNAL LA English DT Meeting Abstract C1 CHR Clemenceau, Caen, France. NR 0 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD SEP-OCT PY 2000 VL 21 IS 4-5 MA 446 BP 378 EP 378 PG 1 WC Psychology, Developmental SC Psychology GA 357DG UT WOS:000089482800439 ER PT J AU Delion, P AF Delion, P TI The baby at risk of autism, according to semiotics SO INFANT MENTAL HEALTH JOURNAL LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD SEP-OCT PY 2000 VL 21 IS 4-5 MA 448 BP 379 EP 379 PG 1 WC Psychology, Developmental SC Psychology GA 357DG UT WOS:000089482800441 ER PT J AU Maestro, S Muratori, F Milone, A Espasa, FP AF Maestro, S Muratori, F Milone, A Espasa, FP TI Psychopathological study of the early onset of autism and PDD derived from home videos SO INFANT MENTAL HEALTH JOURNAL LA English DT Meeting Abstract C1 Univ Pisa, I-56100 Pisa, Italy. Univ Geneva, CH-1211 Geneva 4, Switzerland. NR 0 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD SEP-OCT PY 2000 VL 21 IS 4-5 MA 497 BP 395 EP 395 PG 1 WC Psychology, Developmental SC Psychology GA 357DG UT WOS:000089482800490 ER PT J AU Palacio-Espasa, F Polytarides, V Maestro, S Golse, B Stern, D AF Palacio-Espasa, F Polytarides, V Maestro, S Golse, B Stern, D TI Early onset of developmental psychopathology through the study of home videos - The first year of life of children presenting autism and pervasive developmetal disorders SO INFANT MENTAL HEALTH JOURNAL LA English DT Meeting Abstract C1 Univ Paris 06, F-75252 Paris 05, France. Univ Pisa, I-56100 Pisa, Italy. Univ Geneva, CH-1211 Geneva 4, Switzerland. NYU, New York, NY USA. NR 0 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD SEP-OCT PY 2000 VL 21 IS 4-5 MA 496 BP 395 EP 395 PG 1 WC Psychology, Developmental SC Psychology GA 357DG UT WOS:000089482800489 ER PT J AU Polytarides, V Philippe, A Danon, G Mazet, P AF Polytarides, V Philippe, A Danon, G Mazet, P TI Face-to-face interactive refusal, early signs of infantile autism syndrome in home-video study SO INFANT MENTAL HEALTH JOURNAL LA English DT Meeting Abstract C1 Univ Paris 06, F-75252 Paris 05, France. NR 0 TC 0 Z9 0 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD SEP-OCT PY 2000 VL 21 IS 4-5 MA 498 BP 395 EP 395 PG 1 WC Psychology, Developmental SC Psychology GA 357DG UT WOS:000089482800491 ER PT J AU Geckeler, AS Libby, ME Graff, RB Ahearn, WH AF Geckeler, AS Libby, ME Graff, RB Ahearn, WH TI Effects of reinforcer choice measured in single-operant and concurrent-schedule procedures SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE reinforcement; choice; developmental disabilities AB The effects of choice and no choice of reinforcer on the response rates of 3 children with autism were compared across single-operant and concurrent-schedule procedures. No consistent differences in responding between choice and no-choice components emerged during single-operant phases. During the concurrent-schedule phases, however, all participants had substantially higher rates of responding to the button that led to a choice among reinforcers than to the button that did nor lead to choice. C1 New England Ctr Children, Southborough, MA 01772 USA. Northeastern Univ, Boston, MA 02115 USA. RP Geckeler, AS (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. CR FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Fisher WW, 1997, J APPL BEHAV ANAL, V30, P423, DOI 10.1901/jaba.1997.30-423 Graff RB, 1999, J APPL BEHAV ANAL, V32, P161, DOI 10.1901/jaba.1999.32-161 GRAFF RB, 1998, BEHAV INTERVENT, V13, P249, DOI 10.1002/(SICI)1099-078X(199811)13:4<249::AID-BIN19>3.0.CO;2-1 Lerman DC, 1997, J APPL BEHAV ANAL, V30, P411, DOI 10.1901/jaba.1997.30-411 PACE GM, 1985, J APPL BEHAV ANAL, V18, P249, DOI 10.1901/jaba.1985.18-249 NR 6 TC 3 Z9 4 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD FAL PY 2000 VL 33 IS 3 BP 347 EP 351 DI 10.1901/jaba.2000.33-347 PG 5 WC Psychology, Clinical SC Psychology GA 365YT UT WOS:000089978600013 PM 11051580 ER PT J AU Carr, JE Nicolson, AC Higbee, TS AF Carr, JE Nicolson, AC Higbee, TS TI Evaluation of a brief multiple-stimulus preference assessment in a naturalistic context SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE reinforcer assessment; preference; autism ID REINFORCER AB We evaluated a brief multiple-stimulus preference assessment within the context of an early intervention program for 3 children who had been diagnosed with autism. Subsequent curriculum-based reinforcer evaluations confirmed the predictions of the preference assessments. In addition, eight additional preference assessments that were conducted over a period of 1 month indicated generally stable preferences for 2 of the 3 participants. C1 Univ Nevada, Reno, NV 89557 USA. RP Carr, JE (reprint author), Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. RI Higbee, Thomas/F-5157-2010 CR DeLeon IG, 1996, J APPL BEHAV ANAL, V29, P519, DOI 10.1901/jaba.1996.29-519 GREEN CW, 1991, J APPL BEHAV ANAL, V24, P537, DOI 10.1901/jaba.1991.24-537 Piazza CC, 1996, J APPL BEHAV ANAL, V29, P1, DOI 10.1901/jaba.1996.29-1 Piazza CC, 1996, J APPL BEHAV ANAL, V29, P137, DOI 10.1901/jaba.1996.29-137 Roane HS, 1998, J APPL BEHAV ANAL, V31, P605, DOI 10.1901/jaba.1998.31-605 NR 5 TC 76 Z9 76 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD FAL PY 2000 VL 33 IS 3 BP 353 EP 357 DI 10.1901/jaba.2000.33-353 PG 5 WC Psychology, Clinical SC Psychology GA 365YT UT WOS:000089978600014 PM 11051581 ER PT J AU Luiselli, JK Blew, P Keane, J Thibadeau, S Holzman, T AF Luiselli, JK Blew, P Keane, J Thibadeau, S Holzman, T TI Pharmacotherapy for severe aggression in a child with autism: "open label" evaluation of multiple medications on response frequency and intensity of behavioral intervention SO JOURNAL OF BEHAVIOR THERAPY AND EXPERIMENTAL PSYCHIATRY LA English DT Article DE behavioral pharmacology; developmental disability; aggression ID MENTAL-RETARDATION; SELF-INJURY; FLUOXETINE TREATMENT; ADULTS; RISPERIDONE; CLOZAPINE; DISORDER AB Many persons who have developmental disabilities and challenging behaviors are treated with multiple medications combined with nonpharmacological approaches. However, the comparative effects from pharmacotherapy frequently are not assessed empirically, do not include corollary behavioral measures, and are not evaluated in the long term. The present single-case study incorporated behavioral assessment methodology in an "open label" evaluation of anticonvulsant (clonazepam), beta-blocking (propanolol), and antidepressant (sertraline and clornipramine) medications on severe aggression in a child with autism. Clinically significant reductions in aggressive behavior were attained with the administration of clornipramine and the reductive effects from the medication persisted for 1.7 years. In addition, clornipramine was associated with the elimination of crisis intervention procedures that had been required to manage the child's aggression. These findings add to the clinical literature describing effective treatment of serious behavior disorders in persons with developmental disabilities using antidepressant medication. (C) 2001 Elsevier Science Ltd. All rights reserved. C1 May Inst Inc, Norwood, MA 02062 USA. RP Luiselli, JK (reprint author), May Inst Inc, 1 Commerce Pl, Norwood, MA 02062 USA. CR ASHBERG M, 1987, PSYCHOPHARMACOLOGY 3, P655 BARLOW DH, 1984, SINGLE CASE EXPT DES Bass J N, 1991, J Child Adolesc Psychopharmacol, V1, P331, DOI 10.1089/cap.1991.1.331 Calamari J. E., 1990, BEHAV INTERVENT, V5, P287, DOI 10.1002/bin.2360050407 CONNOR DF, 1998, MENTAL HLTH ASPECTS, V1, P93 GARBER HJ, 1992, J AM ACAD CHILD PSY, V31, P1157, DOI 10.1097/00004583-199211000-00027 Gardner W. I., 1990, HDB BEHAV MODIFICATI, P225 HARRIS SL, 1990, AVERSIVE NONAVERSIVE HITTNER JB, 1994, BEHAV INTERVENT, V23, P99 Horrigan JP, 1997, J AUTISM DEV DISORD, V27, P313, DOI 10.1023/A:1025854532079 Iwata B. 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Behav. Ther. Exp. Psychiatry PD SEP-DEC PY 2000 VL 31 IS 3-4 BP 219 EP 230 DI 10.1016/S0005-7916(01)00007-6 PG 12 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 457HT UT WOS:000170131700005 PM 11494958 ER PT J AU Eliez, S Reiss, AL AF Eliez, S Reiss, AL TI Annotation: MRI neuroimaging of childhood psychiatric disorders: A selective review SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE ADD/ADHD; autistic disorder; brain imaging; depression; schizophrenia.; Tourette syndrome ID DEFICIT-HYPERACTIVITY DISORDER; CORPUS-CALLOSUM MORPHOLOGY; ONSET SCHIZOPHRENIA; MAJOR DEPRESSION; INFANTILE-AUTISM; CAUDATE-NUCLEUS; POSTERIOR-FOSSA; QUANTITATIVE MORPHOLOGY; MORPHOMETRIC ANALYSIS; TOURETTES-SYNDROME AB Over the past 10 years, innovations in physics and computer science have promoted magnetic resonance imaging (MRI) as an essential tool for investigating the biological substrates of psychiatric disorders. Requiring no radiation exposure, MRI is no-rv the preferred imaging technique for pediatric populations. However, the rapid technical advances in MRI pulse sequences, data processing, and analysis have made it increasingly complex for clinicians to compare and critically evaluate MRI research studies. This paper selectively reviews MRI research on five psychiatric conditions occurring in childhood or adolescence: ADHD, autism, childhood-onset schizophrenia, Tourette syndrome, and early-onset depression. The selection of papers reviewed was based on four criteria: the originality of the idea underlying the paper, the quality of the sample and methodologies used, the presence of controversial findings in the paper, and whether the paper was a clear illustration of specific methodological strengths or weaknesses. The tlwo goals of this review paper. are to update clinicians on morphometric brain imaging in child psychiatry and the methodological issues pertaining to image acquisition and analysis, and to promote critical reading of future MRI studies. C1 Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. RP Eliez, S (reprint author), Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, 401 Quarry Rd, Stanford, CA 94305 USA. 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Child Psychol. Psychiatry Allied Discip. PD SEP PY 2000 VL 41 IS 6 BP 679 EP 694 DI 10.1017/S0021963099006095 PG 16 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 359UK UT WOS:000089630300002 PM 11039681 ER PT J AU Willemsen-Swinkels, SHN Bakermans-Kranemburg, MJ Buitelaar, JK van IJzendoorn, MH van Engeland, H AF Willemsen-Swinkels, SHN Bakermans-Kranemburg, MJ Buitelaar, JK van IJzendoorn, MH van Engeland, H TI Insecure and disorganised attachment in children with a pervasive developmental disorder: Relationship with social interaction and heart rate SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Pervasive Developmental Disorder; attachment; autistic disorder; child development; ethology; behavioural measures ID STRANGE SITUATION; YOUNG-CHILDREN; BEHAVIOR; AUTISM; ORGANIZATION; PATTERNS; INFANTS AB This study on children with a Pervasive Developmental Disorder (PDD; N = 32), children with developmental language disorder (N = 22), and normally developing children (N = 28) sought to answer questions concerning attachment and autistic behaviour. We could replicate the finding that children with a PDD are able to develop secure attachment relationships to their primary caregiver. Children with PDD who had an insecure attachment showed fewer social initiatives and responses than children with PDD who had a secure attachment, even when the insecurely and securely attached PDD children were matched on chronological and mental age. Children with both a PDD and mental retardation were more often classified as disorganised. Three findings suggested that a disorganised attachment does not merely reflect the presence of "autistic" behaviour: (1) children with PDD did not reveal higher rates of a disorganised attachment than matched comparison children; (2) having a PDD diagnosis and having a disorganised attachment were found to be associated with opposite effects on an ethological measure of level of behavioural organisation; and (3) a disorganised attachment but not a PDD diagnosis was associated with an increase in heart rate during parting with the caregiver and a decrease in heart rate during reunion. C1 Univ Utrecht, Ctr Med, Dept Child & Adolescent Psychiat, NL-3508 GA Utrecht, Netherlands. Leiden Univ, Leiden, Netherlands. RP Willemsen-Swinkels, SHN (reprint author), Univ Utrecht, Ctr Med, Dept Child & Adolescent Psychiat, F-05126,POB 85500, NL-3508 GA Utrecht, Netherlands. RI van IJzendoorn, Marinus/I-1379-2012; Buitelaar, Jan/E-4584-2012 OI Buitelaar, Jan/0000-0001-8288-7757 CR Ainsworth M. 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Child Psychol. Psychiatry Allied Discip. PD SEP PY 2000 VL 41 IS 6 BP 759 EP 767 DI 10.1111/1469-7610.00663 PG 9 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 359UK UT WOS:000089630300009 PM 11039688 ER PT J AU Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ TI Atypical interference of local detail on global processing in high-functioning autism and Asperger's disorder SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE high-functioning autism; Asperger's disorder; local-global processing; global advantage; local interference; autistic disorder; executive function; laterality; perception ID CHILDREN; PERFORMANCE; CLUMSINESS; PRECEDENCE; TASK; INDIVIDUALS; INFORMATION; EXPLORATION; IMPAIRMENT; ABILITIES AB This study explored the claim that individuals with autism and Asperger's disorder lend to process locally rather than holistically. Participants observed a large or "global" number composed of smaller or "local" numbers. The response was contingent upon the identification or either the large stimulus or the small stimuli. Relative to age, sex, and IQ matched controls, global processing in children and adolescents with autism (N = 12) and Asperger's disorder (N = 12) was more vulnerable when the local stimuli were incongruent. The autism group made more global errors than their matched control group, regardless of whether there was local incongruence. In contrast, the Asperger's disorder group made a similar number of global errors as their respective control group. These results were discussed in relation to an " absence of global precedence " notion, " weak central coherence " theory, and right-hemisphere dysfunction. The neurobiological significance of these findings were discussed in the context of a fronto-striatal model of dysfunction. C1 Monash Univ, Dept Psychol, Neuropsychol Res Unit, Clayton, Vic 3168, Australia. RP Rinehart, NJ (reprint author), Monash Univ, Dept Psychol, Neuropsychol Res Unit, Clayton, Vic 3168, Australia. CR Achenbach TM, 1991, MANUAL CHILD BEHAV C American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S, 1997, HDB AUTISM PERVASIVE, P880 Brian JA, 1996, J CHILD PSYCHOL PSYC, V37, P865, DOI 10.1111/j.1469-7610.1996.tb01482.x ELLIS HD, 1994, EUR CHILD ADOLES PSY, V3, P255 FILOTEO JV, 1994, NEUROPSYCHOLOGY, V8, P210, DOI 10.1037//0894-4105.8.2.210 Fink GR, 1999, NEUROPSYCHOLOGIA, V37, P31 Frith U., 1989, AUTISM EXPLAINING EN Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 GHAZIUDDIN M, 1994, J INTELL DISABIL RES, V38, P519 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P651, DOI 10.1007/BF01046333 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P43, DOI 10.1046/j.1365-2788.1998.00065.x GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 Jolliffe T, 1997, J CHILD PSYCHOL PSYC, V38, P527, DOI 10.1111/j.1469-7610.1997.tb01539.x Klin A., 1997, HDB AUTISM PERVASIVE, P94 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MANJIVIONA J, 1995, J AUTISM DEV DISORD, V25, P23, DOI 10.1007/BF02178165 Manjiviona J., 1999, AUTISM, V3, P327, DOI DOI 10.1177/1362361399003004003 MCKELVEY JR, 1995, J CHILD NEUROL, V10, P310 MOTTRON L, 1993, BRAIN COGNITION, V23, P279, DOI 10.1006/brcg.1993.1060 Mottron L, 1999, J CHILD PSYCHOL PSYC, V40, P203, DOI 10.1017/S0021963098003333 NAVON D, 1977, COGNITIVE PSYCHOL, V9, P353, DOI 10.1016/0010-0285(77)90012-3 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x OZONOFF S, 1994, J CHILD PSYCHOL PSYC, V35, P1015, DOI 10.1111/j.1469-7610.1994.tb01807.x Ozonoff S, 1996, BRAIN LANG, V52, P411, DOI 10.1006/brln.1996.0022 Ozonoff S, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P777, DOI 10.1017/S0021963098002613 Plaisted K, 1999, J CHILD PSYCHOL PSYC, V40, P733, DOI 10.1111/1469-7610.00489 Pomeroy JC, 1998, ASPERGER SYNDROME HI PRIOR M, 1990, J AUTISM DEV DISORD, V20, P581, DOI 10.1007/BF02216063 Proverbio AM, 1998, COGNITIVE BRAIN RES, V6, P321, DOI 10.1016/S0926-6410(97)00039-6 Ring HA, 1999, BRAIN, V122, P1305, DOI 10.1093/brain/122.7.1305 RUMSEY JM, 1988, J CLIN EXP NEUROPSYC, V10, P201, DOI 10.1080/01688638808408236 Sattler J.M., 1992, ASSESSMENT CHILDREN SHAH A, 1983, J CHILD PSYCHOL PSYC, V24, P613, DOI 10.1111/j.1469-7610.1983.tb00137.x SHAH A, 1993, J CHILD PSYCHOL PSYC, V34, P1351, DOI 10.1111/j.1469-7610.1993.tb02095.x SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 TANTAM D, 1988, J CHILD PSYCHOL PSYC, V29, P245, DOI 10.1111/j.1469-7610.1988.tb00713.x Tonge B. J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 Ziatas K, 1998, J CHILD PSYCHOL PSYC, V39, P755, DOI 10.1017/S0021963098002510 NR 43 TC 113 Z9 115 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD SEP PY 2000 VL 41 IS 6 BP 769 EP 778 DI 10.1017/S002196309900596X PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 359UK UT WOS:000089630300010 PM 11039689 ER PT J AU Wolk, L Giesen, J AF Wolk, L Giesen, J TI A phonological investigation of four siblings with childhood autism SO JOURNAL OF COMMUNICATION DISORDERS LA English DT Article DE childhood autism; multiple siblings; phonological investigation ID INFANTILE-AUTISM; LANGUAGE; CHILDREN AB Multiple autistic siblings of four or more are extremely rare. This study carried out a phonological investigation of four siblings in a unique family. Phonological investigations were carried out on four siblings with childhood autism (one female and three males). In addition, behavioral characteristics were described and compared among the four children. The two methods used for speech elicitation were object: naming and spontaneous speech utterances. Data analyses included phonetic inventory and phonological process analyses. Phonological investigations showed that these autistic children, at least the more severely impaired ones, do not only exhibit delayed phonological behavior, but also show some atypical patterns that rarely occur in normal development. Findings from this study reveal five general patterns of phonological behavior, namely: (a) evidence of several phonological processes that are common in normal development; (b) persistence of several phonological processes, such as labialization, cluster reduction, or final consonant deletion, beyond the expected age; (c) evidence of unusual sound changes, such as extensive segment coalescence, frication of liquids, and velarization; (d) evidence of "chronological mismatch" (Grunwell, 1981), which is the notion of the absence of earlier sounds co-occurring with characteristics of later development; and (e) restricted use of contrasts. These findings support earlier work on a single autistic child using phonological investigations (Wolk & Edwards, 1993), but contrast with all previous research suggesting that autistic children exhibit delayed rather than unusual phonological development. Clinical implications are suggested. (C) 2000 by Elsevier Science Inc. C1 Univ Connecticut, Dept Commun Sci, Storrs, CT 06269 USA. RP Wolk, L (reprint author), Univ Connecticut, Dept Commun Sci, U-85,850 Bolton Rd, Storrs, CT 06269 USA. 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Commun. Disord. PD SEP-OCT PY 2000 VL 33 IS 5 BP 371 EP 389 DI 10.1016/S0021-9924(00)00021-6 PG 19 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 369JX UT WOS:000165063100001 PM 11081786 ER PT J AU Waldman, HB Swerdloff, M Perlman, SP AF Waldman, HB Swerdloff, M Perlman, SP TI Understanding the siblings of children with mental retardation SO JOURNAL OF DENTISTRY FOR CHILDREN LA English DT Article ID YOUNGER SIBLINGS; BROTHERS; SISTERS; AUTISM C1 SUNY Stony Brook, Dept Gen Dent, Dent Hlth Serv, Stony Brook, NY 11794 USA. SUNY Stony Brook, Dept Oral & Maxillofacial Surg, Stony Brook, NY 11794 USA. Boston Univ, Goldman Sch Grad Dent, Boston, MA 02215 USA. RP Waldman, HB (reprint author), SUNY Stony Brook, Dept Gen Dent, Dent Hlth Serv, Stony Brook, NY 11794 USA. 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Dent. Child. PD SEP-OCT PY 2000 VL 67 IS 5 BP 345 EP 349 PG 5 WC Dentistry, Oral Surgery & Medicine; Pediatrics SC Dentistry, Oral Surgery & Medicine; Pediatrics GA 368HP UT WOS:000090111900007 ER PT J AU Tanguay, PE AF Tanguay, PE TI Pervasive developmental disorders: A 10-year review SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Review DE pervasive developmental disorders; autism; Asperger's disorder; review ID YOUNG AUTISTIC-CHILDREN; DIAGNOSTIC OBSERVATION SCHEDULE; INFANTILE-AUTISM; MENTAL-RETARDATION; ASPERGER-SYNDROME; DOUBLE-BLIND; JOINT ATTENTION; FACILITATED COMMUNICATION; PSYCHIATRIC-DISORDERS; SOCIAL COMMUNICATION AB Objective: To summarize recent advances about the nature, diagnosis, and treatment of pervasive developmental disorders. Method: Review of Medline databases, books, and book chapters published between July 1989 and November 1999. Results: Clinical and genetic studies support expansion of the concept of autism to include a broader spectrum of social communication handicaps. The prevalence of autism is approximately 1 per 2,000; the prevalence of autism and Asperger's disorder together is 1 per 1,000. The Checklist for Autism in Toddlers is a useful screening instrument for 18-month-old children; the Autism Diagnostic Interview-Revised and the Autism Diagnostic Observation Schedule are instruments of choice for research. Although twin and family studies clearly support genetic factors as important in autism, linkage analysis studies indicate that many genes may be involved. There is no one treatment of choice. Social-pragmatic approaches, augmented by individualized strategies and social coaching, may be best for teaching social communication skills. Pharmacological interventions have a limited role in improving social communication, but selective serotonin reuptake inhibitors and atypical neuroleptic medications may help ameliorate aggression, hyperactivity, and other secondary problems. Conclusions: Private and government agencies must continue to support basic and applied research. C1 Univ Louisville, Sch Med, Dept Psychiat, Div Child & Adolescent Psychiat, Louisville, KY 40292 USA. RP Tanguay, PE (reprint author), Bingham Child Guidance Ctr, 200 E Chestnut St, Louisville, KY 40202 USA. 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Am. Acad. Child Adolesc. Psychiatr. PD SEP PY 2000 VL 39 IS 9 BP 1079 EP 1095 DI 10.1097/00004583-200009000-00007 PG 17 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 348UK UT WOS:000089004700007 PM 10986804 ER PT J AU Gergely, G AF Gergely, G TI Reapproaching Mahler: New perspectives on normal autism, symbiosis, splitting and libidinal object constancy from cognitive developmental theory SO JOURNAL OF THE AMERICAN PSYCHOANALYTIC ASSOCIATION LA English DT Article ID INFANCY; SELF; REPRESENTATION; IMITATION; MIND; BIOFEEDBACK; PERCEPTION; ATTACHMENT; SECURITY; GESTURES AB Margaret Mahler's seminal work on the psychological birth of the infant has generated more critical discussion than most other psychoanalytic theories of early development. But while the empirically, theoretically, and methodologically based criticisms of Mahler's theory are generally justified, her critics fail at times to consider some of the intriguing and creative insights that her theoretical formulations tried to capture. This paper attempts to reformulate these insights using the new conceptual tools that current cognitive developmental theory provides. Mahler's stage of normal autism is reconsidered in the light of contingency detection theory as an initial phase of primary preoccupation with self-generated perfectly response-contingent stimulation. Her concept of normal symbiosis is recast with the help of attachment theory's views on homeostatic regulation and the social biofeedback model of affect-reflective mirroring interactions with parents. Finally, her ideas about the development of splitting and libidinal object constancy are reconsidered according to recent theories of early representational development and mentalization. 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PD FAL PY 2000 VL 48 IS 4 BP 1197 EP 1228 DI 10.1177/00030651000480040801 PG 32 WC Psychiatry; Psychology, Psychoanalysis SC Psychiatry; Psychology GA 393YP UT WOS:000166497500010 PM 11212188 ER PT J AU Tsuchiya, H Hayashi, T AF Tsuchiya, H Hayashi, T TI A possible link between beta-carboline metabolism and infantile autism SO MEDICAL HYPOTHESES LA English DT Article ID HEPATIC-ENCEPHALOPATHY; PSYCHOACTIVE COMPOUNDS; MAMMALIAN BODY; RAT-BRAIN; METHTRYPTOLINE; HYDROXYLATION; ORIGIN AB Benzodiazepine receptors and abnormal hepatic metabolism have been suggested to participate in several neuropsychiatric disorders including autism. Neuropsychoactive beta-carboline alkaloids as the potent ligands for benzodiazepine receptors are endogenously produced and exogenously supplied much more than benzodiazepines. 1-Methyl-1,2,3,4-tetrahydro-beta-carboline, a predominant alkaloid in humans and foodstuffs, is metabolically hydroxylated in liver. 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PD SEP PY 2000 VL 15 IS 4 BP 375 EP 392 PG 18 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 346FV UT WOS:000088860900001 ER PT J AU Castelli, F Happe, F Frith, U Frith, C AF Castelli, F Happe, F Frith, U Frith, C TI Movement and mind: A functional imaging study of perception and interpretation of complex intentional movement patterns SO NEUROIMAGE LA English DT Article DE brain imaging; theory of mind; mentalizing; biological motion; autism ID ANTERIOR CINGULATE; BIOLOGICAL MOTION; SOCIAL CAUSALITY; CORTEX; AUTISM; BRAIN; ACTIVATION; RECOGNITION; LANGUAGE AB We report a functional neuroimaging study with positron emission tomography (PET) in which six healthy adult volunteers were scanned while watching silent computer-presented animations. The characters in the animations were simple geometrical shapes whose movement patterns selectively evoked mental state attribution or simple action description. 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The presence of the 5-HT transporter in platelets, similar to the same structure located in presynaptic serotonergic neurons, has produced a series of studies aimed at assessing its functionality in this disorder, but the ensuing findings are quite controversial. For this reason, we investigated the 5-HT transporter by means of the specific binding of [H-3]-Paroxetine ([H-3]-Par), which is currently considered the first-choice ligand for labeling it, in platelets of 20 autistic children and adolescents, as compared with healthy control subjects, Methods: Twenty children and adolescents of both sexes suffering from autism according to DSM IV criteria were included in the study and compared with a similar group of healthy control subjects. Platelet membranes and the binding of [H-3]-Par were carried out according to standardized protocols. Results: The results showed a significantly higher density of [H-3]-Par binding sites in autistic children than in healthy control subjects. 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Kinderpsychol. Kinderpsychiatr. PD SEP PY 2000 VL 49 IS 7 BP 528 EP 529 PG 2 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 360HN UT WOS:000089660500009 ER PT J AU Jolliffe, T Baron-Cohen, S AF Jolliffe, T Baron-Cohen, S TI Linguistic processing in high-functioning adults with autism or Asperger's syndrome. Is global coherence impaired? SO PSYCHOLOGICAL MEDICINE LA English DT Article ID HIGH-LEVEL AUTISM; TEXT COMPREHENSION; INFANTILE-AUTISM; NORMAL-CHILDREN; DOWNS-SYNDROME; MIND; PERFORMANCE; EXPLORATION; INFERENCES; ABILITIES AB Background. Linguistic processing was explored in normally intelligent adults with either autism or Asperger's syndrome, to test if global coherence was impaired. Global coherence is the ability to establish causal connections and interrelate local chunks into higher-order chunks so that most linguistic elements are linked together thematically. Since individuals with autism are hypothesized to have weak central coherence then one would predict that the clinical groups would have difficulty integrating information globally so as to derive full meaning. Methods. Two experiments were designed to test global coherence. Experiment 1 investigated whether individuals on the autism spectrum condition could arrange sentences coherently. Experiment 2 investigated whether they were less able to use context to make a global inference. Results. The clinical groups were less able to arrange sentences coherently and use context to make a global inference. Conclusions. The results suggest that individuals on the autism spectrum have impaired global coherence. Arranging sentences and making global inferences correlated highly, suggesting that central coherence may be a unitary force in these different tasks. Of the two clinical groups, the autism group had the greater deficit. 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Med. PD SEP PY 2000 VL 30 IS 5 BP 1169 EP 1187 DI 10.1017/S003329179900241X PG 19 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 353ZR UT WOS:000089305800016 PM 12027052 ER PT J AU Pepperberg, IM Sherman, D AF Pepperberg, IM Sherman, D TI Proposed use of two-part interactive modeling as a means to increase functional skills in children with a variety of disabilities SO TEACHING AND LEARNING IN MEDICINE LA English DT Article ID PARROTS PSITTACUS-ERITHACUS; AUTISTIC-CHILDREN; VIDEOTAPED INSTRUCTION; LANGUAGE IMPAIRMENT; NEGATIVE EVIDENCE; SOCIAL BEHAVIORS; TIME-DELAY; PEER; ACQUISITION; STUDENTS AB Purpose: Many behavior modification and intervention programs are based on operant procedures developed for animal subjects, but few use modeling procedures in which one student observes interactions between two proficient trainers. We show how such procedures, which successfully trained Grey parrots (Psittacus erithacus) to produce and comprehend elements of human language, can be adapted for use with children with three types of disabilities: (a) autism with limited social and language skills, (b) developmental delay with physical handicaps and lack of language skills, and (c) hyperactivity with impaired cognitive and social skills. Summary: Children were evaluated before entering the program and outcomes were recorded to determine improvement levels. No child reached totally normative (physical age-appropriate) levels, but all significantly improved their social and communication skills and use of contextually appropriate behavior. Conclusions: A two-trainer modeling system can be a valuable intervention tool for children whose disabilities involve social and communicative skills. C1 Univ Arizona, Dept Ecol & Evolutionary Biol, Tucson, AZ USA. New Found Therapies Inc, Monterey, CA USA. 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PD AUG 25 PY 2000 VL 67 IS 14 BP 1667 EP 1682 DI 10.1016/S0024-3205(00)00763-3 PG 16 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 351RD UT WOS:000089171200001 PM 11021352 ER PT J AU Filipek, PA Accardo, PJ Ashwal, S Baranek, GT Cook, EH Dawson, G Gordon, B Gravel, JS Johnson, CP Kallen, RJ Levy, SE Minshew, NJ Ozonoff, S Prizant, BM Rapin, I Rogers, SJ Stone, WL Teplin, SW Tuchman, RF Volkmar, FR AF Filipek, PA Accardo, PJ Ashwal, S Baranek, GT Cook, EH Dawson, G Gordon, B Gravel, JS Johnson, CP Kallen, RJ Levy, SE Minshew, NJ Ozonoff, S Prizant, BM Rapin, I Rogers, SJ Stone, WL Teplin, SW Tuchman, RF Volkmar, FR TI Practice parameter: Screening and diagnosis of autism - Report of the Quality Standards Subcommittee of the American Academy of Neurology and the Child Neurology Society SO NEUROLOGY LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; BRAIN-STEM RESPONSES; FAMILY HISTORY; YOUNG-CHILDREN; TUBEROUS SCLEROSIS; BEHAVIORAL TREATMENT; FRAGILE-X; HEAD CIRCUMFERENCE; SPECTRUM DISORDERS; EXECUTIVE FUNCTION AB Autism is a common disorder of childhood, affecting 1 in 500 children. Yet, it often remains unrecognized and undiagnosed until or after late preschool age because appropriate tools for routine developmental screening and screening specifically for autism have not been available. Early identification of children with autism and intensive, early intervention during the toddler and preschool years improves outcome for most young children with autism. This practice parameter reviews the available empirical evidence and gives specific recommendations for the identification of children with autism. This approach requires a dual process: 1) routine developmental surveillance and screening specifically for autism to be performed on all children to first identify those at risk for any type of atypical development, and to identify those specifically at risk for autism; and 2) to diagnose and evaluate autism, to differentiate autism from other developmental disorders. C1 Amer Acad Neurol, St Paul, MN 55116 USA. Univ Calif Irvine, Coll Med, Dept Pediat, Irvine, CA 92717 USA. Univ Calif Irvine, Coll Med, Dept Neurol, Irvine, CA 92717 USA. New York Med Coll, Dept Pediat, Valhalla, NY 10595 USA. Loma Linda Univ, Sch Med, Loma Linda, CA USA. Univ N Carolina, Dept Allied Hlth Sci, Chapel Hill, NC USA. Univ N Carolina, Dept Pediat, Chapel Hill, NC USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. Univ Washington, Dept Psychol, Seattle, WA 98195 USA. Johns Hopkins Med Inst, Dept Neurol & Cognit Sci, Baltimore, MD 21205 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Otolaryngol, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10461 USA. Yeshiva Univ Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10461 USA. Univ Texas, Hlth Sci Ctr, Dept Pediat, San Antonio, TX 78284 USA. Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA. Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA USA. Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15261 USA. Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT 84112 USA. Brown Univ, Ctr Study Human Dev, Providence, RI 02912 USA. Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. Vanderbilt Univ, Med Ctr, Dept Pediat, Nashville, TN 37232 USA. Univ Miami, Sch Med, Dept Neurol, Miami, FL USA. Yale Univ, Sch Med, Dept Child Psychiat, New Haven, CT USA. Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. RP Filipek, PA (reprint author), Amer Acad Neurol, 1080 Montreal Ave, St Paul, MN 55116 USA. 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J., 1992. Facial emotion discrimination: I. Task construction and behavioural findings in normal participants. Psychiatry Research 42, 231-240.) consists of standardized black-and-white photographs of Caucasian actors exhibiting happy, sad, and neutral faces. Originally designed for brain-imaging research in emotion recognition in schizophrenia and major depression, it has since been successfully employed in emotion recognition studies on mental retardation and psychosomatic disorders. This article presents new basic psychometric data from three studies with a total of 401 college undergraduates. Content validity, item reliability (test-retest, item-total correlation, item difficulty) and test reliability (internal consistency) were established. Happy and sad items were easier to agree upon than neutral ones. In general, happy items had the highest validity, highest test-retest reliability, and highest item-total correlations. Recognition errors of neutral items were biased toward negative affect. Advantages and limitations of the FDT for clinical research applications are discussed. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved. C1 Ohio State Univ, Nisonger Ctr, Columbus, OH 43210 USA. Univ Trier, Ctr Psychobiol & Psychosomat Res, Trier, Germany. RP Rojahn, J (reprint author), Ohio State Univ, Nisonger Ctr, 1581 Dodd Dr, Columbus, OH 43210 USA. 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PD AUG 21 PY 2000 VL 95 IS 2 BP 169 EP 181 DI 10.1016/S0165-1781(00)00169-4 PG 13 WC Psychiatry SC Psychiatry GA 348BY UT WOS:000088965600008 PM 10963802 ER PT J AU Pascual-Castroviejo, I Pascual, SIP AF Pascual-Castroviejo, I Pascual, SIP TI Cerebral arteritis and psychic involution in children. A report of one case with a good response to treatment SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE acquired aphasia; acquired mental retardation; autism; calcium channel blockers; psychic involution ID LANDAU-KLEFFNER SYNDROME; EPILEPSY AB Objective. To show the importance of the cerebral arteritis as etiology of the language and the intellectual involution in children. Clinical case. A boy started to show psychic and language involution since 18 months of life to arrive to an autistic behavior. After showing normal results in all the studies performed in order to investigate the possible etiologies, cerebral arteriography was performed. Cerebral arteritis affecting especially the right opercular artery was disclosed. Oral nicardipine administration was follow-up of a complete recuperation. Conclusions. Cerebral arteritis is very seldom managed as the cause of intellectual and/or language involution in children as it also occurs with the syndrome of acquired aphasia. However. this pathology has a good response not only to corticoids but also to calcium channel antagonists as it occurred in our patient. C1 Hosp Univ La Paz, Serv Neurol Pediat, E-28046 Madrid, Spain. 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Neurologia PD AUG 16 PY 2000 VL 31 IS 4 BP 311 EP 313 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 355QP UT WOS:000089396600003 PM 11008286 ER PT J AU Prats-Vinas, JM AF Prats-Vinas, JM TI Does the cerebellum play a part in cognitive processes? SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE cerebellum; cognition; frontal lobe ID WILLIAMS-SYNDROME; AUTISM; MRI; DISORDER; MUTISM; BRAIN AB Objective and development. We review the different cognitive and behaviour disorders in whose genesis the cerebellum has been thought to play a part. These disorders include infantile autism, Williams' syndrome, attention-deficit hyperactivity disorder and congenital cerebellar hypoplasia. We also consider the consequences of an acquired cerebellar lesion in the light of the following neuropsychological sequelas. It would seem that the cerebellum is involved in the functioning of the executive system due to its relationship with the prefrontal operative system and in the function of the working memory, and may share some of the characteristics of the acquired frontal syndrome. C1 Hosp Cruces, Unidad Neuropediat, E-48903 Baracaldo, Vizcaya, Spain. CR Apollonio I. 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Neurologia PD AUG 16 PY 2000 VL 31 IS 4 BP 357 EP 359 PG 3 WC Clinical Neurology SC Neurosciences & Neurology GA 355QP UT WOS:000089396600010 PM 11008292 ER PT J AU Calderon-Gonzalez, R Calderon-Sepulveda, RF AF Calderon-Gonzalez, R Calderon-Sepulveda, RF TI Polemic or controversial therapies in the neurodevelopmental disorders SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE alternative therapy; Attention Deficit disorder; autism; controversial therapy; learning disorders; neurodevelopment ID LEARNING-DISABILITIES; FACILITATED COMMUNICATION; CHILDREN; AUTISM; SCIENCE; PROJECT; LENSES AB Objective. To analyze the therapies and methods not scientifically documented that more frequently are offer and used for the treatment of neurodevelopmental disorders. Development. These therapies are divided into three main groups: a) Therapies directed upon brain functioning; b) Therapies directed upon nutritional needs, and c) Others. Parents and close relatives of children with developmental disorders are vulnerable to any person, institution or method that offers a quick and easy solution to their problem. It is a priority that all health professionals are familiar with the unproven therapies, that are offered for the therapy of developmental disorders, so that they can inform, educate and advise correctly to parents and close relatives of their patients. To deal with unproven treatments involves more than analyzing the available scientific data. It is required a comprehension and understanding of the personal and family dynamics in front of a threat of illness or disfunction. Conclusion. Responsible and well informed parents in relation to an unproven therapy should be free and have the right to decide whether or not to use a controversial procedure prior to a scientific determination of its validity; they also must keep in mind that at least some procedures, beside of not been useful, could be harmful for the physical, emotional and economical well-being of the patient and/or his family. C1 Hosp San Jose Tec, Dept Neurol, Monterrey, Nuevo Leon, Mexico. Hosp San Jose Tec, Ctr Neurol Ninos & Adolescentes, Monterrey, Nuevo Leon, Mexico. Hosp San Jose Tec, Dept Pediat, Monterrey, Nuevo Leon, Mexico. 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A significant scan statistic based on the single-marker statistics represents evidence of the presence of a susceptibility gene. For a given length of the scan statistic, we assess its significance by Monte Carlo permutation tests. Comparing P values for varying lengths of scan statistics, we treat the smallest observed P value as our statistic of interest and determine its overall significance level. We applied this method to a genome screen with autism families. The result was informative and surprising: A susceptibility region was found (genome-wide significance level, P = 0.038), which is missed with conventional approaches. C1 Rockefeller Univ, Lab Stat Genet, New York, NY 10021 USA. RP Ott, J (reprint author), Rockefeller Univ, Lab Stat Genet, 1230 York Ave, New York, NY 10021 USA. 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Natl. Acad. Sci. U. S. A. PD AUG 15 PY 2000 VL 97 IS 17 BP 9615 EP 9617 DI 10.1073/pnas.170179197 PG 3 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 345XM UT WOS:000088840500051 PM 10931953 ER PT J AU Toth, EA Worby, C Dixon, JE Goedken, ER Marqusee, S Yeates, TO AF Toth, EA Worby, C Dixon, JE Goedken, ER Marqusee, S Yeates, TO TI The crystal structure of adenylosuccinate lyase from Pyrobaculum aerophilum reveals an intracellular protein with three disulfide bonds SO JOURNAL OF MOLECULAR BIOLOGY LA English DT Article DE lyase; purine biosynthesis; beta-elimination; thermal stability; autism ID TRANSFER RNA-SYNTHETASE; ESCHERICHIA-COLI; BACILLUS-SUBTILIS; ACTIVE-SITE; THIOL; THERMOSTABILITY; IDENTIFICATION; DEHYDROGENASE; POLYMERASE; DEFICIENCY AB Adenylosuccinate lyase catalyzes two separate reactions in the de novo purine biosynthetic pathway. Through its dual action in this pathway, adenylosuccinate lyase plays an integral part in cellular replication and metabolism. Mutations in the human enzyme can result in severe neurological disorders, including mental retardation with autistic features. The crystal structure of adenylosuccinate lyase from the hyperthermophilic archaebacterium Pyrobaculum aerophilum has been determined to 2.1 Angstrom resolution. Although both the fold of the monomer and the architecture of the tetrameric asssembly are similar to adenylosuccinate lyase from the thermophilic eubacterium Thermotoga maritima, the archaebacterial lyase contains unique features. Surprisingly, the structure of adenylosuccinate lyase from P. aerophilum reveals that this intracellular protein contains three disulfide bonds that contribute significantly to its stability against thermal and chemical denaturation. The observation of multiple disulfide bonds in the recombinant form of the enzyme suggests the need for further investigations into whether the intracellular environment of P. aerophilum, and possibly other hyperthermophiles, may be compatible with protein disulfide bond formation. In addition, the protein is shorter in P. aerophilum than it is in other organisms. This abbreviation results from an internal excision of a cluster of helices that may be involved in protein-protein interactions in other organisms and may relate to the observed clinical effects of human mutations in that region. (C) 2000 Academic Press. C1 Univ Calif Los Angeles, Dept Chem & Biochem, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, US DOE, Lab Struct Biol & Mol Med, Los Angeles, CA 90095 USA. Univ Michigan, Sch Med, Dept Biol Chem, Ann Arbor, MI 48109 USA. Univ Calif Berkeley, Dept Mol & Cell Biol, Berkeley, CA 94720 USA. 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Mol. Biol. PD AUG 11 PY 2000 VL 301 IS 2 BP 433 EP 450 DI 10.1006/jmbi.2000.3970 PG 18 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 345TK UT WOS:000088831100015 PM 10926519 ER PT J AU Auranen, M Ylisaukko-oja, T Vanhala, R Nieminen, T Peltonen, L Jarvela, I AF Auranen, M Ylisaukko-oja, T Vanhala, R Nieminen, T Peltonen, L Jarvela, I TI Genome scan of autism spectrum disorders in the Finnish population. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Natl Publ Hlth Inst, Dept Human Mol Genet, FIN-00300 Helsinki, Finland. Univ Helsinki, Dept Med Genet, Helsinki, Finland. Univ Helsinki, Hosp Children & Adolescents, Unit Child Neurol, Helsinki, Finland. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA O70 BP 478 EP 478 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900089 ER PT J AU Liu, J Nyholt, DR Grunn, A Tong, X Brito, M Penchaszadeh, G Ott, J Gilliam, TC AF Liu, J Nyholt, DR Grunn, A Tong, X Brito, M Penchaszadeh, G Ott, J Gilliam, TC TI A genome-wide search for autism predisposing genes in 110 autistic families. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Columbia Univ, Columbia Genome Ctr, New York, NY 10032 USA. Columbia Univ, Dept Psychiat, New York, NY 10032 USA. Columbia Univ, Dept Genet & Dev, New York, NY 10032 USA. Rockefeller Univ, Genet & Dev, New York, NY USA. Rockefeller Univ, Lab Statist Genet, New York, NY 10021 USA. NR 0 TC 1 Z9 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA O71 BP 478 EP 479 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900090 ER PT J AU Basu, S Ashley-Koch, A Wolpert, CM Menold, MM Matsumoto, N Greenblatt, DM Powell, CM Qumsiyeh, MB Cuccaro, ML Ledbetter, DH Green, ED Vance, JM Pericak-Vance, MA Gilbert, JR AF Basu, S Ashley-Koch, A Wolpert, CM Menold, MM Matsumoto, N Greenblatt, DM Powell, CM Qumsiyeh, MB Cuccaro, ML Ledbetter, DH Green, ED Vance, JM Pericak-Vance, MA Gilbert, JR TI Identification of autism susceptibility candidates on 7q. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ N Carolina, Dept Pediat, Chapel Hill, NC USA. Univ S Carolina, W S Hall Inst Psychiat, Columbia, SC 29208 USA. Natl Inst Hlth, NHGRI, Bethesda, MD USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA O73 BP 479 EP 479 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900092 ER PT J AU Folstein, S Santangelo, S AF Folstein, S Santangelo, S CA Collaborative Linkage Study Autism TI Autism LOD on chromosome 7 increased by subset analysis of language. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Tufts New England Med Ctr, Collaborative Linkage Study Autism, Boston, MA 02111 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA O72 BP 479 EP 479 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900091 ER PT J AU Klauck, SM Beyer, KS Benner, A Poustka, F Poustka, A AF Klauck, SM Beyer, KS Benner, A Poustka, F Poustka, A TI Infantile autism - Fine mapping of a candidate region on chromosome 7q and association studies of candidate genes. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Deutsch Krebsforschungszentrum, Mol Genome Anal, D-69120 Heidelberg, Germany. Deutsch Krebsforschungszentrum, D-69120 Heidelberg, Germany. Univ Frankfurt, Dept Child & Adolscent Psychiat, D-60590 Frankfurt, Germany. NR 0 TC 1 Z9 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA O74 BP 479 EP 479 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900093 ER PT J AU Constantino, JN Hudziak, JJ Todd, RD AF Constantino, JN Hudziak, JJ Todd, RD TI The genetic structure of reciprocal social behavior: Support for a population based approach to genetic studies of autism. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Washington Univ, Sch Med, Dept Psychiat, St Louis, MO 63110 USA. NR 0 TC 1 Z9 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA O76 BP 480 EP 480 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900095 ER PT J AU Santangelo, S Ashley-Koch, A Pericak-Vance, M Silverman, J Smith, CJ Buxbaum, JSD AF Santangelo, S Ashley-Koch, A Pericak-Vance, M Silverman, J Smith, CJ Buxbaum, JSD CA CLSA TI Combined analysis of data on chromosome 7q from three autism genome scans. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Tufts Univ, New England Med Ctr, Boston, MA 02111 USA. NR 0 TC 1 Z9 1 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA O75 BP 480 EP 480 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900094 ER PT J AU Gallagher, L Kearney, G Fitzgerald, M Gill, M AF Gallagher, L Kearney, G Fitzgerald, M Gill, M TI Three cases of autism associated with differing chromosomal abnormalities. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 St Jamess Hosp, Trinity Ctr Hlth Sci, Dept Psychiat, Dublin, Ireland. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA P281 BP 543 EP 543 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900323 ER PT J AU Lauritsen, MB Borglum, AD Betancur, C Philippe, A Kruse, TA Leboyer, M Ewald, H AF Lauritsen, MB Borglum, AD Betancur, C Philippe, A Kruse, TA Leboyer, M Ewald, H TI Investigation of two variants in the DOPA decarboxylasse gene in patients with infantile autism. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Hosp Psychiat, Inst Basic Psychiat Res, Dept Psychiat Demog, Aarhus, Denmark. Univ Aarhus, Inst Human Genet, Aarhus, Denmark. INSERM U513, Fac Med, Creteil, France. INSERM U513, Fac Med, Hop A Chenevier & H Mondor, Creteil, France. INSERM U513, Psychiat Serv, Hop A Chenevier & H Mondor, Creteil, France. Odense Univ Hosp, Dept Clin Biochem, KKA, Odense, Denmark. Odense Univ Hosp, Dept Genet, KKA, Odense, Denmark. INSERM U513, Fac Med, Hop A Chenevier & H Mondor, Creteil, France. INSERM U513, Psychiat Serv, Hop A Chenevier & H Mondor, Creteil, France. Hosp Psychiat, Dept Psychiat Demog, Inst Basic Psychiat Res, Aarhus, Denmark. Hosp Psychiat, Dept Biol Psychiat, Inst Basic Psychiat Res, Aarhus, Denmark. EM mbl@dadlnet.dk; anders@humgen.au.dk; betancur@im3.inserm.fr; kinabalu@infonie.fr; tak@imbmed.ou.dk; leboyer@im3.inserm.fr; he@psykiatri.aaa.dk 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 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA P284 BP 543 EP 544 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900326 ER PT J AU Tordjman, S Gutknecht, L Carlier, M Spitz, E Antoine, C Slama, F Cohen, DJ Ferrari, P Roubertoux, P Anderson, GA AF Tordjman, S Gutknecht, L Carlier, M Spitz, E Antoine, C Slama, F Cohen, DJ Ferrari, P Roubertoux, P Anderson, GA TI Serotonin transporter gene (5-HTT, locus SLC6A4) and behavioral phenotypes in autism. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 CNRS UPR 9074, F-45071 Orleans CEDEX 02, France. Univ Paris Sud, Fondation Vallee, Le Kremlin Bicetre, France. Yale Univ, Sch Med, Dept Child Psychiat, New Haven, CT USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA P283 BP 543 EP 543 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900325 ER PT J AU Paterson, AD Vincent, JB Scherer, SW AF Paterson, AD Vincent, JB Scherer, SW TI Parental origin linkage effects on chromosome 7q in autism. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Hosp Sick Children, Dept Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. RI Paterson, Andrew/A-4088-2011 OI Paterson, Andrew/0000-0002-9169-118X NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA P289 BP 545 EP 545 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900331 ER PT J AU Jamain, S Clergue, M Quach, H Fellous, M Bourgeron, T AF Jamain, S Clergue, M Quach, H Fellous, M Bourgeron, T TI Identification of new genes on chromosome 6: Candidates for schizophrenia or autism. SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Meeting Abstract C1 Inst Pasteur, Human Immunogenet Lab, F-75724 Paris 15, France. NR 0 TC 0 Z9 0 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD AUG 7 PY 2000 VL 96 IS 4 MA P392 BP 561 EP 561 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 340ZE UT WOS:000088565900393 ER PT J AU Senior, K AF Senior, K TI Autism: progress and priorities SO LANCET LA English DT News Item CR Filipek PA, 2000, NEUROLOGY, V55, P468 NR 1 TC 3 Z9 3 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD AUG 5 PY 2000 VL 356 IS 9228 BP 490 EP 490 DI 10.1016/S0140-6736(05)74160-X PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 342QY UT WOS:000088657700026 PM 10981900 ER PT J AU Folstein, SE Mankoski, RE AF Folstein, SE Mankoski, RE TI Chromosome 7q: Where autism meets language disorder? SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Editorial Material ID INFANTILE-AUTISM; FAMILY HISTORY; ASPERGERS SYNDROME; CHILDREN; PATTERNS; PARENTS; IMPAIRMENT; TWINS; INDIVIDUALS; SPECTRUM C1 New England Med Ctr, Dept Psychiat, Boston, MA 02111 USA. RP Folstein, SE (reprint author), New England Med Ctr, Dept Psychiat, 750 Washington St,NEMC 1007, Boston, MA 02111 USA. 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PD AUG PY 2000 VL 67 IS 2 BP 278 EP 281 DI 10.1086/303034 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 354YA UT WOS:000089357800003 PM 10889044 ER PT J AU Lai, CSL Fisher, SE Hurst, JA Levy, ER Hodgson, S Fox, M Jeremiah, S Povey, S Jamison, DC Green, ED Vargha-Khadem, F Monaco, AP AF Lai, CSL Fisher, SE Hurst, JA Levy, ER Hodgson, S Fox, M Jeremiah, S Povey, S Jamison, DC Green, ED Vargha-Khadem, F Monaco, AP TI The SPCH1 region on human 7q31: Genomic characterization of the critical interval and localization of translocations associated with speech and language disorder SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID GENE; MAP; CHROMOSOME; DISEASE; AUTISM AB The KE family is a large three-generation pedigree in which half the members are affected with a severe speech and language disorder that is transmitted as an autosomal dominant monogenic trait. In previously published work, we localized the gene responsible (SPCH1) to a 5.6-cM region of 7q31 between D7S2459 and D7S643. In the present study, we have employed bioinformatic analyses to assemble a derailed BAC-/PAC-based sequence map of this interval, containing 152 sequence tagged sites (STSs), 20 known genes, and >7.75 Mb of completed genomic sequence. We screened the affected chromosome 7 from the KE family with 120 of these STSs (average spacing <100 kb), but we did not detect any evidence of a microdeletion. Novel polymorphic markers were generated from the sequence and were used to further localize critical recombination breakpoints in the KE family. This allowed refinement of the SPCH1 interval to a region between new markers 013A and 330B, containing similar to 6.1 Mb of completed sequence. In addition, we have studied two unrelated patients with a similar speech and language disorder, who have de novo translocations involving 7q31. Fluorescence in situ hybridization analyses with BACs/PACs from the sequence map localized the t(5;7)(q22;q31.2) breakpoint in the first patient (CS) to a single clone within the newly refined SPCH1 interval. This clone contains the CAGH44 gene, which encodes a brain-expressed protein containing a large polyglutamine stretch. However, we found that the t(2;7)(p23;q31.3) breakpoint in the second patient (BRD) resides within a BAC clone mapping >3.7 Mb distal to this, outside the current SPCH1 critical interval. Finally, we investigated the CAGH44 gene in affected individuals of the KE family, but we found no mutations in the currently known coding sequence. These studies represent further steps toward the isolation of the first gene to be implicated in the development of speech and language. C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford OX3 7BN, England. Oxford Radcliffe Hosp, Dept Clin Genet, Oxford, England. UCL, Guys Hosp, Genet Ctr, London WC1E 6BT, England. UCL, MRC, Human Biochem Genet Unit, London WC1E 6BT, England. Inst Child Hlth, Cognit Neurosci Unit, London, England. NHGRI, NIH, Bethesda, MD 20892 USA. RP Monaco, AP (reprint author), Univ Oxford, Wellcome Trust Ctr Human Genet, Roosevelt Dr, Oxford OX3 7BN, England. 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J. Hum. Genet. PD AUG PY 2000 VL 67 IS 2 BP 357 EP 368 DI 10.1086/303011 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA 354YA UT WOS:000089357800012 PM 10880297 ER PT J AU Vincent, JB Herbrick, JA Gurling, HMD Bolton, PF Roberts, W Scherer, SW AF Vincent, JB Herbrick, JA Gurling, HMD Bolton, PF Roberts, W Scherer, SW TI Identification of a novel gene on chromosome 7q31 that is interrupted by a translocation breakpoint in an autistic individual SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID DISORDER AB The results of genetic linkage studies for autism have suggested that a susceptibility locus for the disease is located on the long arm of chromosome 7 (7q). An autistic individual carrying a translocation, t(7;13)(q31.3;q21), with the chromosome 7 breakpoint located in the region of 7q implicated by genetic studies was identified. A novel gene known as "RAY1" (or "FAM4A1") was found to be directly interrupted by the translocation breakpoint. The gene, which was found to be encoded by 16 exons with evidence of alternative splicing, spanned greater than or equal to 220 kb of DNA at 7q31.3. Mutation screening of the entire coding region in a set of 27 unrelated autistic individuals failed to identify phenotype-specific variants, suggesting that coding region mutations are unlikely to be involved in the etiology of autism. Apparent homologues of RAY1 have also been identified in mouse, rat, pig, chicken, fruit fly, and nematode. The human and mouse genes share similar splicing patterns, and their predicted protein products are 98% identical. C1 Univ Toronto, Hosp Sick Children, Dept Genet, Toronto, ON M5G 1X8, Canada. Univ Toronto, Hosp Sick Children, Child Dev Ctr, Toronto, ON M5G 1X8, Canada. UCL, Sch Med, Dept Psychiat & Behav Sci, Windeyer Inst Med Sci,Mol Psychiat Lab, London W1N 8AA, England. Univ Cambridge, Dept Psychiat, Cambridge, England. RP Scherer, SW (reprint author), Univ Toronto, Hosp Sick Children, Dept Genet, Room 9107,555 Univ Ave, Toronto, ON M5G 1X8, Canada. EM steve@genet.sickkids.on.ca RI Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013; Gurling, Hugh/A-5029-2010; Bolton, Patrick/E-8501-2010 OI Scherer, Stephen /0000-0002-8326-1999; Bolton, Patrick/0000-0002-5270-6262 CR Akgun E, 1997, MOL CELL BIOL, V17, P5559 Ashley-Koch A, 1999, GENOMICS, V61, P227, DOI 10.1006/geno.1999.5968 Barrett S, 1999, AM J MED GENET, V88, P609 BOLTON P, 1992, PSYCHIATR GENET, V2, P277, DOI 10.1097/00041444-199210000-00005 Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Bailey A, 1998, HUM MOL GENET, V7, P571 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LORD C, 1989, J AUTISM DEV DISORD, V19, P505 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 NR 10 TC 77 Z9 82 PU CELL PRESS PI CAMBRIDGE PA 600 TECHNOLOGY SQUARE, 5TH FLOOR, CAMBRIDGE, MA 02139 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD AUG PY 2000 VL 67 IS 2 BP 510 EP 514 DI 10.1086/303005 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 354YA UT WOS:000089357800027 PM 10889047 ER PT J AU Gras-Vincendon, A Seegmuller, C Bursztejn, C AF Gras-Vincendon, A Seegmuller, C Bursztejn, C TI Autism and theory of mind: a cognitive model to understand symptomatology? SO ANNALES MEDICO-PSYCHOLOGIQUES LA French DT Article DE autism; theory of mind; cognition; deficit ID CHILDS THEORY AB "Theory of Mind" is the ability to attribute mental states to self and others, in order to predict and explain actions. It appears in normally-developing children between 3 and 4 years. Baron-Cohen et al. (1985) showed that most of the autistic children failed the ''Theory of Mind" tasks and this finding was taken as evidence for an autism-specific cognitive deficit, underlying communication and socialization handicaps. The "Theory of Mind" model has a clinical interest for the early detection, the specific diagnosis of autism and for educative and therapeutic uses. However, the "Theory of Mind" deficit hypothese in autism has been criticized: it doesn't account for all the abnormal features of autism. This deficit isn't specific, nor primary, while the early symptoms are present quite before the "Theory of Mind" emergence. Alternative cognitive theor-res appeared executive function deficits and the weak "central coherence ", that attempt to explain some other clinical features of autism. C1 Hop Univ Strasbourg, Serv Psychotherap Enfants & Adolescents, F-67091 Strasbourg, France. RP Gras-Vincendon, A (reprint author), Hop Univ Strasbourg, Serv Psychotherap Enfants & Adolescents, 1 Pl Hop, F-67091 Strasbourg, France. CR BARONCOHEN S, 1993, ANAE, V5, P146 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Fonagy P, 1997, DEV PSYCHOPATHOL, V9, P679 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Happe F, 1996, BRAIN, V119, P1377, DOI 10.1093/brain/119.4.1377 HOBSON RP, 1986, J CHILD PSYCHOL PSYC, V27, P321, DOI 10.1111/j.1469-7610.1986.tb01836.x Pennington BF, 1996, J CHILD PSYCHOL PSYC, V37, P51, DOI 10.1111/j.1469-7610.1996.tb01380.x PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 NR 11 TC 0 Z9 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0003-4487 J9 ANN MED-PSYCHOL JI Ann. Med.-Psychol. PD AUG-SEP PY 2000 VL 158 IS 7 BP 574 EP 576 PG 3 WC Pharmacology & Pharmacy; Psychiatry; Psychology; Psychology, Multidisciplinary SC Pharmacology & Pharmacy; Psychiatry; Psychology GA 363ET UT WOS:000089822700005 ER PT J AU Seegmuller, C Gras-Vincendon, A Bursztejn, C AF Seegmuller, C Gras-Vincendon, A Bursztejn, C TI Theory of mind tasks in pervasive developmental disorders: interest for diagnosis SO ANNALES MEDICO-PSYCHOLOGIQUES LA French DT Article DE autism; pervasive developmental disorder; theory of mind; executive function; verbal abilities; assessment; diagnosis ID AUTISM AB Since the initial report by Baron-Cohen et al., 1985, several studies have confirmed that, compared with normal and retarded children, autistic children exhibited lower performance in "Theory of Mind" tasks. However, it is not clear wether this failure is specific to autism or if it applies also to other patients, since other groups of Pervasive Developmental Disorders have not been extensively explored. In this study, false belief tasks (The "Sally-Ann" test and the "Box of Smarties" test) were administred to 47 children (age range 5.9 to 11.3 years), all attending a day-care psychiatric ward. The children were classified into 3 groups according to ICD-10: Autism, other Pervasive Developmental Disorders (OPDD) and other disorders (no-PDD). The results are consistent with Baron-Cohen's findings: autistic subjects fail more frequently in both false belief tasks; however, while in the "Sally-Ann" test, the difference between the autistic and OPDD group is statistically significant these two group do not differ significatively when the results of the "Box of Smarties" test are considered, because of the high number of failure in the OPDD group. Thus, the "Sally-Ann" task could be used to differentiate autism from other types of PDD, while, if these results are confirmed, the "Box of Smarties" test does not seem suitable for this purpose. Possible implications of verbal skills and/or executive functions in "Theory of Mind" tasks, are discussed. C1 Hop Univ Strasbourg, Serv Psychotherap Enfants & Adolescents, F-67091 Strasbourg, France. RP Seegmuller, C (reprint author), Hop Univ Strasbourg, Serv Psychotherap Enfants & Adolescents, 1 Pl Hop, F-67091 Strasbourg, France. CR Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 FRITH U, 1992, ENIGME AUTISME HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x Prior M, 1998, J CHILD PSYCHOL PSYC, V39, P893, DOI 10.1111/1469-7610.00389 WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 NR 8 TC 0 Z9 0 PU MASSON EDITEUR PI PARIS 06 PA 120 BLVD SAINT-GERMAIN, 75280 PARIS 06, FRANCE SN 0003-4487 J9 ANN MED-PSYCHOL JI Ann. Med.-Psychol. PD AUG-SEP PY 2000 VL 158 IS 7 BP 577 EP 580 PG 4 WC Pharmacology & Pharmacy; Psychiatry; Psychology; Psychology, Multidisciplinary SC Pharmacology & Pharmacy; Psychiatry; Psychology GA 363ET UT WOS:000089822700006 ER PT J AU Blake, C Wang, WQ Cartledge, G Gardner, R AF Blake, C Wang, WQ Cartledge, G Gardner, R TI Middle school students with serious emotional disturbances serve as social skills trainers and reinforcers for peers with SED SO BEHAVIORAL DISORDERS LA English DT Article ID YOUNG ADOLESCENTS; BEHAVIOR; TEACHER; INTERVENTIONS; ATTENTION; CHILDREN; IMPROVE; AUTISM AB In two related studies middle school students with serious emotional disturbances (SED) served as student trainers to teach social interaction skills to peers with SED. Researchers in both studies taught middle school boys to use a formal social skills curriculum in order to teach more positive peer interactions. Study results indicate the desired effects of the peer-based social skills instruction, with some evidence of behavior maintenance and transfer. The findings point to beneficial effects for both peer trainers and student trainees. C1 SW City Sch, Grove City, OH USA. Ohio State Univ, Columbus, OH 43210 USA. RP Blake, C (reprint author), SW City Sch, Grove City, OH USA. 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A., 1999, ED TREATMENT CHILDRE, V22, P19 SACKS S, 1989, BEHAV THER, V20, P619, DOI 10.1016/S0005-7894(89)80139-X STRAIN PS, 1979, J AUTISM DEV DISORD, V9, P41, DOI 10.1007/BF01531291 THOMPSON KL, 1995, ADOLESCENCE, V30, P723 *US DEP ED, 1999, 20 ANN REP C IMPL IN WARGER CL, 1993, PREVENTING SCH FAILU, V37, P21 Wenzel M, 1996, J SCHOOL HEALTH, V66, P125 WOLFBERG PL, 1993, J AUTISM DEV DISORD, V13, P467 NR 22 TC 13 Z9 13 PU COUNCIL CHILDREN BEHAVIORAL DISORDERS PI RESTON PA 1920 ASSOCIATION DR, RESTON, VA 20191-1589 USA SN 0198-7429 J9 BEHAV DISORDERS JI Behav. Disord. PD AUG PY 2000 VL 25 IS 4 BP 280 EP 298 PG 19 WC Psychology, Clinical; Psychology, Educational SC Psychology GA 708ZD UT WOS:000184599500002 ER PT J AU Aldridge, MA Stone, KR Sweeney, MH Bower, TGR AF Aldridge, Michelle A. Stone, Kari R. Sweeney, Melissa H. Bower, T. G. R. TI Preverbal children with autism understand the intentions of others SO DEVELOPMENTAL SCIENCE LA English DT Article AB There is a 'theory of mind' theory of autism. Meltzoff has recently developed a procedure that gives a nonverbal assessment of 'theory of mind'. A group of children with autism and a matched control group of normally developing infants were given three of Meltzoff's tasks and three conventional, gestural imitation tasks. The children with autism showed the expected deficits on gestural imitation, but were significantly better than the normally developing infants on the Meltzoff tasks. The implications of these results for a number of theoretical issues are discussed. C1 [Aldridge, Michelle A.; Stone, Kari R.; Sweeney, Melissa H.] Univ Texas Dallas, Callier Ctr Commun Disorders, Dallas, TX 75235 USA. [Bower, T. G. R.] Univ Texas Dallas, Sch Human Dev, Richardson, TX 75083 USA. RP Aldridge, MA (reprint author), Univ Texas Dallas, Callier Ctr Commun Disorders, 1966 Inwood Rd, Dallas, TX 75235 USA. EM aldridge@utdallas.edu CR BARONCOHEN S, 1993, UNDERSTANDING MINDS BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bower T. G. R., 1982, DEV INFANCY BOWER TGR, 1988, RATIONAL INFANT BUTTERWORTH G, 1987, C INSERM, V146, P185 CHARMAN T, 1994, DEV PSYCHOPATHOL, V6, P403, DOI 10.1017/S0954579400006015 GOPNIK A, 1994, CHILDRENNS EARLY UND Gopnik Alison, 1997, WORDS THOUGHTS THEOR LOVAAS O, 1980, TEACHING DEVELOPMENT Meltzoff A. N., 1993, UNDERSTANDING OTHER Meltzoff A. 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PD AUG PY 2000 VL 3 IS 3 BP 294 EP 301 DI 10.1111/1467-7687.00123 PG 8 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA V80KW UT WOS:000205436200014 ER PT J AU Moore, D McGrath, P Thorpe, J AF Moore, D McGrath, P Thorpe, J TI Computer-aided learning for people with autism - a framework for research and development SO INNOVATIONS IN EDUCATION AND TRAINING INTERNATIONAL LA English DT Article ID COMMUNICATION-SKILLS; CHILDREN; MULTIMEDIA AB There is good evidence that computer-aided learning is well accepted by students with autism and is of great potential benefit to them. Despite the potential, however, the field remains relatively unexplored. This paper therefore proposes a framework for further research and development in the field of computer-aided learning for students with autism. The framework is based around the core deficiencies of autism, namely a social impairment, a communication impairment, rigidity and inflexibility in thinking and a theory of mind deficit. Proposals for computer-aided learning systems for each of these areas are put forward, and our current development work outlined. C1 Leeds Metropolitan Univ, Sch Comp, Leeds LS6 3QS, W Yorkshire, England. RP Moore, D (reprint author), Leeds Metropolitan Univ, Sch Comp, Beckett Pk, Leeds LS6 3QS, W Yorkshire, England. CR ALLEN J, 1995, NATURAL LANGUAGE UND ANTHONY A, 1992, P 7 ANN C TECHN PERS ATTWOOD T, 1986, COMMUNICATION, V20, P9 Attwood T, 1998, ASPERGER SYNDROME GU AUSTIN M, 1997, COMMUNICATION SPR, P21 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BERNARD-OPITZ V, 1990, Annals Academy of Medicine Singapore, V19, P611 Boone R., 1996, FOCUS AUTISM OTHER D, V11, P69 *BRASS NCIP, 1995, NATL CTR IMPR PRACT BROWN W, 1993, CHILDREN ASPERGER SY Buffington DM, 1998, J AUTISM DEV DISORD, V28, P535, DOI 10.1023/A:1026056229214 CARLTON S, 1993, OTHER SIDE AUSTISM CHEN SHA, 1993, MENT RETARD, V31, P368 CLANCY H, 1996, COMPUTER RESELLER NE, V698, P76 Cumine V., 1998, ASPERGER SYNDROME PR Eddon G., 1992, Proceedings of the Johns Hopkins National Search for Computing Applications to Assist Persons with Disabilities (Cat. 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Educ. Train. Int. PD AUG PY 2000 VL 37 IS 3 BP 218 EP 228 PG 11 WC Education & Educational Research SC Education & Educational Research GA 359BN UT WOS:000089591800005 ER PT J AU Gillham, JE Carter, AS Volkmar, FR Sparrow, SS AF Gillham, JE Carter, AS Volkmar, FR Sparrow, SS TI Toward a developmental operational definition of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; diagnosis; Vineland socialization scores ID ADAPTIVE-BEHAVIOR SCALES; DIAGNOSTIC INTERVIEW; DOWN-SYNDROME; CHILDREN; DISORDER; INDIVIDUALS; ADOLESCENTS; PREVALENCE; AGE AB Traditional approaches to diagnosing autism emphasize delays in communication and socialization. Traditional diagnostic schemes typically list symptoms (e.g., lack of eye contact), but provide little guidance on how to incorporate information about developmental level in making a diagnosis. Because standardized measures of adaptive behavior can provide information about children's communication, socialization, and other behavior relative to their age, they may be useful tools for diagnosing autism. This study investigated the ability of the Vineland Adaptive Behavior Scales to identify children with autism. Vineland scores and measures of intellectual functioning were obtained for children with autism, PDDNOS, and other developmental disorders (DD). Discriminant function analyses indicated that the autism and combined nonautism (PDDNOS and DD) groups could be differentiated on the basis of socialization, daily living skills, and serious maladaptive behaviors. Socialization alone accounted fur 48% of the variance in diagnosis. Using regression analyses derived from a large normative sample, adaptive behavior scores were predicted from chronological age (CA) and mental age (MA). Socialization scores in the autism group were substantially below the level predicted from CA or MA. An index derived from the ratio of actual to predicted socialization scores correctly classified 86% of both autism and nonautism cases. Findings suggest that comparison of obtained Vineland socialization scores to those predicted by CA or MA may be useful in clarifying the diagnosis of autism. C1 Univ Penn, Philadelphia, PA 19104 USA. Swarthmore Coll, Swarthmore, PA 19081 USA. Univ Massachusetts, Boston, MA 02125 USA. Yale Univ, New Haven, CT USA. Yale Child Study Ctr, New Haven, CT USA. RP Gillham, JE (reprint author), 3815 Walnut St, Philadelphia, PA 19104 USA. 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Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 269 EP 278 DI 10.1023/A:1005571115268 PG 10 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000001 PM 11039854 ER PT J AU Green, J Gilchrist, A Burton, D Cox, A AF Green, J Gilchrist, A Burton, D Cox, A TI Social and psychiatric functioning in adolescents with Asperger syndrome compared with conduct disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; high-functioning autism; psychosocial functioning; psychiatric disorder; social adaptation; conduct disorder ID SCHIZOID PERSONALITY; AUTISTIC-CHILDREN; ADULT LIFE; CHILDHOOD; VIOLENCE AB Lack of standardized phenotypic definition has made outcome studies of Asperger syndrome (AS) difficult to interpret. This paper reports psychosocial functioning in 20 male adolescents with AS, defined according to current ICD-10 criteria, and a comparison group of 20 male adolescents with severe conduct disorder. Subjects were gathered from clinical referral. Evaluation used standardized interviewer rated assessments of social functioning and psychiatric morbidity. The AS group showed severe impairments in practical social functioning despite good cognitive ability and lack of significant early language delay. High levels of anxiety and obsessional disorders were found in AS; depression, suicidal ideation, tempers, and defiance in both groups. Results are compared with those from other studies. Relevance to clinical ascertainment and treatment is discussed. C1 Booth Hall Childrens Hosp, Dept Child Psychiat, Manchester M9 7AA, Lancs, England. Royal Cornhill Hosp, Aberdeen, Scotland. Guys Hosp, London SE1 9RT, England. RP Green, J (reprint author), Booth Hall Childrens Hosp, Dept Child Psychiat, Manchester M9 7AA, Lancs, England. 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Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 279 EP 293 DI 10.1023/A:1005523232106 PG 15 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000002 PM 11039855 ER PT J AU Bowler, DM Gardiner, JM Grice, SJ AF Bowler, DM Gardiner, JM Grice, SJ TI Episodic memory and remembering in adults with Asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Asperger syndrome; remembering memory; knowing memory ID REPORTING RECOLLECTIVE EXPERIENCES; RECOGNITION MEMORY; AUTISTIC-CHILDREN; AUTONOETIC CONSCIOUSNESS; EXECUTIVE FUNCTIONS; CHILDHOOD AUTISM; INFANTILE-AUTISM; AMNESIC SYNDROME; AGE-DIFFERENCES; DIRECT ACCESS AB A group of adults with Asperger syndrome and an IQ-matched control group were compared in remember versus know recognition memory. Word frequency was also manipulated. Both groups showed superior recognition for low-frequency compared with high-frequency words, and in both groups this word frequency effect occurred in remembering, not in knowing. Nor did overall recognition differ between the two groups. However, recognition in the Asperger group was associated with less remembering, and more knowing, than in the control group. Since remembering reflects autonoetic consciousness, which is: the hallmark of an episodic memory system, these results show that episodic memory is moderately impaired in individuals with Asperger syndrome even when overall recognition performance is not. C1 City Univ London, Dept Psychol, London EC1V 0HB, England. RP Bowler, DM (reprint author), City Univ London, Dept Psychol, Northampton Sq, London EC1V 0HB, England. 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Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 295 EP 304 DI 10.1023/A:1005575216176 PG 10 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000003 PM 11039856 ER PT J AU Bowler, DM Briskman, JA AF Bowler, DM Briskman, JA TI Photographic cues do not always facilitate performance on false belief tasks in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT Annual Conference of the British Psychological Society CY SEP 08-11, 1995 CL GLASGOW, SCOTLAND SP Dev Sect, British Psychol Soc HO UNIV STRATHCLYDE DE false belief tasks; autism ID MIND; REPRESENTATION; 3-YEAR-OLDS; INDIVIDUALS; KNOWLEDGE; ABILITY; GRASP AB Previous studies have indicated that a pictorial representation of a prior belief can help 3-year-old children (Mitchell Br Lacohee, 1991) as well as children with autism (Charman & Lynggaard, 1998) to pass false belief tasks that used the deceptive box or "Smarties" paradigm. The studies reported here attempted to replicate these findings using the unexpected transfer or "Sally-Anne" paradigm, which requires children to predict the actions of a protagonist on the basis of a false belief. Results showed no facilitative effect on "Sally-Anne" task performance for the children with autism or for comparison children of either representational or nonrepresentational cues. This effect was found even in children who benefited from the intervention with the deceptive box paradigm. The findings raise issues regarding the way false belief tasks are conceptualized by experimenters and the demands different false belief paradigms make on children. C1 City Univ London, Dept Psychol, London EC1V 0HB, England. Inst Psychiat, Social & Genet Psychiat Unit, London, England. RP Bowler, DM (reprint author), City Univ London, Dept Psychol, Northampton Sq, London EC1V 0HB, England. CR Baddeley A. 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Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 305 EP 316 DI 10.1023/A:1005552811441 PG 12 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000004 PM 11039857 ER PT J AU Luteijn, E Luteijn, F Jackson, S Volkmar, F Minderaa, R AF Luteijn, E Luteijn, F Jackson, S Volkmar, F Minderaa, R TI The children's social behavior questionnaire for milder variants of PDD problems: Evaluation of the psychometric characteristics SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Children's Social Behavior Questionnaire; psychometric characteristics ID PERVASIVE DEVELOPMENTAL DISORDER; AUTISTIC SPECTRUM DISORDERS; CLASSIFICATION; CHILDHOOD AB The Children's Social Behavior Questionnaire (CSBQ) contains items referring to behavior problems seen in children with milder variants of PDD. Data of large samples of children diagnosed as having high-functioning autism, PDDNOS, ADHD, and other child-psychiatric disorders were gathered. Besides the CSBQ, parents completed the Autism Behavior Check list (ABC) and the Child Behavior Checklist (CBCL). The data provided the basis for scale construction of the CSBQ, a comparison of the CSBQ scales with other instruments and a comparison of groups on scores on the CSBQ. The 5 scales obtained referred to Acting-out behaviors, Social Contact problems, Social Insight problems, Anxious/Rigid behaviors and Stereotypical behaviors. Results show that the CSBQ has good psychometric qualities with respect to both reliability and validity. A comparison of the different groups showed that significant group differences were found on all scales. in general, the autism group received the highest scores, followed by the PDDNOS group and the ADHD group. Exceptions were on the Acting-out scale, where the ADHD group scored highest and on the Social Insight scale, where no significant. difference was found between the PDDNOS group and the ADHD group. 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Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 317 EP 330 DI 10.1023/A:1005527300247 PG 14 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000005 PM 11039858 ER PT J AU Hwang, B Hughes, C AF Hwang, B Hughes, C TI The effects of social interactive training on early social communicative skills of children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; social interactive intervention; social communicative skills ID TIME-DELAY; SPONTANEOUS SPEECH; YOUNG-CHILDREN; BEHAVIORS; VERBALIZATIONS; LANGUAGE AB Growing attention has been directed at the relation between early social communicative skills of children with autism and subsequent development of these children's social and communicative functioning. We reviewed 16 empirical studies that investigated the effects of social interactive interventions designed to increase early social communicative skills of young children with autism by increasing their role as initiator of social interactions. To identify factors relating to treatment effectiveness, we analyzed studies in relation to participant characteristics, settings, target behaviors, training methods, and results. To determine durability of treatment, we analyzed generalization effects across persons, settings, stimuli, and time. Increases were found for social and affective behaviors, nonverbal and verbal communication, eye contact, joint attention, and imitative play. Limited generalization or maintenance of target behaviors was reported. Findings are discussed in relation to critical variables that may relate to treatment effectiveness in future research and practice efforts. C1 Vanderbilt Univ, Dept Special Educ, Nashville, TN 37203 USA. RP Hughes, C (reprint author), Vanderbilt Univ, Dept Special Educ, Box 328 Peabody, Nashville, TN 37203 USA. CR Baker MJ, 1998, J ASSOC PERS SEVERE, V23, P300, DOI 10.2511/rpsd.23.4.300 BILLINGSLEY F, 1980, BEHAV ASSESS, V2, P229 BRANDEKAMP S, 1997, DEV APPROPRIATE PRAC CHARLOP MH, 1985, J APPL BEHAV ANAL, V18, P155, DOI 10.1901/jaba.1985.18-155 CHARLOP MH, 1986, J APPL BEHAV ANAL, V19, P307, DOI 10.1901/jaba.1986.19-307 CHARLOP MH, 1991, J APPL BEHAV ANAL, V24, P747, DOI 10.1901/jaba.1991.24-747 Cooper H. M, 1989, INTEGRATING RES GUID DATTILO J, 1991, J APPL BEHAV ANAL, V24, P369, DOI 10.1901/jaba.1991.24-369 Dawson G., 1990, DEV PSYCHOPATHOL, V2, P151, DOI 10.1017/S0954579400000675 DYER K, 1989, J ASSOC PERS SEVERE, V14, P184 Harris S. 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Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 331 EP 343 DI 10.1023/A:1005579317085 PG 13 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000006 PM 11039859 ER PT J AU Sheinkopf, SJ Mundy, P Oller, DK Steffens, M AF Sheinkopf, SJ Mundy, P Oller, DK Steffens, M TI Vocal atypicalities of preverbal autistic children SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE vocal behavior; autism; preverbal children ID JOINT ATTENTION; COMMUNICATION; LANGUAGE AB This study was designed to evaluate the nature of early vocal behaviors in young children with autism. Recent methodological and conceptual advances in the study of infant preverbal vocalizations were used to provide a detailed examination of the vocal behavior of young preverbal children with autism and comparison children with developmental delays. Results revealed that children with autism did not have difficulty with the expression of well-formed syllables (i.e., canonical babbling). However, children with autism did display significant impairments in vocal quality (i.e., atypical phonation). Specifically, autistic children produced a greater proportion of syllables with atypical phonation than did comparison children. Consistent with prior reports, the children with autism also displayed a deficit in joint attention behaviors. Furthermore, the atypicalities in the vocal behavior of children with autism appeared to be independent of individual differences in joint attention skill, suggesting that a multiple process model may be needed to describe early social-communication impairments in children with autism. Data are discussed in terms of their implications for future theoretical and applied research, including efforts to enhance the specificity of early diagnostic procedures. C1 Univ Miami, Coral Gables, FL 33124 USA. Infant Dev Ctr, Providence, RI USA. Brown Univ, Sch Med, Providence, RI 02912 USA. Univ Maine, Orono, ME 04469 USA. New Mexico State Univ, Las Cruces, NM 88003 USA. RP Mundy, P (reprint author), Univ Miami, 5665 Ponce De Leon Blvd, Coral Gables, FL 33124 USA. 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PD AUG PY 2000 VL 30 IS 4 BP 345 EP 354 DI 10.1023/A:1005531501155 PG 10 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000007 PM 11039860 ER PT J AU Michaelis, RC Copeland-Yates, SA Sossey-Alaoui, K Skinner, C Friez, MJ Longshore, JW Simensen, RJ Schroer, RJ Stevenson, RE AF Michaelis, RC Copeland-Yates, SA Sossey-Alaoui, K Skinner, C Friez, MJ Longshore, JW Simensen, RJ Schroer, RJ Stevenson, RE TI The HOPA gene dodecamer duplication is not a significant etiological factor in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE HOPA gene; dodecamer duplication ID X-CHROMOSOME; MENTAL-RETARDATION; ANDROGEN-RECEPTOR; INFANTILE-AUTISM; ASSOCIATION; FAMILY AB A recent study has suggested that a dodecamer duplication in the HOPA gene in Xq13 may occur in a significant portion of male patients with autism. We have determined the incidence of this duplication in 202 patients from the South Carolina Autism Study. The incidence of the duplication was not significantly different between patients and controls. Three of the female patients inherited the duplication from nonautistic fathers. In addition, there was no systematic skewing of X inactivation in the female patients with the duplication, or in nonautistic mothers and sisters with the duplication. These findings suggest that the dodecamer duplication in the HOPA gene does not play a significant role in the etiology of autism. C1 Greenwood Genet Ctr, JC Self Res Inst, Greenwood, SC 29646 USA. RP Michaelis, RC (reprint author), Greenwood Genet Ctr, JC Self Res Inst, 1 Gregor Mendel Circle, Greenwood, SC 29646 USA. 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Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 355 EP 358 DI 10.1023/A:1005583517994 PG 4 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000008 PM 11039861 ER PT J AU Moore, M Calvert, S AF Moore, M Calvert, S TI Brief report: Vocabulary acquisition for children with autism: Teacher or computer instruction SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE vocabulary acquisition; autism; computer technology AB This study examined the impact of computers on the vocabulary acquisition of young children with autism. Children's attention, motivation, and learning of words was compared in a behavioral program and an educational software program. The educational software program was designed to parallel the behavioral program, but it added perceptually salient qualities such as interesting sounds and object movement. Children with autism were more attentive, moro motivated, and learned more vocabulary in the computer than in the behavioral program. Implications are considered for the development of computer software to teach vocabulary to children who have autism. C1 Georgetown Univ, Dept Psychol, Washington, DC 20057 USA. Georgetown Univ, Commun Culture & Technol Program, Washington, DC 20057 USA. RP Calvert, S (reprint author), Georgetown Univ, Dept Psychol, 37th & O St NW, Washington, DC 20057 USA. CR Calvert S. L., 1999, CHILDRENS JOURNEYS I CALVERT SL, 1989, J EDUC COMPUT RES, V22, P251 HEIMANN M, 1995, J AUTISM DEV DISORD, V25, P459, DOI 10.1007/BF02178294 LOVAAS I, 1981, ME BOOK TEACHING DEV MAURICE C, 1996, BEHAV INTERVENTION Y NR 5 TC 76 Z9 77 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 359 EP 362 DI 10.1023/A:1005535602064 PG 4 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000009 PM 11039862 ER PT J AU Fombonne, E AF Fombonne, E TI Is a large head circumference a sign of autism? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material CR BAILEY A, 1993, LANCET, V341, P1225, DOI 10.1016/0140-6736(93)91065-T Fombonne E, 1999, J AUTISM DEV DISORD, V29, P113, DOI 10.1023/A:1023036509476 Lainhart JE, 1997, J AM ACAD CHILD PSY, V36, P282, DOI 10.1097/00004583-199702000-00019 NR 3 TC 12 Z9 12 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2000 VL 30 IS 4 BP 365 EP 365 DI 10.1023/A:1005591719811 PG 1 WC Psychology, Developmental SC Psychology GA 357CB UT WOS:000089480000012 PM 11039865 ER PT J AU Elia, M Ferri, R Musumeci, SA Panerai, S Bottitta, M Scuderi, C AF Elia, M Ferri, R Musumeci, SA Panerai, S Bottitta, M Scuderi, C TI Clinical correlates of brain morphometric features of subjects with low-functioning autistic disorder SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID EARLY INFANTILE-AUTISM; POSTERIOR-FOSSA; MENTAL-RETARDATION; CHILDHOOD AUTISM; 4TH VENTRICLE; RATING-SCALE; CEREBELLAR; ABNORMALITIES; SIZE; HYPOPLASIA AB Numerous neuropathologic and imaging studies have reported different structural abnormalities in the brains of autistic subjects. However, whether or not the degree of brain abnormality is correlated with the severity of developmental impairment in autistic disorder is still unknown. The midsagittal area of the cerebrum, corpus callosum, midbrain, cerebellar vermis, and vermal lobules VI and VII was measured by means of magnetic resonance imaging in 22 boys with low-functioning autistic disorder and in 11 age-matched normal controls. Morphometric measures were statistically compared between groups and correlated with age and scores on the Psychoeducational Profile-Revised and the Childhood Autism Rating Scale. A significant negative correlation was found between midsagittal area of the cerebrum and age in patients with autistic disorder, and a positive correlation was found between the midsagittal area of the midbrain and some subscales of the Psychoeducational Profile-Revised. C1 OASI Inst, Dept Neurol, I-94018 Troina, Italy. IRCCS, Oasi Inst Res Mental Retardat & Brain Aging, Dept Psychol, Troina, Italy. RP Elia, M (reprint author), OASI Inst, Dept Neurol, Via Conte Ruggero 73, I-94018 Troina, Italy. 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Child Neurol. PD AUG PY 2000 VL 15 IS 8 BP 504 EP 508 DI 10.1177/088307380001500802 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 344HB UT WOS:000088752200002 PM 10961787 ER PT J AU Stein, MT Dixon, SD Cowan, C Wessel, M AF Stein, MT Dixon, SD Cowan, C Wessel, M TI A two-year-old boy with language regression and unusual social interactions SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Editorial Material ID YOUNG-CHILDREN; AUTISM; DISORDER C1 Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA. RP Stein, MT (reprint author), Univ Calif San Diego, Sch Med, San Diego, CA 92103 USA. 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Dev. Behav. Pediatr. PD AUG PY 2000 VL 21 IS 4 BP 285 EP 290 PG 6 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 347ED UT WOS:000088913700006 PM 10972253 ER PT J AU Diesfeld, K AF Diesfeld, K TI Neither consenting nor protesting: an ethical analysis of a man with autism SO JOURNAL OF MEDICAL ETHICS LA English DT Article DE informal admission; autism; discrimination AB This article critically examines the 25 June 1998 decision by the House of lords regarding the psychiatric admission of a man with autism.(1) Mr L was able neither to consent to, nor refuse, that admission and the disposition of his case illuminates the current debate regarding best interests of vulnerable adults by the judiciary and the psychiatric profession. This article begins with the assumption that hospitalisation was nor the optimum response to Mr L's condition, provides alternative approaches to the interpretation of best interest and examines principles of liberty, anti-discrimination, and equal protection. C1 Univ Kent, Sch Law, Kent Law Clin Mental Hlth & Learning Disabil, Canterbury, Kent, England. RP Diesfeld, K (reprint author), Univ Kent, Sch Law, Kent Law Clin Mental Hlth & Learning Disabil, Canterbury, Kent, England. CR DURAND BM, 1990, SEVERE BEHAV PROBLEM, P19 EMERSON E, 1990, SEVERE LEARNING DISA, P7 Fennell Philip, 1998, Med Law Rev, V6, P322, DOI 10.1093/medlaw/6.3.322 GOODING C, 1996, BLACKSTONES GUIDE DI HODGSON J, 1999, J MENTAL HLTH LAW, V1, P23 MURPHY G, 1990, SEVERE LEARNING DISA, P37 POLYVIOU PG, 1980, EQUAL PROTECTION LAW, P1 Schopp R.F., 1996, LAW THERAPEUTIC KEY, P723 NR 8 TC 1 Z9 1 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0306-6800 J9 J MED ETHICS JI J. Med. Ethics PD AUG PY 2000 VL 26 IS 4 BP 277 EP 281 DI 10.1136/jme.26.4.277 PG 5 WC Ethics; Medical Ethics; Social Issues; Social Sciences, Biomedical SC Social Sciences - Other Topics; Medical Ethics; Social Issues; Biomedical Social Sciences GA 344MP UT WOS:000088763700011 PM 10951924 ER PT J AU State, MW Lombroso, PJ Pauls, DL Leckman, JF AF State, MW Lombroso, PJ Pauls, DL Leckman, JF TI The genetics of childhood psychiatric disorders: A decade of progress SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Review DE genetics; childhood psychiatric disorders; autism; dyslexia; attention-deficit/hyperactivity disorder; Tourette's disorder ID DEFICIT HYPERACTIVITY DISORDER; FRAGILE-X-SYNDROME; DOPAMINE TRANSPORTER GENE; QUANTITATIVE-TRAIT LOCUS; LA-TOURETTE SYNDROME; TRINUCLEOTIDE REPEAT EXPANSION; AFFECTED RELATIVE PAIRS; PRADER-WILLI SYNDROMES; RECEPTOR D4 DRD4; PAST 10 YEARS AB Objective: To review the literature over the past decade on the genetics of childhood neuropsychiatric disorders. Method: A computerized search was performed for articles published in the past decade, and selected papers were highlighted. Results: The past decade of research has illuminated the complex genetics of early-onset mental disorders. Advances in statistical methodologies and laboratory-based gene-hunting techniques are laying the foundation for a deeper understanding of both the biological and environmental factors that contribute to mental illness. Researchers are on the verge of identifying and characterizing genetic vulnerabilities involved in common childhood psychiatric syndromes. Conclusions: Although the study of the genetics of childhood psychiatric disorders has advanced significantly over the past decade, considerable work remains. The identification of genes conferring vulnerability to psychiatric illnesses will have the potential to transform the field by providing insight into both biological and environmental determinants that contribute to serious developmental and psychiatric disorders in children and adolescents. These advances promise new understanding and new avenues for prevention and treatment. They will also present physicians and families with significant clinical and ethical challenges. C1 Yale Univ, Ctr Child Study, Sch Med, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dept Genet, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dept Psychol, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dept Pediat, New Haven, CT 06520 USA. Yale Univ, Sch Med, Childrens Clin Res Ctr, New Haven, CT 06520 USA. RP Leckman, JF (reprint author), Yale Univ, Ctr Child Study, Sch Med, 230 S Frontage Rd,POB 207900, New Haven, CT 06520 USA. 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PD AUG PY 2000 VL 24 IS 6 BP 581 EP 604 DI 10.1016/S0149-7634(00)00025-7 PG 24 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 347YH UT WOS:000088956400001 PM 10940436 ER PT J AU Mouridsen, SE Rich, B Isager, T AF Mouridsen, SE Rich, B Isager, T TI A comparative study of genetic and neurobiological findings in disintegrative psychosis and infantile autism SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE disintegrative psychosis; infantile autism; validity ID DSM-IV; CHILDHOOD; DISORDERS; INDIVIDUALS; PARENTS; ISSUES AB Although disintegrative psychosis (DP) was first described in 1908, the validity of the syndrome has not yet been fully documented. To investigate the validity of DP as defined in ICD-9, 13 cases of DP were compared with 39 cases of infantile autism with reference to lifetime parental psychopathology, neuroradiological findings and genetic abnormalities. The groups were matched for gender, age, intellectual level and social class. Apart from a significantly higher rate of electroencephalogram abnormalities in the disintegrative group there was very little in the neurobiological background to support a clear distinction between DP and infantile autism. C1 Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. Roskilde Hosp, Roskilde, Denmark. Univ Copenhagen, Glostrup Hosp, DK-2600 Glostrup, Denmark. RP Mouridsen, SE (reprint author), Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. 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PD AUG PY 2000 VL 54 IS 4 BP 441 EP 446 DI 10.1046/j.1440-1819.2000.00734.x PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 356BU UT WOS:000089424800009 PM 10997861 ER PT J AU Lewine, JD Provencal, SL Hill, D Davis, JT Funke, M Huang, M Orrison, WW AF Lewine, JD Provencal, SL Hill, D Davis, JT Funke, M Huang, M Orrison, WW TI Magnetoencephalographic assessment of patients with autism SO PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Univ Utah, Salt Lake City, UT 84112 USA. NR 0 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 USA SN 0048-5772 J9 PSYCHOPHYSIOLOGY JI Psychophysiology PD AUG PY 2000 VL 37 SU 1 BP S10 EP S10 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 364PJ UT WOS:000089900500042 ER PT J AU Baving, L Schmidt, MH AF Baving, L Schmidt, MH TI Psychological tests between aspirations and reality in intelligence diagnostics SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE psychological testing; standards; intelligence; diagnostics; children ID KAUFMAN ASSESSMENT BATTERY; CHILDREN K-ABC; GERMAN-SPEAKING CHILDREN; PSYCHOMETRIC PROPERTIES; TEST I-S-T-70; WISC-R; AUTISM; ADAPTATION; PROFILE; RAVEN AB Objectives: The U.S.-American standards of quality for psychological diagnostics tests were published in 1998 in German translation under the title "Standards fur padagogisches und psychologisches Testen". The relevance of these Standards for studies of psychological testing in child and adolescent psychiatry is discussed. Important intelligence tests will be assessed on the basis of these standards for studies of psychological testing in children and adolescents. Methods: Relevant standards were presented and discussed. The intelligence tests HAWIK-R, HAWIK-III K-ABC, AID, PSB, I-S-T 70, SPM, CFT 20: CMM-LB, SON-R 2 1/2-7, SON-R 5 1/2-17 were analyzed with regard to whether or not they fulfilled the Standards under inclusion Of the test manuals, test reviews, and empirical studies from the literature. Results The intelligence tests listed differ widely in the extent to which they meet the Standards. Conclusions: The Standards appear, at least in part, to be relevant to studies Of psychological testing in child and adolescent psychiatry. 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PD AUG PY 2000 VL 28 IS 3 BP 163 EP 176 DI 10.1024//1422-4917.28.3.163 PG 14 WC Psychiatry SC Psychiatry GA 346ZY UT WOS:000088902800003 PM 11008342 ER PT J AU Beversdorf, DQ Smith, BW Crucian, GP Anderson, JM Keillor, JM Barrett, AM Hughes, JD Felopulos, GJ Bauman, ML Nadeau, SE Heilman, KM AF Beversdorf, DQ Smith, BW Crucian, GP Anderson, JM Keillor, JM Barrett, AM Hughes, JD Felopulos, GJ Bauman, ML Nadeau, SE Heilman, KM TI Increased discrimination of "false memories" in autism spectrum disorder SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID OLDER ADULTS; ILLUSORY MEMORIES; RECOGNITION; YOUNGER AB Individuals with autism spectrum disorder (ASD) have impaired ability to use context, which may manifest as alterations of relatedness within the semantic: network. However, impairment in context use may be more difficult to detect in high-functioning adults with ASD. To test context use in this population, we examined the influence of context on memory by using the "false memory" test. In the false memory task, lists of words were presented to high-functioning subjects with ASD and matched controls. Each list consists of words highly related to an index word not on the list. Subjects are then given a recognition test. Positive responses to the index words represent false memories. We found that individuals with ASD are able to discriminate false memory items from true items significantly better than are control subjects. Memory in patients with ASD may be more accurate than in normal individuals under certain conditions. These results also suggest that semantic representations comprise a less distributed network in high-functioning adults with ASD. Furthermore, these results may be related to the unusually high memory capacities found in some individuals with ASD. Research directed at defining the range of tasks performed superiorly by high-functioning individuals with ASD will be important for optimal vocational rehabilitation. C1 Ohio State Univ, Med Ctr, Dept Neurol, Columbus, OH 43210 USA. Baystate Med Ctr, Springfield, MA 01199 USA. Univ Florida, Coll Med, Dept Neurol, Gainesville, FL 32610 USA. Def & Civil Inst Environm Med, Toronto, ON M3M 3B9, Canada. Penn State Univ, Coll Med, Dept Med, Div Neurol, Hershey, PA 17033 USA. Uniformed Serv Univ Hlth Sci, Dept Neurol, Bethesda, MD 20814 USA. Massachusetts Gen Hosp, Dept Child Psychiat, Boston, MA 02114 USA. Massachusetts Gen Hosp, Dept Pediat Neurol, Boston, MA 02114 USA. Ctr Geriatr Res Educ & Clin, Gainesville, FL 32610 USA. Dept Vet Adm Med Ctr, Neurol Serv, Gainesville, FL 32610 USA. Brain Rehabil Ctr, Gainesville, FL 32610 USA. RP Beversdorf, DQ (reprint author), Ohio State Univ, Med Ctr, Dept Neurol, 1654 Upham Dr, Columbus, OH 43210 USA. 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PD JUL 18 PY 2000 VL 97 IS 15 BP 8734 EP 8737 DI 10.1073/pnas.97.15.8734 PG 4 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 335YF UT WOS:000088273900098 PM 10900024 ER PT J AU Gallup, R AF Gallup, R TI The MMR question SO LANCET LA English DT Letter ID ASSOCIATION; MEASLES; AUTISM C1 Autism Autoimmun Project, Lake Hiawatha, NJ 07034 USA. RP Gallup, R (reprint author), Autism Autoimmun Project, Lake Hiawatha, NJ 07034 USA. CR Singh VK, 1998, CLIN IMMUNOL IMMUNOP, V89, P105, DOI 10.1006/clin.1998.4588 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 2000, LANCET, V355, P1379 NR 4 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD JUL 8 PY 2000 VL 356 IS 9224 BP 161 EP 162 DI 10.1016/S0140-6736(05)73172-X PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 331UG UT WOS:000088036600043 PM 10963267 ER PT J AU Smith, T Groen, AD Wynn, JW AF Smith, T Groen, AD Wynn, JW TI Randomized trial of intensive early intervention for children with pervasive developmental disorder SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID BEHAVIORAL TREATMENT; AUTISTIC-CHILDREN; YOUNG AUTISM; PROJECT AB Young children with pervasive developmental disorder were randomly assigned to intensive treatment or parent training. The intensive treatment group (7 with autism, 8 with pervasive developmental disorder not otherwise specified-NOS) averaged 24.52 hours per week of individual treatment for one year, gradually reducing hours over the next 1 to 2 years. The parent training group (7 with autism, 6 with pervasive developmental disorder NOS) received 3 to 9 months of parent training. The groups appeared similar at intake on all measures; however, at follow-up the intensive treatment group outperformed the parent training group on measures of intelligence, visual-spatial skills, language, and academics, though not adaptive functioning or behavior problems. Children with pervasive developmental disorder NOS may have gained more than those with autism. C1 Washington State Univ, Dept Psychol, Pullman, WA 99164 USA. Metropolitan State Coll, Denver, CO 80204 USA. Univ Calif Los Angeles, Los Angeles, CA USA. RP Smith, T (reprint author), Washington State Univ, Dept Psychol, POB 644820, Pullman, WA 99164 USA. 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J. Ment. Retard. PD JUL PY 2000 VL 105 IS 4 BP 269 EP 285 DI 10.1352/0895-8017(2000)105<0269:RTOIEI>2.0.CO;2 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 336XR UT WOS:000088328700006 PM 10934569 ER PT J AU Bobee, S Mariette, E Tremblay-Leveau, H Caston, J AF Bobee, S Mariette, E Tremblay-Leveau, H Caston, J TI Effects of early midline cerebellar lesion on cognitive and emotional functions in the rat SO BEHAVIOURAL BRAIN RESEARCH LA English DT Article DE cerebellum; motor activity; attention; anxiety; emotional behavior; neophobia; autism; rat ID LURCHER MUTANT MICE; NICTITATING-MEMBRANE RESPONSE; LONG-TERM HABITUATION; EQUILIBRIUM BEHAVIOR; AUDITORY INFORMATION; SPATIAL ORIENTATION; AUTISTIC PATIENTS; INFANTILE-AUTISM; ACOUSTIC STARTLE; GUINEA-PIG AB Midline lesion of the cerebellum was performed in young 10-day-old DA/HAN strained (pigmented) rats. Once adults, the lesioned animals were subjected to a series of behavioral tests and their performances were compared with those of control (nonlesioned) rats. Compared with controls, the spontaneous motor activity of the lesioned rats was higher, they showed persevering behavior and did not pay attention to environmental distracters. In anxiety and social discrimination tests, disinhibition tendencies were obvious, which suggested that the animals were less dependent on the context. These abnormalities were most likely due to early midline lesion of the cerebellum and not to a deficit in maternal care before weaning, since the dams took care of the lesioned and control pups similarly. From these results, it can be concluded that the cerebellar vermis is involved in motor control, attentional capabilities and emotional behavior. 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Brain Res. PD JUL PY 2000 VL 112 IS 1-2 BP 107 EP 117 DI 10.1016/S0166-4328(00)00166-2 PG 11 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 324PE UT WOS:000087629900012 PM 10862941 ER PT J AU Clark, AF AF Clark, AF TI Neuropsychiatry of children and adolescents including psychoses, obsessive-compulsive disorder and physical illness SO CURRENT OPINION IN PSYCHIATRY LA English DT Article ID RETT-SYNDROME; ELECTROCONVULSIVE-THERAPY; CHILDHOOD DISORDERS; GENETICS; AUTISM; PSYCHIATRY; ATTITUDES; MIND; AGE AB This paper reviews key developments in the physical aspects of child psychiatric practice. It concentrates on the implications of increasing knowledge of the genetic bases of disorders, advances in understanding within the pervasive developmental disorders, and physical modalities of treatment. Curr Opin Psychiatry 13:403-407. (C) 2000 Lippincott Williams & Wilkins. C1 Univ Manchester, Salford NHS Trust, Mental Hlth Serv, Dept Adolescent Psychiat, Manchester M25 3BL, Lancs, England. RP Clark, AF (reprint author), Univ Manchester, Salford NHS Trust, Mental Hlth Serv, Dept Adolescent Psychiat, Bury New Rd, Manchester M25 3BL, Lancs, England. 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Opin. Psychiatr. PD JUL PY 2000 VL 13 IS 4 BP 403 EP 407 DI 10.1097/00001504-200007000-00007 PG 5 WC Psychiatry SC Psychiatry GA 327WD UT WOS:000087816400007 ER PT J AU Douville, O AF Douville, O TI On the threshold of the figurable. Autism, childhood psychosis and body techniques SO EVOLUTION PSYCHIATRIQUE LA French DT Book Review CR ALLOUCH E, 1999, SEUIL FIGURABLE AUTI NR 1 TC 0 Z9 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD JUL-SEP PY 2000 VL 65 IS 3 BP 631 EP 634 PG 4 WC Psychiatry SC Psychiatry GA 369HB UT WOS:000165058900027 ER PT J AU Agathon, M AF Agathon, M TI Supporting the families of children with autism. SO EVOLUTION PSYCHIATRIQUE LA French DT Book Review CR Randall P., 1999, SUPPORTING FAMILIES NR 1 TC 0 Z9 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD JUL-SEP PY 2000 VL 65 IS 3 BP 654 EP 654 PG 1 WC Psychiatry SC Psychiatry GA 369HB UT WOS:000165058900054 ER PT J AU Dutoit, MS AF Dutoit, MS TI Exploration of autism SO EVOLUTION PSYCHIATRIQUE LA French DT Book Review CR LELORD G, 1998, EXPLORATION AUTISME NR 1 TC 0 Z9 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS CEDEX 15 PA 23 RUE LINOIS, 75724 PARIS CEDEX 15, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD JUL-SEP PY 2000 VL 65 IS 3 BP 668 EP 668 PG 1 WC Psychiatry SC Psychiatry GA 369HB UT WOS:000165058900073 ER PT J AU Posey, DJ McDougle, CJ AF Posey, DJ McDougle, CJ TI The pharmacotherapy of target symptoms associated with autistic disorder and other pervasive developmental disorders SO HARVARD REVIEW OF PSYCHIATRY LA English DT Review ID OBSESSIVE-COMPULSIVE DISORDER; DEFICIT HYPERACTIVITY DISORDER; SEVERE MENTAL-RETARDATION; DOUBLE-BLIND; OPEN-LABEL; SCHIZOPHRENIC CHILDREN; INFANTILE-AUTISM; YOUNG-CHILDREN; SELF-INJURY; OPEN-TRIAL AB Research into the pharmacotherapy of autistic disorder has steadily increased over the past two decades. Several psychoactive medications have shown efficacy for selected symptoms of autistic disorder and can be used to augment critical educational and behavioral interventions that are the mainstays of treatment. A comprehensive review of medication trials conducted In individuals with autistic disorder and other pervasive developmental disorders is presented. The typical antipsychotic haloperidol is the best-studied medication in autistic disorder but is associated with a high rate of dyskinesias. investigations to date suggest that the atypical antipsychotics such as risperidone have efficacy for certain symptoms of autistic disorder and may be better tolerated than typical antipsychotics. Preliminary results from trials with serotonin-reuptake inhibitors are favorable, although efficacy has not been demonstrated in younger age groups. Recent controlled studies of naltrexone suggest that the drug has minimal efficacy. In two small controlled Investigations, clonidine was more effective than placebo for a variety of symptoms, including hyperactivity and irritability; in one of these studies, however, the majority of patients relapsed within several months. Psychostimulants reduced hyperactivity and irritability in one small double-blind crossover study in children with autistic disorder, although these agents are frequently reported to exacerbate irritability, insomnia, and aggression in clinical populations. Recent controlled trials of secretin have not shown efficacy compared to placebo. Several other medications, including buspirone, mood stabilizers, and beta-blockers, have produced symptom reduction in some open-label studies and may warrant controlled investigation. C1 Indiana Univ, Sch Med, Dept Psychiat, Sect Child & Adolescent Psychiat, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), James Whitcomb Riley Hosp Children, 702 Barnhill Dr,Room 3701, Indianapolis, IN 46202 USA. CR Abenhaim L, 1996, NEW ENGL J MED, V335, P609, DOI 10.1056/NEJM199608293350901 Aman M. 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Rev. Psychiatr. PD JUL-AUG PY 2000 VL 8 IS 2 BP 45 EP 63 DI 10.1093/hrp/8.2.45 PG 19 WC Psychiatry SC Psychiatry GA 327YH UT WOS:000087821700001 PM 10902094 ER PT J AU DeGangi, GA Breinbauer, C Roosevelt, JD Porges, S Greenspan, S AF DeGangi, GA Breinbauer, C Roosevelt, JD Porges, S Greenspan, S TI Prediction of childhood problems at three years in children experiencing disorders of regulation during infancy SO INFANT MENTAL HEALTH JOURNAL LA English DT Article ID ATTACHMENT; RISK AB The objective of this study was to determine if symptoms of regulatory disorder (RD) during infancy were related to clinical status at three years. Two age-matched RD groups based on severity (N = 10 in mild RD group; N = 22 in moderate-severe RD group) and an age-matched control group (N = 38) were evaluated at 7 and 30 months. A fourth group with pervasive developmental disorders (N = 18) also were tested. Problems with self-regulation, including sleep, feeding, state control, self-calming, sensory reactivity, mood regulation, and emotional and behavioral control, were documented during infancy. Children were retested at 36 months in their development, behavior, and play. Two child psychiatrists unfamiliar with the subjects' diagnostic classification during infancy provided diagnoses at 36 months. At 36 months, 60% of children with mild regulatory disorders did not meet criteria for any disorders, while 95% of infants with moderate regulatory disorders had diagnoses that fell into two diagnostic clusters: (1) delays in motor, language, and cognitive development and (2) parent-child relational problems. Most toddlers in the pervasive developmental disorder group were diagnosed as having PDD or autism with mental retardation or borderline intelligence at 36 months. Early symptoms are discussed as they relate to later diagnostic outcomes for the clinical samples. 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E., 1987, PSYCHIAT MED, V4, P149 McCarthy D., 1972, MCCARTHY SCALES CHIL PORGES SW, 1991, DEV AFFECT REGULATIO PORGES SW, IN PRESS PSYCHONEURO Rutter M., 1977, CHILD PSYCHIAT MODER, P3 SROUFE LA, 1983, CHILD DEV, V54, P1615, DOI 10.1111/j.1467-8624.1983.tb00078.x WALKER E, 1983, CHILD DEV, V54, P1269, DOI 10.1111/j.1467-8624.1983.tb00546.x ZERO TO THREE, 1994, DIAGNOSTIC CLASSIFIC NR 38 TC 50 Z9 52 PU MICHIGAN ASSN INFANT MENTAL HEALTH PI E LANSING PA MICHIGAN STATE UNIV DEPT PSYCHOLOGY, E LANSING, MI 48824-1117 USA SN 0163-9641 J9 INF MENTAL HLTH J JI Infant Ment. Health J. PD JUL PY 2000 VL 21 IS 3 BP 156 EP 175 DI 10.1002/1097-0355(200007)21:3<156::AID-IMHJ2>3.0.CO;2-D PG 20 WC Psychology, Developmental SC Psychology GA 339XY UT WOS:000088504200002 ER PT J AU Roth-Hanania, R Busch-Rossnagel, N Higgins-D'Alessandro, A AF Roth-Hanania, R Busch-Rossnagel, N Higgins-D'Alessandro, A TI Development of self and empathy in early infancy: Implications for atypical development SO INFANTS AND YOUNG CHILDREN LA English DT Article DE atypical development; autism; empathy development; prosocial behavior; self-concept development ID JOINT ATTENTION; 1ST YEAR; AUTISM; CHILDREN; RECOGNITION; PERSPECTIVE; DEFICITS; MOTHERS; OTHERS AB It is widely accepted that an essential process in the normal development of infants is their growing capacity to relate to others. Empathy is a unique form of relating to others. It is present at birth and gradually develops during infancy, through childhood, and into adolescence. Infants exhibit various behavioral forms of empathic concern toward others in distress. Empathic responses grow both in frequency and complexity during the first two years of life. Theoretical perspectives on empathy development propose that empathy responses are largely dependent on the development of sense of self. Several empirical explorations have established a correlation between self and empathy development during the first years of life. Understanding the relationship between development of sense of self and that of empathy is crucial not only for broadening our currently somewhat limited knowledge base regarding typical development in these areas, but also for our understanding atypical development. Autistic children are observed to have a general deficit in development of empathic capacity as well as great difficulty in developing both physical and representational sense of self. 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PD JUL PY 2000 VL 13 IS 1 BP 1 EP 14 PG 14 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 327ZT UT WOS:000087824900003 ER PT J AU [Anonymous] AF [Anonymous] TI Imagine a world without meaning ... now learn the reality with Ages of Autism SO JOURNAL OF ADVANCED NURSING LA English DT News Item NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0309-2402 J9 J ADV NURS JI J. Adv. Nurs. PD JUL PY 2000 VL 32 IS 1 BP 8 EP 8 PG 1 WC Nursing SC Nursing GA 329WY UT WOS:000087932500014 ER PT J AU Sandler, RH Finegold, SM Bolte, ER Buchanan, CP Maxwell, AP Vaisanen, ML Nelson, MN Wexler, HM AF Sandler, RH Finegold, SM Bolte, ER Buchanan, CP Maxwell, AP Vaisanen, ML Nelson, MN Wexler, HM TI Short-term benefit from oral vancomycin treatment of regressive-onset autism SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 4th International Symposium on Brain-Gut Interactions CY JUL, 1998 CL LA JOLLA, CALIFORNIA ID SPECTRUM PARENTERAL ANTIBIOTICS; D-LACTIC ACIDOSIS; COLONIZATION RESISTANCE; INTESTINAL MICROFLORA; FECAL FLORA; CHILDREN; BOTULISM; MICE; COLITIS; INFANCY AB In most cases symptoms of autism begin in early infancy. However, a subset of children appears to develop normally until a clear deterioration is observed. Many parents of children with "regressive"-onset autism have noted antecedent antibiotic exposure followed by chronic diarrhea. We speculated that, in a subgroup of children, disruption of indigenous gut flora might promote colonization by one or more neurotoxin-producing bacteria, contributing, at least in part, to their autistic symptomatology To help test this hypothesis, II children with regressive-onset autism were recruited for an intervention trial using a minimally absorbed oral antibiotic. Entry criteria included antecedent broad-spectrum antimicrobial exposure followed by chronic persistent diarrhea, deterioration of previously acquired skills, and then autistic features. Short-term improvement was noted using multiple pre- and post-therapy evaluations. These included coded, paired videotapes scored by a clinical psychologist blinded to treatment status; these noted improvement in 8 of 10 children studied. Unfortunately, these gains had largely waned at follow-up. Although the protocol used is not suggested as useful therapy, these results indicate that a possible gut flora-brain connection warrants further investigation, as it might lead to greater pathophysiologic insight and meaningful prevention or treatment in a subset of children with autism. C1 Rush Childrens Hosp, Rush Med Coll, Sect Pediat Gastroenterol & Nutr, Chicago, IL 60612 USA. Rush Childrens Hosp, Sect Pediat Psychol, Chicago, IL 60612 USA. Univ Calif Los Angeles, Sch Med, Infect Dis Sect, Los Angeles, CA USA. Univ Calif Los Angeles, Sch Med, Res Serv, Los Angeles, CA USA. RP Sandler, RH (reprint author), Rush Childrens Hosp, Rush Med Coll, Sect Pediat Gastroenterol & Nutr, 1725 W Harrison Ave,Ste 946, Chicago, IL 60612 USA. 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Child Neurol. PD JUL PY 2000 VL 15 IS 7 BP 429 EP 435 DI 10.1177/088307380001500701 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 333AM UT WOS:000088106600001 PM 10921511 ER PT J AU Mawhood, L Howlin, P Rutter, M AF Mawhood, L Howlin, P Rutter, M TI Autism and developmental receptive language disorder - a comparative follow-up in early adult life. I: Cognitive and language outcomes SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE adulthood; autistic disorder; follow-up studies; intelligence; language; language disorder; social behaviour ID LONG-TERM CONSISTENCY; INFANTILE-AUTISM; SPEECH/LANGUAGE PROFILES; DIAGNOSTIC INTERVIEW; FAMILY HISTORY; IMPAIRMENT; CHILDREN; INDIVIDUALS; PARENTS; PRESCHOOLERS AB In this paper we compare adult outcome in a group of young men with autism and a group with developmental receptive language disorders. The two groups were first assessed in early childhood, when aged 7 to 8 years of age. Although matched at that time for nonverbal IQ (mean 92-93) and expressive language ability, the Autism group was significantly more impaired on most measures of social and communication skills and stereotyped behaviours. A later follow-up, in mid-childhood, suggested that although the groups were still quite distinct, social and behavioural problems had become more apparent in the Language group. The current study was completed when the participants were aged, on average, 23 to 24 years. The findings indicated that verbal IQ and receptive language scores had improved significantly more in the Autism group than in the Language group over time. Moreover, although the Language group were less severely impaired in their social use of language, many showed a number of abnormal features in this domain. There were no differences between the groups on tests of reading or spelling. Discriminant function analysis, which had clearly distinguished between the groups as children, now showed much greater overlap between them. Regression analysis indicated that although early language ability appeared to be related to outcome in the Autism group, in the Language group there was little association between measures of childhood functioning and later progress. The implications of these findings for understanding the nature of the underlying deficit in autism and the relationship between the two disorders are discussed. C1 St George Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. Inst Psychiat, London, England. RP Howlin, P (reprint author), St George Hosp, Sch Med, Dept Psychol, Cranmer Terrace, London SW17 0RE, England. RI Howlin, Patricia/A-7622-2011; Rutter, Michael/C-8570-2013 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARAM DM, 1984, J SPEECH HEAR RES, V27, P232 AUGUST GJ, 1981, BRIT J PSYCHIAT, V138, P416, DOI 10.1192/bjp.138.5.416 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAIRD TD, 1985, J AUTISM DEV DISORD, V15, P315, DOI 10.1007/BF01531501 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BARTAK L, 1977, J AUTISM CHILD SCHIZ, V7, P383, DOI 10.1007/BF01540396 Beitchman J., 1996, LANGUAGE LEARNING BE Beitchman JH, 1996, J AM ACAD CHILD PSY, V35, P815, DOI 10.1097/00004583-199606000-00022 BEITCHMAN JH, 1994, J AM ACAD CHILD PSY, V33, P1322, DOI 10.1097/00004583-199411000-00015 Beitchman JH, 1996, J AM ACAD CHILD PSY, V35, P804, DOI 10.1097/00004583-199606000-00021 BEITCHMAN JH, 1992, CAN J PSYCHIAT, V37, P151 BIRD J, 1995, J CHILD PSYCHOL PSYC, V37, P391 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 Bishop D. V. M., 1987, LANGUAGE DEV DISORDE, P16 Bishop D. V. 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PD JUL PY 2000 VL 41 IS 5 BP 547 EP 559 DI 10.1017/S002196309900579X PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 336TD UT WOS:000088318300003 PM 10946748 ER PT J AU Howlin, P Mawhood, L Rutter, M AF Howlin, P Mawhood, L Rutter, M TI Autism and developmental receptive language disorder - a follow-up comparison in early adult life. II: Social, behavioural, and psychiatric outcomes SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Review DE adulthood; autistic disorder; follow-up studies; intelligence; language; language disorder; social behaviour ID LONG-TERM CONSISTENCY; INFANTILE-AUTISM; FAMILY HISTORY; SPEECH/LANGUAGE PROFILES; DIAGNOSTIC INTERVIEW; CHILDREN; IMPAIRMENT; SPEECH; SCHIZOPHRENIA; INDIVIDUALS AB This paper focuses on general social functioning in two groups of young men, one with autism and one with developmental receptive language disorders, who were first assessed at the ages of 7-8 years. At that time, although matched for nonverbal IQ (mean 92-93) and expressive language, the Language group showed significantly fewer social and behavioural problems. At follow-up, when aged on average, 23 to 24 years, the Autism group continued to show significantly more impairments in terms of stereotyped behaviour patterns, social relationships, jobs, and independence. However, problems in all these areas were also common in the Language group. Many still lived with their parents, few had close friends or permanent jobs, and ratings of social interaction indicated abnormalities in a number of different areas. On a composite measure of social competence only 10% of the Language group was assessed as having severe social difficulties compared to 74% of the Autism group. Nevertheless, 65% were rated as having moderate social problems and only 25% were rated as being of near/normal social functioning. Two individuals in the Language group, but none in the Autism group, had also developed a florid paranoid psychosis in late adolescence. As in the follow-up of cognitive and linguistic functioning (see Mawhood et al., 2000, this volume, pp. 547-559), discriminant function analysis, which had clearly distinguished between the groups as children, now showed much greater overlap between them. Regression analysis indicated that although early language ability appeared to be related to outcome in the Autism group, there was little association between any measures of childhood functioning and prognosis in the Language group. Theoretically, these findings have implications for our understanding of the nature of autism and other pervasive language disorders, and of the relationship between them. Practically, they demonstrate the very persistent problems experienced by individuals with developmental language disorders, and their need for much greater help and support than is presently available. C1 St George Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. Inst Psychiat, London, England. RP Howlin, P (reprint author), St George Hosp, Sch Med, Dept Psychol, Cranmer Terrace, London SW17 0RE, England. 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YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD JUL PY 2000 VL 41 IS 5 BP 561 EP 578 DI 10.1017/S0021963099005806 PG 18 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 336TD UT WOS:000088318300004 PM 10946749 ER PT J AU Szatmari, P MacLean, JE Jones, MB Bryson, SE Zwaigenbaum, L Bartolucci, G Mahoney, WJ Tuff, L AF Szatmari, P MacLean, JE Jones, MB Bryson, SE Zwaigenbaum, L Bartolucci, G Mahoney, WJ Tuff, L TI The familial aggregation of the lesser variant in biological and nonbiological relatives of PDD probands: a family history study SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Asperger's disorder; autistic disorder; family history; genetics ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISTIC INDIVIDUALS; INFANTILE-AUTISM; TWIN; CHILDREN; RELIABILITY; PHENOTYPE; SIBLINGS; PARENTS; PAIRS AB Objective. To determine the risk of the lesser variant (or PDD-like traits) in the biological and nonbiological second- and third-degree relatives of PDD probands using a screening questionnaire and to investigate the extent to which the risk of the lesser variant differs according to various characteristics of the proband. Method: The sample consists of a series of 34 nuclear families with 2 affected PDD children (multiplex, MPX), 44 families with a single PDD child (simplex, SPX), and 14 families who adopted a PDD child. Data on characteristics of the lesser variant in 1362 biological and 337 nonbiological second- and third-degree relatives were collected from parents by telephone interview and from several maternal and paternal relatives by questionnaire. Results: All components of the lesser variant were more common in biological relatives (BR) than nonbiological relatives (NBR), confirming the familial aggregation of the traits. Proband characteristics associated with an increased risk of the lesser variant in relatives were a higher level of functioning and coming from a MPX family. Conclusions: These findings on the familial aggregation of the lesser variant suggest that the genes for PDD also confer susceptibility to the lesser variant and that PDD may be a genetically heterogeneous disorder. C1 McMaster Univ, Hamilton, ON, Canada. RP Szatmari, P (reprint author), Chedoke McMaster Hosp, Dept Psychiat, Patterson Bldg,POB 2000,Stn A, Hamilton, ON L8N 3Z5, Canada. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANDREASEN NC, 1977, ARCH GEN PSYCHIAT, V34, P1229 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAIRD TD, 1985, J AUTISM DEV DISORD, V15, P315, DOI 10.1007/BF01531501 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x CHAPMAN TF, 1994, AM J PSYCHIAT, V151, P574 COHEN NJ, 1993, J CHILD PSYCHOL PSYC, V34, P545, DOI 10.1111/j.1469-7610.1993.tb01035.x FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x GIBBONS LE, 1993, AM J EPIDEMIOL, V137, P654 GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 KOSTEN TA, 1992, J PSYCHIAT RES, V26, P135, DOI 10.1016/0022-3956(92)90005-9 LANDA R, 1992, PSYCHOL MED, V22, P245 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 LEVINE M, 1986, LEITER INT PERFORMAN LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MACLEAN JE, IN PRESS J AM ACAD C, V38, P746 Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 MERIKANGAS KR, 1987, APA ANN REV, V6, P625 NARAYAN S, 1990, J AUTISM DEV DISORD, V20, P523, DOI 10.1007/BF02216057 PICKLES A, 1995, AM J HUM GENET, V57, P717 Piven J, 1997, AM J PSYCHIAT, V154, P185 PIVEN J, 1990, J AM ACAD CHILD PSY, V29, P177, DOI 10.1097/00004583-199003000-00004 RITVO ER, 1985, AM J PSYCHIAT, V142, P74 SMALLEY SL, 1995, AM J MED GENET, V60, P19, DOI 10.1002/ajmg.1320600105 STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x Szatmari P, 1999, GENET EPIDEMIOL, V16, P368, DOI 10.1002/(SICI)1098-2272(1999)16:4<368::AID-GEPI4>3.0.CO;2-A Szatmari P, 1996, AM J MED GENET, V67, P354, DOI 10.1002/(SICI)1096-8628(19960726)67:4<354::AID-AJMG7>3.0.CO;2-M SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 SZATMARI P, 1995, AM J MED GENET, V60, P282, DOI 10.1002/ajmg.1320600405 SZATMARI P, 1998, AUTISM Wechsler D., 1967, MANUAL WECHSLER PRES Wechsler D., 1974, MANUAL WECHSLER INTE Wechsler D, 1981, WAIS R MANUAL WECHSL NR 34 TC 79 Z9 81 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH STREET, NEW YORK, NY 10011-4211 USA SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD JUL PY 2000 VL 41 IS 5 BP 579 EP 586 DI 10.1017/S0021963099005831 PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 336TD UT WOS:000088318300005 PM 10946750 ER PT J AU Rieffe, C Terwogt, MM AF Rieffe, C Terwogt, MM TI Deaf children's understanding of emotions: Desires take precedence SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE child development; emotion recognition; hearing loss; theory of mind ID FALSE BELIEFS; MIND; COMMUNICATION; KNOWLEDGE; REPRESENTATION; CONVERSATION; AUTISM AB Deaf children frequently have trouble understanding other people's emotions. It has been suggested that an impaired theory of mind can account for this. This research focused on the spontaneous use of mental states in explaining other people's emotions by 6- and 10-year-old deaf children as compared to their hearing peers. Within both age-groups deaf children referred to others' beliefs as often as their hearing peers and their references to desires even exceeded those of hearing children. This relative priority for the expression of desires is discussed in terms of possible communicative patterns of deaf children. The specific problems that deaf children meet in their daily communication might explain their abundance of desire-references: plausibly, they give a high priority to stress their own desires and needs unambiguously. C1 Free Univ Amsterdam, Dept Child Psychol, NL-1081 BT Amsterdam, Netherlands. RP Rieffe, C (reprint author), Free Univ Amsterdam, Dept Child Psychol, Vd Boechorststr 1, NL-1081 BT Amsterdam, Netherlands. CR BARDEN RC, 1980, J PERS SOC PSYCHOL, V39, P368 BARONCHEN S, 1995, MINDBLINDNESS ESSAY BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Boucher J., 1996, THEORIES THEORIES MI, P223 Brown PM, 1997, VOLTA REV, V99, P5 Carruthers P., 1996, THEORIES THEORIES MI, P257 CLARK MD, 1996, J DEAF STUDIES DEAF, V1, P180 DARBYSHIRE JO, 1977, VOLTA REV, V79, P19 Frijda N. H., 1986, EMOTIONS Gregory S., 1976, DEAF CHILD HIS FAMIL HAPPE FGE, 1993, COGNITION, V48, P101, DOI 10.1016/0010-0277(93)90026-R HARRIS AE, 1978, DEAF CHILDREN DEV PE, P217 Harris P., 1989, COGNITION EMOTION, V3, P379, DOI DOI 10.1080/02699938908412713 Harris P. L, 1996, THEORIES THEORIES MI, P200 Harris P. 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PD JUL PY 2000 VL 41 IS 5 BP 601 EP 608 DI 10.1017/S0021963099005843 PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 336TD UT WOS:000088318300007 PM 10946752 ER PT J AU Farmer, M AF Farmer, M TI Language and social cognition in children with specific language impairment SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE language; social behaviour; social cognition; specific language impairment; theory of mind ID FALSE BELIEF; MIND DEVELOPMENT; INDIVIDUAL-DIFFERENCES; PRESCHOOL-CHILDREN; CONCEPTUAL DEFICIT; 2ND-ORDER BELIEFS; JOINT ATTENTION; YOUNG-CHILDREN; COMMUNICATION; AUTISM AB This study explored the links between the development of language and the development of social cognition. Measures of language, phonological short-term memory, social cognition, and social competence of two groups of children with specific language impairment (SLI), one group attending a special school, the other attending integrated educational placements, were compared with those of chronological and language age-matched normally developing peers (N = 8 in each group). Significant differences between the scores of normally developing children and the scores of the group of children with SLI who attended the special school were found for social cognition and ratings of social competence. Children with SLI from integrated placements did not differ significantly from other groups on these measures. Assessments of language development and phonological short-term memory were not related to social cognition and social competence. Models of the possible relationship between social cognition and language development in children with SLI are discussed. 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PD JUL PY 2000 VL 41 IS 5 BP 627 EP 636 DI 10.1017/S0021963099005788 PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 336TD UT WOS:000088318300009 PM 10946754 ER PT J AU Moore, SJ Turnpenny, P Quinn, A Glover, S Lloyd, DJ Montgomery, T Dean, JCS AF Moore, SJ Turnpenny, P Quinn, A Glover, S Lloyd, DJ Montgomery, T Dean, JCS TI A clinical study of 57 children with fetal anticonvulsant syndromes SO JOURNAL OF MEDICAL GENETICS LA English DT Article DE fetal anticonvulsant syndrome; fetal valproate syndrome; teratogen; birth defects ID EXPOSED IN-UTERO; VALPROATE SYNDROME; EPILEPTIC MOTHERS; CARBAMAZEPINE MONOTHERAPY; CONGENITAL-MALFORMATIONS; ANTIEPILEPTIC DRUGS; HYDANTOIN SYNDROME; SPINA-BIFIDA; PREGNANCY; WOMEN AB Background-Anticonvulsants taken in pregnancy are associated with an increased risk of malformations and developmental delay in the children. To evaluate the pattern of abnormalities associated with prenatal anticonvulsant exposure further, we undertook a clinical study of 57 children with fetal anticonvulsant syndromes. Methods-Fifty two children were ascertained through the Fetal Anticonvulsant Syndrome Association and five were referred to the Aberdeen Medical Genetics Service. Pregnancy and medical history were obtained through a standardised questionnaire and interview and the children were examined. Results-Thirty four (60%) were exposed in utero to valproate alone, four (7%) to carbamazepine alone, four (7%) to phenytoin alone, and 15 (26%) to more than one anticonvulsant. Forty six (81%) reported behavioural problems, 22 (39%) with hyperactivity or poor concentration of whom four (7%) had a diagnosis of attention deficit and hyperactivity disorder. Thirty four (60%) reported two or more autistic features, of whom four had a diagnosis of autism and two of Asperger's syndrome. Forty four (77%) had learning difficulties, 46 (81%) had speech delay, 34 (60%) had gross motor delay, and 24 (42%) had fine motor delay. Nineteen (33%) had glue ear and 40 (70%) had joint laxity involving all sizes of joints. Of 46 who had formal ophthalmic evaluation, 16 (34%) had myopia. Conclusions-Speech delay, joint laxity, glue ear, and myopia are common in the fetal anticonvulsant syndromes and autistic features and hyperactivity form part of the behavioural phenotype. C1 Sch Med, Dept Med Genet, Aberdeen AB25 2ZD, Scotland. Royal Devon & Exeter Hosp, Dept Med Genet, Exeter EX2 5DW, Devon, England. Royal Devon & Exeter Hosp, Dept Ophthalmol, Exeter EX2 5DW, Devon, England. Aberdeen Matern Hosp, Dept Neonatal Med, Aberdeen, Scotland. Univ Newcastle Upon Tyne, Dept Human Genet, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. RP Dean, JCS (reprint author), Sch Med, Dept Med Genet, Aberdeen AB25 2ZD, Scotland. 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Med. Genet. PD JUL PY 2000 VL 37 IS 7 BP 489 EP 497 DI 10.1136/jmg.37.7.489 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 333XZ UT WOS:000088157200002 PM 10882750 ER PT J AU Leggio, MG Silveri, MC Petrosini, L Molinari, M AF Leggio, MG Silveri, MC Petrosini, L Molinari, M TI Phonological grouping is specifically affected in cerebellar patients: a verbal fluency study SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article DE cerebellum; language; cluster analysis ID SPEECH PRODUCTION; LESION; DEGENERATION; HYPOPLASIA; ATROPHY; DISEASE; AUTISM AB Objectives-Recent clinical and functional neuroimaging evidence points towards a cerebellar role in verbal production. At present it is not clear how the cerebellum participates in language production. The aim was to investigate the influence of cerebellar lesions on verbal fluency abilities with specific focus on the verbal searching strategies employed by patients with cerebellar damage. Methods-Twenty five patients with focal or degenerative cerebellar disease and 14 control subjects were tested in a timed verbal fluency task requiring word production under forced (phonemic or semantic) conditions. To analyse the verbal searching strategy employed, semantic and phonemic cluster analyses were also performed. Results-Performances of cerebellar patients were comparable with those of controls in the semantic task; conversely their performances were significantly impaired when tested in the letter task. Cluster analysis results showed that the verbal fluency impairment is linked to specific damage of phonemically related retrieval strategies. Conclusion-Cerebella damage impairs verbal fluency by specifically affecting phonemic rule performances while sparing semantic rule ones. These findings underline the importance of the cerebellar computing properties in strategy development in the linguistic domain. C1 Univ Rome La Sapienza, Dept Psychol, I-00185 Rome, Italy. IRCSS S Lucia, Rome, Italy. Catholic Univ, Neurol Inst, Rome, Italy. RP Leggio, MG (reprint author), Univ Rome La Sapienza, Dept Psychol, Via Dei Marsi 78, I-00185 Rome, Italy. 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Neurol. Neurosurg. Psychiatry PD JUL PY 2000 VL 69 IS 1 BP 102 EP 106 DI 10.1136/jnnp.69.1.102 PG 5 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA 330UR UT WOS:000087980000020 PM 10864613 ER PT J AU [Anonymous] AF [Anonymous] TI Practice parameters for the assessment and treatment of children, adolescents, and adults with autism and other pervasive developmental disorders (vol 38, pg 32S, 1999) SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Correction CR [Anonymous], 1999, J AM ACAD CHILD ADOL, V38, p32S NR 1 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0890-8567 EI 1527-5418 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. 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PD JUL PY 2000 VL 93 IS 7 BP 351 EP 355 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 332JL UT WOS:000088070500005 PM 10928021 ER PT J AU Richardson, AJ Ross, MA AF Richardson, AJ Ross, MA TI Fatty acid metabolism in neurodevelopmental disorder: a new perspective on associations between attention-deficit/hyperactivity disorder, dyslexia, dyspraxia and the autistic spectrum SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID MAGNETIC-RESONANCE SPECTROSCOPY; DEFICIT HYPERACTIVITY DISORDER; SCHIZOPHRENIC-PATIENTS; CHILD-PSYCHIATRY; OMEGA-3-FATTY-ACIDS; SUPPLEMENTATION; ABNORMALITIES; GENETICS; BOYS AB There is increasing evidence that abnormalities of fatty acid and membrane phospholipid metabolism play a part in a wide range of neurodevelopmental and psychiatric disorders. This proposal is discussed here in relation to attention-deficit/hyperactivity disorder (ADHD), dyslexia, developmental coordination disorder (dyspraxia) and the autistic spectrum. These are among the most common neurodevelopmental disorders of childhood, with significant implications for society as well as for those directly affected. However, controversy still surrounds both the identification and management of these conditions, and while their aetiology is recognized as being complex and multifactorial, little progress has yet been made in elucidating predisposing factors at the biological level. An overview is provided here of the contents of this Special Issue, which contains a selection of reports from a unique multidisciplinary workshop involving both researchers and clinicians. Its purpose was to explore the possibility that ADHD, dyslexia, dyspraxia and autism fall within a phospholipid spectrum of disorders. This proposal could explain the high degree of co-morbidity between these conditions, their aggregation within families and relation to other psychiatric disorders, and a range of associated features that are already well known at a clinical level. The existing evidence for fatty acid abnormalities in these disorders is summarized, and new approaches are outlined that have the potential to improve both the identification and the management of these and related neurodevelopmental and psychiatric conditions. (C) 2000 Harcourt Publishers Ltd. C1 Univ Oxford, Physiol Lab, Oxford OX1 3PT, England. Imperial Coll Sch Med, MRC, Ctr Clin Sci, MRI Unit, London, England. Highland Psychiat Res Fdn, Inverness, Scotland. RP Richardson, AJ (reprint author), Univ Oxford, Physiol Lab, Parks Rd, Oxford OX1 3PT, England. 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Essent. Fatty Acids PD JUL-AUG PY 2000 VL 63 IS 1-2 BP 1 EP 9 DI 10.1054/plef.2000.0184 PG 9 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA 356DK UT WOS:000089428900001 PM 10970706 ER PT J AU Jones, GS AF Jones, GS TI Autistic spectrum disorder: diagnostic difficulties SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID ASPERGERS SYNDROME AB Recognition of the autistic spectrum disorders is becoming more widespread amongst basic scientists, clinicians, and the general population. The term does not imply anything about pathology or aetiology, although it has proved to be a useful concept clinically. From Kanner's classical autism the concept has widened in scope to include milder and more subtle impairments. From a clinical perspective, there are many alternative diagnoses in an individual with autistic-like symptoms, and thorough investigation is necessary to exclude these. (C) 2000 Harcourt Publishers Ltd. C1 Woodlands Hosp, Aberdeen AB15 9PR, Scotland. RP Jones, GS (reprint author), Woodlands Hosp, Craigton Rd, Aberdeen AB15 9PR, Scotland. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BERNEY P, 2000, B J PSYCH, V176, P20 GESCHWIND DH, 1998, CNS SPECTRUMS, V3, P40 Ghaziuddin M., 1992, EUROPEAN CHILD ADOLE, V1, P209 Gillberg C., 1991, AUTISM ASPERGER SYND, P122, DOI 10.1017/CBO9780511526770.004 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x HOWLIN P, 1997, AUTISM PREPARING ADU, P217 KOLVIN I, 1971, BRIT J PSYCHIAT, V118, P381, DOI 10.1192/bjp.118.545.381 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Leo Kanner, 1973, CHILDHOOD PSYCHOSIS NAGY J, 1986, J AUTISM DEV DISORD, V16, P351, DOI 10.1007/BF01531664 NORDIN V, 1998, ACTA PSYCHIAT SCAND, V97, P999 TANTAM D, 1988, BRIT J PSYCHIAT, V153, P783, DOI 10.1192/bjp.153.6.783 WING L, 1997, LANCET, V350, P1791 WING L, 1996, CLIN DEV MED, V139 WING L, 1981, PSYCHOL MED, V11, P115 Wolff S., 1995, LONERS LIFE PATH UNU World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 19 TC 5 Z9 5 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD JUL-AUG PY 2000 VL 63 IS 1-2 BP 33 EP 36 DI 10.1054/plef.2000.0188 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA 356DK UT WOS:000089428900005 PM 10970710 ER PT J AU Trevarthen, C AF Trevarthen, C TI Autism as a neurodevelopmental disorder affecting communication and learning in early childhood: prenatal origins, post natal course and effective educational support SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article AB Colwyn Trevarthen, working on autism, discussed the importance of time, rhythm and temporal processing in brain function. The brains of new born infants show highly coherent and coordinated patterns of activity over time, and their rhythms are remarkably similar to those of adults. Since the cortex has not yet developed, this coordination must be subcortical in origin. The likely source is the emotional motor system. He noted that the cerebellum might regulate the intricate timing of the development and expression of emotional communication. He also pointed out that emotional and motivational factors have often been seriously neglected in psychology (largely owing to a misplaced focus on 'cognition' as some isolated entity) and emphasized the potential importance of empathetic support and music therapy in helping autistic children. (C) 2000 Harcourt Publishers Ltd. C1 Univ Edinburgh, Dept Psychol, Edinburgh EH8 9JZ, Midlothian, Scotland. RP Trevarthen, C (reprint author), Univ Edinburgh, Dept Psychol, 7 George Sq, Edinburgh EH8 9JZ, Midlothian, Scotland. CR Aitken K. 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Essent. Fatty Acids PD JUL-AUG PY 2000 VL 63 IS 1-2 BP 41 EP 46 DI 10.1054/plef.2000.0190 PG 6 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA 356DK UT WOS:000089428900007 PM 10970712 ER PT J AU Ward, PE AF Ward, PE TI Potential diagnostic aids for abnormal fatty acid metabolism in a range of neurodevelopmental disorders SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article ID NIACIN SKIN FLUSH; SCHIZOPHRENIC-PATIENTS; HYPERACTIVITY; BREATH; DEFICIENT; CHILDREN; MONKEYS; HUMANS; BOYS AB Disorders of neurodevelopment include attention deficit hyperactivity disorder, dyspraxia, dyslexia and autism. There is considerable co-morbidity of these disorders and their identification often presents difficulties to those making a diagnosis. This is especially difficult when a multidisciplinary approach is not adopted. All of these disorders have been reported as associated with fatty acid abnormalities ranging from genetic abnormalities in the enzymes involved in phospholipid metabolism to symptoms reportedly improved following dietary supplementation with long chain fatty acids. If definitive disorders of lipid metabolism could be defined then the diagnosis and subsequent management of neurodevelopmental disorders might be transformed. In the identification of those disorders of development which involve lipid metabolism, there are now several tests, measures of lipid metabolism, which could be useful. (C) 2000 Harcourt Publishers Ltd. C1 Highland Psychiat Res Fdn, Inverness IV2 3ED, Scotland. RP Ward, PE (reprint author), Highland Psychiat Res Fdn, Green House,Beechwood Business Pk N, Inverness IV2 3ED, Scotland. 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Essent. Fatty Acids PD JUL-AUG PY 2000 VL 63 IS 1-2 BP 65 EP 68 DI 10.1054/plef.2000.0193 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA 356DK UT WOS:000089428900010 PM 10970715 ER PT J AU Noterdaeme, M Mildenberger, K Sitter, S Amorosa, H AF Noterdaeme, M Mildenberger, K Sitter, S Amorosa, H TI Examination of communicative and interactive behavior in children with autism and speech disorders SO PSYCHIATRISCHE PRAXIS LA German DT Meeting Abstract C1 Heckscher Klin, Abt Teilleistungsgestorte & Verhaltensauffallige, Munich, Germany. LMU, Ins Kinder & Jugendpsychiat, Munich, Germany. CR BARTAK L, 1975, BRIT J PSYCHIAT, V126, P127, DOI 10.1192/bjp.126.2.127 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 RUTTER M, 1992, SPECIFIC SPEECH AND LANGUAGE DISORDERS IN CHILDREN : CORRELATES, CHARACTERISTICS AND OUTCOMES, P63 NR 4 TC 0 Z9 0 PU GEORG THIEME VERLAG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0303-4259 J9 PSYCHIAT PRAX JI Psychiatr. Prax. PD JUL PY 2000 VL 27 SU 1 BP S12 EP S13 PG 2 WC Psychiatry SC Psychiatry GA 335WA UT WOS:000088266700016 ER PT J AU Eaves, RC Campbell, HA Chambers, D AF Eaves, RC Campbell, HA Chambers, D TI Criterion-related and construct validity of the pervasive developmental disorders rating scale and the autism behavior checklist SO PSYCHOLOGY IN THE SCHOOLS LA English DT Article ID DSM-III; CHILDREN; INSTRUMENTS AB This study investigated the validity of the Autism Behavior Checklist (ABC; Krug, Arick, & Almond, 1993) and the Pervasive Developmental Disorders Rating Scale (PDDRS; Eaves, 1993a). Both instruments are screening devices designed to measure characteristics of individuals with autistic disorder or, more broadly, pervasive developmental disorders. Results showed that the total scores of the ABC and PDDRS measure significantly overlapping constructs (r = .80). Further, both instruments significantly discriminated between participants with autistic disorder and children with diagnoses frequently confused with autistic disorder. Both instruments provided re spectable indices for classification accuracy (PDDRS overall accuracy = 88%, ABC overall accuracy = 80%). Finally, the ABC and PDDRS agreed in their classifications of 85% of the 136 participants; a phi coefficient based on the instruments' nominal classifications of the participants equaled .68 (p < .001). (C) 2000 John Wiley & Sons, Inc. C1 Auburn Univ, Dept Rehabil & Special Educ, Haley Ctr 1228, Auburn, AL 36849 USA. RP Eaves, RC (reprint author), Auburn Univ, Dept Rehabil & Special Educ, Haley Ctr 1228, Auburn, AL 36849 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CREAK M, 1964, INFANTILE AUTISM EAVES R. C., 1993, Recent advances in special education and rehabilitation, P3 Eaves R. 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The system is responsible for our adaptive responses (initiation, execution, or withholding) to environmental situations, and the above disorders, involving effectively excessive release ol withholding of various types of response, are all a consequence of changes in specific frontostriatal regions. The disorders all have a genetic component, and their persistence in the genome indicates that their clinical manifestations may also he associated, perhaps in low levels in close relatives, with certain adaptive advantages in given situations. Thus autism is associated with computational careers, depression with literary creativity, SCZ with lateral thinking and the Odyssean personality, ADHD with an lee-Age readiness to respond, OCD with a focused range of interests, and TS with competitive sports and jazz improvisation. The disorders are all highly cumorbid, and which one predominantly manifests may depend on how the frontostriatal system happens to he compromised as a result of inherited genetic predispositions and environmental contingency. We review the adaptive nature of the various subclinical manifestations and the evidence for concomitant phenomena (possibly epiphenomena): alterations in structural, functional, and behavioral lateralization in each syndrome. Indeed it is not clear that altered lateralization in frontostriatal disorders of a neurodevelopmental origin generally has any adaptive significance; it may often simply serve as a marker for altered regulatory function of the frontostriatal system, alterations which in low genetic dosage or penetrance continue to play an adoptive role in clinically unaffected close relatives of probands, hut which, in high dosage or penetrance in the probands themselves, are generally deleterious. (C) 2000 Academic Press. 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PD JUN 15 PY 2000 VL 73 IS 2 BP 297 EP 320 DI 10.1006/brln.2000.2308 PG 24 WC Audiology & Speech-Language Pathology; Linguistics; Neurosciences; Psychology, Experimental SC Audiology & Speech-Language Pathology; Linguistics; Neurosciences & Neurology; Psychology GA 325HH UT WOS:000087669800008 PM 10856179 ER PT J AU Donnelly, SL Wolpert, CM Menold, MM Bass, MP Gilbert, JR Cuccaro, ML DeLong, GR Pericak-Vance, MA AF Donnelly, SL Wolpert, CM Menold, MM Bass, MP Gilbert, JR Cuccaro, ML DeLong, GR Pericak-Vance, MA TI Female with autistic disorder and monosomy X (Turner syndrome): Parent-of-origin effect of the X chromosome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autistic disorder; Turner syndrome; imprinting; social cognition ID PERVASIVE DEVELOPMENTAL DISORDERS; INACTIVATION PATTERNS; BEHAVIOR PROBLEMS; SEX-DIFFERENCES; CHILDREN; PHENOTYPE; LOCUS AB We have ascertained and examined a pa. tient with autistic disorder (AD) and monosomy X (Turner syndrome), The patient met Diagnostic and Statistical Manual of Mental Disorders (DSM-TV)/International Classification of Diseases (ICD-10) criteria for AD verified by the Autism Diagnostic Interview-Revised. The patient exhibited both social and verbal deficits and manifested the classical physical features associated with monosomy X, Skuse et al, [1997: Nature 387:705-708] reported three such cases of AD and monosomy X in their study of Turner syndrome and social cognition, They observed that monosomy X females with a maternally inherited X chromosome had reduced social cognition when compared with monosomy X females with a paternally inherited X chromosome, All three cases of AD and monosomy X were maternally inherited. Based on their data, they suggested that there was a gene for social cognition on the X chromosome that is imprinted and not expressed when the X chromosome is of maternal origin. Thus, we conducted parent-of-origin studies in our AD/monosomy X patient by genotyping X chromosome markers in the patient and her family. We found that the patient's X chromosome was of maternal origin. These findings represent the fourth documented case of maternal inheritance of AD and monosomy X and provide further support for the hypothesis that parent-of-origin of the X chromosome influences social cognition. Am. J, Med, Genet. (Neuropsychiatr, Genet,) 96:312-316, 2000. (C) 2000 Wiley-Liss, Inc. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. WS Hall Psychiat Inst, Columbia, SC USA. Duke Univ, Med Ctr, Div Pediat Neurol, Durham, NC USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Box 3445,Carl Bldg, Durham, NC 27710 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BENDER BG, 1994, ATYPICAL COGNITIVE D, P197 Buchanan L, 1998, DEV NEUROPSYCHOL, V14, P341 Busque L, 1996, BLOOD, V88, P59 Cuccaro M. 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J. Med. Genet. PD JUN 12 PY 2000 VL 96 IS 3 BP 312 EP 316 DI 10.1002/1096-8628(20000612)96:3<312::AID-AJMG16>3.0.CO;2-8 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 320DP UT WOS:000087386700016 PM 10898907 ER PT J AU Wolpert, CM Menold, MM Bass, MP Qumsiyeh, MB Donnelly, SL Ravan, SA Vance, JM Gilbert, JR Abramson, RK Wright, HH Cuccaro, ML Pericak-Vance, MA AF Wolpert, CM Menold, MM Bass, MP Qumsiyeh, MB Donnelly, SL Ravan, SA Vance, JM Gilbert, JR Abramson, RK Wright, HH Cuccaro, ML Pericak-Vance, MA TI Three probands with autistic disorder and isodicentric chromosome 15 SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE maternally derived; de novo; isodicentric chromosome 15q; gamma-aminobutyric acid receptor (GABA) ID PRADER-WILLI-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; CHILD PSYCHIATRIC-DISORDERS; ANGELMAN SYNDROME; MENTAL-RETARDATION; INFANTILE-AUTISM; GENETIC-FACTORS; INV DUP(15); HYPOMELANOSIS; ITO AB We have identified three unrelated probands with autistic disorder (AD) and isodicentric chromosomes that encompass the proximal region of 15q11.2. All three probands met the Diagnostic and Statistical Manual of Mental Disorders, fourth edition [DSM-IV; American Psychiatric Association, 1994], and International Classification of Diseases (ICD-10) diagnostic criteria for AD, confirmed with the Autism Diagnostic Interview -Revised (ADI-R), Chromosome analysis revealed the following karyotypes: 47,XX, +idic(15)(q11.2), 47,XX, +idic(15) (q11.2), and 47,XY,+idic(15)(q11.2). Haplotype analysis of genotypic maker data in the probands and their parents showed that marker chromosomes in all three instances were of maternal origin. Comparison of the clinical findings of the three AD probands with case reports in the published literature (N = 20) reveals a clustering of physical and developmental features, Specifically, these three probands and the majority of reported probands in the literature exhibited hypotonia (n = 13), seizures (n = 13), and delayed gross motor development (n = 13). In addition, clustering of the following clinical signs was seen with respect to exhibited speech delay (n = 13), lack of social reciprocity (n = 11), and stereotyped behaviors (n = 12), Collectively, these data provide further evidence for the involvement of chromosome 15 in AD as well as present preliminary data suggesting a clustering of clinical features in AD probands with proximal 15q anomalies. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:365-372, 2000. (C) 2000 Wiley-Liss, Inc. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Med, Durham, NC 27710 USA. Duke Univ, Med Ctr, Dept Pathol & Pediat, Durham, NC USA. Univ S Carolina, WS Hall Psychiat Inst, Columbia, SC 29208 USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Carl Bldg,Box 3445, Durham, NC 27710 USA. 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J. Med. Genet. PD JUN 12 PY 2000 VL 96 IS 3 BP 365 EP 372 DI 10.1002/1096-8628(20000612)96:3<365::AID-AJMG25>3.0.CO;2-X PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 320DP UT WOS:000087386700025 PM 10898916 ER PT J AU Croen, LA Grether, JK Hoogstrate, J Selvin, S AF Croen, LA Grether, JK Hoogstrate, J Selvin, S TI Epidemiologic characteristics of full syndrome autism in California. SO AMERICAN JOURNAL OF EPIDEMIOLOGY LA English DT Meeting Abstract C1 Calif Birth Defects Monitoring Program, Emeryville, CA 94608 USA. NR 0 TC 0 Z9 0 PU OXFORD UNIV PRESS INC PI CARY PA JOURNALS DEPT, 2001 EVANS RD, CARY, NC 27513 USA SN 0002-9262 J9 AM J EPIDEMIOL JI Am. J. Epidemiol. 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The personalities of the participants often were described as friendly, good-natured, and cheerful, but they did not differ empirically on a standardized measure of personality structure from typically developing comparison children, even after controlling for the effects of IQ Specifically, higher rates of agreeableness and extraversion were not confirmed, though these constructs do not correspond perfectly with the traits of affability and gregariousness described in earlier published case studies of FC syndrome. In terms of neuropsychological assessment, the boys had relatively less developed language, fine motor, and executive function skills, and visual-spatial abilities were a relative strength. Limitations and suggestions for future research are discussed. (C) 2000 Wiley-Liss, Inc. C1 Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA. Univ Utah, Autism Specialty Clin, Salt Lake City, UT 84112 USA. Univ Erlangen Nurnberg, Inst Human Genet, D-8520 Erlangen, Germany. 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PD SUM PY 2000 VL 97 IS 2 BP 112 EP 118 DI 10.1002/1096-8628(200022)97:2<112::AID-AJMG2>3.0.CO;2-D PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 377WG UT WOS:000165548800002 PM 11180218 ER PT J AU Bardoni, B Mandel, JL Fisch, GS AF Bardoni, B Mandel, JL Fisch, GS TI FMR1 gene and fragile X syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Review DE fragile X syndrome; FMR1 gene; FMRP; mental retardation; phenotype; genotype ID MENTAL-RETARDATION PROTEIN; PROSPECTIVE MULTICENTER ANALYSIS; PREMATURE OVARIAN FAILURE; NUCLEAR EXPORT SIGNALS; SELECTIVE RNA-BINDING; FULL MUTATION; CELL-PROLIFERATION; POINT MUTATION; CGG REPEATS; KH DOMAIN AB Taxonomic features of fragile X syndrome (FXS) associated with the fragile X mutation have evolved over several decades. Males are more severely impacted cognitively than females, but both show declines in IQ scores as they age. Although many males with FXS exhibit autistic-like features, autism does not occur more frequently in males with FXS than among males with mental retardation (MR). FXS is caused by inactivation of the FMR1 gene located on Xq27.3. FMRP, the protein produced by FMR1, has been detected in most organs and in brain. In cells, it is located primarily in cytoplasm and contains motifs found in RNA-binding proteins. The FMRP N-terminal contains a functional nuclear localization signal which permits the protein to shuttle between cytoplasm and nucleus. FMR1 knockout mice show subtle behavioral and visual-spatial difficulties. Analysis of their brain tissue suggests absence of FMRP impairs synaptic maturation. Individuals with the fragile premutation produce FMRP, and the phenotype associated with the premutation has been controversial. However, there seems to be a higher incidence of premature ovarian failure in women with the premutation than is found in the general female population. 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J. Med. Genet. PD SUM PY 2000 VL 97 IS 2 BP 153 EP 163 DI 10.1002/1096-8628(200022)97:2<153::AID-AJMG7>3.0.CO;2-M PG 11 WC Genetics & Heredity SC Genetics & Heredity GA 377WG UT WOS:000165548800007 PM 11180223 ER PT J AU Burack, J Zelazo, PD Iarocci, G AF Burack, J Zelazo, PD Iarocci, G TI Speculations about systemic and modular approaches to the development of cognition in autism. SO BRAIN AND COGNITION LA English DT Meeting Abstract C1 McGill Univ, Montreal, PQ H3A 2T5, Canada. Univ Toronto, Toronto, ON, Canada. NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0278-2626 J9 BRAIN COGNITION JI Brain Cogn. 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PD JUN-AUG PY 2000 VL 43 IS 1-3 BP 7 EP 8 PG 2 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 316FU UT WOS:000087157600006 ER PT J AU Mottron, L AF Mottron, L TI Cognitive deficit in autism: Specific or distributed? SO BRAIN AND COGNITION LA English DT Meeting Abstract C1 Univ Montreal, Montreal, PQ H3C 3J7, Canada. NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC 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 JUN-AUG PY 2000 VL 43 IS 1-3 BP 11 EP 11 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 316FU UT WOS:000087157600016 ER PT J AU O'Riordan, M AF O'Riordan, M TI Reduced perception of similarity in autism. SO BRAIN AND COGNITION LA English DT Meeting Abstract C1 Univ Cambridge, Cambridge CB2 1TN, England. NR 0 TC 1 Z9 1 PU ACADEMIC PRESS INC 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 JUN-AUG PY 2000 VL 43 IS 1-3 BP 11 EP 12 PG 2 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 316FU UT WOS:000087157600018 ER PT J AU Tager- Flusberg, H AF Tager- Flusberg, H TI On the relationship between language, theory of mind, and executive functions in high and low functioning children with autism. SO BRAIN AND COGNITION LA English DT Meeting Abstract C1 Univ Massachusetts, Amherst, MA 01003 USA. Eunice Kennedy Shriver Ctr Mental Retardat Inc, Waltham, MA 02452 USA. RI Tager-Flusberg, Helen/D-5265-2009 NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC 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 JUN-AUG PY 2000 VL 43 IS 1-3 BP 15 EP 15 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 316FU UT WOS:000087157600028 ER PT J AU Cole, K Mitchell, P AF Cole, K Mitchell, P TI Siblings in the development of executive control and a theory of mind SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID FALSE-BELIEF TASKS; CHILDRENS DIFFICULTY; STRATEGIC DECEPTION; YOUNG-CHILDREN; WINDOWS TASK; PRESCHOOLERS; BEHAVIOR; ABILITY; AUTISM AB The purpose of the study was to determine whether the relationship between siblings and theory of mind might be mediated by executive abilities. The participants were 119 children from a lower income community, between the ages of 3 and 5, who completed an executive function battery and tests of an understanding of mind. The correlation data suggested a link between siblings and executive control and between cheery of mind and executive control but, surprisingly, not between siblings and cheery of mind. A further experiment with 71 children indirectly highlighted the potential contaminating influence of socio;economic status (SES) on the sibling advantage in theory of mind. Multiple regression analyses, controlling for age and verbal IQ, discriminated between the types of executive processes most likely to predict performance in mental understanding. The implications of this result are discussed in terms of a 'primary' and 'secondary' executive deficit account. C1 Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England. Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Cole, K (reprint author), Dept Clin Psychol, Bangor LL57 2PW, Gwynedd, Wales. CR BROWN A, 1989, METACOGNITION MOTIVA, P65 Bruner J. 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Projects discussed included a study assessing impulsive temperament in eating disorder patients, a study on serotonin. receptor sensitivity in autism, a study of sleep EEG abnormalities tit OCD, a study of dissociation tit pathological gamblers, papers on aspects of schizo-obsessive patients, a study addressing biological alterations lit OCD, data from a new family study on OCD, data from a molecular genetic study of OCD, a factor analytic study of Tourette disorder, a study hypothesizing the existence of an OCD continuum, and, finally, a paper on early- vs late-onset OCD. 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SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID HARMFUL DYSFUNCTION; INDIVIDUAL-DIFFERENCES; MENTAL DISORDER; NORMAL-CHILDREN; MIND; ADULTS; DEFICITS; BELIEFS; PHENOTYPE; FEELINGS AB This article considers whether Asperger syndrome (AS) or high-functioning autism (HFA) necessarily leads to disability or whether AS/HFA simply leads to "difference." It concludes that the term "difference" in relation to AS/HFA is a more neutral, value-free, and fairer description than terms such as "impairment," "deficiency," or "disability"; that the term "disability" only applies to the lower functioning cases of autism; but that the term "disability" may need toe retained for AS/HFA as long as the legal framework provides financial and other support only for individuals with a disability. Two models are summarized which attempt to define in what way individuals with AS/HFA are "different": the central coherence model, and the folk psychology-folk physics model. The challenge for research is to test the value of such models and to precisely characterize the differences in cognitive style. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. 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Psychopathol. PD SUM PY 2000 VL 12 IS 3 BP 489 EP 500 DI 10.1017/S0954579400003126 PG 12 WC Psychology, Developmental SC Psychology GA 355DM UT WOS:000089370400012 PM 11014749 ER PT J AU Wang, PP Woodin, MF Kreps-Falk, R Moss, EM AF Wang, PP Woodin, MF Kreps-Falk, R Moss, EM TI Research on behavioral phenotypes: velocardiofacial syndrome (deletion 22q11.2) SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID CARDIO-FACIAL SYNDROME; FRAGILE-X; MENTAL-RETARDATION; WORKING-MEMORY; PROFILES; CHILDREN; MICRODELETIONS; ADOLESCENTS; DIGEORGE; AUTISM C1 Childrens Seashore House, Philadelphia, PA 19104 USA. RP Wang, PP (reprint author), Childrens Seashore House, 3405 Civ Ctr Blvd, Philadelphia, PA 19104 USA. 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Med. Child Neurol. PD JUN PY 2000 VL 42 IS 6 BP 422 EP 427 DI 10.1017/S0012162200000785 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 325RY UT WOS:000087691200013 PM 10875531 ER PT J AU London, E Etzel, RA AF London, E Etzel, RA TI The environment as an etiologic factor in autism: A new direction for research SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE autism; autism epidemiology; autism etiology; children; developmental disorders; retinoids; gene-environment interaction; Hox genes ID VITAMIN-A INTAKE; INFANTILE-AUTISM; INDIVIDUALS; RETINOIDS; DISORDER; DEFECTS; PARENTS AB Autism is one of a group of developmental disorders that have devastating lifelong effects on its victims. Despite the severity of the disease and the fact that it is relatively common (15 in 10,000), there is still little understanding of its etiology. Although believed to be highly genetic, no abnormal genes have been found. Recent findings in autism and in related disorders point to the possibility that the disease is caused by a gene-environment interaction. Epidemiologic studies indicate that: the number of cases of autism is increasing dramatically each year. it is not clear whether this is due to a real increase in the disease or whether this is an artifact of ascertainment. A new theory regarding the etiology of autism suggests that it may be a disease of very early fetal development (approximately day 20-24 of gestation). This theory has initiated new lines of investigation into developmental genes. Environmental exposures during pregnancy could cause or contribute to autism based on the neurobiology of these genes. C1 Natl Alliance Autism Res, Princeton, NJ 08540 USA. Univ Med & Dent New Jersey, New Brunswick, NJ USA. USDA, Food Safety & Inspect Serv, Div Epidemiol & Risk Assessment, Washington, DC 20250 USA. 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Health Perspect. PD JUN PY 2000 VL 108 SU 3 BP 401 EP 404 PG 4 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 326RK UT WOS:000087748400006 PM 10852835 ER PT J AU Goldman, LR Koduru, S AF Goldman, LR Koduru, S TI Chemicals in the environmental and developmental toxicity to children: A public health and policy perspective SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Article DE chemical testing; child health; developmental disabilities; neurotoxicity; pesticides; risk assessment ID NORMAL BIRTH-WEIGHT; CEREBRAL-PALSY; AUTISM; DISABILITIES; EPIDEMIOLOGY; INFANTS; RISK AB There are numerous pesticides and toxic chemicals in the environment that have yet to be evaluated for potential to cause developmental neurotoxicity. Recent legislation and testing initiatives provide an impetus to generating more information about potential hazards to children. In the United States, the 1996 Food Quality Protection Act (FQPA) required the U.S. Environmental Protection Agency (U.S. EPA) to make a finding that a pesticide food use is safe for children. In addition, the law requires U.S. EPA to incorporate an additional 10-fold factor in risk assessments for pesticide residue tolerances to take into account the special sensitivities of infants and children as well as incomplete data with respect to toxicity and exposures. The potential of chemicals in food and drinking water to cause endocrine disruption will also be examined via the Endocrine Disrupter Screening and Testing Program required by the FQPA and the 1996 Safe Drinking Water Act. in addition, a new Voluntary chemical information program will provide screening-level information for the some 2,800 high-volume chemicals in commerce in the United States. These initiatives will need to be accompanied by research focused on developmental toxicity for children, including developmental disabilities. Developmental disabilities exact a large toll on children's health in the United States. Three major developmental disabilities-autism cerebral palsy, and severe mental retardation-each affect substantial numbers of children. We know very little about the etiology of these conditions. A number of priority areas for research are suggested, including a large environmental prospective study of developmental neurotoxicity. C1 Johns Hopkins Univ, Sch Hyg & Publ Hlth, Baltimore, MD 21205 USA. RP Goldman, LR (reprint author), Johns Hopkins Univ, Sch Hyg & Publ Hlth, 624 N Broadway,Room 441, Baltimore, MD 21205 USA. 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Health Perspect. PD JUN PY 2000 VL 108 SU 3 BP 443 EP 448 DI 10.2307/3454535 PG 6 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 326RK UT WOS:000087748400014 PM 10852843 ER PT J AU Rice, D Barone, S AF Rice, D Barone, S TI Critical periods of vulnerability for the developing nervous system: Evidence from humans and animal models SO ENVIRONMENTAL HEALTH PERSPECTIVES LA English DT Review DE abnormal neurological development; apoptosis; behavioral testing methodology; delayed neurotoxicity; differentiation; migration; myelination; neurobiological substrates of function; neuronal plasticity; neurotrophic factor; primate; rodent ID FETAL ALCOHOL SYNDROME; LEVEL LEAD-EXPOSURE; VISUAL RECOGNITION MEMORY; FACTOR MESSENGER-RNA; SCHEDULE-CONTROLLED BEHAVIOR; ENDOGENOUS OPIOID SYSTEMS; PRIMATE CEREBRAL-CORTEX; GROWTH-FACTOR RECEPTOR; PROGRAMMED CELL-DEATH; RAT-BRAIN DEVELOPMENT AB Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis). Evidence from numerous sources demonstrates that neural development extends from the embryonic period through adolescence. In general, the sequence of events is comparable among species, although the time scales are considerably different. Developmental exposure of animals or humans to numerous agents (e.g., X-ray irradiation, methylazoxymethanol, ethanol, lead, methyl mercury, or chlorpyrifos) demonstrates that interference with one or more of these developmental processes can lead to developmental neurotoxicity. Different behavioral domains (e.g., sensory, motor, and various cognitive functions) are subserved by different brain areas. Although there are important differences between the rodent and human brain, analogous structures can be identified. Moreover, the ontogeny of specific behaviors can be used to draw inferences regarding the maturation of specific brain structures or neural circuits in rodents and primates, including humans. Furthermore, Various clinical disorders in humans (e.g., schizophrenia, dyslexia, epilepsy, and autism) may also be the result of interference with normal ontogeny of developmental processes in the nervous system. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function. This concern is compounded by the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans. C1 US EPA, Cellular & Mol Toxicol Branch, Div Neurotoxicol, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA. US EPA, Natl Ctr Environm Assessment, Washington, DC 20460 USA. RP Barone, S (reprint author), US EPA, Cellular & Mol Toxicol Branch, Div Neurotoxicol, Natl Hlth & Environm Effects Res Lab, Res Triangle Pk, NC 27711 USA. 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Health PD SUM PY 2000 VL 29 IS 2 BP 32 EP 43 PG 12 WC Health Policy & Services; Psychiatry; Psychology SC Health Care Sciences & Services; Psychiatry; Psychology GA 353BC UT WOS:000089253000003 ER PT J AU Peeters, T AF Peeters, T TI The role of training in developing services for persons with autism and their families SO INTERNATIONAL JOURNAL OF MENTAL HEALTH LA English DT Article C1 TEACCH, Opleidingscentrum Autisme Ctr Training Autism, B-2140 Borgerhout, Antwerp, Belgium. RP Peeters, T (reprint author), TEACCH, Opleidingscentrum Autisme Ctr Training Autism, Laar 61, B-2140 Borgerhout, Antwerp, Belgium. 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Health PD SUM PY 2000 VL 29 IS 2 BP 44 EP 59 PG 16 WC Health Policy & Services; Psychiatry; Psychology SC Health Care Sciences & Services; Psychiatry; Psychology GA 353BC UT WOS:000089253000004 ER PT J AU Magerotte, G AF Magerotte, G TI From quality of services to quality of life of persons with autism - Contributions to research, training, and community services of the University of Mons-Hainaut SO INTERNATIONAL JOURNAL OF MENTAL HEALTH LA English DT Article ID BEHAVIORAL TREATMENT; EARLY INTERVENTION; CHILDREN C1 Univ Mons, Fac Psychol & Educ, Dept Orthoped, B-7000 Mons, Belgium. RP Magerotte, G (reprint author), Univ Mons, Fac Psychol & Educ, Dept Orthoped, Pl Parc 18, B-7000 Mons, Belgium. 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H., 1989, NONAVERSIVE INTERVEN MONTREUIL N, 1987, COMPORTEMENT HUMAIN, V1, P65 MONTREUIL N, 1994, PRATIQUE INTERVENTIO NIHIRA K, 1972, AAMD ADAPTIVE BEHAV ONEIL RE, 1990, FUNCTIONAL ANAL PROB Ramey CT, 1998, AM PSYCHOL, V53, P109, DOI 10.1037/0003-066X.53.2.109 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 RUTTER M, 1968, J CHILD PSYCHOL PSYC, V9, P1, DOI 10.1111/j.1469-7610.1968.tb02204.x Rutter M., 1978, AUTISM REAPPRAISAL C SCHOPLER E, 1998, PSYCHOL FRANCAISE, V43, P209 Schopler E., 1988, CHILDHOOD AUTISM RAT Schopler E, 1994, PROFIL PSYCHOEDUCATI SCHULER AL, 1989, SEMINARS SPEECH LANG, V10, P51, DOI 10.1055/s-0028-1082489 WEHMEYER ML, 1992, EDUC TRAIN MENT RET, V27, P302 Willis CM, 1998, EUR J DERMATOL, V8, P8 1998, J ASS PERSONS SEVERE, V23 NR 42 TC 0 Z9 0 PU M E SHARPE INC PI ARMONK PA 80 BUSINESS PARK DR, ARMONK, NY 10504 USA SN 0020-7411 J9 INT J MENT HEALTH JI Int. J. Ment. Health PD SUM PY 2000 VL 29 IS 2 BP 60 EP 77 PG 18 WC Health Policy & Services; Psychiatry; Psychology SC Health Care Sciences & Services; Psychiatry; Psychology GA 353BC UT WOS:000089253000005 ER PT J AU Fuentes, J Gallano, I Gallano, I AF Fuentes, J Gallano, I Gallano, I TI Applying TEACCH in developing autism services in Spain - The GAUTENA project SO INTERNATIONAL JOURNAL OF MENTAL HEALTH LA English DT Article C1 GAUTENA, San Sebastian 20080, Spain. RP Fuentes, J (reprint author), GAUTENA, POB 1000, San Sebastian 20080, Spain. NR 0 TC 1 Z9 1 PU M E SHARPE INC PI ARMONK PA 80 BUSINESS PARK DR, ARMONK, NY 10504 USA SN 0020-7411 J9 INT J MENT HEALTH JI Int. J. Ment. Health PD SUM PY 2000 VL 29 IS 2 BP 78 EP 88 PG 11 WC Health Policy & Services; Psychiatry; Psychology SC Health Care Sciences & Services; Psychiatry; Psychology GA 353BC UT WOS:000089253000006 ER PT J AU Hultman, CM Cnattingius, S Sparen, P AF Hultman, CM Cnattingius, S Sparen, P TI Early risk factors for infantile autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Uppsala Univ, Dept Neurosci, Uppsala, Sweden. Karolinska Inst, Stockholm, Sweden. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 106 EP 106 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388801033 ER PT J AU Basil, C Reyes, S Rosell, C Soro-Camats, E AF Basil, C Reyes, S Rosell, C Soro-Camats, E TI Literacy development among children with multiple handicaps or autism: Evaluating an intervention program in Barcelona SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Barcelona, Dept Psychol, Barcelona, Spain. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 111 EP 111 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388801080 ER PT J AU Tager-Flusberg, H AF Tager-Flusberg, H TI Language and theory of mind development in children with autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract RI Tager-Flusberg, Helen/D-5265-2009 NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 111 EP 112 PG 2 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388801082 ER PT J AU Russel, J AF Russel, J TI The role of agency in the development of self-awareness: Clues from autism. SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Dept Expt Psychol, Cambridge, England. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 183 EP 183 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388801793 ER PT J AU Ostlin, AK d'Escury, AC Janols, LO Lunell, K Van der Molen, M von Knorring, AL AF Ostlin, AK d'Escury, AC Janols, LO Lunell, K Van der Molen, M von Knorring, AL TI Meta-representation in children with autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Child & Adolescent Psychiat, Uppsala, Sweden. Univ Uppsala, Child & Adolescent Psychiat, Uppsala, Sweden. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 196 EP 196 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388801914 ER PT J AU Bowler, DM Berthoud-Papandropou, I Kilcher, H AF Bowler, DM Berthoud-Papandropou, I Kilcher, H TI Metalinguistic awareness in children with and without autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 City Univ London, Dept Psychol, London, England. Univ Geneva, CH-1211 Geneva 4, Switzerland. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 297 EP 298 PG 2 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388802908 ER PT J AU Akande, D AF Akande, D TI The effect of self-monitoring in black children with autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Potchefstroom Univ Christian Higher Educ, Vanderbijlpark, South Africa. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 356 EP 356 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388803491 ER PT J AU Crawley, TFO Martin, F AF Crawley, TFO Martin, F TI Cognitive and visual processes in autism: Visual memory, global precedence and central coherence SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Tasmania, Hobart, Tas, Australia. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 421 EP 421 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388804130 ER PT J AU Olivar, JS Belinchon Carmona, M AF Olivar, JS Belinchon Carmona, M TI Referential communication in children with autism and Down's syndrome: Efficiency as listeners SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Valladolid, E-47002 Valladolid, Spain. Univ Autonoma Madrid, E-28049 Madrid, Spain. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 431 EP 431 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388804232 ER PT J AU Tjus, T Strid, K AF Tjus, T Strid, K TI Positive changes in syntactical reading errors in children with autism after multimedia training SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Gothenburg Univ, Dept Psychol, Gothenburg, Sweden. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD JUN-AUG PY 2000 VL 35 IS 3-4 SI SI BP 431 EP 431 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 337XP UT WOS:000088388804229 ER PT J AU Miller, N Neuringer, A AF Miller, N Neuringer, A TI Reinforcing variability adolescents with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; operant variability; response stereotypy; percentile reinforcement; noncontingent reinforcement ID BEHAVIORAL VARIABILITY; NONCONTINGENT REINFORCEMENT; DIFFERENTIAL REINFORCEMENT; CHILDREN; OPERANT; CREATIVITY; FREQUENCY; SELECTION; SCHEDULE; REDUCE AB Five adolescents with autism, 5 adult control participants, and 4 child controls received rewards for varying their sequences of responses while playing a computer game. In preceding and following phases, rewards were provided at approximately the same rate but were independent of variability. The most important finding was that, when reinforced, variability increased significantly in all groups. Reinforced variability could provide the necessary behavioral substrate for individuals with autism to learn new responses. C1 Reed Coll, Dept Psychol, Portland, OR 97202 USA. RP Neuringer, A (reprint author), Reed Coll, Dept Psychol, Portland, OR 97202 USA. 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Autism Dev. Disord. PD JUN PY 2000 VL 30 IS 3 BP 181 EP 182 PG 2 WC Psychology, Developmental SC Psychology GA 360NL UT WOS:000089674100001 ER PT J AU Laushey, KM Heflin, LJ AF Laushey, KM Heflin, LJ TI Enhancing social skills of kindergarten children with autism through the training of multiple peers as tutors SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE social skills; autism; peer tutors ID STUDENTS; PRESCHOOLERS; DISABILITIES; EDUCATION; BEHAVIOR; VALIDITY AB Many students with autism are being served in inclusive settings. Early intervention programs, traditionally home-based, are beginning to create center-based options which incorporate typically developing peers. One of the arguments for the use of inclusive programs is that students with autism will benefit from their exposure to and interactions with typical peers. Unfortunately, research suggests that in inclusive settings, typical peers and peers with autism do not always interact without prompting from an adult. This study used an ABAB design to determine if a peer buddy approach in which all students were trained to interact in dyads would increase non-adult-directed interactions. Data collected on the students with autism indicate that the peer buddy approach significantly increased their appropriate social interactions. Follow-up data on one of the students indicates generalization of appropriate social interactions to a new classroom. C1 Georgia State Univ, Dept Educ Psychol & Special Educ, Atlanta, GA 30303 USA. RP Laushey, KM (reprint author), Georgia State Univ, Dept Educ Psychol & Special Educ, Univ Plaza, Atlanta, GA 30303 USA. CR Alberto P. A., 1999, APPL BEHAV ANAL TEAC American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Attwood T., 1998, ASPERGERS SYNDROME G BARRON AM, 1991, EDUC RES, V33, P174 Bergan J. 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Autism Dev. Disord. PD JUN PY 2000 VL 30 IS 3 BP 183 EP 193 DI 10.1023/A:1005558101038 PG 11 WC Psychology, Developmental SC Psychology GA 360NL UT WOS:000089674100002 PM 11055455 ER PT J AU Rieffe, C Terwogt, MM Stockmann, L AF Rieffe, C Terwogt, MM Stockmann, L TI Understanding atypical emotions among children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high functioning children with autism; theory of mind; emotions, multiple complex developmental disorder ID HIGH-FUNCTIONING CHILDREN; MIND; CLASSIFICATION; ABNORMALITIES; CONVERSATION; BELIEFS AB Children with autism are said to be poor mind readers: They have a limited understanding of the role that mental states play in determining emotions and behavior. In this research, 23 high-functioning children from the autistic spectrum (M age 9 years 3 months), 42 6-year-old controls, and 43 10-year-old controls were presented with six emotion-evoking stories and they were asked to explain protagonists' typical and atypical emotions. In the case of typical emotions, as expected on the basis of the mindblind hypothesis, children from the autistic spectrum gave few mental state explanations, referring to fewer than even the 6-year-old control group. However, in the case of atypical emotions, the autistic group performed as well as the 10-year-old controls. Their explanations for the atypical emotions demonstrate that children from the autistic spectrum indeed have the capacity to mind read (with respect to both desires and beliefs), although they do not always use this capacity in the same way as normally developing children. It is argued that the mind-reading capacity of high-functioning children from the autistic spectrum might be basically intact; unused in everyday circumstances but not necessarily defective. C1 Free Univ Amsterdam, Amsterdam, Netherlands. Paedal Inst, Duivendrecht, Netherlands. RP Rieffe, C (reprint author), Free Univ Amsterdam, Amsterdam, Netherlands. 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PD JUN PY 2000 VL 30 IS 3 BP 195 EP 203 DI 10.1023/A:1005540417877 PG 9 WC Psychology, Developmental SC Psychology GA 360NL UT WOS:000089674100003 PM 11055456 ER PT J AU Lord, C Risi, S Lambrecht, L Cook, EH Leventhal, BL DiLavore, PC Pickles, A Rutter, M AF Lord, C Risi, S Lambrecht, L Cook, EH Leventhal, BL DiLavore, PC Pickles, A Rutter, M TI The Autism Diagnostic Observation Schedule-Generic: A standard measure of social and communication deficits associated with the spectrum of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE Autism Diagnostic Observation Schedule; PDDNOS; non-autistic-spectrum diagnoses; expressive language skill ID DISORDER; INTERVIEW; CHILDREN AB The Autism Diagnostic Observation Schedule-Generic (ADOS-G) is a semistructured, standardized assessment of social interaction, communication, play, and imaginative use of materials for individuals suspected of having autism spectrum disorders. The observational schedule consists of four 30-minute modules, each designed to be administered to different individuals according to their level of expressive language. Psychometric data are presented for 223 children and adults with Autistic Disorder (autism), Pervasive Developmental Disorder Not Otherwise Specified (PDDNOS) or nonspectrum diagnoses. Within each module, diagnostic groups were equivalent on expressive language level. Results indicate substantial interrater and test-retest reliability for individual items, excellent interrater reliability within domains and excellent internal consistency. Comparisons of means indicated consistent differentiation of autism and PDDNOS from nonspectrum individuals, with some, but less consistent, differentiation of autism from PDDNOS. A priori operationalization of DSM-IV/ICD-10 criteria, factor analyses, and ROC curves were used to generate diagnostic algorithms with thresholds set for autism and broader autism spectrum/PDD. Algorithm sensitivities and specificities for autism and PDDNOS relative to nonspectrum disorders were excellent, with moderate differentiation of autism from PDDNOS. C1 Univ Chicago, Chicago, IL 60637 USA. Univ N Carolina, Chapel Hill, NC USA. Univ Manchester, Manchester, Lancs, England. Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London, England. RP Lord, C (reprint author), Univ Chicago, Chicago, IL 60637 USA. RI Pickles, Andrew/A-9625-2011; Rutter, Michael/C-8570-2013 OI Pickles, Andrew/0000-0003-1283-0346; CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAILEY A, 1995, PSYCHOL MED, V25, P63 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 CRONBACH LJ, 1951, PSYCHOMETRIKA, V16, P297 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Dunn L. M., 1981, PEABODY PICTURE VOCA Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd Elliott C. D., 1990, DIFFERENTIAL ABILITI HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x KOBAYASHI R, 1992, J AUTISM DEV DISORD, V22, P395, DOI 10.1007/BF01048242 KRUSKAL WH, 1952, J AM STAT ASSOC, V47, P583 LANDIS JR, 1977, BIOMETRICS, V33, P159, DOI 10.2307/2529310 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x Mahoney WJ, 1998, J AM ACAD CHILD PSY, V37, P278, DOI 10.1097/00004583-199803000-00012 MESIBOV G, 1994, BEHAV ISSUES AUTISM Mullen E, 1995, MULLEN SCALES EARLY Murray H., 1938, EXPLORATIONS PERSONA Raven J. C., 1956, GUIDE USING COLOURED Raven J.C., 1960, GUIDE USING STANDARD SCHEFFE H, 1953, BIOMETRIKA, V40, P87, DOI 10.1093/biomet/40.1-2.87 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SIEGEL B, 1989, J AM ACAD CHILD PSY, V28, P542, DOI 10.1097/00004583-198907000-00013 *STAT CORP, 1997, STAT STATS SOFTW REL Wechsler D., 1991, MANUAL WECHSLER INTE Wechsler D., 1984, MANUAL WECHSLER ADUL World Health Organization, 1993, INT CLASS DIS 10 REV NR 30 TC 2500 Z9 2510 PU KLUWER ACADEMIC/PLENUM PUBL 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 JUN PY 2000 VL 30 IS 3 BP 205 EP 223 DI 10.1023/A:1005592401947 PG 19 WC Psychology, Developmental SC Psychology GA 360NL UT WOS:000089674100004 PM 11055457 ER PT J AU Heavey, L Phillips, W Baron-Cohen, S Rutter, M AF Heavey, L Phillips, W Baron-Cohen, S Rutter, M TI The Awkward Moments Test: A naturalistic measure of social understanding in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE theory of mind; mind-reading ability ID EXECUTIVE DYSFUNCTION; COGNITIVE PHENOTYPE; ASPERGERS SYNDROME; NORMAL-CHILDREN; VERBAL-ABILITY; MIND; PARENTS; AGE; DISORDER; DEFICITS AB Details are given of a new advanced theory of mind task, developed to approximate che demands of real-life mentalizing in able individuals with autism. Excerpts of films showing characters in social situations were presented. with participants required to answer questions on characters' mental states and on control, nonsocial questions. When compared with control participants, adults with high-functioning autism and Asperger syndrome were most impaired in their ability to answer the questions requiring mind-reading ability. Although the present findings have implications for task modification, such naturalistic, dynamic stimuli are held to offer an important means of studying subtle difficulties in mentalistic understanding. C1 Inst Psychiat, MRC, Child Psychiat Unit, London SE13 4AF, England. Univ Cambridge, Cambridge, England. RP Heavey, L (reprint author), Inst Psychiat, MRC, Child Psychiat Unit, De Crespigny Pk,Denmark Hill, London SE13 4AF, England. RI Rutter, Michael/C-8570-2013 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 1980, DIAGN STAT MAN MENT Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BAILEY A, 1995, PSYCHOL MED, V25, P63 BARONCOHEN S, 1989, J AUTISM DEV DISORD, V19, P579, DOI 10.1007/BF02212859 BaronCohen S, 1997, J COGNITIVE NEUROSCI, V9, P548, DOI 10.1162/jocn.1997.9.4.548 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bauminger N, 1999, J AUTISM DEV DISORD, V29, P81, DOI 10.1023/A:1025974701090 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 Cramer D., 1994, INTRO STAT SOCIAL RE CRAWFORD JR, 1992, BRIT J CLIN PSYCHOL, V31, P191 Frith U., 1983, BRIT J DEV PSYCHOL, V1, P329, DOI 10.1111/j.2044-835X.1983.tb00906.x Frith U., 1989, AUTISM EXPLAINING EN HAPPE FGE, 1994, J CHILD PSYCHOL PSYC, V35, P1461, DOI 10.1111/j.1469-7610.1994.tb01287.x Happe F., 1994, AUTISM INTRO PSYCHOL HAPPE F, 1998, BPS DEV SECT C LANC 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 Happe FGE, 1998, DEV PSYCHOL, V34, P358, DOI 10.1037//0012-1649.34.2.358 HEAVEY L, 1999, UNPUB THEORY MIND EX Hughes C, 1997, PSYCHOL MED, V27, P209, DOI 10.1017/S0033291796004308 Hughes C, 1999, J CHILD PSYCHOL PSYC, V40, P705, DOI 10.1017/S0021963099004023 HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LESLIE AM, 1988, BRIT J DEV PSYCHOL, V6, P315 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1107, DOI 10.1111/j.1469-7610.1991.tb00352.x OZONOFF S, 1993, J AUTISM DEV DISORD, V23, P429, DOI 10.1007/BF01046049 Piven J, 1997, J CHILD PSYCHOL PSYC, V38, P1011, DOI 10.1111/j.1469-7610.1997.tb01618.x Rutter M., 1978, AUTISM REAPPRAISAL C SODIAN B, 1992, J CHILD PSYCHOL PSYC, V33, P591, DOI 10.1111/j.1469-7610.1992.tb00893.x SPARREVOHN R, 1995, J CHILD PSYCHOL PSYC, V36, P249, DOI 10.1111/j.1469-7610.1995.tb01823.x TAGERFLUSBERG H, 1992, CHILD DEV, V63, P161, DOI 10.1111/j.1467-8624.1992.tb03604.x VOLKMAR F, 1997, HDB AUTISM PERVASIVE Wechsler D, 1981, WECHSLER ADULT INTEL World Health Organisation, 1992, ICD 10 CLASS MENT BE Yirmiya N, 1996, J CHILD PSYCHOL PSYC, V37, P1003, DOI 10.1111/j.1469-7610.1996.tb01497.x NR 41 TC 76 Z9 78 PU KLUWER ACADEMIC/PLENUM PUBL 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 JUN PY 2000 VL 30 IS 3 BP 225 EP 236 DI 10.1023/A:1005544518785 PG 12 WC Psychology, Developmental SC Psychology GA 360NL UT WOS:000089674100005 PM 11055458 ER PT J AU Bodfish, JW Symons, FJ Parker, DE Lewis, MH AF Bodfish, JW Symons, FJ Parker, DE Lewis, MH TI Varieties of repetitive behavior in autism: Comparisons to mental retardation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; mental retardation; repetitive behavior ID NEUROLEPTIC-RELATED DYSKINESIAS; OBSESSIVE-COMPULSIVE DISORDER; SELF-INJURY; CHILDREN; STEREOTYPIES; PREVALENCE; AKATHISIA; MOVEMENT; ADULTS; SCALE AB Systematic study of abnormal repetitive behaviors in autism has been lacking despite the diagnostic significance of such behavior. The occurrence of specific topographies of repetitive behaviors as well as their severity was assessed in individuals with mental retardation with and without autism. The occurrence of each behavior category, except dyskinesias, was higher in the autism group and autistic subjects exhibited a significantly greater number of topographies of stereotypy and compulsions. Both groups had significant patterns of repetitive behavior cooccurrence. Autistic subjects had significantly greater severity ratings for compulsions, stereotypy, and self-injury. Repetitive behavior severity also predicted severity of autism. Although abnormal repetition is not specific to autism, an elevated pattern of occurrence and severity appears to characterize the disorder. C1 Univ Florida, Dept Psychiat, Gainesville, FL 32610 USA. Western Carolina Ctr, Human Dev Res & Training Inst, Morganton, NC 28655 USA. Univ N Carolina, Frank Porter Graham Child Dev Ctr, Chapel Hill, NC 27599 USA. RP Lewis, MH (reprint author), Univ Florida, Dept Psychiat, POB 100256, Gainesville, FL 32610 USA. 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Autism Dev. Disord. PD JUN PY 2000 VL 30 IS 3 BP 237 EP 243 DI 10.1023/A:1005596502855 PG 7 WC Psychology, Developmental SC Psychology GA 360NL UT WOS:000089674100006 PM 11055459 ER PT J AU Handen, BL Johnson, CR Lubetsky, M AF Handen, BL Johnson, CR Lubetsky, M TI Efficacy of methylphenidate among children with autism and symptoms of attention-deficit hyperactivity disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; methylphenidate; ADHD ID MENTALLY-RETARDED CHILDREN; SCHIZOPHRENIC CHILDREN; ADHD; RETARDATION; DEXTROAMPHETAMINE; BEHAVIOR AB Thirteen children (ages 5.6 to 11.2 years) with autism and symptoms of attention-deficit hyperactivity disorder (ADHD) participated in a double-blind, placebo-controlled crossover study of methylphenidate (0.3 and 0.6 mg/kg per dose). Eight subjects responded positively, based upon a minimum 50% decrease on the Conners Hyperactivity Index. Ratings of stereotypy and inappropriate speech, which are often associated with autistic core features, also decreased. However, no changes were found on the Child Autism Rating Scale, a global assessment of autistic symptomotology. Significant adverse side effects occurred in some children including social withdrawal and irritability, especially at the 0.6 mg/kg dose. Results suggest that methylphenidate can be efficacious for children with autism and ADHD symptoms. However, this group of children seems to be particularly susceptible to adverse side effects. C1 Western Psychiat Inst & Clin, Merck Program, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Pittsburgh, PA USA. RP Handen, BL (reprint author), Western Psychiat Inst & Clin, Merck Program, 3811 OHara St, Pittsburgh, PA 15213 USA. 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PD JUN PY 2000 VL 30 IS 3 BP 245 EP 255 DI 10.1023/A:1005548619694 PG 11 WC Psychology, Developmental SC Psychology GA 360NL UT WOS:000089674100007 PM 11055460 ER PT J AU Yeates-Frederikx, MHM Nijman, H Logher, E Merckelbach, HLGJ AF Yeates-Frederikx, MHM Nijman, H Logher, E Merckelbach, HLGJ TI Birth patterns in mentally retarded autistic patients SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE birth patterns; seasonality; autism ID INFANTILE-AUTISM; SEASON; SCHIZOPHRENIA; HYPOTHESIS; DISORDER AB Some studies claim to have shown that, compared to the general population, autistic children are born more often in the spring. The current study sought to replicate this finding in a large Dutch sample of mentally retarded autistic patients. Birth data for 1,031 patients with a diagnosis of "Infantile Austism" or "other psychoses with origin specific to childhood" were compared to those of the Dutch national population. Separate analyses were performed on diagnostic subgroups (i.e., infantile autism vs. other psychoses with origin specific to childhood), gender, and intelligence. No evidence was found to suggest that autism is characterized by a deviant birth pattern. C1 Psychiat Hosp Welterhof, Dienst Bestuursondersteuning, NL-6401 CX Heerlen, Netherlands. Maastricht Univ, Dept Expt Psychol, Maastricht, Netherlands. Riagg OZL, Ed Dept Child & Adolescent Psychiat, Heerlen, Netherlands. RP Yeates-Frederikx, MHM (reprint author), Psychiat Hosp Welterhof, Dienst Bestuursondersteuning, POB 4436, NL-6401 CX Heerlen, Netherlands. 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PD JUN PY 2000 VL 30 IS 3 BP 257 EP 262 DI 10.1023/A:1005500803764 PG 6 WC Psychology, Developmental SC Psychology GA 360NL UT WOS:000089674100008 PM 11055461 ER PT J AU Zuddas, A Di Martino, A Muglia, P Cianchetti, C AF Zuddas, A Di Martino, A Muglia, P Cianchetti, C TI Long-term risperidone for pervasive developmental disorder: Efficacy, tolerability, and discontinuation SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Article ID CHILDHOOD-ONSET SCHIZOPHRENIA; INDUCED TARDIVE-DYSKINESIA; AUTISTIC DISORDER; YOUNG-CHILDREN; DOUBLE-BLIND; WEIGHT-GAIN; OPEN-LABEL; ADOLESCENTS; ADULTS; TRIAL AB To investigate the safety (e.g., weight gain, liver function, extrapyramidal side effects, and seizures) and efficacy of the long-term use of risperidone in children and adolescents and to ascertain the effects of drug withdrawal in a semi-naturalistic prospective, subjects with autism or pervasive developmental disorders not otherwise specified (PDDNOS) were treated with risperidone for 6 months after which parents were given the option of continuing for a further 6 months (final assessment at 12 months). Behavioral rating included Childhood Autism Rating Scale (CARS), Child Psychiatric Rating Scale (CPRS), Clinical Global Impression (CGI), and Child-Global Assessment Scale (C-GAS). Risperidone significantly ameliorated behavioral symptoms of PDD in 10 out of 11 subjects, with the effects on core symptoms being of smaller amplitude and of slower onset. No loss of effectiveness was observed in patients who continued risperidone for 12 months, while a relapse of associated behavioral symptoms occurred in the others. Weight gain was common, although the rate of increase lessened over a period of time; after drug withdrawal, considerable weight loss was observed in the patient who had previously shown the most significant increase. After 6 months of therapy, two patients developed facial dystonia: this disappeared after reducing dosage in one case, after drug discontinuation in the other. Amenorrhea was also observed, but no changes in liver function, blood tests or EEG were reported. The data indicate that risperidone is an effective and relatively safe drug for long term treatment of behavioral disruption in autistic children and adolescents. C1 Univ Cagliari, Dept Neurosci, I-09124 Cagliari, Italy. RP Zuddas, A (reprint author), Univ Cagliari, Dept Neurosci, Via Osped 119, I-09124 Cagliari, Italy. 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PD SUM PY 2000 VL 10 IS 2 BP 79 EP 90 DI 10.1089/cap.2000.10.79 PG 12 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 335HC UT WOS:000088237200004 PM 10933118 ER PT J AU Graf, WD Marin-Garcia, J Gao, HG Pizzo, S Naviaux, RK Markusic, D Barshop, BA Courchesne, E Haas, RH AF Graf, WD Marin-Garcia, J Gao, HG Pizzo, S Naviaux, RK Markusic, D Barshop, BA Courchesne, E Haas, RH TI Autism associated with the mitochondrial DNA G8363A transfer RNA(Lys) mutation SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID RAGGED-RED FIBERS; MYOCLONUS EPILEPSY; TRNA(LYS); DUPLICATION; FAMILIES; DISORDER; DISEASE; 15Q AB We report a family with a heterogeneous group of neurologic disorders associated with the mitochondrial DNA G8363A transfer ribonucleic acid (RNA)(Lys) mutation. The phenotype of one child in the family was consistent with autism. During his second year of life, he lost previously acquired language skills and developed marked hyperactivity with toe-walking, abnormal reciprocal social interaction, stereotyped mannerisms, restricted interests, self-injurious behavior, and seizures. Brain magnetic resonance imaging (MRI) and repeated serum lactate studies were normal. His older sister developed signs of Leigh syndrome with progressive ataxia, myoclonus, seizures, and cognitive regression. Her laboratory studies revealed increased MRI T-2-weighted signal in the putamen and posterior medulla, elevated lactate in serum and cerebrospinal fluid, and absence of cytochrome c oxidase staining in muscle histochemistry. Molecular analysis in her revealed the G8363A mutation of the mitochondrial transfer RNA(Lys) gene in blood (82% mutant mitochondrial DNA) and muscle (86%). The proportions of mutant mitochondrial DNA from her brother with autism were lower (blood 60%, muscle 61%). It is Likely that the origin of his autism phenotype is the pathogenic G8363A mitochondrial DNA mutation. This observation suggests that certain mitochondrial point mutations could be the basis for autism in some individuals. C1 Univ Washington, Dept Pediat, Seattle, WA 98195 USA. Univ Washington, Dept Neurol, Seattle, WA 98195 USA. Mol Cardiol Inst Inc, Highland Pk, NJ USA. Univ Calif San Diego, Dept Pediat, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA. RP Graf, WD (reprint author), Childrens Hosp & Reg Med Ctr, Dept Pediat, Div Genet & Dev, Mail Stop 47,4800 Sand Point Way NE, Seattle, WA 98105 USA. 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Child Neurol. PD JUN PY 2000 VL 15 IS 6 BP 357 EP 361 DI 10.1177/088307380001500601 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 321QG UT WOS:000087465700001 PM 10868777 ER PT J AU Buoni, S Sorrentino, L Farnetani, MA Pucci, L Fois, A AF Buoni, S Sorrentino, L Farnetani, MA Pucci, L Fois, A TI The syndrome of inv dup (15): Clinical, electroencephalographic, and imaging findings SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID ANGELMAN SYNDROME; CHROMOSOME 15Q; DUPLICATION; MUTATIONS; EPILEPSY; MARKER; AUTISM; AGE AB The clinical and laboratory data of four pediatric patients and one adult patient with inverted duplication (inv dup) (15) are reported. The most evident findings were dysmorphic features with frontal bossing; genital abnormalities, such as macropenis or hypospadias; mental retardation; autistic behavior, and seizures. Two additional adults with inv dup (15) front other institutions were also diagnosed in our laboratory. Seizures and mental retardation were the reasons for their referral. The clinical picture of inv dup (15) seems to be quite variable since the phenotype can also be normal. However, karyotyping and fluorescent in-situ hybridization, focused in particular on chromosome 15, appear to be indicated in patients with dysmorphic phenotypes, such as the one present in our patients, and in subjects with early-onset seizures and psychomotor retardation with autistic features. C1 Univ Siena, Inst Pediat Clin, I-53100 Siena, Italy. RP Fois, A (reprint author), Univ Siena, Inst Pediat Clin, Viale Bracci, I-53100 Siena, Italy. 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Child Neurol. PD JUN PY 2000 VL 15 IS 6 BP 380 EP 385 DI 10.1177/088307380001500605 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 321QG UT WOS:000087465700006 PM 10868780 ER PT J AU Ringman, JM Jankovic, J AF Ringman, JM Jankovic, J TI Occurrence of tics in Asperger's syndrome and autistic disorder SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM; LA-TOURETTE SYNDROME; IDIOT-SAVANT; CHILDREN; ABNORMALITIES; ADULTS; BLIND; BOYS AB Asperger's syndrome is a condition in the autistic spectrum in which language development is normal. Patients with Asperger's syndrome frequently exhibit repetitive movements (stereotypies), and can have motor and phonic ties in addition to other behavioral abnormalities. We present 12 patients with autistic spectrum disorders who were referred to our Movement Disorders Clinic for evaluation of ties. Eight of the 12 had normal language development and therefore met criteria for Asperger's syndrome. All patients exhibited stereotypic movements; in addition, seven had ties and six of these met diagnostic criteria for Tourette syndrome. Of the six patients with clinical features of both Asperger's syndrome and Tourette syndrome, three had severe congenital sensory deficits. The autistic patients in our series were clinically heterogenous and though ties were clearly present, other aberrant movements demonstrated by them were harder to classify. Our series confirms the wide range of clinical manifestations in Asperger's syndrome and autism, including ties and other features of Tourette syndrome. Furthermore, it suggests that sensory deprivation contributes to the development of adventitious movements in this population. C1 Univ Calif Irvine, Sch Med, Dept Neurol, Irvine, CA 92717 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. RP Jankovic, J (reprint author), Univ Calif Irvine, Sch Med, Dept Neurol, Irvine, CA 92717 USA. 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PD JUN PY 2000 VL 15 IS 6 BP 394 EP 400 DI 10.1177/088307380001500608 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 321QG UT WOS:000087465700009 PM 10868783 ER PT J AU Mason, BW Donnelly, PD AF Mason, BW Donnelly, PD TI Impact of a local newspaper campaign on the uptake of the measles mumps and rubella vaccine SO JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH LA English DT Article ID AUTISM C1 Iechyd Morgannwg Hlth, Swansea SA1 1LT, W Glam, Wales. RP Mason, BW (reprint author), Iechyd Morgannwg Hlth, 41 High St, Swansea SA1 1LT, W Glam, Wales. 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Community Health PD JUN PY 2000 VL 54 IS 6 BP 473 EP 474 DI 10.1136/jech.54.6.473 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 319NC UT WOS:000087347200015 PM 10818125 ER PT J AU Ahearn, W Callison, T Ortman, M AF Ahearn, W Callison, T Ortman, M TI Behavioural treatment of food selectivity in a child with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 New England Ctr Children, Southborough, MA USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 010 BP 191 EP 191 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700011 ER PT J AU Akerstrom, B AF Akerstrom, B TI Adults with autism and mental retardation: A life-span perspective SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Mid Sweden Univ, Dept Hlth Sci, Ostersund, Sweden. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 013 BP 192 EP 192 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700014 ER PT J AU Bang, M AF Bang, M TI A theory of mind deficit in autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Woosuk Univ, Dept Special Educ, Chonju, South Korea. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 041 BP 199 EP 199 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700042 ER PT J AU Beadle-Brown, J Murphy, G AF Beadle-Brown, J Murphy, G TI Long-term outcome in people with severe intellectual disabilities and/or autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Kent Canterbury, Tizard Ctr, Canterbury, Kent, England. NR 0 TC 2 Z9 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 057 BP 203 EP 203 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700058 ER PT J AU Brereton, AB Tonge, BJ Einfeld, SE AF Brereton, AB Tonge, BJ Einfeld, SE TI Longitudinal study of change in emotional and behavioural problems in young people with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Monash Univ, Monash Med Ctr, Ctr Dev Psychiat, Clayton, Vic 3168, Australia. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 120 BP 219 EP 219 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700121 ER PT J AU Brown, T Galliver, B Stevenage, S Remington, B AF Brown, T Galliver, B Stevenage, S Remington, B TI Perception of biomechanical motion in children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Southampton, Dept Psychol, Southampton SO9 5NH, Hants, England. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 130 BP 221 EP 221 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700131 ER PT J AU Cotton, S Richdale, AL AF Cotton, S Richdale, AL TI Sleep problems in Down syndrome, Prader-Willi syndrome and autism spectrum disorders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 La Trobe Univ, Fac Hlth Sci, Bundoora, Vic 3083, Australia. La Trobe Univ, Sch Psychol Sci, Bundoora, Vic 3083, Australia. RMIT Univ, Dept Psychol & Intellectual Disabil Studies, Bundoora, Vic, Australia. NR 0 TC 2 Z9 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 232 BP 248 EP 248 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700233 ER PT J AU Dawson, G Osterling, J Carver, L Panagiotides, H Meltzoff, A Gray, J McPartland, J AF Dawson, G Osterling, J Carver, L Panagiotides, H Meltzoff, A Gray, J McPartland, J TI Neuropsychological and electrophysiological indices of brain dysfunction in autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Washington, Seattle, WA 98195 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 271 BP 258 EP 258 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700272 ER PT J AU De Bal, C Stichting, A AF De Bal, C Stichting, A TI Assessment of hearing problems in people with profound intellectual disability and autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Kinsbergen Gehandicaptenzorg Prov Antwerpen Vzw H, Gierle, Belgium. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 281 BP 261 EP 261 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700282 ER PT J AU Dowrick, PW Buggey, T AF Dowrick, PW Buggey, T TI Creating futures through video self-modelling behavioural interventions: Social and academic development in challenging behaviours and autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Hawaii, Ctr Disabil Studies, Honolulu, HI 96822 USA. Univ Memphis, Memphis, TN 38152 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 310 BP 268 EP 269 PN 3-4 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700311 ER PT J AU Ferraz, P Assumpcao, F AF Ferraz, P Assumpcao, F TI Autism in a group of patients with phenylketonuria SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 APAE SP, Sao Paulo, Brazil. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 361 BP 282 EP 282 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700362 ER PT J AU Foxx, RM AF Foxx, RM TI Successful autism treatment: The confluence of science and expertise SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Penn State Univ Harrisburg, Harrisburg, PA USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 378 BP 286 EP 287 PN 3-4 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700379 ER PT J AU Gray, K Tonge, B AF Gray, K Tonge, B TI Early features of autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Monash Univ, Ctr Dev Psychiat & Psychol, Melbourne, Vic 3004, Australia. NR 0 TC 2 Z9 2 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 427 BP 299 EP 299 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700428 ER PT J AU Green, G AF Green, G TI Science, pseudoscience and antiscience in autism treatment SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 New England Ctr Children, Southborough, MA USA. Eunice Kennedy Shriver Ctr Mental Retardat Inc, Waltham, MA 02154 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 429 BP 300 EP 300 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700430 ER PT J AU Green, G Parkin, J AF Green, G Parkin, J TI Nonverbal assessment of cognitive skills in autism and severe mental retardation SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 New England Ctr Children, Southborough, MA USA. Eunice Kennedy Shriver Ctr Mental Retardat Inc, Southborough, MA USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 430 BP 300 EP 300 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700431 ER PT J AU Grether, JK Nelson, KB Croen, L Dambrosia, J Dickens, BF Phillips, TM AF Grether, JK Nelson, KB Croen, L Dambrosia, J Dickens, BF Phillips, TM TI Neuropeptides and neurotrophins in the neonatal blood of children with mental retardation, autism or cerebral palsy SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Calif Birth Defects Monitoring Prog, Emeryville, CA 94608 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 431 BP 300 EP 300 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700432 ER PT J AU Hastings, R Brown, A Johnson, E AF Hastings, R Brown, A Johnson, E TI Stress of UK parents running home-based behavioural intervention programmes for their young children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Southampton, Southampton, Hants, England. RI Hastings, Richard/D-9657-2013; Charman, Tony/A-2085-2014 OI Hastings, Richard/0000-0002-0495-8270; Charman, Tony/0000-0003-1993-6549 NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 465 BP 309 EP 309 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700466 ER PT J AU Iarocci, G Burack, JA Shore, D AF Iarocci, G Burack, JA Shore, D TI Global and local perception in autism: The role of basic and higher-order attention SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 McGill Univ, Montreal, PQ H3A 1Y2, Canada. Baycrest Med Ctr, Toronto, ON, Canada. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 543 BP 329 EP 329 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700544 ER PT J AU Kraijer, D AF Kraijer, D TI Screening autism/pervasive developmental disorder in intellectual disability: the Scale of Pervasive Developmental Disorder in the Mentally Retarded SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Ctr Hendrik van Boeijen, Assen, Netherlands. Fdn Res Dev Disabil, Assen, Netherlands. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 639 BP 355 EP 355 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700640 ER PT J AU Krauss, MM Robison, D Seltzer, M Makuch, R AF Krauss, MM Robison, D Seltzer, M Makuch, R TI Therapeutic treatments and service utilization among individuals with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Brandeis Univ, Waltham, MA 02254 USA. Univ Wisconsin, Madison, WI USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 641 BP 356 EP 356 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700642 ER PT J AU Liddell, J Martinez, D AF Liddell, J Martinez, D TI Families of children with autism as advocates and local experts in rural and geographically isolated communities SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ New Mexico, Ctr Dev & Disabil, Albuquerque, NM USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 678 BP 365 EP 365 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700679 ER PT J AU Magana, S Seltzer, MM Krauss, MW AF Magana, S Seltzer, MM Krauss, MW TI An ethnographic study of Puerto Rican mothers caring for a child with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Brandeis Univ, Waltham, MA 02254 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 726 BP 377 EP 378 PN 3-4 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700727 ER PT J AU Magerotte, G Willaye, E AF Magerotte, G Willaye, E TI Positive behaviour support and quality of life: A new way to support the people with a mental handicap and/or autism in French-speaking Europe? SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Mons, Dept Special Educ, Univ Specialized Serv People Autism, B-7000 Mons, Belgium. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 727 BP 378 EP 378 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700728 ER PT J AU Ogata, B Trahms, C Lucas, B Schwartz, I AF Ogata, B Trahms, C Lucas, B Schwartz, I TI A behaviour-based approach to food refusal in children with autism and pervasive developmental disorder SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Washington, CHDD, Seattle, WA 98195 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 870 BP 414 EP 415 PN 3-4 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700871 ER PT J AU Orsmond, G Seltzer, MM Krauss, M Leavitt, L AF Orsmond, G Seltzer, MM Krauss, M Leavitt, L TI Symptoms of autism across the course of life SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Brandeis Univ, Waltham, MA USA. Univ Wisconsin, Madison, WI 53706 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 889 BP 419 EP 419 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700890 ER PT J AU Paparella, T D'Angiola, N Kasari, C AF Paparella, T D'Angiola, N Kasari, C TI Emergence of joint attention and requesting skills in young children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Los Angeles, CA USA. Childrens Hosp, Los Angeles, CA 90027 USA. NR 0 TC 1 Z9 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 901 BP 422 EP 423 PN 3-4 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700902 ER PT J AU Richdale, AL AF Richdale, AL TI Treatment of sleep problems in children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Royal Melbourne Inst Technol, Dept Psychol & Intellectual Disabil Studies, Bundoora, Vic, Australia. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 972 BP 441 EP 441 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700973 ER PT J AU Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ TI A comparison of executive functioning in high-functioning autism and Asperger disorder using tasks sensitive to inhibitory and set-shifting deficits SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Monash Univ, Dept Psychol, Clayton, Vic 3168, Australia. Monash Univ, Ctr Dev Psychiat, Melbourne, Vic, Australia. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 976 BP 442 EP 442 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700977 ER PT J AU Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ AF Rinehart, NJ Bradshaw, JL Moss, SA Brereton, AV Tonge, BJ TI An examination of left-hemisphere anomalies in high-functioning autism and Asperger disorder using executive function and visual-perceptual paradigms SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Monash Univ, Dept Psychol, Clayton, Vic 3168, Australia. Monash Univ, Ctr Dev Psychiat, Melbourne, Vic, Australia. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 977 BP 442 EP 442 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697700978 ER PT J AU Schellenberg, GD Dawson, G Wijsman, EM AF Schellenberg, GD Dawson, G Wijsman, EM TI Genetic studies of autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Washington, Seattle, WA USA. Vet Affairs Puget Sound Hlth Care Syst, Seattle, WA USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1020 BP 453 EP 453 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701020 ER PT J AU Schreck, KA AF Schreck, KA TI Co-occurrence of sleep problems and the behavioural characteristics of autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Penn State Univ, Harrisburg, PA USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1023 BP 454 EP 454 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701023 ER PT J AU Schweigert, P Rowland, C AF Schweigert, P Rowland, C TI Tangible symbols, tangible outcomes in communication intervention for children with autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Oregon Hlth Sci Univ, Oregon Inst Disabil & Dev, Portland, OR 97201 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1034 BP 456 EP 456 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701034 ER PT J AU Seidel, M Symalla, R AF Seidel, M Symalla, R TI Co-occurrence of autism and epilepsy: Theoretical aspects and practical demands on care SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 von Bodelschwinghsche Anstalten Bethel, Bielefeld, Germany. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1038 BP 457 EP 457 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701038 ER PT J AU Seltzer, MM Krauss, MW Shattuck, P AF Seltzer, MM Krauss, MW Shattuck, P TI Maternal involvement with individuals with autism after placement SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Brandeis Univ, Heller Sch, Waltham, MA 02254 USA. Univ Wisconsin, Madison, WI USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1039 BP 457 EP 458 PN 3-4 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701039 ER PT J AU Seltzer, MM Kraus, MW Orsmond, GI AF Seltzer, MM Kraus, MW Orsmond, GI TI Stress and coping: A comparison of mothers of adults with autism versus mothers of adults with Down syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Brandeis Univ, Heller Sch, Waltham, MA 02254 USA. Univ Wisconsin, Madison, WI USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1040 BP 458 EP 458 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701040 ER PT J AU Sigman, M AF Sigman, M TI Continuity and change in the development of children with autism and Down syndrome SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90024 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1063 BP 464 EP 464 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701063 ER PT J AU Stavrou, L AF Stavrou, L TI Efforts to educate and incorporate a child with autism and blindness in a normal kindergarten SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Ionnina, Lab Special & Curat Educ, Ionnina, Greece. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1101 BP 473 EP 474 PN 3-4 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701101 ER PT J AU Symalla, R Seidel, MV AF Symalla, R Seidel, MV TI Implementation of special services for people with autism in an institution for individuals with disabilities SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Bodelschwinghsche Anstalten Bethel, Bielefeld, Germany. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1130 BP 481 EP 481 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701130 ER PT J AU Unis, A Dawson, G Osterling, J Munson, J AF Unis, A Dawson, G Osterling, J Munson, J TI Effectiveness of secretin for reducing symptoms of autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Washington, Seattle, WA 98195 USA. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1192 BP 497 EP 497 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701192 ER PT J AU Urwand, S Haag, G AF Urwand, S Haag, G TI A clinical locating grid of the evolutionary stages of child autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 IMP Champrosay, Draveil, France. INSERM, Paris, France. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1195 BP 498 EP 498 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701195 ER PT J AU Webb, E Thompsen, W Morey, J Fraser, WI Butler, C Barber, M AF Webb, E Thompsen, W Morey, J Fraser, WI Butler, C Barber, M TI A prevalence study of Asperger syndrome and high-functioning autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Univ Wales Coll Med, Dept Psychol Med & Child Hlth, Cardiff CF4 4XN, S Glam, Wales. NR 0 TC 1 Z9 1 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 MA 1252 BP 513 EP 513 PN 3-4 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701252 ER PT J AU Kraijer, D AF Kraijer, D TI Stereotyped behaviour, autism and intellectual disability SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Meeting Abstract C1 Ctr Hendrik Van Boeijen, Assen, Netherlands. Fdn Res Dev Disabil, Assen, Netherlands. NR 0 TC 0 Z9 0 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD JUN-AUG PY 2000 VL 44 BP 527 EP 528 PN 3-4 PG 2 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 343HV UT WOS:000088697701305 ER PT J AU Wilson, B Smith, DS AF Wilson, B Smith, DS TI Music therapy assessment in school settings: A preliminary investigation SO JOURNAL OF MUSIC THERAPY LA English DT Article ID CHILDREN; HOPELESSNESS; DISABILITIES; PERCEPTION; AGE AB The present investigation was undertaken in response to music therapists working in school settings for information relating to the availability of music therapy assessments and the feasibility of standardizing an assessment instrument for music therapists to use in school settings. Five research questions were identified, and the music therapy literature was surveyed to compile responses to those questions. Three different online data bases (ERIC, PsycINFO, and Article 1st) were used, covering articles published between 1980 and 1997 Individual hand searches were done of the Arts in Psychotherapy, Journal of Music Therapy, Journal of Research in Music Education, Journal of the International Association of Music for the Handicapped, Music Therapy and Music Therapy Perspectives. The questions and responses were as follows: 1. Which music-based assessment tools are being used with children with disabilities? Little commonality in assessment fools being used by music therapists and researchers was discovered. Of the fetal 41 studies, 20 (49%) reported using a "named" or "titled" assessment tool, and in the remaining 51% of studies, the authors reported using an untitled, and usually experimenter-designed, original assessment tool. 2 Have certain assessments been used in more than one study? Very limited replication of existing assessments was found. Of the 16 "named" assessments, only 3 were found to be used in more than one research study. 3. Are the actual assessments published along with the articles describing their use? Only 3 of the 20 studies using named assessments were published along with the journal article. Of the remaining 21 studies using original, experimenter-designed assessment tools, only 6 (28%) had the assessment instrument published with the article. 4. What is the primary purpose for using the assessment? Six primary purposes emerged from the review of the literature: to compare with data obtained from other assessment measures or from other populations (39%), as a baseline or pretest measure (29%), to determine eligibility for services or the receipt of treatment (12%), to determine the psychometric properties of the assessment (7%), suitability of the instrument for the given population (7%), and the identification of musical preferences (5%). 5. What are the musical or nonmusic elements being assessed? Musical elements were: music perception (37%), musical aptitude (29%), musical preferences (12%), and attention to/enjoyment of music (2%). Nonmusical behaviors/responses were: self-expression (10%), motor responses (10%), behavioral responses (7%), cognitive development (2%), and acts of communication (2%). 6. What subject populations are being assessed? Subject populations were: children with developmental disabilities/mental retardation (44%), children with autism (10%), children with hearing impairments (17%), "psychiatric" clients or emotionally disturbed (22%), individuals described as "handicapped" (5%), individuals with physical disabilities (2%), and a student with a speech impairment (2%). Nondisabled individuals were also included in 12 of the aforementioned studies. C1 Western Michigan Univ, Kalamazoo, MI 49008 USA. RP Wilson, B (reprint author), Western Michigan Univ, Kalamazoo, MI 49008 USA. 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Music Ther. PD SUM PY 2000 VL 37 IS 2 BP 95 EP 117 PG 23 WC Music; Rehabilitation SC Music; Rehabilitation GA 336LW UT WOS:000088304600002 PM 10932124 ER PT J AU Starkstein, SE Vazquez, S Vrancic, D Nanclares, V Manes, F Piven, J Plebst, C AF Starkstein, SE Vazquez, S Vrancic, D Nanclares, V Manes, F Piven, J Plebst, C TI SPECT findings in mentally retarded autistic individuals SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID CHILDHOOD AUTISM; BRAIN; DEFICITS; MRI AB The authors examined specific deficits of cerebral blood perfusion in autistic patients as measured with [Tc-99m]HMPAO single-photon emission computed tomography (SPECT). The study, conducted in an outpatient clinic setting, included a consecutive series of 30 patients with autism and 14 patients with mental retardation but no autism comparable in chronological age, mental age, height, weight, and head circumference. All participants were examined with a comprehensive psychiatric and neuropsychological battery and received a [Tc-99m]HMPAO SPECT scan. Autistic patients had significantly lower perfusion than the control group in the following brain regions: right temporal lobe (basal and inferior areas), occipital lobes, thalami, and left basal ganglia. The study demonstrated significant perfusion deficits in specific brain areas of moderately to severely mentally retarded autistic patients. C1 FLENI, Raul Carrea Inst Neurol Res, Dept Neuropsychiat, Div Child Psychiat, RA-1428 Buenos Aires, DF, Argentina. FLENI, Raul Carrea Inst Neurol Res, Div Nucl Med, RA-1428 Buenos Aires, DF, Argentina. Univ Iowa, Sch Med, Dept Psychiat, Iowa City, IA 52242 USA. RP Starkstein, SE (reprint author), FLENI, Raul Carrea Inst Neurol Res, Dept Neuropsychiat, Div Child Psychiat, Montaneses 2325, RA-1428 Buenos Aires, DF, Argentina. 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Neuropsychiatr. Clin. Neurosci. PD SUM PY 2000 VL 12 IS 3 BP 370 EP 375 DI 10.1176/appi.neuropsych.12.3.370 PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 343BX UT WOS:000088682800010 PM 10956571 ER PT J AU Bower, C Leonard, H Petterson, B AF Bower, C Leonard, H Petterson, B TI Intellectual disability in Western Australia SO JOURNAL OF PAEDIATRICS AND CHILD HEALTH LA English DT Article DE autism; Down syndrome; intellectual disability; record linkage; time trends ID CONGENITAL-RUBELLA SYNDROME; MENTAL-RETARDATION; PREVALENCE; IMPACT; VACCINATION; CHILDREN; AUTISM; MILD AB Objective: To investigate the prevalence of intellectual disability in Western Australia (WA), its causes, prevention, and trends over time. Methodology: Data from an administrative database of intellectual disability in WA were used to report on the trends in intellectual disability in childhood. Results: The prevalence of intellectual disability was 8.3 per 1000 live births in 1980-90. For half the cases, there was no known cause for the intellectual disability. Down syndrome accounted for 14 to 15% of all cases. Since the introduction of newborn screening, no WA-born child participating in the screening program has been diagnosed with intellectual disability as a result of either phenylketonuria or congenital hypothyroidism. The rate of autism spectrum disorders rose from three to six per 10 000 in the 1980-83 WA birth cohort to 10-13 per 10 000 for the 1989-92 cohort. Conclusions: Recent linkage of this administrative database to the WA Maternal and Child Health Research Data Base provides a unique opportunity for more detailed investigation of intellectual disability and its risk factors in a large, well-ascertained population of children. C1 TVW Telethon Inst Child Hlth Res, Div Epidemiol, W Perth, WA 6872, Australia. Disabil Serv Commiss, W Perth, WA 6872, Australia. RP Bower, C (reprint author), TVW Telethon Inst Child Hlth Res, Div Epidemiol, POB 855, W Perth, WA 6872, Australia. 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Paediatr. Child Health PD JUN PY 2000 VL 36 IS 3 BP 213 EP 215 DI 10.1046/j.1440-1754.2000.00480.x PG 3 WC Pediatrics SC Pediatrics GA 317LQ UT WOS:000087227200003 PM 10849218 ER PT J AU Baird, G Charman, T Baron-Cohen, S Cox, A Swettenham, J Wheelwright, S Drew, A AF Baird, G Charman, T Baron-Cohen, S Cox, A Swettenham, J Wheelwright, S Drew, A TI A screening instrument for autism at 18 months of age: A 6-year follow-up study SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; pervasive developmental disorder; Asperger's syndrome; screening ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDHOOD AUTISM; CHILDREN; CLASSIFICATION; EPIDEMIOLOGY; INDIVIDUALS AB Objectives: A population of 16,235 children aged 18 months was screened using the Checklist for Autism in Toddlers (CHAT) to identify childhood autism (CA). Two further screening procedures were conducted at age 3 and 5 years. The population was followed up at age 7 years in order to establish the sensitivity, specificity, and positive predictive value of the instrument. Method: A brief checklist assessing joint attention and pretend play behaviors was administered by primary health care practitioners when the children were 18 months old. Follow-up methods included screening through parents and health practitioners and checking medical and educational records. Results: Nineteen cases of CA were successfully identified by the CHAT at 18 months. At follow-up a total of 50 cases of CA were identified via all surveillance methods. Thus, the CHAT has a sensitivity of 38% and a specificity of 98% for identifying CA. The positive predictive value of the instrument was maximized by concentration on the highest-risk group. Repeated screening 1 month later increased the positive predictive value to 75% for identification of CA but reduced the sensitivity to 20%, although the specificity was close to 100%. The screen also identified cases of pervasive developmental disorder as well as children with language and other developmental disorders. Conclusions: The CHAT can be used to identify cases of autism and related pervasive developmental disorders at 18 months of age. It is emphasized that the CHAT is not a diagnostic instrument but can identify potential cases of autism spectrum disorders for a full diagnostic assessment. C1 Guys Hosp, Newcomen Ctr, London SE1 9RT, England. Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 3EB, England. UCL, Dept Human Commun & Sci, London, England. RP Charman, T (reprint author), UCL, Behav Sci Unit, Inst Child Hlth, 30 Guilford St, London WC1N 1EH, England. 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Acad. Child Adolesc. Psychiatr. PD JUN PY 2000 VL 39 IS 6 BP 694 EP 702 DI 10.1097/00004583-200006000-00007 PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 319FQ UT WOS:000087331200007 PM 10846303 ER PT J AU Megson, MN AF Megson, MN TI Is autism a G-alpha protein defect reversible with natural vitamin A? SO MEDICAL HYPOTHESES LA English DT Article AB Autism may be a disorder linked to the disruption of the G-alpha protein, affecting retinoid receptors in the brain. A study of 60 autistic children suggests that autism may be caused by inserting a G-alpha protein defect, the pertussis toxin found in the DPT vaccine, into genetically at-risk children. This toxin separates the G-alpha protein from retinoid receptors. Those most at risk report a family history of at least one parent with a pre-existing G-alpha protein defect, including night blindness, pseudohypoparathyroidism or adenoma of the thyroid or pituitary gland. Natural vitamin A may reconnect the retinoid receptors critical for vision, sensory perception, language processing and attention. Autism spectrum disorders have increased from 1 in 10 000 in 1978 to 1 in 300 in some US communities in 1999. Recent evidence indicates that autism is a disorder of the nervous system and the immune system, affecting multiple metabolic pathways. (C) 2000 Harcourt Publishers Ltd. C1 Virginia Commonwealth Univ, Med Coll Virginia Hosp, Pediat & Adolescent Abil Ctr, Richmond, VA 23226 USA. RP Megson, MN (reprint author), Virginia Commonwealth Univ, Med Coll Virginia Hosp, Pediat & Adolescent Abil Ctr, 7229 Forest Ave,Suite 211, Richmond, VA 23226 USA. 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Hypotheses PD JUN PY 2000 VL 54 IS 6 BP 979 EP 983 DI 10.1054/mehy.1999.0999 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 333NA UT WOS:000088135100017 PM 10867750 ER PT J AU Maes, B Fryns, JP Ghesquiere, P Borghgraef, M AF Maes, B Fryns, JP Ghesquiere, P Borghgraef, M TI Phenotypic checklist to screen for fragile X syndrome in people with mental retardation SO MENTAL RETARDATION LA English DT Article ID NEW-YORK-STATE; RETARDED MEN; AUTISM; LANGUAGE; PROGRAM; MALES; FMR-1 AB The development of a phenotypic checklist for identifying people with fragile X syndrome is described. The checklist was designed to identify people with developmental disabilities of unknown causes for molecular genetic testing for fragile X syndrome. The list consists of 28 items (7 on physical characteristics and 21 on behavioral features). 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Retard. PD JUN PY 2000 VL 38 IS 3 BP 207 EP 215 DI 10.1352/0047-6765(2000)038<0207:PCTSFF>2.0.CO;2 PG 9 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 325AZ UT WOS:000087655300002 PM 10900928 ER PT J AU Kim, SJ Gonen, D Hanna, GL Leventhal, BL Cook, EH AF Kim, SJ Gonen, D Hanna, GL Leventhal, BL Cook, EH TI Deletion polymorphism in the coding region of the human NESP55 alternative transcript of GNAS1 SO MOLECULAR AND CELLULAR PROBES LA English DT Article DE NESP55; GNAS1; polymorphism; SNP; LSAL; serotonin ID RAT-BRAIN; GENE; PEPTIDE AB NESP55, a novel member of the chromogranins, was originally implicated as a precursor of a peptide LSAL with 5-HT1B receptor antagonist activity. In humans, NESP55 (MIM 139320) is encoded by an alternative transcript of GNAS1, the gene encoding the guanine nucleotide-binding alpha subunit of G(s). As a results of the potential relevance of NESP55 to serotoninergic neurotransmission, we screened its sequence using genomic DNA pools from autistic disorder, obsessive-compulsive disorder (OCD) probands and control subjects. Six single nucleotide polymorphisms (SNPs) were identified and the allele frequencies of those SNPs were determined. In addition, a 24-bp in-frame deletion in the coding region was found in one of the OCD probands. To further investigate its pattern of inheritance and the relevance to studied phenotypes, we genotyped 123 total subjects from autism, OCD and attention deficit hyperactivity disorder (ADHD) families. The deletion was detected only in one OCD family and followed Mendelian inheritance. All subjects with the deletion were heterozygous. However, there are no specific behavioural or physical alterations in the subjects with this deletion variant. 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Probes PD JUN PY 2000 VL 14 IS 3 BP 191 EP 194 DI 10.1006/mcpr.2000.0300 PG 4 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology SC Biochemistry & Molecular Biology; Biotechnology & Applied Microbiology; Cell Biology GA 330NL UT WOS:000087968100007 PM 10860717 ER PT J AU Turner, M Barnby, G Bailey, A AF Turner, M Barnby, G Bailey, A TI Genetic clues to the biological basis of autism SO MOLECULAR MEDICINE TODAY LA English DT Review ID SEROTONIN TRANSPORTER; FAMILY HISTORY; DISORDER; LINKAGE; TWIN AB Autism, the prototypical pervasive developmental disorder, is characterized by impaired communication and social interaction, and by repetitive interests and behaviours,The core disorder probably affects around 5:10 000 individuals, of whom some three-quarters are male, Onset is in the first three years of life, and the disorder is associated with lifelong disabilities. 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Med. Today PD JUN PY 2000 VL 6 IS 6 BP 238 EP 244 DI 10.1016/S1357-4310(00)01712-3 PG 7 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 322JQ UT WOS:000087506800009 PM 10840382 ER PT J AU Sandman, CA Hetrick, W Talyor, D Marion, S Chicz-DeMet, A AF Sandman, CA Hetrick, W Talyor, D Marion, S Chicz-DeMet, A TI Uncoupling of proopiomelanocortin (POMC) fragments is related to self-injury SO PEPTIDES LA English DT Article DE self-injury; autism; beta-endorphin; naltrexone; ACTH; POMC; opioids ID PLASMA BETA-ENDORPHIN; BLOOD-BRAIN-BARRIER; SENSORY NEURONS; NALTREXONE; PEPTIDES; MORPHINE; STEREOTYPY; DEPENDENCE; TOLERANCE; BEHAVIOR AB Proopiomelanocortin (POMC) contains several interesting, behaviorally active peptides. Release patterns of these fragments have been related to bizarre episodes of self-injurious behavior (SIB) among autistic individuals. Moreover, elevation in P-endorphin (PE) but not ACTH levels was associated with a positive response to an acutely administered, centrally acting opioid blocker among autistic individuals exhibiting SIE. In the present study, POMC fragments were measured in 12 self-injurious patients before and after long term (3 month) treatment with an opiate blocker naltrexone (NTX). POMC fragments were sampled from blood collected at the beginning of the baseline and placebo-controlled treatment phases of the study. Results indicated that the co-release (coupling) of POMC fragments were stable over time and the profile of POMC fragments in plasma predicted the effectiveness of a CNS acting drug in autistic subjects who self-injure. (C) 2000 Elsevier Science Inc. All rights reserved. C1 Univ Calif Irvine, Dept Psychiat & Human Behav, Irvine, CA 92717 USA. Fairview Dev Ctr, Costa Mesa, CA USA. Indiana Univ, Dept Psychol, Bloomington, IN USA. RP Sandman, CA (reprint author), Univ Calif Irvine, Dept Psychiat & Human Behav, Irvine, CA 92717 USA. 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A 14-year-old autistic male with severe mental retardation was given melatonin at a dose of 6 mg at 9:00 pm (C1) or 11:00 pm(C2). His parents kept a sleep diary. In C1, he often experienced early morning waking and fragmented night sleep but in C2, night sleep was prolonged and sleep-wake rhythm was improved. Suitable medication time, therefore, improved the sleep-wake rhythm. C1 Kaga Welf Inst, Tokyo, Japan. RP Hayashi, E (reprint author), 1-7-2 Kaga,Itabashi Ku, Tokyo 1730003, Japan. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th JAN JE, 1995, DEV MED CHILD NEUROL, V37, P279 JAN JE, 1994, DEV MED CHILD NEUROL, V36, P97 Richdale A., 1995, EU CHILD ADOLESC PSY, V4, P1, DOI 10. 1007/BF01980456 NR 4 TC 24 Z9 24 PU BLACKWELL SCIENCE ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 1323-1316 J9 PSYCHIAT CLIN NEUROS JI Psychiatry Clin. Neurosci. PD JUN PY 2000 VL 54 IS 3 BP 383 EP 384 DI 10.1046/j.1440-1819.2000.00725.x PG 2 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 377LQ UT WOS:000165515400059 PM 11186124 ER PT J AU [Anonymous] AF [Anonymous] TI The cost of autism SO PSYCHOLOGIST LA English DT News Item NR 0 TC 0 Z9 0 PU BRITISH PSYCHOLOGICAL SOC PI LEICESTER PA ST ANDREWS HOUSE, 48 PRINCESS RD EAST, LEICESTER LE1 7DR, LEICS, ENGLAND SN 0952-8229 J9 PSYCHOLOGIST JI Psychologist PD JUN PY 2000 VL 13 IS 6 BP 285 EP 285 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 353BZ UT WOS:000089255000004 ER PT J AU Koller, R AF Koller, R TI Sexuality and adolescents with autism SO SEXUALITY AND DISABILITY LA English DT Article DE sexuality education; adolescence; self-pleasuring; sexual abuse ID INDIVIDUALS; PERSPECTIVE; KNOWLEDGE; ATTITUDES; DISORDER; CHILDREN AB Appropriate education in sexuality is critical to the development of a person's positive self-esteem. The development of a healthy self-image may overcome potential feelings of depression and loneliness for the person with autism. This paper addresses the need for and challenges to providing sexuality education to individuals with autism. Tt summarizes teaching methods and approaches which have proven to be successful with this population. C1 Univ Utah, Dept Special Educ, Salt Lake City, UT 84112 USA. RP Koller, R (reprint author), 1698 N 725 W, Woods Cross, UT 84087 USA. 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PD SUM PY 2000 VL 18 IS 2 BP 125 EP 135 DI 10.1023/A:1005567030442 PG 11 WC Rehabilitation SC Rehabilitation GA 350HF UT WOS:000089094400004 ER PT J AU Strain, PS Hoyson, M AF Strain, PS Hoyson, M TI The need for longitudinal, intensive social skill intervention: LEAP follow-up outcomes for children with autism SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article AB In this article, we suggest the need to embed social skills intervention within the more general context of long-term early intervention efforts that promote all dimensions of developmental performance. Although the field has advanced on many fronts during the last 30 years, we believe that the limits of isolated social skills training over brief periods of time have been reached. To support the call for more comprehensive and intensive intervention efforts, we offer preliminary results from an 18-year study to address the social and related needs of young children with autism. Contrary to the usually gloomy picture of social skills intervention evaluated across time and contexts, the former clients of the LEAP program demonstrate evidence of sustained growth and development over nearly two decades. C1 Univ Colorado, Denver, CO 80202 USA. RP Strain, PS (reprint author), CCEL, 1380 Lawrence St,Suite 650, Denver, CO 80217 USA. CR BUELL J, 1968, J APPL BEHAV ANAL, V1, P167, DOI 10.1901/jaba.1968.1-167 Carta J., 1990, ED TREATMENT CHILDRE, V13, P298 Carta J. J., 1988, EARLY INTERVENTION I, P217 Cordisco L., 1986, J DIVISION EARLY CHI, V10, P10 DODGE DT, 1988, CREATIVE CURRICULUM HARRIS FR, 1964, J EDUC PSYCHOL, V55, P95 Hoyson M., 1985, J DIVISION EARLY CHI, V8, P157 Kohler F. W., 1990, J EARLY INTERVENTION, V14, P327 KOHLER FW, 1992, BEHAV MODIF, V16, P525, DOI 10.1177/01454455920164005 KOHLER FW, 1996, PRACTICAL APPROACHES, P23 KOHLER FW, 1990, CLIN PSYCHOL REV, V10, P441, DOI 10.1016/0272-7358(90)90047-E LeMay D. 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PD SUM PY 2000 VL 20 IS 2 BP 116 EP 122 DI 10.1177/027112140002000207 PG 7 WC Education, Special SC Education & Educational Research GA 330LK UT WOS:000087963400008 ER PT J AU Lamb, JA Moore, J Bailey, A Monaco, A AF Lamb, JA Moore, J Bailey, A Monaco, A TI Autism: recent molecular genetic advances (vol 5, pg 861, 2000) SO HUMAN MOLECULAR GENETICS LA English DT Correction RI Monaco, Anthony/A-4495-2010; Bailey, Anthony/J-2860-2014 OI Monaco, Anthony/0000-0001-7480-3197; Bailey, Anthony/0000-0003-4257-972X CR Lamb JA, 2000, HUM MOL GENET, V9, P861, DOI 10.1093/hmg/9.6.861 NR 1 TC 2 Z9 2 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0964-6906 J9 HUM MOL GENET JI Hum. Mol. Genet. PD MAY 22 PY 2000 VL 9 IS 9 BP 1461 EP 1461 PG 1 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 319RD UT WOS:000087354800021 ER PT J AU Fatemi, SH Cuadra, AE El-Fakahany, EE Sidwell, RW Thuras, P AF Fatemi, SH Cuadra, AE El-Fakahany, EE Sidwell, RW Thuras, P TI Prenatal viral infection causes alterations in nNOS expression in developing mouse brains SO NEUROREPORT LA English DT Article DE human influenza; neuronal nitric oxide synthase; neurotoxicity; prenatal; schizophrenia ID NITRIC-OXIDE SYNTHASE; NEONATAL MICE; IN-UTERO; INFLUENZA; SCHIZOPHRENIA; HIPPOCAMPI; INDUCTION; EXPOSURE; CELLS; NOS AB Epidemiological evidence points to prenatal viral infection being responsible for some forms of schizophrenia and autism. We hypothesized that prenatal human influenza viral infection in day 9 pregnant mice may cause changes in the levels of neuronal nitric oxide synthase (nNOS), an important molecule involved in synaptogenesis and excitotoxicity, in neonatal brains. Brains from 35- and 56-day-old mice were prepared for SDS-gel electrophoresis and Western blotting using polyclonal anti nNOS antibody. Quantification of nNOS showed time and region-dependent changes in the levels of nNOS protein. Mean rostral brain area value from prenatally infected animals showed a significant (p = 0.067) increase of 147% in nNOS levels at 35 days postnatally, with an eventual 29% decrease on day 56. Middle and caudal brain areas showed reductions in nNOS in experimental mice at 35 and 56 days, with a significant 27% decrease in nNOS in the middle segment of day 56 brains (p = 0.016). Significant interactions were found between group membership and brain area (Wilks lambda = 0.440, F(2.9)= 5.72, p = 0.025); there was also a significant interaction between brain area, group and age (Wilks lambda = 0.437, F(2.9) = 5.79, P = 0.024). These results provide further support for the notion that prenatal viral infection affects brain development adversely via the pathological involvement of nNOS expression. NeuroReport 11:1493-1496 (C) 2000 Lippincott Williams & Wilkins. C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. Utah State Univ, Inst Antiviral Res, Logan, UT 84322 USA. RP Fatemi, SH (reprint author), Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Box 392 Mayo Bldg,420 Delaware St SE, Minneapolis, MN 55455 USA. CR AKBARIAN S, 1993, ARCH GEN PSYCHIAT, V50, P169 Andreasen NC, 1999, ARCH GEN PSYCHIAT, V56, P781, DOI 10.1001/archpsyc.56.9.781 Baader SL, 1996, J NEUROSCI, V16, P1440 Bolanos JP, 1997, J NEUROCHEM, V68, P2227 CARINAMALLARD E, 1999, SCHIZOPHR RES, V40, P11 Cuadra AE, 1998, J NEUROCHEM, V71, P571 Deng XL, 1999, BRAIN RES, V851, P254, DOI 10.1016/S0006-8993(99)02087-9 EMAMIAN ES, 1999, BIOL PSYCHIAT, V45, P265 Fatemi SH, 1998, BRAIN RES, V800, P1, DOI 10.1016/S0006-8993(98)00450-8 Fatemi SH, 1998, SYNAPSE, V29, P84, DOI 10.1002/(SICI)1098-2396(199805)29:1<84::AID-SYN8>3.0.CO;2-7 Fatemi SH, 1999, MOL PSYCHIATR, V4, P145, DOI 10.1038/sj.mp.4000520 Gonzalez-Hernandez T, 1999, J NEUROSCI RES, V55, P198, DOI 10.1002/(SICI)1097-4547(19990115)55:2<198::AID-JNR7>3.0.CO;2-M Harada S, 1999, BRAIN RES, V821, P322, DOI 10.1016/S0006-8993(99)01124-5 HORNIG M, 1999, P 5 S NEUR NEUR SCHI, P48 Ikeda M, 1999, J NEUROSCI RES, V55, P352, DOI 10.1002/(SICI)1097-4547(19990201)55:3<352::AID-JNR10>3.0.CO;2-3 Moore PK, 1997, TRENDS PHARMACOL SCI, V18, P204, DOI 10.1016/S0165-6147(97)01064-X Nicotera P, 1997, TRENDS PHARMACOL SCI, V18, P189, DOI 10.1016/S0165-6147(97)90619-2 OGILVIE P, 1995, FASEB J, V9, P799 SUSSER ES, 1999, PRENATAL EXPOSURES S, P1 Takei N, 1996, BIOL PSYCHIAT, V40, P817, DOI 10.1016/0006-3223(95)00592-7 Tueting P, 1999, NEUROREPORT, V10, P1329, DOI 10.1097/00001756-199904260-00032 Weiss SW, 1998, J NEUROSCI, V18, P1725 WRIGHT P, 1995, AM J PSYCHIAT, V152, P1714 Wu AG, 1999, BRAIN RES, V850, P249, DOI 10.1016/S0006-8993(99)02138-1 NR 24 TC 52 Z9 53 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD MAY 15 PY 2000 VL 11 IS 7 BP 1493 EP 1496 DI 10.1097/00001756-200005150-00026 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 316WN UT WOS:000087191200028 PM 10841364 ER PT J AU Novotny, S Hollander, E Allen, A Mosovich, S Aronowitz, B Cartwright, C DeCaria, C Dolgoff-Kaspar, R AF Novotny, S Hollander, E Allen, A Mosovich, S Aronowitz, B Cartwright, C DeCaria, C Dolgoff-Kaspar, R TI Increased growth hormone response to sumatriptan challenge in adult autistic disorders SO PSYCHIATRY RESEARCH LA English DT Article DE autism; Asperger's disorder; serotonin; sumatriptan; growth hormone ID WHOLE-BLOOD SEROTONIN; BINDING-SITES; DOUBLE-BLIND; CHILDREN; HYPERSEROTONINEMIA; ANTIBODIES; RELATIVES; PLACEBO AB Serotonergic (5-HT) abnormalities have been documented in autism. To assess sensitivity of the 5-HT1d receptor, growth hormone response to the 5-HT1d receptor agonist sumatriptan was studied in adult autistic patients and matched normal controls. In this study, 11 adult patients with autism or Asperger's disorder were compared with nine matched controls. All subjects were randomized to single dose sumatriptan (6 mg SQ) and placebo challenges, separated by a 1-week interval, and growth hormone was measured before and during the challenges. The results showed a highly significant diagnosis x drug x time interaction on repeated measure analysis covaried for baseline. This suggests that autistic patients had significantly greater growth hormone response to sumatriptan than normal controls, independent of placebo effects. Therefore, abnormalities in 5-HT regulation in autism may be related to increased sensitivity of the 5-HT1d inhibitory receptor in autism. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved. 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PD MAY 15 PY 2000 VL 94 IS 2 BP 173 EP 177 DI 10.1016/S0165-1781(00)00134-7 PG 5 WC Psychiatry SC Psychiatry GA 319UD UT WOS:000087360000008 PM 10808042 ER PT J AU Partington, M Mowat, D Einfeld, S Tonge, B Turner, G AF Partington, M Mowat, D Einfeld, S Tonge, B Turner, G TI Genes on the X chromosome are important in undiagnosed mental retardation SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE intellectual disability; male/female ratio; X linkage; nonsyndromic X-linked mental retardation; community survey ID MAJOR INTELLECTUAL TRAITS; POPULATION PREVALENCE; DISABILITY; CHILDREN; PSYCHOPATHOLOGY; ADOLESCENTS; FAMILIES; LINKAGE AB The clinical genetic diagnosis was reviewed in 429 subjects with intellectual disability in the Australian Child and Adolescent Development (ACAD) study of behavioural problems. With minor differences, the overall "general distribution by causation" was similar to that to that found by the Consensus Conference of the American College of Medical Genetics in 1995, There was a significant male excess in the whole series which was shown to reside in those with "autism," those with undiagnosed nonsyndromic mental retardation (NSMR) and those with X-linked monogenic disorders. It is argued that a substantial proportion of undiagnosed NSMR is caused by genes on the X chromosome. Some of the practical problems of assigning individuals to diagnostic groups are discussed. Am. J, Med. Genet, 92:57-61, 2000, (C) 2000 Wiley-Liss, Inc. C1 Hunter Genet, Hunter Area Hlth Serv, Newcastle, NSW, Australia. Univ Newcastle, Newcastle, NSW 2308, Australia. S Eastern Sydney Area Hlth Serv, Child & Adolescent Psychiat Programs, Sydney, NSW, Australia. Univ Sydney, Sydney, NSW 2006, Australia. Monash Med Ctr, Ctr Dev Psychiat, Clayton, Vic 3168, Australia. 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PD MAY 1 PY 2000 VL 92 IS 1 BP 57 EP 61 DI 10.1002/(SICI)1096-8628(20000501)92:1<57::AID-AJMG10>3.0.CO;2-0 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 303UV UT WOS:000086444000010 PM 10797424 ER PT J AU Santosh, PJ AF Santosh, PJ TI Neuroimaging in child and adolescent psychiatric disorders SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article DE neuroimaging; psychiatry; psychopathology ID DEFICIT HYPERACTIVITY DISORDER; BRAIN-DEVELOPMENT; TOURETTE SYNDROME; CAUDATE-NUCLEUS; INTELLIGENCE; MORPHOLOGY; ASYMMETRY; BINDING; AUTISM; MIND AB Neuroimaging in child psychiatry is a rapidly developing field and the number of different techniques being used is increasing rapidly. This review describes the current status of neuroimaging in childhood psychopathology and discusses limitations of the various studies. as yet, no specific and consistent abnormality has been detected in childhood psychiatric disorders. Obsessive compulsive disorder has shown the most consistent findings so far, with orbitofrontal cortex and the caudate nucleus being implicated. Better understanding of the corticostriatal neural networks will shed more light on the neurodevelopmental disorders of childhood. C1 Inst Psychiat, London SE5 8AF, England. RP Santosh, PJ (reprint author), Inst Psychiat, Denmark Hill, London SE5 8AF, England. 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Dis. Child. PD MAY PY 2000 VL 82 IS 5 BP 412 EP 419 DI 10.1136/adc.82.5.412 PG 8 WC Pediatrics SC Pediatrics GA 316EE UT WOS:000087154000020 PM 10799438 ER PT J AU Riva, D Giorgi, C AF Riva, D Giorgi, C TI The cerebellum contributes to higher functions during development - Evidence from a series of children surgically treated for posterior fossa tumours SO BRAIN LA English DT Article DE cerebellum; social behaviour; frontal functions; language; intelligence; children AB We present data on the intellectual, language and executive functions of 26 children who had undergone surgery for the removal of cerebellar hemisphere or vermal tumours, The children tumours presented with disturbances of sequential memory and language processing, whereas those with left cerebellar tumours showed deficits on tests of spatial and visual sequential memory. The vermal with right cerebellar tumours presented with disturbances of auditory lesions led to two profiles: (i) post-surgical mutism, which evolved into speech disorders or language disturbances similar to agrammatism; and (ii) behavioural disturbances ranging from irritability to behaviours reminiscent of autism. These data are consistent with the recently acknowledged role of the cerebellum as a modulator of mental and social functions, and suggest that this role is operative early in childhood. C1 Ist Nazl Neurol C Besta, Dev Neurol Div, I-20133 Milan, Italy. Carlo Besta Natl Neurol Inst, Stereotact & Funct Neurosurg Unit, Milan, Italy. RP Riva, D (reprint author), Ist Nazl Neurol C Besta, Dev Neurol Div, Via Celoria 11, I-20133 Milan, Italy. NR 0 TC 327 Z9 335 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD MAY PY 2000 VL 123 BP 1051 EP 1054 DI 10.1093/brain/123.5.1051 PN 5 PG 4 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 323TK UT WOS:000087580900018 PM 10775549 ER PT J AU Riva, D Giorgi, C AF Riva, D Giorgi, C TI The cerebellum contributes to higher functions during development - Evidence from a series of children surgically treated for posterior fossa tumours SO BRAIN LA English DT Article DE cerebellum; social behaviour; frontal functions; language; intelligence; children ID UNILATERAL BRAIN-LESIONS; RHESUS-MONKEY; PROJECTIONS; MUTISM; AUTISM; SYSTEM; CORTEX; ABNORMALITIES; ACTIVATION; DIASCHISIS AB We present data on the intellectual, language and executive functions of 26 children who had undergone surgery for the removal of cerebellar hemisphere or vermal tumours. The children with right cerebellar tumours presented with disturbances of auditory sequential memory and language processing, whereas those with left cerebellar tumours showed deficits on tests of spatial and visual sequential memory. The vermal lesions led to two profiles: (i) post-surgical mutism, which evolved into speech disorders or language disturbances similar to agrammatism; and (ii) behavioural disturbances ranging from irritability to behaviours reminiscent of autism. These data are consistent with the recently acknowledged role of the cerebellum as a modulator of mental and social functions, and suggest that this role is operative early in childhood. C1 Ist Nazl Neurol Carlo Besta, Dev Neurol Div, I-20133 Milan, Italy. Ist Nazl Neurol Carlo Besta, Stereotact & Funct Neurosurg Unit, Milan, Italy. RP Riva, D (reprint author), Ist Nazl Neurol Carlo Besta, Dev Neurol Div, Via Celoria 11, I-20133 Milan, Italy. 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J. Psychiat.-Rev. Can. Psychiat. PD MAY PY 2000 VL 45 IS 4 BP 363 EP 368 PG 6 WC Psychiatry SC Psychiatry GA 320AE UT WOS:000087378200005 PM 10813070 ER PT J AU Fisman, S Wolf, L Ellison, D Freeman, T AF Fisman, S Wolf, L Ellison, D Freeman, T TI A longitudinal study of siblings of children with chronic disabilities SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Article DE sibling adjustment; disability; parental distress ID DISABLED-CHILDREN; HANDICAPPED-CHILDREN; EXCEPTIONAL-CHILDREN; SOCIAL-ADJUSTMENT; CHRONIC ILLNESS; DOWNS-SYNDROME; STRESS; PARENTS; AUTISM; FAMILY AB Objective: To examine the unaffected siblings of 2 different groups with chronic disabilities, pervasive developmental disorder (PDD) and Down syndrome (DS), over 3 years, comparing their adjustment with each other and with the siblings of a nondisabled group. Method: This study examines 137 siblings of children with PDD, children with DS, and developmentally normal children (control group) initially and 127 siblings at follow-up 3 years later. Their adjustment is measured by the Survey Diagnostic Instrument (SDI), completed by caregivers and teachers. Predictor variables include sibling self-perception, social support, and relationship with sibling, as indicated by siblings; caregiver psychosocial factors such as parental stress, caregiver depression, and marital relationship, family systems characteristics as viewed by both caregiver and sibling; and difficulty that disabled child causes as perceived by the primary caregiver. Results: Significantly more adjustment problems are found in the siblings of PDD children at both times when compared with siblings of DS and control children. Caregivers of PDD children report the highest levels of distress and depression, and this persists over time. 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J. Psychiat.-Rev. Can. Psychiat. PD MAY PY 2000 VL 45 IS 4 BP 369 EP 375 PG 7 WC Psychiatry SC Psychiatry GA 320AE UT WOS:000087378200006 PM 10813071 ER PT J AU Mundy, P Card, J Fox, N AF Mundy, P Card, J Fox, N TI EEG correlates of the development of infant joint attention skills SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Article DE EEG; joint attention; infant development ID VISUAL-ATTENTION; NONVERBAL-COMMUNICATION; BRAIN; CHILDREN; MECHANISMS; LANGUAGE; AUTISM; ACQUISITION; COHERENCE; ASYMMETRY AB The development of the capacity for social attention coordination, or "joint attention," is a major milestone of infancy. Data from a recent study of handicapped infants have raised the hypothesis that the tendency to initiate bids for joint attention may reflect processes associated with the frontal cortex to a greater extent than other forms of infant attention coordination (R. Caplan et al., 1993). This hypothesis was examined in a longitudinal study of 32 normally developing infants. The results indicated that EEG data at 14 months indicative of left frontal, as well as left and right central cortical activity, was associated with the tendency to initiate joint attention bids (IJA) at 14 and 18 months. In contrast, a pattern of left parietal activation and right parietal deactivation at 14 months was associated with the development of the capacity to respond to the joint attention bids (RJA) of others of 14 and 18 months. These results were interpreted to be consistent with a general anterior-posterior model of attention development (M. Posner & S. Petersen, 1990). The implications of these results for current conceptualizations of joint attention development, as well as for understanding the disturbance of joint attention skill development in autism are discussed. (C) 2000 John Wiley & Sons Inc. Dev Psychobiol 36: 325-338, 2000. C1 Univ Miami, Dept Psychol, Miami, FL 33146 USA. Univ Maryland, Dept Human Dev, College Pk, MD 20740 USA. RP Mundy, P (reprint author), Univ Miami, Dept Psychol, Miami, FL 33146 USA. 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PD MAY PY 2000 VL 36 IS 4 BP 325 EP 338 DI 10.1002/(SICI)1098-2302(200005)36:4<325::AID-DEV7>3.0.CO;2-F PG 14 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA 310DF UT WOS:000086810700007 PM 10797253 ER PT J AU Rookard, CJ AF Rookard, CJ TI Fluoride and autism: is there a connection? SO FLUORIDE LA English DT Editorial Material NR 0 TC 0 Z9 0 PU INT SOC FLUORIDE RESEARCH PI AUCKLAND 4 PA 81A LANDSCAPE RD, MT EDEN, AUCKLAND 4, NEW ZEALAND SN 0015-4725 J9 FLUORIDE JI Fluoride PD MAY PY 2000 VL 33 IS 2 BP 99 EP 100 PG 2 WC Public, Environmental & Occupational Health; Toxicology SC Public, Environmental & Occupational Health; Toxicology GA 373PF UT WOS:000165297300006 ER PT J AU Miller, JN Ozonoff, S AF Miller, JN Ozonoff, S TI The external validity of Asperger disorder: Lack of evidence from the domain of neuropsychology SO JOURNAL OF ABNORMAL PSYCHOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; NONVERBAL LEARNING-DISABILITIES; AUTISM DIAGNOSTIC INTERVIEW; INFANTILE-AUTISM; RIGHT-HEMISPHERE; EXECUTIVE FUNCTION; HANOI PERFORMANCE; MOTOR IMPAIRMENT; TEMPORAL-LOBE; CHILDREN AB The present study compared individuals with high-functioning autism (HFA) and Asperger disorder (AD) in intellectual, motor, visuospatial, and executive function domains. Participants with AD demonstrated significantly higher Verbal and Full Scale IQ scores, significantly larger Verbal-Performance IQ discrepancies, and significantly better visual-perceptual skills than those with HFA. Once the superior intellectual abilities of the AD group were controlled (both statistically through analysis of covariance and by examining IQ-matched subgroups of HFA and AD participants), no significant group differences in motor, visuospatial, or executive functions were evident, save a marginally significant trend toward poorer fine motor performance in the AD group. This suggests that AD may simply be "high-IQ autism" and that separate names for the disorders may not be warranted. The relation of these findings to theories of autism and AD are discussed. C1 Univ Utah, Dept Psychol, Salt Lake City, UT 84112 USA. RP Ozonoff, S (reprint author), Univ Utah, Dept Psychol, 390 S 1530 E,Room 502, Salt Lake City, UT 84112 USA. 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Y., 1992, HIGH FUNCTIONING IND, P11 WEBER RC, 1992, EXCEPT CHILDREN, V59, P77 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WEINTRAUB S, 1983, ARCH NEUROL-CHICAGO, V40, P463 WELSH M, 1995, J GEN PSYCHOL, V122, P69 WELSH MC, 1990, CHILD DEV, V61, P1697, DOI 10.1111/j.1467-8624.1990.tb03560.x WELSH MC, 1991, DEV NEUROPSYCHOL, V7, P131 Wing L, 1991, AUTISM ASPERGER SYND, P93, DOI DOI 10.1017/CB09780511526770.003 WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1993, INT CLASS DIS NR 81 TC 119 Z9 122 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0021-843X J9 J ABNORM PSYCHOL JI J. Abnorm. Psychol. PD MAY PY 2000 VL 109 IS 2 BP 227 EP 238 DI 10.1037/0021-843X.109.2.227 PG 12 WC Psychology, Clinical; Psychology, Multidisciplinary SC Psychology GA 328ZA UT WOS:000087880600007 PM 10895561 ER PT J AU Pickles, A Starr, E Kazak, S Bolton, P Papanikolaou, K Bailey, A Goodman, R Rutter, M AF Pickles, A Starr, E Kazak, S Bolton, P Papanikolaou, K Bailey, A Goodman, R Rutter, M TI Variable expression of the autism broader phenotype: Findings from extended pedigrees SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autism; broader phenotype; familial loading; phenotypic profile; X-linkage; imprinted X-linkage; sex difference ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; FAMILY HISTORY; PSYCHIATRIC-DISORDERS; INFANTILE-AUTISM; PARENTS; CHILDREN; TWIN; INDIVIDUALS; INTERVIEW AB Factors influencing the rate, form, and severity of phenotypic expression among relatives of autistic probands are examined. Family history data on 3095 first- and second-degree relatives and cousins from 149 families with a child with autism and 36 families with a child with Down syndrome are studied. The results provide further evidence of an increased risk among autism relatives for the broadly defined autism phenotype. Of proband characteristics, severity of autism and obstetric optimality were confirmed as being related to familial loading for probands with speech. There was little variation in loading among probands lacking speech. The type of phenotypic profile reported in relatives appeared little influenced by characteristics of the relative or the proband, except for variation by degree of relative, parental status of relative, and perhaps proband's birth optimality score. Phenotypic rates among parents suggested reduced fitness for the severest and more communication-related forms of expression but not for the more mild and social forms of expression. Patterns of expression within the families did not support a simple X-linked nor an imprinted X-linked mode of inheritance. The basis for sex differences in rates of expression is discussed. C1 Univ London Kings Coll, MRC, Child Psychiat Unit, London, England. Univ London Kings Coll, Inst Psychiat, London, England. Univ Windsor, Windsor, ON N9B 3P4, Canada. Univ Cambridge, Cambridge CB2 1TN, England. Orta Dogu Tekn Univ, Ankara, Turkey. Aghia Sophia Childrens Hosp, Athens, Greece. RP Pickles, A (reprint author), Univ Manchester, Sch Epidemiol & Hlth Sci, Manchester M13 9PT, Lancs, England. 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PD MAY PY 2000 VL 41 IS 4 BP 491 EP 502 DI 10.1017/S0021963099005557 PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 315VV UT WOS:000087134400010 PM 10836679 ER PT J AU Leevers, HJ Harris, PL AF Leevers, HJ Harris, PL TI Counterfactual syllogistic reasoning in normal 4-year-olds, children with learning disabilities, and children with autism SO JOURNAL OF EXPERIMENTAL CHILD PSYCHOLOGY LA English DT Article; Proceedings Paper CT Meeting of the Society-for-Research-in-Child-Development CY APR 05-06, 1997 CL WASHINGTON, D.C. SP Soc Res Child Dev DE logical reasoning; autism; syllogistic reasoning; counterfactual thought; intentional understanding ID PRETEND PLAY; MIND; IMAGINATION; COMPETENCE; DEFICITS AB Instruction encouraging imagery improves logical reasoning with counterfactual premises by normal preschool children, In contrast, children with autism have been reported to reason accurately with counterfactual premises in the absence of such instruction (F. J. Scott. S. Baron-Cohen, & A. M. Leslie, 1999). To investigate this: pattern of findings, we compared the performance of children with autism. children with learning disabilities, and normally developing 4-year-olds, who were given reasoning problems both with and without instruction in two separate testing sessions 2 to 3 weeks apart. Overall, instruction to use imagery led to persistent logical performance. However, children with autism displayed a distinctive pattern of responding, performing around chance levels, showing a simple response bias, and rarely justifying their responses by elaborating on the premises. We propose that instruction boosts logical performance by clarifying the experimenter's intention that a false proposition be accepted as a basis for reasoning and that children with autism have difficulty grasping this intention. (C) 2000 Academic Press. C1 Rutgers State Univ, Ctr Mol & Behav Neurosci, Aidekman Res Ctr, Newark, NJ 07102 USA. Univ Oxford, Oxford, England. RP Leevers, HJ (reprint author), Rutgers State Univ, Ctr Mol & Behav Neurosci, Aidekman Res Ctr, 197 Univ Ave, Newark, NJ 07102 USA. CR BARONCOHEN S, 1989, J AUTISM DEV DISORD, V19, P579, DOI 10.1007/BF02212859 Bishop D. V. M, 1982, TEST RECEPTION GRAMM Braine M. D. S., 1983, HDB CHILD PSYCHOL, V3, P263 Braine M. D. 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Exp. Child Psychol. PD MAY PY 2000 VL 76 IS 1 BP 64 EP 87 DI 10.1006/jecp.1999.2542 PG 24 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 307PH UT WOS:000086661400004 PM 10764526 ER PT J AU Ohnishi, T Matsuda, H Nishikawa, M Kunihiro, T Uema, T AF Ohnishi, T Matsuda, H Nishikawa, M Kunihiro, T Uema, T TI Abnormal regional cerebral blood flow in childhood autism. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 Natl Ctr Neurol & Psychiat, Kodaira, Tokyo, Japan. NR 0 TC 0 Z9 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 2000 VL 41 IS 5 SU S MA 911 BP 202P EP 202P PG 1 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 364KW UT WOS:000089892400805 ER PT J AU Ryu, YH Lee, JD Shin, EJ Jeon, TJ Yoon, PH Kim, DI AF Ryu, YH Lee, JD Shin, EJ Jeon, TJ Yoon, PH Kim, DI TI Usefulness of Tc-99m ECD Brain SPECT in autism spectrum disorders. SO JOURNAL OF NUCLEAR MEDICINE LA English DT Meeting Abstract C1 Yonsei Univ, Coll Med, Seoul, South Korea. NR 0 TC 0 Z9 0 PU SOC NUCLEAR MEDICINE INC PI RESTON PA 1850 SAMUEL MORSE DR, RESTON, VA 20190-5316 USA SN 0161-5505 J9 J NUCL MED JI J. Nucl. Med. PD MAY PY 2000 VL 41 IS 5 SU S MA 913 BP 202P EP 203P PG 2 WC Radiology, Nuclear Medicine & Medical Imaging SC Radiology, Nuclear Medicine & Medical Imaging GA 364KW UT WOS:000089892400807 ER PT J AU Accardo, PJ Roseman, B AF Accardo, PJ Roseman, B TI By any other name SO JOURNAL OF PEDIATRICS LA English DT Editorial Material ID AUTISM C1 New York Med Coll, Westchester Inst Human Dev, Valhalla, NY 10595 USA. RP Accardo, PJ (reprint author), New York Med Coll, Westchester Inst Human Dev, Valhalla, NY 10595 USA. CR ACCARDO P, 1988, CLIN PEDIATR, V27, P41, DOI 10.1177/000992288802700108 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Shenoy S, 2000, J PEDIATR-US, V136, P682, DOI 10.1067/mpd.2000.105355 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 NR 4 TC 1 Z9 1 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD MAY PY 2000 VL 136 IS 5 BP 576 EP 577 DI 10.1067/mpd.2000.106780 PG 2 WC Pediatrics SC Pediatrics GA 313DW UT WOS:000086985900005 PM 10802486 ER PT J AU Shenoy, S Arnold, S Chatila, T AF Shenoy, S Arnold, S Chatila, T TI Response to steroid therapy in autism secondary to autoimmune lymphoproliferative syndrome SO JOURNAL OF PEDIATRICS LA English DT Article ID FAS GENE-MUTATIONS; LANDAU-KLEFFNER SYNDROME; LYMPHOCYTE APOPTOSIS; LIGAND EXPRESSION; DISORDERS; CHILDREN; AUTOANTIBODIES; BRAIN; VIRUS; DEFICIENCY AB We report a child who developed autoimmune lymphoproliferative syndrome (ALPS) secondary to a heterozygous dominant negative mutation in the death domain of the Fas receptor. Previously developmentally normal, he had symptoms of autism with rapid regression in developmental milestones coincident with the onset of lymphoproliferation and autoimmune hemolytic anemia. Low-dose steroid therapy induced early and complete remission in the ALPS phenotype. There was subjective improvement, followed by objective improvement in speech and developmental milestones. We propose that autism may be part of the autoimmune disease spectrum of ALPS in this child, and this case represents a novel manifestation and target organ involvement in this disease. C1 Washington Univ, Sch Med, Div Pediat Hematol Oncol, Dept Pediat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Div Neurol, Dept Pediat, St Louis, MO 63110 USA. Washington Univ, Sch Med, Div Hematol Immunol, Dept Pediat, St Louis, MO 63110 USA. St Louis Childrens Hosp, St Louis, MO 63178 USA. RP Shenoy, S (reprint author), Washington Univ, Sch Med, Div Pediat Hematol Oncol, Dept Pediat, Box 8116,660 S Euclid Ave, St Louis, MO 63110 USA. CR Benkerrou M, 1997, EUR J IMMUNOL, V27, P2043, DOI 10.1002/eji.1830270831 Bettinardi A, 1997, BLOOD, V89, P902 Connolly AM, 1999, J PEDIATR-US, V134, P607, DOI 10.1016/S0022-3476(99)70248-9 Dianzani U, 1997, BLOOD, V89, P2871 Drappa J, 1996, NEW ENGL J MED, V335, P1643, DOI 10.1056/NEJM199611283352204 Fattal-Valevski A, 1999, DEV MED CHILD NEUROL, V41, P21, DOI 10.1017/S0012162299000055 Feinstein C, 1998, J AUTISM DEV DISORD, V28, P393, DOI 10.1023/A:1026000404855 FISHER GH, 1995, CELL, V81, P935, DOI 10.1016/0092-8674(95)90013-6 FIUCCI G, 1994, IMMUNOGENETICS, V39, P437 French LE, 1996, J CELL BIOL, V133, P335, DOI 10.1083/jcb.133.2.335 Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 Infante AJ, 1998, J PEDIATR-US, V133, P629, DOI 10.1016/S0022-3476(98)70102-7 Jerome KR, 1998, J VIROL, V72, P436 Kraus MD, 2000, PEDIATR DEVEL PATHOL, V3, P101, DOI 10.1007/s100240050014 LeDeist F, 1996, LANCET, V348, P719, DOI 10.1016/S0140-6736(96)02293-3 LERMAN P, 1991, DEV MED CHILD NEUROL, V33, P257 MARESCAUX C, 1990, EPILEPSIA, V31, P768, DOI 10.1111/j.1528-1157.1990.tb05518.x Nordin V, 1998, DEV MED CHILD NEUROL, V40, P587 PLIOPLYS AV, 1994, NEUROPSYCHOBIOLOGY, V29, P12, DOI 10.1159/000119056 Plioplys AV, 1998, J CHILD NEUROL, V13, P79 Ray RB, 1998, J BIOL CHEM, V273, P2256, DOI 10.1074/jbc.273.4.2256 RIEUXLAUCAT F, 1995, SCIENCE, V268, P1347, DOI 10.1126/science.7539157 Saas P, 1997, J CLIN INVEST, V99, P1173, DOI 10.1172/JCI119273 Seshagiri S, 1997, P NATL ACAD SCI USA, V94, P13606, DOI 10.1073/pnas.94.25.13606 SINGH VK, 1993, BRAIN BEHAV IMMUN, V7, P97, DOI 10.1006/brbi.1993.1010 Singh VK, 1997, PEDIATR NEUROL, V17, P88, DOI 10.1016/S0887-8994(97)00045-3 Singh VK, 1998, CLIN IMMUNOL IMMUNOP, V89, P105, DOI 10.1006/clin.1998.4588 Sneller MC, 1997, BLOOD, V89, P1341 SNELLER MC, 1992, J CLIN INVEST, V90, P334, DOI 10.1172/JCI115867 STEFANATOS GA, 1995, J AM ACAD CHILD PSY, V34, P1107, DOI 10.1097/00004583-199508000-00022 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 vanGent T, 1997, J CHILD PSYCHOL PSYC, V38, P337 Volkmar FR, 1998, J AUTISM DEV DISORD, V28, P457, DOI 10.1023/A:1026012707581 Wu JG, 1996, J CLIN INVEST, V98, P1107, DOI 10.1172/JCI118892 NR 34 TC 24 Z9 24 PU MOSBY-ELSEVIER PI NEW YORK PA 360 PARK AVENUE SOUTH, NEW YORK, NY 10010-1710 USA SN 0022-3476 EI 1097-6833 J9 J PEDIATR-US JI J. Pediatr. PD MAY PY 2000 VL 136 IS 5 BP 682 EP 687 DI 10.1067/mpd.2000.105355 PG 6 WC Pediatrics SC Pediatrics GA 313DW UT WOS:000086985900023 PM 10802504 ER PT J AU Kadesjo, B Gillberg, C AF Kadesjo, B Gillberg, C TI Tourette's disorder: Epidemiology and comorbidity in primary school children SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE Tourette's disorder; prevalence; comorbidity; attention-deficit/hyperactivity disorder; autism; Asperger's disorder; obsessive-compulsive disorder; deficits in attention; motor control; and perception ID SWEDISH 7-YEAR-OLD CHILDREN; ASPERGER-SYNDROME; AUTISTIC DISORDER; AGE-CHILDREN; PREVALENCE; POPULATION; CLUMSINESS; ADHD AB Objective: To study prevalence and comorbidity of Tourette's disorder in the general population of children and in a clinical setting. Method: School-age children in the general population and children attending a county-wide tic disorder clinic were screened and examined by the same doctor. Behavioral-psychometric instruments with demonstrated reliability and validity were used. Results: Depending on the sample characteristics, 0.15% to 1.1% of all children had Tourette's disorder. Boys outnumbered girls by 4:1 through 6:1.Attention deficits and empathy/autism spectrum problems (including Asperger's disorder) were Very common, each type of comorbidity affecting approximately two thirds of individuals with Tourette's disorder. Overall behavior problem scores were high, and affected children exhibited a marked degree of functional impairment. Conclusions: Tourette's disorder is a common disorder with high rates of significant comorbidity. in most cases, attention deficits and empathy problems are likely to cause more suffering than the tics per se. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, SE-41345 Gothenburg, Sweden. RP Gillberg, C (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, SE-41345 Gothenburg, Sweden. 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Am. Acad. Child Adolesc. Psychiatr. PD MAY PY 2000 VL 39 IS 5 BP 548 EP 555 DI 10.1097/00004583-200005000-00007 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 308DC UT WOS:000086694400007 PM 10802971 ER PT J AU Beck, L AF Beck, L TI Facing autism: Reasons for hope, encouragement for parents, guidance for help. SO LIBRARY JOURNAL LA English DT Book Review C1 Indian Valley Publ Lib, Telford, PA 18969 USA. RP Beck, L (reprint author), Indian Valley Publ Lib, Telford, PA 18969 USA. CR HAMILTON LM, 2000, FACING AUTISM REASON 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 MAY 1 PY 2000 VL 125 IS 8 BP 138 EP 138 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 317DB UT WOS:000087210100163 ER PT J AU Manning, JT Bundred, PE AF Manning, JT Bundred, PE TI The ratio of 2nd to 4th digit length: A new predictor of disease predisposition? SO MEDICAL HYPOTHESES LA English DT Article ID MYOCARDIAL-INFARCTION; BREAST-CANCER; SEX-HORMONES; TESTOSTERONE; MUTATION; MEN AB The ratio between the length of the 2nd and 4th digits is: (a) fixed in utero; (b) lower in men than in women; (c) negatively related to testosterone and sperm counts; and (d) positively related to oestrogen concentrations. Prenatal levels of testosterone and oestrogen have been implicated in infertility, autism, dyslexia, migraine, stammering, immune dysfunction, myocardial infarction and breast cancer. We suggest that 2D:4D ratio is predictive of these diseases and may be used in diagnosis, prognosis and in early life-style interventions which may delay the onset of disease or facilitate its early detection. (C) 2000 Harcourt Publishers Ltd. C1 Univ Liverpool, Sch Biol Sci, Liverpool L69 3BX, Merseyside, England. Univ Liverpool, Dept Primary Care, Liverpool L69 3BX, Merseyside, England. RP Manning, JT (reprint author), Univ Liverpool, Sch Biol Sci, Liverpool L69 3BX, Merseyside, England. 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Hypotheses PD MAY PY 2000 VL 54 IS 5 BP 855 EP 857 DI 10.1054/mehy.1999.1150 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 322AE UT WOS:000087487100038 PM 10859702 ER PT J AU Auranen, M Nieminen, T Majuri, S Vanhala, R Peltonen, L Jarvela, I AF Auranen, M Nieminen, T Majuri, S Vanhala, R Peltonen, L Jarvela, I TI Analysis of autism susceptibility gene loci on chromosomes 1p, 4p, 6q, 7q, 13q, 15q, 16p, 17q, 19q and 22q in Finnish multiplex families SO MOLECULAR PSYCHIATRY LA English DT Article DE genetic analysis; sib-pair analysis; isolated population; susceptibility genes ID BREAST-CANCER FAMILIES; SEROTONIN TRANSPORTER; GENOMEWIDE SCAN; BRCA2 MUTATIONS; LOW PROPORTION; DISORDER; LINKAGE; SCLEROSIS; SCREEN; MAPS AB The role of genetic factors in the etiology of the autistic spectrum of disorders has clearly been demonstrated. Ten chromosomal regions, on chromosomes Ip, 4p, 6q, 7q, 13q, 15q, 16p, 17q, 19q and 22q have potentially been linked to autism.(1-8) We have analyzed these chromosomal regions in a total of 17 multiplex families with autism originating from the isolated Finnish population by pairwise linkage analysis and sib-pair analysis. Mild evidence for putative contribution was found only with the Ip chromosomal region in the susceptibility to autism. Our data suggest that additional gene loci exist for autism which will be detectable in and even restricted to the isolated Finnish population. C1 Natl Publ Hlth Inst, Dept Human Mol Genet, FIN-00300 Helsinki, Finland. Univ Helsinki, Dept Med Genet, Helsinki, Finland. Univ Helsinki, Unit Child Neurol, Hosp Children & Adolescents, Helsinki, Finland. Vaalijala Inst, Outpatient Ctr Dev Disorders, Nenonpelto, Finland. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA 90095 USA. RP Auranen, M (reprint author), Natl Publ Hlth Inst, Dept Human Mol Genet, Mannerheimintie 166, FIN-00300 Helsinki, Finland. 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Psychiatr. PD MAY PY 2000 VL 5 IS 3 BP 320 EP 322 DI 10.1038/sj.mp.4000708 PG 3 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 325DL UT WOS:000087661000017 PM 10889536 ER PT J AU Baron-Cohen, S Ring, HA Bullmore, ET Wheelwright, S Ashwin, C Williams, SCR AF Baron-Cohen, S Ring, HA Bullmore, ET Wheelwright, S Ashwin, C Williams, SCR TI The amygdala theory of autism SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE autism; Kluver-Bucy syndrome; functional magnetic resonance imaging; amygdala ID TEMPORAL POLYSENSORY AREA; EARLY INFANTILE-AUTISM; FACIAL EXPRESSIONS; ASPERGER-SYNDROME; RHESUS-MONKEY; WILLIAMS-SYNDROME; NEURAL SUBSTRATE; SOCIAL-BEHAVIOR; BRAIN; RECOGNITION AB Brothers (Brothers L. Concepts in Neuroscience 1990;1:27-51) proposed a network of neural regions that comprise the "social brain", which includes the amygdala. Since the childhood psychiatric condition of autism involves deficits in "social intelligence", it is plausible that autism may be caused by an amygdala abnormality. In this paper we review the evidence for a social function of the amygdala. This includes reference to the Kluver-Bucy syndrome (which Hetzler and Griffin suggested may serve as an animal model of autism). We then review evidence for an amygdala deficit in people with autism, who are well known to have deficits in social behaviour. This includes a detailed summary of our recent functional magnetic resonance imaging (fMRI) study involving judging from the expressions of another person's eyes what that other person might be thinking or feeling. In this study, patients with autism or AS did not activate the amygdala when making mentalistic inferences from the eyes, whilst people without autism did show amygdala activity. The amygdala is therefore proposed to be one of several neural regions that are abnormal in autism. 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PD MAY PY 2000 VL 24 IS 3 BP 355 EP 364 DI 10.1016/S0149-7634(00)00011-7 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 312FC UT WOS:000086931700005 PM 10781695 ER PT J AU Ingram, JL Peckham, SM Tisdale, B Rodier, PM AF Ingram, JL Peckham, SM Tisdale, B Rodier, PM TI Prenatal exposure of rats to valproic acid reproduces the cerebellar anomalies associated with autism SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Article DE autism; valproic acid; cerebellum; Purkinje cells ID STEREOLOGICAL METHODS; INFANTILE-AUTISM; BRAIN-STEM; NEURONS; ORIGIN AB Abnormalities in anatomy and function of the cranial nerve motor nuclei have been demonstrated in some people with autism and can be modeled in rats by exposure to valproic acid during neural tube closure. Reductions in Purkinje cell number and cerebellar volume, particularly or the posterior lobe, have also been reported in people with autism. Thus, a stereological examination of cerebellar morphology was undertaken in valproate-exposed rats. Compared to controls, rats exposed to a single dose of 600-mg/kg sodium valproate on embryonic day 12.5 had significantly fewer Purkinje cells in the cerebellar vermis and a reduction short of significant in the hemispheres. The diminished cell numbers reflect reductions in tissue volume throughout the cerebellum, rather than cell density, which was unaffected in all regions. Within the vermis. the reduction in volume was significantly greater in the posterior lobe than in the anterior lobe. The results parallel those reported for human cases of autism. (C) 2000 Elsevier Science Inc. All rights reserved. C1 Univ Rochester, Sch Med & Dent, Dept Obstet & Gynecol, Rochester, NY 14642 USA. RP Rodier, PM (reprint author), Univ Rochester, Sch Med & Dent, Dept Obstet & Gynecol, Rochester, NY 14642 USA. 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PD MAY-JUN PY 2000 VL 22 IS 3 BP 319 EP 324 DI 10.1016/S0892-0362(99)00083-5 PG 6 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA 321RZ UT WOS:000087469600001 PM 10840175 ER PT J AU Coplan, J AF Coplan, J TI Counseling parents regarding prognosis in autistic spectrum disorder SO PEDIATRICS LA English DT Article DE autism; autistic spectrum disorder; pervasive developmental disorder; Asperger syndrome; developmental disability ID PERVASIVE DEVELOPMENTAL DISORDERS; FOLLOW-UP; CHILDREN AB A triaxial model for autistic spectrum disorder (ASD) is presented, incorporating age, degree of intelligence, and severity of autistic features. As the name implies, ASD can vary in degree of expression from minimal to profound. Furthermore, the symptoms of ASD change in predictable ways with the passage of time. For example, echolalia during early childhood may be replaced by verbal literalism and difficulty with verbal humor during later childhood or adolescence. The prognosis for children with ASD is governed by the joint impact of the degree of expression of ASD and the degree of developmental delay, if any. All combinations of ASD and intellect are possible (ie, severe ASD plus severe mental retardation, severe ASD plus normal general intelligence, and so forth). The relationship among these 3 parameters-severity of ASD, level of general intelligence, and change in symptom expression over time, is represented schematically as a 3-dimensional graph. The utility of this graph as a counseling tool, and as the basis for future research on the prognosis of ASD are discussed. C1 Univ Penn, Childrens Hosp Philadelphia, Childrens Seashore House, Sch Med,Dept Pediat, Philadelphia, PA 19104 USA. RP Coplan, J (reprint author), Univ Penn, Childrens Hosp Philadelphia, Childrens Seashore House, Sch Med,Dept Pediat, 3405 Civic Ctr Blvd, Philadelphia, PA 19104 USA. 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PD MAY PY 2000 VL 42 IS 5 BP 28 EP 55 PG 28 WC Education & Educational Research SC Education & Educational Research GA 366DV UT WOS:000089990300003 ER PT J AU [Anonymous] AF [Anonymous] TI Measles, MMR, and autism: the confusion continues SO LANCET LA English DT Editorial Material CR WAKEFIELD, 1999, LANCET, V353, P2026 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 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 0140-6736 EI 1474-547X J9 LANCET JI Lancet PD APR 22 PY 2000 VL 355 IS 9213 BP 1379 EP 1379 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 310LN UT WOS:000086829800001 ER PT J AU Singh, VK Lin, SX AF Singh, VK Lin, SX TI Autoantibodies to myelin markers and autoantigen therapy in autism. SO FASEB JOURNAL LA English DT Meeting Abstract C1 Utah State Univ, Dept Biol, Logan, UT 84322 USA. Univ Michigan, Ann Arbor, MI 48109 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 APR 20 PY 2000 VL 14 IS 6 SU S BP A1251 EP A1251 PG 1 WC Biochemistry & Molecular Biology; Biology; Cell Biology SC Biochemistry & Molecular Biology; Life Sciences & Biomedicine - Other Topics; Cell Biology GA 307FQ UT WOS:000086643101995 ER PT J AU Horvath, K AF Horvath, K TI Secretin treatment for autism SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Univ Maryland, Baltimore, MD 21201 USA. RP Horvath, K (reprint author), Univ Maryland, Baltimore, MD 21201 USA. CR Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 NR 3 TC 4 Z9 4 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 20 PY 2000 VL 342 IS 16 BP 1216 EP 1216 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 305DG UT WOS:000086523700015 PM 10777376 ER PT J AU Rimland, B AF Rimland, B TI Secretin treatment for autism SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Autism Res Inst, San Diego, CA 92116 USA. RP Rimland, B (reprint author), Autism Res Inst, San Diego, CA 92116 USA. CR Lord C., 1997, HDB AUTISM PERVASIVE, P460 VOLKMAR, HDB AUTISM PERVASIVE Volkmar FR, 1999, NEW ENGL J MED, V341, P1842, DOI 10.1056/NEJM199912093412412 NR 3 TC 1 Z9 1 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 20 PY 2000 VL 342 IS 16 BP 1216 EP 1217 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 305DG UT WOS:000086523700016 PM 10777377 ER PT J AU Herlihy, WC AF Herlihy, WC TI Secretin treatment for autism SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Repligen Corp, Needham, MA 02494 USA. RP Herlihy, WC (reprint author), Repligen Corp, Needham, MA 02494 USA. CR JOHANNES L, 1999, WALL STREET J 1209 KRUG D, 1993, AUSTISM SCREENING IN NR 2 TC 1 Z9 1 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 20 PY 2000 VL 342 IS 16 BP 1217 EP 1217 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 305DG UT WOS:000086523700017 PM 10777378 ER PT J AU Said, SI Bodanszky, M AF Said, SI Bodanszky, M TI Secretin treatment for autism SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 SUNY Stony Brook, Stony Brook, NY 11794 USA. Case Western Reserve Univ, Cleveland, OH 44106 USA. RP Said, SI (reprint author), SUNY Stony Brook, Stony Brook, NY 11794 USA. CR BODANSZKY M, 1978, INT J PEPT PROT RES, V12, P69 ONDETTI MA, 1968, BIOCHEMISTRY-US, V7, P4069, DOI 10.1021/bi00851a040 Said SI, 1996, J CLIN INVEST, V97, P2163, DOI 10.1172/JCI118655 SAID SI, 1970, SCIENCE, V169, P1217, DOI 10.1126/science.169.3951.1217 NR 4 TC 0 Z9 0 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 20 PY 2000 VL 342 IS 16 BP 1217 EP 1218 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 305DG UT WOS:000086523700018 PM 10777379 ER PT J AU Sandler, A AF Sandler, A TI Secretin treatment for autism - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Thoms Rehabil Hosp, Asheville, NC 28803 USA. RP Sandler, A (reprint author), Thoms Rehabil Hosp, Asheville, NC 28803 USA. NR 0 TC 1 Z9 1 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 20 PY 2000 VL 342 IS 16 BP 1218 EP 1218 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 305DG UT WOS:000086523700019 ER PT J AU Volkmar, F AF Volkmar, F TI Secretin treatment for autism - Reply SO NEW ENGLAND JOURNAL OF MEDICINE LA English DT Letter C1 Yale Univ, Sch Med, New Haven, CT 06520 USA. RP Volkmar, F (reprint author), Yale Univ, Sch Med, 333 Cedar St, New Haven, CT 06520 USA. CR MCDOUGLE CJ, 1998, AUTISM PERVASIVE DEV, P169 OWLEY T, 1999, DOUBLE BLIND PLACEBO NR 2 TC 1 Z9 1 PU MASSACHUSETTS MEDICAL SOC PI WALTHAM PA WALTHAM WOODS CENTER, 860 WINTER ST,, WALTHAM, MA 02451-1413 USA SN 0028-4793 J9 NEW ENGL J MED JI N. Engl. J. Med. PD APR 20 PY 2000 VL 342 IS 16 BP 1218 EP 1218 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 305DG UT WOS:000086523700020 ER PT J AU Buxbaum, JD Silverman, JM Smith, CJ Kilifarski, MA Reichert, JG Song, CY Lawlor, B Greenberg, DA Davis, KL AF Buxbaum, JD Silverman, JM Smith, CJ Kilifarski, MA Reichert, JG Song, CY Lawlor, B Greenberg, DA Davis, KL TI Genetics of autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2000 VL 47 IS 8 SU S MA 30 BP 9S EP 9S DI 10.1016/S0006-3223(00)00288-2 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 304ZW UT WOS:000086515200028 ER PT J AU Hardan, A Minshew, NJ Mallikarjun, M Keshavan, MS AF Hardan, A Minshew, NJ Mallikarjun, M Keshavan, MS TI Brain volume in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Univ Pittsburgh, Western Psychiat Inst & Clin, Pittsburgh, PA 15213 USA. NR 0 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2000 VL 47 IS 8 SU S MA 331 BP 99S EP 100S DI 10.1016/S0006-3223(00)00595-3 PG 2 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 304ZW UT WOS:000086515200327 ER PT J AU Hardan, A Minshew, NJ Keshavan, MS AF Hardan, A Minshew, NJ Keshavan, MS TI Corpus callosum size in autism SO BIOLOGICAL PSYCHIATRY LA English DT Meeting Abstract C1 Univ Pittsburgh, Med Ctr, Western Psychiat Inst & Clin, Pittsburgh, PA USA. NR 0 TC 1 Z9 1 PU ELSEVIER SCIENCE INC PI NEW YORK PA 655 AVENUE OF THE AMERICAS, NEW YORK, NY 10010 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD APR 15 PY 2000 VL 47 IS 8 SU S MA 332 BP 100S EP 100S DI 10.1016/S0006-3223(00)00596-5 PG 1 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 304ZW UT WOS:000086515200328 ER PT J AU Nelson, KB Grether, JK Croen, LA Dambrosia, JM Dickens, BF Hansen, RL Phillips, TM AF Nelson, KB Grether, JK Croen, LA Dambrosia, JM Dickens, BF Hansen, RL Phillips, TM TI Neuropeptides and neurotrophins in neonatal blood of children with autism, mental retardation, or cerebral palsy SO NEUROLOGY LA English DT Meeting Abstract NR 0 TC 4 Z9 4 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0028-3878 J9 NEUROLOGY JI Neurology PD APR 11 PY 2000 VL 54 IS 7 SU 3 BP A247 EP A247 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 305UA UT WOS:000086557800657 ER PT J AU McCabe, KA Smith, VL LePore, M AF McCabe, KA Smith, VL LePore, M TI Intentionality detection and "mindreading": Why does game form matter? SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID EXTENSIVE FORM; RECIPROCITY AB By around the age of 4 years, children "can work out what people might know, think or believe" based on what they say or do. This is called "mindreading," which builds upon the human ability to infer the intentions of others. Came theory makes a strong assumption about what individual A can expect about B's intentions and vice versa, viz, that each is a self-interested opponent of the other and will reliably analyze games by using such basic principles as dominance and backward induction, and behave as if the normal form of an extensive form game is equivalent to the latter. But the extensive form allows intentions to be detected from actual sequential play and is therefore not necessarily equivalent psychologically to the normal form. We discuss Baron-Cohen's theory of the mindreading system [Baron-Cohen, S. (1995) Mindblindness: An Essay on Autism and Theory of Mind (MIT Press, Cambridge, MA)] to motivate the comparison of behavior in an extensive form game with its corresponding normal form. As in the work of Rapoport [Rapoport, A. (1997) Int. J. Game Theory 26, 113-136] and Schotter et al. [Schotter, A., Wiegelt K. & Wilson, C. (1994) Games Econ. Behav. 6, 445-468], we find consistent differences in behavior between the normal and extensive forms, In particular, we observe attempts to cooperate, and in some treatments we observe the achievement of cooperation, occurring more frequently in the extensive form. Cooperation in this context requires reciprocity, which is more difficult to achieve by means of intentionality detection in the normal as opposed to the extensive form games we study. C1 Univ Arizona, Econ Sci Lab, Tucson, AZ 85721 USA. Univ Rochester, Dept Polit Sci, Rochester, NY 14627 USA. 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PD APR 11 PY 2000 VL 97 IS 8 BP 4404 EP 4409 DI 10.1073/pnas.97.8.4404 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 304AV UT WOS:000086461100110 PM 10760306 ER PT J AU Miles, JH Hillman, RE AF Miles, JH Hillman, RE TI Value of a clinical morphology examination in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; clinical morphology; minor physical anomalies; dysmorphology; sex ratio; brain MRI ID MINOR PHYSICAL ANOMALIES; PERVASIVE DEVELOPMENTAL DISORDER; GENETIC DISORDER; INFANTILE-AUTISM; YOUNG-CHILDREN; TWIN; MALFORMATIONS; ABNORMALITIES; EPIDEMIOLOGY; PAIRS AB In an effort to delineate more homogeneous autism subgroups for genetic study, we evaluated 133 consecutive individuals referred to the University of Missouri Autism Center. Each index case underwent a diagnostic evaluation, including a clinical morphology examination, laboratory studies, brain MRI, EEG, and collection of historical, medical, and family data. The 71% (94/133) who fulfilled DSM-IV and CARS autism diagnostic criteria were included in this study. Six of 94 were diagnosed with a known genetic disorder. Of the remaining 88 with apparently "idiopathic autism," 58% (51/88) were phenotypically normal, 22% (19/88) were clearly abnormal, and for 20% (18/88) the clinical morphology examination was equivocal. The percentage of phenotypically abnormal individuals is higher than generally thought and disagrees with the perception that children with autism are usually normally formed. The phenotypically abnormal individuals were 10 times more likely to be diagnosed with a known genetic syndrome (21% vs. 2%) and were more than twice as likely (29% vs. 14%) to have structurally abnormal brain MRIs than the phenotypically normal propositi, Moreover, the male to female ratio correlated with the presence of physical anomalies. The total study group had a male to female ratio of 4.2:1; the morphologically normal subgroup, defined on the basis of a normal physical examination, had a sex ratio of 7.5:1 and the normal subgroup, defined on the basis of both a normal physical examination and a structurally normal brain by MRI had a 23:1 sex ratio. For the phenotypically abnormal subgroup, the sex ratio was 1.7:1, Since differences in sex ratio are presumably a reflection of differences in genetic constitution, we postulate that the phenotypically normal subgroup of individuals with "idiopathic autism" is genetically different from the phenotypically abnormal individuals and that differences in the sex ratio in different autism populations is one indicator of a population's genetic heterogeneity. (C) 2000 Wiley-Liss, Inc. C1 Univ Missouri, Childrens Hosp, Columbia, MO USA. RP Miles, JH (reprint author), Univ Missouri, 1 Hosp Dr, Columbia, MO USA. 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J. Med. Genet. PD APR 10 PY 2000 VL 91 IS 4 BP 245 EP 253 DI 10.1002/(SICI)1096-8628(20000410)91:4<245::AID-AJMG1>3.0.CO;2-2 PG 9 WC Genetics & Heredity SC Genetics & Heredity GA 301HM UT WOS:000086304800001 PM 10766977 ER PT J AU Pilowsky, T Yirmiya, N Arbelle, S Mozes, T AF Pilowsky, T Yirmiya, N Arbelle, S Mozes, T TI Theory of mind abilities of children with schizophrenia, children with autism, and normally developing children SO SCHIZOPHRENIA RESEARCH LA English DT Article DE autism; schizophrenia; theory of mind (ToM) ID MENTAL-RETARDATION; INDIVIDUALS; DECEPTION; BELIEFS; PEOPLE; TASK; AGE AB Theory of mind (ToM) abilities of children with schizophrenia, children with high functioning autism, and normally developing children, matched on mental age (MA), verbal MA, and performance MA, were compared. Both clinical groups were matched on chronological age as well, whereas the normally developing children were younger. A fact belief task, a value belief task, a deception task, and a false belief task were administered. The three groups did not differ on the fact belief task. Children with autism performed more poorly than normally developing children on value belief and false belief tasks, and more poorly than individuals with schizophrenia on the deception task. Children with schizophrenia performed more poorly than normally developing children only on the false belief task. Overall, the group with autism passed significantly fewer tasks compared to the normally developing group. ToM abilities correlated with verbal abilities for individuals with autism. The ToM abilities of children with paranoid schizophrenia and children with undifferentiated or disorganized schizophrenia did not differ. Findings strengthen the notion of a limited understanding of ToM in schizophrenia, and support the notion that ToM deficits, although more severe in autism, are not unique to autism. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hebrew Univ Jerusalem, Jerusalem, Israel. Ben Gurion Univ Negev, IL-84105 Beer Sheva, Israel. Ness Ziona Mental Hlth Ctr, Ness Ziona, Israel. RP Yirmiya, N (reprint author), Hebrew Univ Jerusalem, Jerusalem, Israel. 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Res. PD APR 7 PY 2000 VL 42 IS 2 BP 145 EP 155 DI 10.1016/S0920-9964(99)00101-2 PG 11 WC Psychiatry SC Psychiatry GA 301YQ UT WOS:000086338500007 PM 10742652 ER PT J AU Warburton, P Baird, G Chen, W Morris, K Jacobs, BW Hodgson, S Docherty, Z AF Warburton, P Baird, G Chen, W Morris, K Jacobs, BW Hodgson, S Docherty, Z TI Support for linkage of autism and specific language impairment to 7q3 from two chromosome rearrangements involving band 7q31 SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE specific developmental disorders of speech and language; chromosome 7; fluorescence in situ hybridisation mapping ID FAMILY HISTORY; DISORDER; SPEECH; TWIN; MAP AB Childhood autism is characterised by impairments in communication and reciprocal social interaction together with restricted/stereotyped interests, which are evident before 3 years of age. Specific developmental disorders of speech and language (SDDSL) are characterised by impairment in the development of expressive and/or receptive language skills which is not associated with intellectual, sensory, physical, or neurological impairment. Family and twin studies indicate a substantial genetic component in the aetiology of both disorders, They also reveal increased rates of SDDSL in relatives of autistic individuals, suggesting that this phenotype can represent one manifestation of the genetic liability for autism. Modelling of the recurrence risk for autism and milder phenotypes, such as SDDSL, suggest that three or four epistatic loci may be aetiologically involved, A recently published linkage study of an exceptional family with an apparently dominantly inherited SDDSL implicated chromosome band 7q31 as the site of the putative susceptibility locus (SPCH1). This region of chromosome 7 also shows strong linkage in multiplex families with autism. We present two individuals (one has autism, the other SDDSL) with different, apparently balanced chromosome rearrangements involving a breakpoint at 7q31,3, Fluorescence in situ hybridisation was used to localise the breakpoints to an similar to 1 cM interval between CFTR and D7S643. Our findings may be of interest and relevance to the genetic aetiology of autism, and helpful in the search for susceptibility loci for SDDSL and autism. (C) 2000 Wiley-Liss, Inc. C1 Guys Hosp, Guys Kings & St Thomas Sch Med, Div Med & Mol Genet, London SE1 9RT, England. Guys Hosp, Newcomen Ctr, London SE1 9RT, England. Maudsley Hosp, Dept Child & Adolescent Psychiat, London SE5 8AZ, England. Bethlem Royal Hosp, Beckenham, Kent, England. RP Warburton, P (reprint author), Guys Hosp, Guys Kings & St Thomas Sch Med, Div Med & Mol Genet, 8th Floor Guys Tower, London SE1 9RT, England. 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PD APR 3 PY 2000 VL 96 IS 2 BP 228 EP 234 DI 10.1002/(SICI)1096-8628(20000403)96:2<228::AID-AJMG20>3.0.CO;2-G PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 299BN UT WOS:000086176100020 PM 10893502 ER PT J AU Schultz, RT Gauthier, I Klin, A Fulbright, RK Anderson, AW Volkmar, F Skudlarski, P Lacadic, C Cohen, DJ Gore, JC AF Schultz, RT Gauthier, I Klin, A Fulbright, RK Anderson, AW Volkmar, F Skudlarski, P Lacadic, C Cohen, DJ Gore, JC TI Abnormal ventral temporal cortical activity during face discrimination among individuals with autism and Asperger syndrome SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Article; Proceedings Paper CT 1998 Biological Psychiatry Meeting CY MAY 28, 1998 CL TORONTO, CANADA ID HUMAN EXTRASTRIATE CORTEX; PERVASIVE DEVELOPMENTAL DISORDERS; POSITRON EMISSION TOMOGRAPHY; HUMAN AMYGDALA; VISUAL-CORTEX; RECOGNITION; PERCEPTION; CHILDREN; LESIONS; MONKEYS AB Background: Recognition of individual faces is an integral part of both interpersonal interactions and successful functioning within a social group. Therefore, it is of considerable interest that individuals with autism and related conditions have selective deficits in face recognition (sparing nonface object recognition). Method: We used functional magnetic resonance imaging (fMRI) to study face and subordinate-level object perception in 14 high-functioning individuals with autism or Asperger syndrome (the autism group), in comparison with 2 groups of matched normal controls (normal control group 1 [NC1] and normal control group 2 [NC2]) (n = 14 for each). Regions of interest (ROIs) were defined in NC1 and then applied in comparisons between NC2 and the autism group. Regions of interest were also defined in NC2 and then applied to comparisons between NC1 and the autism group as a replication study. Results: In the first set of comparisons, we found significant task X group interactions for the size of activation in the right fusiform gyrus (FC) and right inferior temporal gyri (ITG). 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M., 1988, ASSESSMENT CHILDREN Saunders RC, 1998, NATURE, V393, P169, DOI 10.1038/30245 SCHACTER DL, 1995, NATURE, V376, P587, DOI 10.1038/376587a0 SERGENT J, 1992, BRAIN, V115, P15, DOI 10.1093/brain/115.1.15 Sparrow S, 1984, VINELAND ADAPTIVE BE TANTAM D, 1989, J CHILD PSYCHOL PSYC, V30, P623, DOI 10.1111/j.1469-7610.1989.tb00274.x Tarr MJ, 1998, COGNITION, V67, P1, DOI 10.1016/S0010-0277(98)00026-2 VALENTINE T, 1988, BRIT J PSYCHOL, V79, P471 VOLKMAR FR, 1989, J CHILD PSYCHOL PSYC, V30, P591, DOI 10.1111/j.1469-7610.1989.tb00270.x WEBSTER MJ, 1991, NEUROREPORT, V2, P769, DOI 10.1097/00001756-199112000-00010 Wechsler D., 1992, MANUAL WECHSLER INTE, V3rd Wechsler D., 1981, MANUAL WECHSLER ADUL World Health Organization, 1992, INT CLASS DIS NR 73 TC 529 Z9 534 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD APR PY 2000 VL 57 IS 4 BP 331 EP 340 DI 10.1001/archpsyc.57.4.331 PG 10 WC Psychiatry SC Psychiatry GA 302LG UT WOS:000086366100009 PM 10768694 ER PT J AU Pierce, K Courchesne, E AF Pierce, K Courchesne, E TI Exploring the neurofunctional organization of face processing in autism SO ARCHIVES OF GENERAL PSYCHIATRY LA English DT Editorial Material ID HUMAN EXTRASTRIATE CORTEX; RECOGNITION; SIZE C1 Univ Calif San Diego, Dept Neurosci, Res Neurosci Autism Lab, La Jolla, CA 92037 USA. RP Pierce, K (reprint author), Univ Calif San Diego, Dept Neurosci, Res Neurosci Autism Lab, Mail Code 0217,8110 La Jolla Shore Dr,Room 201B, La Jolla, CA 92037 USA. CR ALLISON T, 1994, J NEUROPHYSIOL, V71, P821 Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 Bauman ML, 1994, NEUROBIOLOGY AUTISM, P119 Clark VP, 1996, NEUROIMAGE, V4, P1, DOI 10.1006/nimg.1996.0025 COURCHESNE E, 1994, DEV PSYCHOPATHOL, V6, P697, DOI 10.1017/S0954579400004740 Courchesne E, 1999, NEUROLOGY, V52, P1057 Dolan RJ, 1997, NATURE, V389, P596, DOI 10.1038/39309 EGAAS B, 1995, ARCH NEUROL-CHICAGO, V52, P794 Farah MJ, 1996, BEHAV BRAIN RES, V76, P181, DOI 10.1016/0166-4328(95)00198-0 Gauthier I, 1999, NAT NEUROSCI, V2, P568, DOI 10.1038/9224 GOURCHESNE E, 1999, CHANGING NERVOUS SYS, P292 Kanwisher N, 1997, J NEUROSCI, V17, P4302 MURAKAMI JW, 1989, ARCH NEUROL-CHICAGO, V46, P689 Puce A, 1998, J NEUROSCI, V18, P2188 Quartz SR, 1997, BEHAV BRAIN SCI, V20, P537 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 NR 16 TC 15 Z9 15 PU AMER MEDICAL ASSOC PI CHICAGO PA 515 N STATE ST, CHICAGO, IL 60610 USA SN 0003-990X J9 ARCH GEN PSYCHIAT JI Arch. Gen. Psychiatry PD APR PY 2000 VL 57 IS 4 BP 344 EP 346 DI 10.1001/archpsyc.57.4.344 PG 3 WC Psychiatry SC Psychiatry GA 302LG UT WOS:000086366100010 PM 10768695 ER PT J AU Smith, T Antolovich, M AF Smith, T Antolovich, M TI Parental perceptions of supplemental interventions received by young children with autism in intensive behavior analytic treatment SO BEHAVIORAL INTERVENTIONS LA English DT Article; Proceedings Paper CT Annual Meeting of the Association-of-Behavior-Analysis CY MAY, 1996 CL SAN FRANCISCO, CALIFORNIA SP Assoc Behav Anal ID SOCIAL VALIDITY; PSYCHOTHERAPY AB Parents of children with autism in applied behavior analytic treatment were surveyed on their use and perceptions of supplemental treatments. In study 1, respondents (N = 121) reported enrolling their children in an average of seven supplemental interventions, most commonly non-behavior-analytic speech therapies (85%), megavitamins (61%), Sensory Integration Therapy (56%), and elimination diets (50%). In study 2, parents (N = 24) were interviewed about these four interventions and typically reported little or no benefit. Factors that parents cited as influencing their decision to obtain supplemental interventions for their children varied substantially, depending on the individual intervention. Because of the extensive use of unvalidated interventions that parents deemed unhelpful, it seems important to reduce children's participation in such interventions. However, because of the diverse influences on parents' decisions to obtain the interventions; a multifaceted strategy may be needed. Copyright (C) 2000 John Wiley & Sons, Ltd. C1 Washington State Univ, Dept Psychol, Pullman, WA 99164 USA. RP Smith, T (reprint author), Washington State Univ, Dept Psychol, POB 644820, Pullman, WA 99164 USA. CR AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 ARENDT RE, 1988, AM J MENT RETARD, V92, P401 Ayres A. J., 1972, SENSORY INTEGRATION Berk L. E., 2000, CHILD DEV Bettelheim B., 1967, EMPTY FORTRESS Biklen D., 1993, COMMUNICATION UNBOUN CAMPBELL M, 1995, J AM ACAD CHILD PSY, V34, P1124, DOI 10.1097/00004583-199509000-00008 Charlop-Christy M. H., 1997, TREAT CHILD AUTISM CROOK WG, 1987, J LEARN DISABIL, V20, P260 DEMYER MK, 1981, SCHIZOPHRENIA BULL, V7, P388 Deslauriers A. M., 1969, YOUR CHILD IS ASLEEP Green G, 1996, BEHAV INTERVENTION Y, P29 GREENSPAN SI, 1992, ZERO 3, V13, P1 HART BM, 1968, J APPL BEHAV ANAL, V1, P109, DOI 10.1901/jaba.1968.1-109 JACOBSON JW, 1995, AM PSYCHOL, V50, P750, DOI 10.1037//0003-066X.50.9.750 Jacobson NS, 1996, AM PSYCHOL, V51, P1031, DOI 10.1037/0003-066X.51.10.1031 Kaufman B. N, 1976, SON RISE Lambert Michael J., 1994, HDB PSYCHOTHERAPY BE, V4th, P143 Matson JL, 1996, RES DEV DISABIL, V17, P433, DOI 10.1016/S0891-4222(96)00030-3 MCGEE JJ, 1990, PERSPECTIVES USE NON, P215 New York State Department of Health Early Intervention Program, 1999, NEW YORK STAT DEP HL, V4217 Prizant B. M., 1997, HDB AUTISM PERVASIVE, P572 Rimland B., 1994, AM J SPEECH-LANG PAT, V3, P16 RIMLAND B, 1987, NEUROBIOLOGICAL ISSU, P390 RIMLAND B, 1998, AUTISM RES REV INT, V12, P1 Rimland B, 1996, J AUTISM DEV DISORD, V26, P237, DOI 10.1007/BF02172019 SCHWARTZ IS, 1991, J APPL BEHAV ANAL, V24, P189, DOI 10.1901/jaba.1991.24-189 SELIGMAN MEP, 1995, AM PSYCHOL, V50, P965, DOI 10.1037//0003-066X.50.12.965 Smith T., 1996, BEHAV INTERVENTION Y, P45 Smith T, 1999, CLIN PSYCHOL-SCI PR, V6, P33, DOI 10.1093/clipsy/6.1.33 SMITH T, IN PRESS PRESCHOOL E Wechsler D., 1989, WECHSLER PRESCHOOL P Welch M G, 1987, Pa Med, V90, P47 Wilcox MJ, 1998, TRANSITIONS PRELINGU, P385 WOLF MM, 1978, J APPL BEHAV ANAL, V11, P203, DOI 10.1901/jaba.1978.11-203 Zager D., 1999, AUTISM IDENTIFICATIO NR 36 TC 31 Z9 31 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD APR-JUN PY 2000 VL 15 IS 2 BP 83 EP 97 DI 10.1002/(SICI)1099-078X(200004/06)15:2<83::AID-BIN47>3.0.CO;2-W PG 15 WC Psychology, Clinical SC Psychology GA 305FT UT WOS:000086529300001 ER PT J AU Romano, JP Roll, D AF Romano, JP Roll, D TI Expanding the utility of behavioral momentum for youth with developmental disabilities SO BEHAVIORAL INTERVENTIONS LA English DT Article ID FUNCTIONAL-ANALYSIS; NONCOMPLIANCE; COVARIATION; CHILDREN AB Non-compliance with requests in educational or therapeutic settings interferes with teaching and learning. Recent studies indicate that the probability of compliance can be increased when short sequences of requests with a high probability of compliance are followed by a request less likely to be followed by compliance. The high probability command sequence (HPCS) consists of requests that produce compliance rates of 80% or more. For some individuals with severe disabilities it is difficult to find sufficient number of requests that result in 80% compliance. This study assessed the effects of two levels of high probability request sequences on compliance with subsequent low probability requests. The three participants (ages 7, 11, and 20) met the diagnostic criteria for autism and/or severe to profound mental retardation. Results showed that both high (>80% compliance) and medium (50-70% compliance) request sequences produced increases in compliance to subsequent requests that had produced low compliance rates (<40%) during baseline. No systematic differences were observed between high and medium probability sequences. Copyright (C) 2000 John Wiley & Sons, Ltd. C1 Dev Disabil Inst, Smithtown, NY 11787 USA. Long Isl Univ, Brookville, NY USA. RP Romano, JP (reprint author), Dev Disabil Inst, 99 Hollywood Dr, Smithtown, NY 11787 USA. CR BARLOW DH, 1984, SINGLE SUBJECT EXPT Carr E. G., 1994, COMMUNICATION BASED CARR EG, 1976, J ABNORM CHILD PSYCH, V4, P139, DOI 10.1007/BF00916518 CARR EG, 1994, J APPL BEHAV ANAL, V27, P393, DOI 10.1901/jaba.1994.27-393 CATALDO MF, 1986, ANAL INTERVEN DEVEL, V6, P265, DOI 10.1016/S0270-4684(86)80009-X Davis CA, 1996, J APPL BEHAV ANAL, V29, P471, DOI 10.1901/jaba.1996.29-471 DAVIS CA, 1993, J APPL BEHAV ANAL, V26, P619 DUCHARME JM, 1994, J APPL BEHAV ANAL, V27, P639, DOI 10.1901/jaba.1994.27-639 IWATA BA, 1982, ANAL INTERVEN DEVEL, V2, P3, DOI 10.1016/0270-4684(82)90003-9 IWATA BA, 1990, PERSPECTIVES USE NON IWATA BA, 1994, J APPL BEHAV ANAL, V27, P413, DOI 10.1901/jaba.1994.27-413 MACE FC, 1988, J APPL BEHAV ANAL, V21, P123, DOI 10.1901/jaba.1988.21-123 Mace FC, 1997, J APPL BEHAV ANAL, V30, P1, DOI 10.1901/jaba.1997.30-1 MACE FC, 1991, RES DEV DISABIL, V12, P155, DOI 10.1016/0891-4222(91)90004-C MACE FC, 1991, J APPL BEHAV ANAL, V24, P553, DOI 10.1901/jaba.1991.24-553 NEVIN JA, 1983, J EXP ANAL BEHAV, V39, P49, DOI 10.1901/jeab.1983.39-49 PARRISH JM, 1986, J APPL BEHAV ANAL, V19, P241, DOI 10.1901/jaba.1986.19-241 RUSSO DC, 1981, J APPL BEHAV ANAL, V14, P209, DOI 10.1901/jaba.1981.14-209 VOLKMAR FR, 1982, J AUTISM DEV DISORD, V12, P35, DOI 10.1007/BF01531672 ZARCONE JR, 1994, J APPL BEHAV ANAL, V27, P649, DOI 10.1901/jaba.1994.27-649 NR 20 TC 2 Z9 2 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD APR-JUN PY 2000 VL 15 IS 2 BP 99 EP 111 DI 10.1002/(SICI)1099-078X(200004/06)15:2<99::AID-BIN48>3.0.CO;2-K PG 13 WC Psychology, Clinical SC Psychology GA 305FT UT WOS:000086529300002 ER PT J AU Rapp, JT Dozier, CL Carr, JE Patel, MR Enloe, KA AF Rapp, JT Dozier, CL Carr, JE Patel, MR Enloe, KA TI Functional analysis of hair manipulation: A replication and extension SO BEHAVIORAL INTERVENTIONS LA English DT Article ID SELF-INJURY; BEHAVIOR AB In a multi-phase investigation, we assessed the problematic hair manipulation of a four-year-old male diagnosed with autism. In phase 1, a functional analysis of hair manipulation resulted in high levels of responding during a no-interaction condition, while near-zero levels were observed in other conditions. In phase 2, hair manipulation was reduced to near-zero levels during a condition in which Billy wore gloves on his hands to attenuate digital-tactile stimulation. In phase 3, a stimulus preference assessment indicated that object manipulation competed with hair manipulation, and that wearing gloves did not alter the amount of time that Billy manipulated preferred objects. The results are discussed in the context of interventions that achieve their effects via reinforcer substitutability or competition. Copyright (C) 2000 John Wiley & Sons, Ltd. C1 Univ Nevada, Reno, NV 89557 USA. RP Rapp, JT (reprint author), Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. CR CHRISTENSON GA, 1991, AM J PSYCHIAT, V148, P365 DeLeon IG, 1999, J APPL BEHAV ANAL, V32, P111, DOI 10.1901/jaba.1999.32-111 ELLINGSON SA, IN PRESS J APPL BEHA FAVELL JE, 1982, ANAL INTERVEN DEVEL, V2, P83, DOI 10.1016/0270-4684(82)90007-6 FRIMAN PC, 1993, PEDIATRICS, V91, P784 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Lerman DC, 1999, J APPL BEHAV ANAL, V32, P1, DOI 10.1901/jaba.1999.32-1 Long ES, 1999, J DEV PHYS DISABIL, V11, P295, DOI 10.1023/A:1021862723409 Miltenberger RG, 1998, J APPL BEHAV ANAL, V31, P447, DOI 10.1901/jaba.1998.31-447 Miltenberger RG, 1999, J APPL BEHAV ANAL, V32, P119, DOI 10.1901/jaba.1999.32-119 Rapp JT, 1999, J APPL BEHAV ANAL, V32, P329, DOI 10.1901/jaba.1999.32-329 RAPP JT, IN PRESS BEHAV MODIF RAPP JT, 1998, J APPL BEHAV ANAL, V31, P135 RINCOVER A, 1979, J APPL BEHAV ANAL, V12, P221, DOI 10.1901/jaba.1979.12-221 STANLEY MA, 1995, BEHAV RES THER, V33, P179, DOI 10.1016/0005-7967(94)E0018-E NR 15 TC 4 Z9 4 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD APR-JUN PY 2000 VL 15 IS 2 BP 121 EP 133 DI 10.1002/(SICI)1099-078X(200004/06)15:2<121::AID-BIN49>3.0.CO;2-O PG 13 WC Psychology, Clinical SC Psychology GA 305FT UT WOS:000086529300004 ER PT J AU Newman, B Reinecke, DR Meinberg, DL AF Newman, B Reinecke, DR Meinberg, DL TI Self-management of varied responding in three students with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article ID TREATMENT PACKAGE AB One of the aspects of autism that is often held up as a hallmark of the disorder is a desire for sameness. Students with autism often show a marked lack of variability in language and play skills. The same behavioral patterns are repeated perseveratively, rather than attempting new patterns. In the current study, students diagnosed with autism were taught to self-manage varied responding. Using a multiple baseline design, three children with autism were taught to self-monitor and then to self-manage in order to increase variability in play and social language. All three students demonstrated marked increases in variability during self-management phases. These gains were maintained at one month follow-up. Copyright (C) 2000 John Wiley & Sons, Ltd. C1 Assoc Manhattan Autist Children, New York, NY USA. Fred S Keller Sch, New York, NY USA. RP Newman, B (reprint author), AMA, 25 W 17th St, New York, NY 10011 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th GOETZ EM, 1973, J APPL BEHAV ANAL, V6, P209, DOI 10.1901/jaba.1973.6-209 KOEGEL RL, 1990, J APPL BEHAV ANAL, V23, P119, DOI 10.1901/jaba.1990.23-119 Malott R. W., 1989, RULE GOVERNED BEHAV, P269 MATSON FW, 1971, HUMANIST, V31, P7 NEWMAN B, 1995, BEHAV DISORDERS, V20, P195 Newman B, 1996, EDUC TRAIN MENT RET, V31, P304 Newman B., 1997, BEHAV INTERVENT, V12, P149, DOI 10.1002/(SICI)1099-078X(199707)12:3<149::AID-BRT173>3.0.CO;2-M Skinner B. F, 1953, SCI HUMAN BEHAV STAHMER AC, 1992, J APPL BEHAV ANAL, V25, P447, DOI 10.1901/jaba.1992.25-447 NR 10 TC 18 Z9 18 PU JOHN WILEY & SONS LTD PI W SUSSEX PA BAFFINS LANE CHICHESTER, W SUSSEX PO19 1UD, ENGLAND SN 1072-0847 J9 BEHAV INTERVENT JI Behav. Intervent. PD APR-JUN PY 2000 VL 15 IS 2 BP 145 EP 151 DI 10.1002/(SICI)1099-078X(200004/06)15:2<145::AID-BIN50>3.3.CO;2-V PG 7 WC Psychology, Clinical SC Psychology GA 305FT UT WOS:000086529300006 ER PT J AU Thony, B Auerbach, G Blau, N AF Thony, B Auerbach, G Blau, N TI Tetrahydrobiopterin biosynthesis, regeneration and functions SO BIOCHEMICAL JOURNAL LA English DT Review DE cyclohydrolase; dehydratase; dihydropteridine; nitric oxide; 6-pyruvoyl-tetrahydropterin; sepiapterin ID GTP-CYCLOHYDROLASE-I; 6-PYRUVOYL TETRAHYDROPTERIN SYNTHASE; NITRIC-OXIDE SYNTHASE; AMINO-ACID HYDROXYLASES; PTERIN-4-ALPHA-CARBINOLAMINE DEHYDRATASE/DIMERIZATION COFACTOR; DIHYDROPTERIDINE REDUCTASE DEFICIENCY; TRANSCRIPTIONAL COACTIVATOR DCOH; FEEDBACK REGULATORY PROTEIN; PHENYLALANINE-HYDROXYLASE; SEPIAPTERIN REDUCTASE AB Tetrahydrobiopterin (BH(4)) cofactor is essential for various processes, and is present in probably every cell or tissue of higher organisms. BH(4) is required for various enzyme activities, and for less defined functions at the cellular level. The pathway for the de novo biosynthesis of BH(4) from GTP involves GTP cyclohydrolase I, 6-pyruvoyl-tetrahydropterin synthase and sepiapterin reductase. Cofactor regeneration requires pterin-4a-carbinolamine-dehydratase and dihydropteridine reductase. Based on gene cloning, recombinant expression, mutagenesis studies, structural analysis of crystals and NMR studies, reaction mechanisms for the biosynthetic and recycling enzymes were proposed. With regard to the regulation of cofactor biosynthesis, the major controlling point is GTP cyclohydrolase I, the expression of which may be under the control of cytokine induction. In the liver at least, activity is inhibited by BH(4), but stimulated by phenylalanine through the GTP cyclohydrolase I feedback regulatory protein. The enzymes that depend on BH(4) are the phenylalanine, tyrosine and tryptophan hydroxylases, the latter two being the rate-limiting enzymes for catecholamine and 5-hydroxytryptamine (serotonin) biosynthesis, all NO synthase isoforms and the glyceryl-ether mono-oxygenase. On a cellular level, BH(4) has been found to be a growth or proliferation factor for Crithidia fasciculata, haemopoietic cells and various mammalian cell lines. In the nervous system, BH(4) is a self-protecting factor for NO, or a general neuroprotecting factor via the NO synthase pathway, and has neurotransmitter-releasing function. With regard to human disease, BH(4) deficiency due to autosomal recessive mutations in all enzymes (except sepiapterin reductase) have been described as a cause of hyperphenylalaninaemia. 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J. PD APR 1 PY 2000 VL 347 BP 1 EP 16 DI 10.1042/0264-6021:3470001 PN 1 PG 16 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 309WQ UT WOS:000086792600001 PM 10727395 ER PT J AU Carper, RA Courchesne, E AF Carper, RA Courchesne, E TI Inverse correlation between frontal lobe and cerebellum sizes in children with autism SO BRAIN LA English DT Article DE magnetic resonance imaging; cerebrum; vermis; neuroanatomy; autism ID CEREBRAL BLOOD-FLOW; INFANTILE-AUTISM; MENTAL-RETARDATION; CHILDHOOD AUTISM; SOCIAL-BEHAVIOR; WORKING-MEMORY; BRAIN-STEM; CORTEX; ACTIVATION; BLIND AB Certain cognitive and behavioural deficits suggest that the frontal lobe functions abnormally in patients with autism, but little anatomical research is available to either verify or refute this. 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They also review studies on why parents do not follow this proven advice. The contribution of the risks of other environmental factors are also reviewed. Also discussed are commentaries from a study reviewed last on the link between a prolonged QT electrocardiogram interval and sudden infant death syndrome. Church provides a cogent and timely review of the reported effectiveness of hormone secretin effectiveness in treating children with autism, This newly proposed treatment has been in the spotlight of the lay public, the popular media, and the scientific community, In short order, secretin as a treatment for autism has moved from a chance observation to the subject of a double-blind, placebo-controlled study, Curr Opin Pediatr 2000, 12:179-183 (C) 2000 Lippincott Williams & Wilkins, Inc. C1 SUNY Syracuse, Upstate Med Univ, Syracuse, NY 13202 USA. RP Blatt, SD (reprint author), SUNY Syracuse, Upstate Med Univ, 90 Presidential Plaza, Syracuse, NY 13202 USA. 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PD APR PY 2000 VL 12 IS 2 BP 179 EP 183 DI 10.1097/00008480-200004000-00017 PG 5 WC Pediatrics SC Pediatrics GA 298WX UT WOS:000086163500017 PM 10763770 ER PT J AU Stromme, P Diseth, TH AF Stromme, P Diseth, TH TI Prevalence of psychiatric diagnoses in children with mental retardation: data from a population-based study SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID FRAGILE-X-SYNDROME; DISORDERS; EPIDEMIOLOGY; ADOLESCENTS; BEHAVIOR; AUTISM AB The main purpose of the study was to estimate the prevalence of psychiatric diagnoses in children with mental retardation (MR) (IQ less than or equal to 70). All children born between 1980 and 1985 (N=30 037) in Akershus County, Norway, were screened for possible MR and assessed with either IQ tests or standardized developmental tests. A total of 178 children, 79 with severe mental retardation (SMR) (IQ<50) and 99 with mild mental retardation (MMR) (IQ 50 to 70) were included for further study, Psychiatric symptomatology was assessed as a standard part of the neurodevelopmental examination, which included a semistructured parent interview, a clinical child interview, and retrieval of the charts of previous child psychiatric examinations. Psychiatric diagnoses were classified according to the International Classification of Disease (ICD-10). In total, 65 (37%) of the total population with MR (95% confidence intervals 29 to 44) were registered to have psychiatric diagnoses, the most common being hyperkinesia (n=28) and pervasive developmental disorder (n=15). Psychiatric diagnoses were present in 42% of the population with SMR and 33% of the population with MMR (p=0.4). Of all children found to have a psychiatric diagnosis, approximately one-third had previously been examined by a child psychiatrist and indicated a previously unrecognized need for these services to children with MR. C1 Univ Oslo, Natl Hosp, Rikshosp, Dept Paediat,Sect Child Neurol, N-0027 Oslo, Norway. Univ Oslo, Natl Hosp, Rikshosp, Dept Paediat,Div Child & Adolescent Psychiat, N-0027 Oslo, Norway. RP Stromme, P (reprint author), Univ Oslo, Natl Hosp, Rikshosp, Dept Paediat,Sect Child Neurol, N-0027 Oslo, Norway. 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PD APR PY 2000 VL 42 IS 4 BP 266 EP 270 DI 10.1017/S0012162200000451 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 308KG UT WOS:000086709600009 PM 10795566 ER PT J AU Kawashima, H Mori, T Kashiwagi, Y Takekuma, K Hoshika, A Wakefield, A AF Kawashima, H Mori, T Kashiwagi, Y Takekuma, K Hoshika, A Wakefield, A TI Detection and sequencing of measles virus from peripheral mononuclear cells from patients with inflammatory bowel disease and autism SO DIGESTIVE DISEASES AND SCIENCES LA English DT Article DE measles; inflammatory bowel disease; pervasive developmental disorder ID POLYMERASE-CHAIN-REACTION; CROHNS-DISEASE; VACCINE STRAIN; GENOME; INFECTION; CHILDREN; RNA AB It has been reported that measles virus may be present in the intestine of patients with Crohn's disease. Additionally, a new syndrome has been reported in children with autism who exhibited developmental regression and gastrointestinal symptoms (autistic enterocolitis), in some cases soon after MMR vaccine. It is not known whether the virus, if confirmed to be present in these patients, derives from either wild strains or vaccine strains. In order to characterize the strains that may be present, we have carried out the detection of measles genomic RNA in peripheral mononuclear cells (PBMC) in eight patients with Crohn's disease, three patients with ulcerative colitis, and nine children with autistic enterocolitis. As controls, we examined healthy children and patients with SSPE, SLE, HIV-1 (a total of eight cases). RNA was purified from PBMC by Ficoll-paque, followed by reverse transcription using AMV; cDNAs were subjected to nested PCR for detection of specific regions of the hemagglutinin (H) and fusion (F) gene regions. Positive samples were sequenced directly, in nucleotides 8393-8676 (H region) or 5325-5465 (from noncoding F to coding F region). One of eight patients with Crohn disease, one of three patients with ulcerative colitis, and three of nine children with autism, were positive. Controls were all negative. The sequences obtained from the patients with Crohn's disease shared the characteristics with wild-strain virus. The sequences obtained from the patients with ulcerative colitis and children with autism were consistent with being vaccine strains. The results were concordant with the exposure history of the patients. Persistence of measles virus was confirmed in PBMC in some patients with chronic intestinal inflammation. C1 Tokyo Med Univ, Dept Paediat, Shinjuku Ku, Tokyo 160, Japan. Kitasato Inst, Dept Virol, Tokyo 108, Japan. Royal Free Hosp, Sch Med, Dept Med, London, England. RP Kawashima, H (reprint author), Tokyo Med Univ, Dept Paediat, Shinjuku Ku, 6-7-1 Nishishinjuku, Tokyo 160, Japan. 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Dis. Sci. PD APR PY 2000 VL 45 IS 4 BP 723 EP 729 DI 10.1023/A:1005443726670 PG 7 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 299TX UT WOS:000086214900015 PM 10759242 ER PT J AU Mas, C Bourgeois, F Bulfone, A Levacher, B Mugnier, C Simonneau, M AF Mas, C Bourgeois, F Bulfone, A Levacher, B Mugnier, C Simonneau, M TI Cloning and expression analysis of a novel gene, RP42, mapping to an autism susceptibility locus on 6q16 SO GENOMICS LA English DT Article ID 3'-UTR SEQUENCE MOTIF; FAMILY; PATTERNS; ENHANCER; BOX AB We isolated a novel mouse gene, RP42, in a systematic search for genes expressed in proliferating neuroblasts whose human orthologs map to suspectibility loci for autism. This gene is intronless and encodes a putative 259-amino-acid protein that exhibits 30-36% overall sequence identity to a fission yeast and a nematode protein (GenPept Accession Nos. CAA17006 and CAB54261). Nevertheless, no homology to any known gene was found. RP42 has developmentally regulated expression, particularly in proliferating neuroblasts from which neocortical neurons originate. Its human ortholog is located in a cluster of embryonic neuronally expressed genes on the 6q16 chromosome, making it a positional candidate susceptibility gene for autism, (C) 2000 Academic Press. C1 Hop Robert Debre, INSERM, Neurogenet E9935, F-75019 Paris, France. TIGEM, Milan, Italy. Univ Paris 05, F-75006 Paris, France. RP Simonneau, M (reprint author), Hop Robert Debre, INSERM, Neurogenet E9935, 48 Blvd Serurier, F-75019 Paris, France. CR Anderson SA, 1997, SCIENCE, V278, P474, DOI 10.1126/science.278.5337.474 Bulfone A, 1998, HUM MOL GENET, V7, P1997, DOI 10.1093/hmg/7.13.1997 Ema M, 1996, MOL CELL BIOL, V16, P5865 Fan CM, 1996, MOL CELL NEUROSCI, V7, P1, DOI 10.1006/mcne.1996.0001 GIBBONS RJ, 1995, CELL, V80, P837, DOI 10.1016/0092-8674(95)90287-2 HATTEN ME, 1999, FUNDAMENTAL NEUROSCI Hogue DL, 1999, GENOMICS, V59, P18, DOI 10.1006/geno.1999.5847 Bailey A, 1998, HUM MOL GENET, V7, P571 KOZAK M, 1991, J BIOL CHEM, V266, P19867 Lai EC, 1998, DEVELOPMENT, V125, P4077 Lai EC, 2000, DEVELOPMENT, V127, P291 Lai EC, 1997, DEVELOPMENT, V124, P4847 Liang P, 1997, Methods Mol Biol, V85, P3 Philippe A, 1999, HUM MOL GENET, V8, P805, DOI 10.1093/hmg/8.5.805 Piven J, 1997, CURR OPIN NEUROBIOL, V7, P708, DOI 10.1016/S0959-4388(97)80093-1 Villard L, 1996, NAT GENET, V12, P359, DOI 10.1038/ng0496-359 Villard L, 1997, GENOMICS, V43, P149, DOI 10.1006/geno.1997.4793 NR 17 TC 11 Z9 13 PU ACADEMIC PRESS INC PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0888-7543 J9 GENOMICS JI Genomics PD APR 1 PY 2000 VL 65 IS 1 BP 70 EP 74 DI 10.1006/geno.2000.6126 PG 5 WC Biotechnology & Applied Microbiology; Genetics & Heredity SC Biotechnology & Applied Microbiology; Genetics & Heredity GA 309AZ UT WOS:000086746200010 PM 10777668 ER PT J AU Kim, SJ Cook, EH AF Kim, Soo-Jeong Cook, Edwin H., Jr. TI Novel de novo Nonsense Mutation of MECP2 in a Patient with Rett Syndrome SO HUMAN MUTATION LA English DT Article DE Rett syndrome; MECP2; autism; X-chromosome inactivation; XCI AB Because of the recent identification of several mutations of methyl-CpG-binding protein 2 (MECP2) in patients with Rett syndrome (RTT), a patient with suspected RTT from an autism clinic was screened for mutations. She was found to have a novel heterozygous nonsense mutation, 129C>T (Q19X), which leads to the most severely truncated MECP2 protein reported to date. Sequencing of parental DNA revealed the mutation was de novo. The patient was not affected with microcephaly or hyperventilation, but had other features of Rett syndrome including severe mental retardation and symptoms of autistic disorder. Moderately skewed X-chromosome inactivation (XCI) may have contributed to her relatively mild phenotype. (C) 2000 Wiley-Liss, Inc. C1 [Kim, Soo-Jeong; Cook, Edwin H., Jr.] Univ Chicago, Lab Dev Neurosci, Dept Psychiat, Chicago, IL 60637 USA. RP Cook, EH (reprint author), Univ Chicago, Lab Dev Neurosci, Dept Psychiat, MC 3077,5841 S Maryland Ave, Chicago, IL 60637 USA. EM ed@yoda.bsd.uchicago.edu FU National Institutes of Health [R01 MH 52223]; Jean Young and Walden W. Shaw Foundation FX Contract grant sponsor: National Institutes of Health; Contract grant number: R01 MH 52223Zhi-Ying Yang and David Gonen provided expert technical assistance. The study was supported in part by the Jean Young and Walden W. Shaw Foundation. S.-J. Kim is a Daniel X. Freedman Psychiatric Research Fellow. CR ALLEN RC, 1992, AM J HUM GENET, V51, P1229 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Amir RE, 1999, NAT GENET, V23, P185 Cook EH, 1997, AM J HUM GENET, V60, P928 Ellaway C, 1998, J CHILD NEUROL, V13, P448 GILLBERG C, 1989, J AUTISM DEV DISORD, V19, P545, DOI 10.1007/BF02212857 HAGBERG B, 1983, ANN NEUROL, V14, P471, DOI 10.1002/ana.410140412 Hendrich B, 1999, MAMM GENOME, V10, P906, DOI 10.1007/s003359901112 LEWIS JD, 1992, CELL, V69, P905, DOI 10.1016/0092-8674(92)90610-O Nan XS, 1998, NATURE, V393, P386 OLSSON B, 1987, DEV MED CHILD NEUROL, V29, P429 Sirianni N, 1998, AM J HUM GENET, V63, P1552, DOI 10.1086/302105 Wan MM, 1999, AM J HUM GENET, V65, P1520, DOI 10.1086/302690 NR 13 TC 23 Z9 23 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 1059-7794 J9 HUM MUTAT JI Hum. Mutat. PD APR PY 2000 VL 15 IS 4 BP 382 EP + DI 10.1002/(SICI)1098-1004(200004)15:4<382::AID-HUMU16>3.0.CO;2-8 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA V23XT UT WOS:000208376200006 PM 10737989 ER PT J AU Donlan, C Masters, J AF Donlan, C Masters, J TI Correlates of social development in children with communication disorders: the concurrent predictive value of verbal short-term memory span SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE short-term memory; social skill; communication disorders ID LANGUAGE IMPAIRMENT; WORKING-MEMORY; AUTISTIC-CHILDREN; INFANTILE-AUTISM; ACQUISITION; VOCABULARY; DEFICIT; AGE AB Linguistic and cognitive correlates of social skill were examined in a clinically selected sample of children with communication disorders. Thirty-two children aged between 5 and 10 years were assessed using a questionnaire-based sociability scale. Specially designed measures of verbal and visuo-spatial short-term memory span were administered, as well as standardized tests of grammatical and lexical comprehension. Multiple regression analyses revealed strong prediction of social skill from STM measures but not from comprehension scores. The prediction was based on a striking negative correlation between serial word span and sociability. This word-span measure could offer a useful tool in the assessment of children with communication disorders. However, attention is drawn to the substantial number of children in the sample whose patterns of cognitive, Linguistic and social skill are not clearly differentiated. It is suggested that: assessment should aim to specify as clearly as possible individual patterns of strength and weakness and avoid unwarranted categorization. C1 UCL, Dept Human Commun Sci, London WC1N 1PG, England. RP Donlan, C (reprint author), UCL, Dept Human Commun Sci, Chandler House,2 Wakefield St, London WC1N 1PG, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BADDELEY AD, 1974, RECENT ADV LEARNING, V3 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BARTAK L, 1975, BRIT J PSYCHIAT, V126, P127, DOI 10.1192/bjp.126.2.127 Benetto L, 1996, CHILD DEV, V67, P1816 BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 Bishop D. V. M., 1997, UNCOMMON UNDERSTANDI BISHOP DVM, 1999, IN PRESS DEV PSYCHOP Bishop DVM, 1983, TEST RECEPTION GRAMM BISHOP DVM, 1992, J CHILD PSYCHOL PSYC, V3, P3 Bishop DVM, 1996, J CHILD PSYCHOL PSYC, V37, P391, DOI 10.1111/j.1469-7610.1996.tb01420.x CARROLL JB, 1973, J VERB LEARN VERB BE, V12, P563, DOI 10.1016/S0022-5371(73)80036-2 ContiRamsden G, 1997, J SPEECH LANG HEAR R, V40, P765 Cowan N., 1996, MODELS SHORT TERM ME Cowan N, 1996, TOP LANG DISORD, V17, P1 Dunn L M., 1982, BRIT PICTURE VOCABUL Gathercole S. 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J. Lang. Commun. Disord. PD APR-JUN PY 2000 VL 35 IS 2 BP 211 EP 226 PG 16 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 304PE UT WOS:000086492000003 PM 10912252 ER PT J AU Capps, I Losh, M Thurber, C AF Capps, I Losh, M Thurber, C TI "The frog ate the bug and made his mouth sad": Narrative competence in children with autism SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article DE autism; narrative; theory of mind; conversational competence ID MIND; INDIVIDUALS; DEFICITS; STATES AB This study compares the narrative abilities of 13 children with autism, 13 children with developmental delays, and 13 typically developing children matched on language ability. Although groups did not differ in their use of causal language or internal state terms, children with autism and children with developmental delays were less likely than typical children to identify the causes of characters' internal states. Rather, they tended simply to label emotions and explain actions. Children with autism and children with developmental delays also relied on a more restricted range of evaluative devices, which both convey point of view and maintain listener involvement. In addition, the narrative abilities of children with autism were linked to performance on measures of theory of mind and an index of conversational competence, whereas this was not the case among children with developmental delays. Findings are discussed in relation to the social, cognitive, and emotional underpinnings and consequences of narrative activity. C1 Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA. Phillips Exeter Acad, Exeter, Devon, England. RP Losh, M (reprint author), Univ Calif Berkeley, Dept Psychol, 3210 Tolman Hall 1650, Berkeley, CA 94720 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT BAMBERG M, 1991, DISCOURSE PROCESS, V14, P277 BAMBERG M, 1991, J COGNITIVE PSYCHOTH, V5, P275 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x Baron-Cohen S., 1993, UNDERSTANDING OTHER BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bellugi U., 1990, DEV PSYCHOPATHOL, V2, P367, DOI DOI 10.1017/S0954579400005782 Berman R. A., 1994, RELATING EVENTS NARR Bruner J, 1986, ACTUAL MINDS POSSIBL Bruner J. 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S., 1996, INTERACTION SOCIAL C, P329 Ricoeur Paul, 1988, TIME NARRATIVE Schopler E., 1986, CHILDHOOD AUTISM RAT Semel E., 1987, CLIN EVALUATION LANG SIGMAN R, 1999, MONOGRAPHS SOC RES C, V64 TAGERFLUSBERG H, 1992, CHILD DEV, V63, P161, DOI 10.1111/j.1467-8624.1992.tb03604.x TAGERFLUSBERG H, 1994, J CHILD PSYCHOL PSYC, V35, P1059, DOI 10.1111/j.1469-7610.1994.tb01809.x Tager-Flusberg H., 1993, UNDERSTANDING OTHER TAGERFLUSBERG H, 1995, BRIT J DEV PSYCHOL, V13, P45 TAGERFLUSBERG H, 1995, APPL PSYCHOLINGUIST, V16, P241, DOI 10.1017/S0142716400007281 Thorndike RL, 1986, STANFORD BINET INTEL Tingey C., 1987, NEW PERSPECTIVES DOW, P233 WANG PP, 1994, J CLIN EXP NEUROPSYC, V16, P317, DOI 10.1080/01688639408402641 WHITE H, 1981, VALUE NARRATIVITY RE WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 NR 47 TC 25 Z9 25 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0091-0627 J9 J ABNORM CHILD PSYCH JI J. Abnorm. Child Psychol. PD APR PY 2000 VL 28 IS 2 BP 193 EP 204 PG 12 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 313QE UT WOS:000087009700007 ER PT J AU Chez, MG Buchanan, CP Bagan, BT Hammer, MS McCarthy, KS Ovrutskaya, I Nowinski, CV Cohen, ZS AF Chez, MG Buchanan, CP Bagan, BT Hammer, MS McCarthy, KS Ovrutskaya, I Nowinski, CV Cohen, ZS TI Secretin and autism: A two-part clinical investigation SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE secretin; autism ID PERVASIVE DEVELOPMENTAL DISORDER AB Recent anecdotal reports have touted the gastrointestinal (GI) hormone secretin as a treatment modality for autism, though there is little clinical evidence or literature to support its viability. We undertook a two-pac? clinical trial to investigate these claims. Fifty six patients (49 boys, 7 girls, mean age = 6.4 years, SD = 2.7) enrolled in an open-label trial of secretin, during which they received one injection of the hormone (2 IU/kg). All subjects were evaluated by their parents at baseline and follow-up visits (3-6 weeks later, M = 3.7, SD = 1.4 weeks) with Childhood Autism Rating Scales (CARS). Thirty-four patients were labeled with Pervasive Developmental Disorder Not Otherwise Specified, and 22 met diagnostic criteria for Autistic Disorder. Forty-five patients were concurrently on other drug treatments. At follow-up, some reported minimal but potentially significant improvements including changes in GI symptoms, expressive and/or receptive language function, and improved awareness and social interactions. No adverse effects were reported or observed. Subsequently, 17 of the most responsive patients from Study 1 began a double-blind trial that also included 8 newly enrolled patients. Patients in this second study were alternatively entered into one of two groups and received injections of secretin or placebo with crossover at 4 weeks. Patients from Study 1 entered into Study 2 at an average of 6.5 (SD = 0.8) weeks after beginning Study 1. Results of both inquiries indicate that although treatment with secretin was reported to cause transient changes in speech and behavior in some children, overall it produced few clinically meaningful changes when compared to children given placebo injections. C1 Lake Forest Hosp, Lake Forest, IL 60045 USA. RP Chez, MG (reprint author), 800 Westmoreland Rd,Suite 100, Lake Forest, IL 60045 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bardenstein R, 1998, NEUROLOGY, V50, pA86 CHEZ M, 1997, ANN NEUROL, V42, P509 Chez M, 1998, NEW DEVELOPMENTS IN CHILD NEUROLOGY, P695 CHEZ MG, 1997, EPILEPSIA, V38, P50 CHEZ MG, 1998, J DEV LEARNING DISOR, V2, P217 Chez MG, 1998, ANN NEUROL, V44, P539 CHEZ MG, 1996, NEUROLOGY, V46, pA115 Chugani DC, 1999, ANN NEUROL, V45, P287, DOI 10.1002/1531-8249(199903)45:3<287::AID-ANA3>3.0.CO;2-9 HAPPE F, 1991, J CHILD PSYCHOL PSYC, V32, P1167, DOI 10.1111/j.1469-7610.1991.tb00356.x Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Kienle G S, 1996, Altern Ther Health Med, V2, P39 Maris E, 1998, PSYCHOL METHODS, V3, P309, DOI 10.1037/1082-989X.3.3.309 Montgomery GH, 1997, PAIN, V72, P107, DOI 10.1016/S0304-3959(97)00016-X Perry R, 1998, J CHILD ADOL PSYCHOP, V8, P247, DOI 10.1089/cap.1998.8.247 PLIOPLYS AV, 1994, ARCH PEDIAT ADOL MED, V148, P220 Schopler E., 1988, CHILDHOOD AUTISM RAT STEFANATOS GA, 1995, J AM ACAD CHILD PSY, V34, P1107, DOI 10.1097/00004583-199508000-00022 TRAUNER DA, 1997, ANN NEUROL, V42, P465 VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 NR 20 TC 65 Z9 65 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 87 EP 94 DI 10.1023/A:1005443119324 PG 8 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000002 PM 10832772 ER PT J AU Rimland, B AF Rimland, B TI Comments on "secretin and autism: A two-part clinical investigation" by M. G. Chez et al. SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material NR 0 TC 5 Z9 5 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 95 EP 95 DI 10.1023/A:1005447203394 PG 1 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000003 PM 10832773 ER PT J AU Chez, MG Buchanan, CP AF Chez, MG Buchanan, CP TI Reply to B. Rimland's "Comments on 'secretin and autism: A two-part clinical investigation'" SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material RP Chez, MG (reprint author), 800 Westmoreland Rd,Suite 100, Lake Forest, IL 60045 USA. CR Bolte ER, 1998, MED HYPOTHESES, V51, P133, DOI 10.1016/S0306-9877(98)90107-4 CHEZ MG, 1998, J DEV LEARNING DISOR, V2, P217 Deonna T, 1995, Semin Pediatr Neurol, V2, P254, DOI 10.1016/S1071-9091(95)80004-2 SANDLER RH, 1999, IN PRESS J CHILD NEU Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 6 TC 3 Z9 3 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 97 EP 98 DI 10.1023/A:1005499220232 PG 2 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000004 ER PT J AU Arnold, LE Aman, MG Martin, A Collier-Crespin, A Vitiello, B Tierney, E Asarnow, R Bell-Bradshaw, F Freeman, PJ Gates-Ulanet, P Klin, A McCracken, JT McDougle, CJ McGough, JJ Posey, DJ Scahill, L Swiezy, NB Ritz, L Volkmar, F AF Arnold, LE Aman, MG Martin, A Collier-Crespin, A Vitiello, B Tierney, E Asarnow, R Bell-Bradshaw, F Freeman, PJ Gates-Ulanet, P Klin, A McCracken, JT McDougle, CJ McGough, JJ Posey, DJ Scahill, L Swiezy, NB Ritz, L Volkmar, F TI Assessment in multisite randomized clinical trials of patients with autistic disorder: The autism RUPP network SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; clinical trials; risperidone ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; INFANTILE-AUTISM; DOUBLE-BLIND; WEIGHT-GAIN; FOLLOW-UP; CHILDREN; METHYLPHENIDATE; PERFORMANCE; RISPERIDONE AB Assessment of autistic disorder (autism) symptoms, primary and secondary, poses more challenging problems than ordinarily found in multisite randomized clinical trial (RCT) assessments. For example, subjects may be uncommunicative and extremely heterogeneous in problem presentation, and current pharmacological treatments are not likely to alter most core features of autism. The Autism Research Units on Pediatric Psychopharmacology (RUPP Autism Network) resolved some of these problems during the design of a risperidone RCT in children/adolescents. The inappropriateness of the usual anchors for a Clinical Global Impression of Severity (CGI-S) was resolved by defining uncomplicated autism without secondary symptoms as a CGI-S of 3, mildly ill. The communication problems, compromising use of the patient as an informant, were addressed by several strategies, including careful questioning of care providers, rating scales, laboratory tests, and physical exams. The broad subject heterogeneity requires outcome measures sensitive to individual change over a wide spectrum of treatment response and side effects. The problems of neuropsychologically testing nonverbal, lower functioning, sometimes noncompliant subjects requires careful instrument selection/adaptation and flexible administration techniques. The problems of assessing low-end IQs, neglected by most standardized test developers, was resolved by an algorithm of test hierarchy. Scarcity of other autism-adapted cognitive and neuropsychological tests and lack of standardization required development of a new, specially adapted battery. Reliability on the Autism Diagnostic Interview (currently the most valid diagnostic instrument) and other clinician instruments required extensive cross-site training (in-person, videotape, and teleconference sessions). Definition of a treatment responder required focus on individually relevant target symptoms, synthesis of possible modest improvements in many domains, and acceptance of attainable though imperfect goals. The assessment strategy developed is implemented in a RCT of risperidone (McDougle et al., 2000) for which the design and other methodological challenges are described elsewhere (Scahill et al., 2000). Some of these problems and solutions are partially shared with RCTs of other treatments and other disorders. C1 Indiana Univ, Bloomington, IN 47405 USA. Johns Hopkins Univ, Kennedy Krieger Inst, Baltimore, MD 21218 USA. Ohio State Univ, Columbus, OH 43210 USA. Univ Calif Los Angeles, Los Angeles, CA 90024 USA. Yale Univ, New Haven, CT 06520 USA. RP Arnold, LE (reprint author), 479 S Galena Rd, Sunbury, OH 43074 USA. CR ALLISON D, 1998, SCI P AM PSYCH ASS A ALPHERTS W, 1997, FEPSY NEUROPSYCHOLOG Alpherts WCJ, 1990, EPILEPSIA S4, V31, P35 Aman MG, 1996, J DEV PHYS DISABIL, V8, P347, DOI 10.1007/BF02578400 AMAN MG, 1985, AM J MENT DEF, V89, P485 AMAN MG, 1991, J AM ACAD CHILD PSY, V30, P816, DOI 10.1016/S0890-8567(10)80022-X AMAN MG, 1986, J ABNORM CHILD PSYCH, V14, P441, DOI 10.1007/BF00915437 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th AMERY W, 1997, AM COLL NEUR 36 AN M, P188 ANDERSON GM, 1987, J CHILD PSYCHOL PSYC, V28, P885, DOI 10.1111/j.1469-7610.1987.tb00677.x ANDO H, 1979, J AUTISM DEV DISORD, V9, P83, DOI 10.1007/BF01531295 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAILEY A, 1993, J CHILD PSYCHOL PSYC, V34, P673, DOI 10.1111/j.1469-7610.1993.tb01064.x BARKLEY RA, 1991, J ABNORM CHILD PSYCH, V19, P149, DOI 10.1007/BF00909976 Barnes TRE, 1998, INT CLIN PSYCHOPHARM, V13, pS49, DOI 10.1097/00004850-199803003-00009 Benvenga MJ, 1997, DRUG DEVELOP RES, V41, P48 Bromel T, 1998, MOL PSYCHIATR, V3, P76, DOI 10.1038/sj.mp.4000352 CAMPBELL M, 1985, PSYCHOPHARMACOL BULL, V21, P1047 CAMPBELL M, 1993, J AM ACAD CHILD PSY, V32, P1283, DOI 10.1097/00004583-199311000-00024 DELIS C, 1994, CALIFORNIA VERBAL LE DOUGLAS VI, 1986, J CHILD PSYCHOL PSYC, V27, P191, DOI 10.1111/j.1469-7610.1986.tb02283.x Dunn L. 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Autism Dev. Disord. PD APR PY 2000 VL 30 IS 2 BP 99 EP 111 DI 10.1023/A:1005451304303 PG 13 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000005 PM 10832774 ER PT J AU Davidovitch, M Glick, L Holtzman, G Tirosh, E Safir, MP AF Davidovitch, M Glick, L Holtzman, G Tirosh, E Safir, MP TI Developmental regression in autism: Maternal perception SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; developmental regression; maternal reports ID CHILDHOOD DISINTEGRATIVE DISORDER; AGE; ONSET AB Developmental regression among children with autism is a common phenomenon of unknown origin. The purpose of this study was to identify the differences between children with autism who reportedly regressed with those who did not regress. A representative group of 39 mothers were interviewed (40 children-1 pair of twin girls) about familial, pregnancy, perinatal, as well as medical history and developmental milestones. The study focused on mothers' perceptions of developmental regression. Nineteen children (47.5%) regressed in verbal and nonverbal communication and social but not in motor abilities. Mean age of regression was 24 months, with ii children who regressed before and 8 after this age. No significant differences were reported by mothers of children who did or did not regress. More mothers of children who regressed, than those of children who did not, expressed guilt feelings regarding the development of autism, and almost all of them had an "explanation" for the possible mechanisms that might have influenced their children's developmental course. In conclusion, developmental regression in our population appears to be a typical event in the natural course of autism. There is little difference between those children who regressed and those who did not regress in maternal perceptions and reports of development, family, and medical history. C1 Bnai Zion Med Ctr, Hannah Khoushy Child Dev Ctr, IL-31048 Haifa, Israel. Technion Israel Inst Technol, Bruce Rappaport Fac Med, IL-31096 Haifa, Israel. Univ Haifa, Dept Psychol, IL-31905 Haifa, Israel. RP Davidovitch, M (reprint author), Bnai Zion Med Ctr, Hannah Khoushy Child Dev Ctr, 47 Golomb St POB 4940, IL-31048 Haifa, Israel. CR *AM PSYCH ASS, 1987, DAIGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BROWN J, 1995, J AUTISM DEV DISORD, V25, P305, DOI 10.1007/BF02179291 Burd L, 1998, DEV MED CHILD NEUROL, V40, P702 DAVIDOVITCH M, 2000, UNPUB AUTISM INCIDEN De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 HOSHINO Y, 1987, JPN J PSYCHIAT NEUR, V41, P237 Kobayashi R, 1998, ACTA PSYCHIAT SCAND, V98, P296, DOI 10.1111/j.1600-0447.1998.tb10087.x KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 Militerni R, 1997, DEV BRAIN DYSFUNCT, V10, P67 *OFF POP CENS SURV, 1971, CLASS OCC Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 ROGERS SJ, 1990, J AM ACAD CHILD PSY, V29, P863, DOI 10.1097/00004583-199011000-00004 RUTTER M, 1987, LANGUAGE DEV DISORDE, P206 SAS, 1982, SAS US GUID STAT, P584 SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 VOLKMAR FR, 1989, J CHILD PSYCHOL PSYC, V30, P717, DOI 10.1111/j.1469-7610.1989.tb00784.x VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 NR 19 TC 79 Z9 79 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 113 EP 119 DI 10.1023/A:1005403421141 PG 7 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000006 PM 10832775 ER PT J AU Zwaigenbaum, L Szatmari, P Mahoney, W Bryson, S Bartolucci, G MacLean, J AF Zwaigenbaum, L Szatmari, P Mahoney, W Bryson, S Bartolucci, G MacLean, J TI High functioning autism and childhood disintegrative disorder in half brothers SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE childhood disintegrative disorder; autism; half-brothers ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; SPEECH LOSS; DSM-IV; TWIN; INDIVIDUALS; PHENOTYPE; DEMENTIA; SUBTYPES; BEHAVIOR AB Childhood Disintegrative Disorder (CDD) is grouped with autism as a subtype of Pervasive Developmental Disorder (PDD) in ICD-10 and DSM-IV. This is the first report of autism and CDD cosegregating within a sibship. J. P. and M. P. are half-brothers with the same mother. J. P. is an 18-year-old with impairments in communication, social reciprocity, and stereotypies and was diagnosed with autism. M. P. is a 7-year-old who developed normally to 2 years 4 months. He then underwent a profound regression, becoming nonverbal and socially withdrawn, and lost adaptive skills. Investigations did not reveal any neurodegenerative process. M. P. was diagnosed with CDD. The rarity of the two conditions suggests a shared transmissible mechanism. The implications for autism/PDD genetic studies are discussed. C1 McMaster Univ, Dept Pediat, Hamilton, ON L8N 3Z5, Canada. McMaster Univ, Dept Psychiat, Hamilton, ON, Canada. Univ York, Dept Psychol, N York, ON, Canada. RP Zwaigenbaum, L (reprint author), McMaster Univ, Dept Pediat, 1200 Main St W, Hamilton, ON L8N 3Z5, Canada. 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Autism Dev. Disord. PD APR PY 2000 VL 30 IS 2 BP 121 EP 126 DI 10.1023/A:1005455505211 PG 6 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000007 PM 10832776 ER PT J AU Schreck, KA Mulick, JA AF Schreck, KA Mulick, JA TI Parental report of sleep problems in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE mental retardation; autism; sleep disorders ID MENTAL HANDICAP; RETARDATION; PATTERNS AB This research evaluated parent reports of sleep behaviors of four groups of children: those with Autism or Pervasive Developmental Disorders, those with General Mental Retardation alone, those attending Special Education classes (with no MR diagnosis), and a control group of similar aged children without a developmental diagnosis. Diagnostic classification and demographic information were determined through parent report, report of classroom registration, and the Gilliam Autism Rating Scale (Gilliam, 1995). To evaluate sleeping behavior the study used a 28-item, five-factor scale (Behavioral Evaluation of Disorders of Sleep/BEDS; Schreck, 1997/1998) constructed from the diagnostic criteria for childhood sleep disorders found in the International Classification of Sleep Disorders: Diagnostic and Coding Manual (ICSD, American Sleep Disorders Association, 1990). Findings suggest that reports of parents with children with autistic characteristics exhibit expected quantities of sleep, but parent perception of their sleep difficulties and sleep quality is different for children with autism than for children in all other study groups. C1 Penn State Harrisburg, Middletown, PA 17057 USA. Childrens Hosp, Dept Pediat Psychol, Columbus, OH 43205 USA. Ohio State Univ, Columbus, OH 43205 USA. RP Schreck, KA (reprint author), Penn State Harrisburg, W157 Olmsted Bldg,777 Harrisburg Pike, Middletown, PA 17057 USA. 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R., 1993, EUROPEAN CHILD ADOLE, V2, P75 SADEH A, 1994, J CONSULT CLIN PSYCH, V62, P63, DOI 10.1037//0022-006X.62.1.63 SCHRECK KA, 1997, DISS ABSTR INT, V58, P3934 SCHROEDER CS, 1991, ASSESSMENT TREATMENT SHELDON H, 1992, PEDIAT SLEEP MED SIMONDS JF, 1982, J AM ACAD CHILD PSY, V21, P383, DOI 10.1016/S0002-7138(09)60942-0 *SPSS, 1995, STAT PACK SOC SCI RE STORES G, 1992, J CHILD PSYCHOL PSYC, V33, P1303, DOI 10.1111/j.1469-7610.1992.tb00951.x WOLF M, 1964, BEHAV RES THER, V1, P305 Zapella M, 1993, DEV MED CHILD NEUROL, V35, P826 NR 33 TC 87 Z9 88 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 127 EP 135 DI 10.1023/A:1005407622050 PG 9 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000008 PM 10832777 ER PT J AU Harris, SL Handleman, JS AF Harris, SL Handleman, JS TI Age and IQ at intake as predictors of placement for young children with autism: A four- to six-year follow-up SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autistic disorder; age; IQ; placement in special education; applied behavior analysis ID INTERVENTION AB The predictive power of age and IQ at time of admission to an intensive treatment program using applied behavior analysis were examined in a 4- to 6-year follow-up of educational placement. Twenty-seven children with autistic disorder who were between the ages of 31 and 65 months and had IQs on the Stanford Binet between 35 and 109 at time of admission to the Douglass Developmental Disabilities Center were followed up 4 to 6 years after they left the preschool. The results showed that having a higher IQ at intake (M = 78) and being of younger age (M = 42 months) were both predictive of being in a regular education class after discharge, whereas having a lower IQ (M = 46) and being older at intake (M = 54 months) were closely related to placement in a special education classroom. The results are interpreted as pointing to the need for very early intervention for children with Autistic Disorder. It is also emphasized that older children and those with lower IQs in the present study showed measurable gains in IQ from treatment. The data should not be taken to suggest that children older than 4 years of age do not merit high quality treatment. C1 Rutgers State Univ, Grad Sch Appl & Profess Psychol, Piscataway, NJ 08854 USA. RP Harris, SL (reprint author), Rutgers State Univ, Grad Sch Appl & Profess Psychol, 152 Frelinghuysen Rd, Piscataway, NJ 08854 USA. CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT ANDERSON SR, 1994, PRESCHOOL ED PROGRAM, P15 Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 FENSKE EC, 1985, ANAL INTERVEN DEVEL, V5, P49, DOI 10.1016/S0270-4684(85)80005-7 Gresham FM, 1998, J AUTISM DEV DISORD, V28, P5, DOI 10.1023/A:1026002717402 Harris SL, 1990, SPECIAL SERVICES SCH, V6, P135 HARRIS SL, 1991, J AUTISM DEV DISORD, V21, P281, DOI 10.1007/BF02207325 Lord C., 1994, PRESCHOOL ED PROGRAM, P87 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 McClannahan L. E., 1994, PRESCHOOL ED PROGRAM, P107 Schopler E., 1986, CHILDHOOD AUTISM RAT Schopler E, 1998, J AUTISM DEV DISORD, V28, P3, DOI 10.1023/A:1026064700564 SHEINKOPF SJ, 1998, J AUTISM DEV DISORD, V28, P1524 Thorndike RL, 1986, STANFORD BINET INTEL NR 14 TC 205 Z9 211 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 137 EP 142 DI 10.1023/A:1005459606120 PG 6 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000009 PM 10832778 ER PT J AU Glasberg, BA AF Glasberg, BA TI The development of siblings' understanding of autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE sibling's understanding of autism ID CHILDRENS CONCEPTS; COGNITIVE-DEVELOPMENT; ILLNESS; ADJUSTMENT AB While professionals commonly advocate sharing information about autism spectrum disorders with siblings, no guidelines currently exist that describe what types of information might be relevant for siblings at different ages. To address this issue, the interviewing method described by Bibace and Walsh (1979, 1980), which measures cognitive sophistication in thinking about illness, was adapted to examine perspectives on autism spectrum disorders. Sixty-three siblings of individuals with autism or related disorders were interviewed using this measure. Parents were given the same interview as their child, and asked to predict their child's responses. Children's reasoning became more mature with age, but developed at a delayed rate compared to norms for illness concepts. Although accurate in estimating their child's understanding of the definition and cause of their sibling's diagnosis, parents tended to overestimate their child's understanding of the disorder's impact. C1 Rutgers State Univ, Douglas Dev Disabilities Ctr, Piscataway, NJ 08854 USA. RP Glasberg, BA (reprint author), Rutgers State Univ, Douglas Dev Disabilities Ctr, Piscataway, NJ 08854 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAGENHOLM A, 1991, J MENT DEFIC RES, V35, P291 BELCHIC JK, 1995, PHIL C DEV DIS PAR P BERRY SL, 1993, J PEDIATR PSYCHOL, V18, P83, DOI 10.1093/jpepsy/18.1.83 Bibace R, 1979, HLTH PSYCHOL HDB, P285 BIBACE R, 1980, PEDIATRICS, V66, P912 BREWSTER AB, 1982, PEDIATRICS, V69, P355 Brodzinsky D M, 1981, J Pediatr Psychol, V6, P177, DOI 10.1093/jpepsy/6.2.177 Brodzinsky DM, 1986, THINKING FAMILY VIEW, P205 BURBACH DJ, 1986, HEALTH PSYCHOL, V5, P307, DOI 10.1037//0278-6133.5.3.307 CARANDANG MLA, 1979, AM J ORTHOPSYCHIAT, V49, P474 Cooper J., 1987, APPL BEHAV ANAL DONOVAN AM, 1988, AM J MENT RETARD, V92, P502 DYSON LL, 1989, J PEDIATR PSYCHOL, V14, P215, DOI 10.1093/jpepsy/14.2.215 GLASBERG BA, 1996, M NEW JERS CTR OUTR GOLD N, 1993, J AUTISM DEV DISORD, V23, P147, DOI 10.1007/BF01066424 Harris Sandra L., 1994, SIBLINGS CHILDREN AU HOLMES N, 1991, J AUTISM DEV DISORD, V21, P159, DOI 10.1007/BF02284757 Lazarus R. 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Autism Dev. Disord. PD APR PY 2000 VL 30 IS 2 BP 143 EP 156 DI 10.1023/A:1005411722958 PG 14 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000010 PM 10832779 ER PT J AU Werner, E Dawson, G Osterling, J Dinno, N AF Werner, E Dawson, G Osterling, J Dinno, N TI Brief report: Recognition of autism spectrum disorder before one year of age: A retrospective study based on home videotapes SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID PHONOLOGICAL DEVELOPMENT; CHILDREN; INFANCY; 1ST C1 Univ Washington, Ctr Human Dev & Disabil, Seattle, WA 98195 USA. RP Werner, E (reprint author), Univ Washington, Ctr Human Dev & Disabil, Box 357920, Seattle, WA 98195 USA. CR ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 ADRIEN JL, 1991, J AUTISM DEV DISORD, V21, P43, DOI 10.1007/BF02206996 American Psychiatric Association, 1987, DIAGN STAT MAN MENT Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 CAMP BW, 1987, J PEDIATR PSYCHOL, V12, P321, DOI 10.1093/jpepsy/12.3.321 Dawson G, 1998, CHILD DEV, V69, P1276, DOI 10.2307/1132265 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 Dawson G., 1997, EFFECTIVENESS EARLY, P307 LOSCHE G, 1990, J CHILD PSYCHOL PSYC, V31, P749, DOI 10.1111/j.1469-7610.1990.tb00815.x MCCALL R, 1977, MONOGRAPHS SOC RES C, V42, P108 MUNDY P, 1986, J CHILD PSYCHOL PSYC, V27, P657, DOI 10.1111/j.1469-7610.1986.tb00190.x ORNITZ EM, 1977, J AUTISM CHILD SCHIZ, V7, P207, DOI 10.1007/BF01538999 OSTERLING J, 1999, 1999 M SOC RES CHILD OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 SIEGEL B, 1988, J DEV BEHAV PEDIATR, V9, P199 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 Stern D., 1985, INTERPERSONAL WORLD Stoel-Gammon C, 1992, PHONOLOGICAL DEV MOD, P439 STOELGAMMON C, 1984, J CHILD LANG, V11, P247 VIHMAN MM, 1986, APPL PSYCHOLINGUIST, V7, P3, DOI 10.1017/S0142716400007165 NR 20 TC 201 Z9 206 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 157 EP 162 DI 10.1023/A:1005463707029 PG 6 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000011 PM 10832780 ER PT J AU Klin, A Lang, J Cicchetti, DV Volkmar, FR AF Klin, A Lang, J Cicchetti, DV Volkmar, FR TI Brief report: Interrater reliability of clinical diagnosis and DSM-IV criteria for autistic disorder: Results of the DSM-IV autism field trial SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; INTERVIEW C1 Yale Child Study Ctr, New Haven, CT 06520 USA. RP Klin, A (reprint author), Yale Child Study Ctr, 230 S Frontage Rd, New Haven, CT 06520 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 CICCHETTI DV, 1981, AM J MENT DEF, V86, P127 CICCHETTI DV, 1981, EDUC PSYCHOL MEAS, V41, P189, DOI 10.1177/001316448104100119 COHEN J, 1960, EDUC PSYCHOL MEAS, V20, P37, DOI 10.1177/001316446002000104 Ferry D, 1998, ARION, V6, P32 Fleiss JL, 1978, APPLIED PSYCHOL MEAS, V2, P113, DOI 10.1177/014662167800200111 Fleiss JL, 1981, STAT METHODS RATES P Fombonne E, 1998, AUTISM PERVASIVE DEV, P32 GOODMAN R, 1991, J CHILD PSYCHOL PSYC, V32, P551, DOI 10.1111/j.1469-7610.1991.tb00331.x KLIN A, 1997, HDB AUTISM PERVASIVE, P411 LORD C, 1996, UNPUB AUTISM DIAGNOS Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 MATTISON R, 1979, ARCH GEN PSYCHIAT, V36, P1217 RUTTER M, 1978, J AUTISM CHILD SCHIZ, V8, P139, DOI 10.1007/BF01537863 SPITZER RL, 1990, J AM ACAD CHILD PSY, V29, P855, DOI 10.1097/00004583-199011000-00003 SPITZER RL, 1988, ARCH GEN PSYCHIAT, V45, P871 STZATMARI P, 1992, J AUTISM DEV DISORD, V22, P507 Volkmar F. R., 1997, HDB AUTISM PERVASIVE, P5 VOLKMAR FR, 1995, J AM ACAD CHILD PSY, V34, P1092, DOI 10.1097/00004583-199508000-00020 VOLKMAR FR, 1994, AM J PSYCHIAT, V151, P1361 VOLKMAR FR, 1992, J AUTISM DEV DISORD, V22, P657, DOI 10.1007/BF01046334 World Health Organisation (WHO), 1993, INT CLASS DIS NR 24 TC 86 Z9 88 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 163 EP 167 DI 10.1023/A:1005415823867 PG 5 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000012 PM 10832781 ER PT J AU Iwanaga, R Kawasaki, C Tsuchida, R AF Iwanaga, R Kawasaki, C Tsuchida, R TI Brief report: Comparison of sensory-motor and cognitive function between autism and Asperger syndrome in preschool children SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID LEARNING-DISABILITIES; CLUMSINESS C1 Ibaraki Prefectural Univ Hlth Sci, Ibaraki, Osaka, Japan. Sasesbo Ctr Child Dev, Nagasaki, Japan. Nagasaki Univ, Sch Allied Med Sci, Nagasaki 852, Japan. RP Iwanaga, R (reprint author), Ibaraki Prefectural Univ Hlth Sci, Ibaraki, Osaka, Japan. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Bonnet K, 1996, J CHILD NEUROL, V11, P483 BURGOINE E, 1983, BRIT J PSYCHIAT, V143, P261, DOI 10.1192/bjp.143.3.261 Ehlers S, 1997, J CHILD PSYCHOL PSYC, V38, P207, DOI 10.1111/j.1469-7610.1997.tb01855.x Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 Ghaziuddin M, 1996, J AUTISM DEV DISORD, V26, P585, DOI 10.1007/BF02172348 GHAZIUDDIN M, 1994, J INTELL DISABIL RES, V38, P519 GHAZIUDDIN M, 1992, J AUTISM DEV DISORD, V22, P651, DOI 10.1007/BF01046333 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P43, DOI 10.1046/j.1365-2788.1998.00065.x GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 Gillberg C, 1996, EUR CHILD ADOLES PSY, V5, P67 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x MANJIVIONA J, 1995, J AUTISM DEV DISORD, V25, P23, DOI 10.1007/BF02178165 Miyahara M, 1997, J AUTISM DEV DISORD, V27, P595, DOI 10.1023/A:1025834211548 Ramberg C, 1996, EUR J DISORDER COMM, V31, P387 SAS Institute Inc, 1988, SAS US GUID Sparrow S, 1984, VINELAND ADAPTIVE BE SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P709 TANTAM D, 1990, J AM ACAD CHILD PSY, V29, P892, DOI 10.1097/00004583-199011000-00008 Tsuchida R., 1989, JAPANESE VERSION MIL WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1993, ICD10 CLASS MENT BEH NR 24 TC 21 Z9 22 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 169 EP 174 DI 10.1023/A:1005467807937 PG 6 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000013 PM 10832782 ER PT J AU Dawson, G AF Dawson, G TI What is Childhood Disintegrative Disorder, how is it different from autism, and what is believed to be its cause? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter CR ZAIGENBAUM L, 2000, J AUTISM DEV DISORD, V30, P121 NR 1 TC 6 Z9 6 PU KLUWER ACADEMIC/PLENUM PUBL 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 2000 VL 30 IS 2 BP 177 EP 177 PG 1 WC Psychology, Developmental SC Psychology GA 315TL UT WOS:000087129000015 PM 10832784 ER PT J AU Nasr, A Roy, M AF Nasr, A Roy, M TI Association of a balanced chromosomal translocation (4;12)(q21.3; q15), affective disorder and autism SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE affective disorder; autism; balanced translocation; monozygotic twins ID BIPOLAR AFFECTIVE-DISORDER; FAMILY HISTORY; ABERRATIONS; CHILDREN; ILLNESS AB This case report describes a set of monozygotic twins with severe intellectual disability, autism and affective disorder with a balanced translocation between chromosomes 4 and 12. Their mother, who carries the same balanced translocation, had severe postnatal depression. The association between autism affective disorder and these chromosome break points has not been reported previously. The implications are discussed. C1 Heath Lane Hosp, W Bromwich B7I 2BQ, W Midlands, England. Queen Elizabeth Psychiat Hosp, Birmingham B15 2QZ, W Midlands, England. RP Roy, M (reprint author), Heath Lane Hosp, W Bromwich B7I 2BQ, W Midlands, England. CR Baysal BE, 1998, AM J MED GENET, V81, P81, DOI 10.1002/(SICI)1096-8628(19980207)81:1<81::AID-AJMG15>3.0.CO;2-S Blackwood DHR, 1996, NAT GENET, V12, P427, DOI 10.1038/ng0496-427 COLLINS FS, 1992, NAT GENET, V1, P3, DOI 10.1038/ng0492-3 CRADDOCK N, 1994, BRIT J PSYCHIAT, V164, P507, DOI 10.1192/bjp.164.4.507 DELONG GR, 1988, J AUTISM DEV DISORD, V18, P593 DeLong GR, 1998, DEV MED CHILD NEUROL, V40, P551 DELONG R, 1994, DEV MED CHILD NEUROL, V36, P674 Ewald H, 1998, PSYCHIATR GENET, V8, P131, DOI 10.1097/00041444-199800830-00002 FAHSOLD R, 1991, CLIN GENET, V40, P326 GILLBERG C, 1992, CLIN DEV MED, V126 HOLLAND T, 1990, PSYCHIAT RES, V32, P1, DOI 10.1016/0165-1781(90)90129-S LAINHART JE, 1994, J AUTISM DEV DISORD, V24, P587, DOI 10.1007/BF02172140 Lauritsen M, 1999, J CHILD PSYCHOL PSYC, V40, P335, DOI 10.1017/S0021963098003710 LOPREIATO JO, 1992, J DEV BEHAV PEDIATR, V13, P281 Overhauser J, 1998, PSYCHIATR GENET, V8, P53, DOI 10.1097/00041444-199800820-00004 Schroer RJ, 1998, AM J MED GENET, V76, P327, DOI 10.1002/(SICI)1096-8628(19980401)76:4<327::AID-AJMG8>3.0.CO;2-M STCLAIR D, 1990, LANCET, V336, P13, DOI 10.1016/0140-6736(90)91520-K Vostanis P., 1994, Psychiatric Genetics, V4, P109, DOI 10.1097/00041444-199422000-00008 NR 18 TC 2 Z9 3 PU BLACKWELL SCIENCE LTD PI OXFORD PA P O BOX 88, OSNEY MEAD, OXFORD OX2 0NE, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD APR PY 2000 VL 44 BP 170 EP 174 DI 10.1046/j.1365-2788.2000.00239.x PN 2 PG 5 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 326TH UT WOS:000087751400009 PM 10898381 ER PT J AU Riva, D AF Riva, D TI Cerebellar contribution to behaviour and cognition in children SO JOURNAL OF NEUROLINGUISTICS LA English DT Article DE cerebellum; children; higher functions; autism; developmental disorders ID POSTERIOR-FOSSA SURGERY; RHESUS-MONKEY; INFANTILE-AUTISM; PROJECTIONS; HYPOPLASIA; MUTISM; CORTEX; BRAIN; DEFICITS; ATROPHY AB Many studies have confirmed the role of the cerebellum in the organisation of superior brain functions in adults. Congenital cerebellar alterations, particularly global hypoplasia of the vermis or selective hypoplasia of some vermian lobules, are frequently observed in children with neurological diseases. These anatomical alterations are associated with neuropsychological or developmental disorders that often give rise to pictures of various degrees of mental insufficiency of varying severity with behavioural changes that may even lead to autism. Hypoplasia of the VI and VII vermian lobules are accompanied by autistic-like pictures, whereas damage to the VIII, IX and X lobules is associated with attention disturbances. Studies of normally intelligent children with acquired cerebellar lesions (mainly tumours) have made it possible to reveal different neuropsychological profiles depending on the lesioned site: lesions of the vermis are related to behavioural and verbal production disturbances, whereas those affecting the cerebellar hemispheres are associated with patterns of side-specific cognitive dysfunctions. (C) 2000 Elsevier Science Ltd. All rights reserved. C1 Inst Nazl Neurol C Besta, Div Neurol Sviluppo, I-20133 Milan, Italy. RP Riva, D (reprint author), Inst Nazl Neurol C Besta, Div Neurol Sviluppo, Via Celoria 11, I-20133 Milan, Italy. 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Neurolinguist. PD APR-JUL PY 2000 VL 13 IS 2-3 BP 215 EP 225 DI 10.1016/S0911-6044(00)00012-9 PG 11 WC Linguistics; Neurosciences; Psychology, Experimental SC Linguistics; Neurosciences & Neurology; Psychology GA 318JD UT WOS:000087279500008 ER PT J AU Schmit, J Alper, S Raschke, D Ryadak, D AF Schmit, J Alper, S Raschke, D Ryadak, D TI Effects of using a photographic cueing package during routine school transitions with a child who has autism SO MENTAL RETARDATION LA English DT Article AB Making successful transitions from one activity to another is difficult for many children, particularly those who have cognitive, language, or behavioral disabilities, Appropriately terminating one activity and initiating another in a timely fashion is a skill important for young children to learn prior to entering kindergarten. The efficacy of teaching a young child labeled as having autism to make successful transitions in daily routines in three different school settings through the use of photographic cue package was examined. A multiple baseline across-settings design was used to evaluate the efficacy of the intervention, Implications for the use of photographic cue packages in reaching a variety of activities to young children are discussed. C1 Univ No Iowa, Dept Special Educ, Educ Ctr 150A, Cedar Falls, IA 50614 USA. Univ Florida, Dept Special Educ, Gainesville, FL 32611 USA. RP Schmit, J (reprint author), POB 194, Cascade, IA 52033 USA. CR Bondy A. S., 1994, FOCUS AUTISTIC BEHAV, V9, P1, DOI DOI 10.1177/108835769400900301 Carr E. G., 1994, COMMUNICATION BASED CARTA JJ, 1987, ADV BEHAVIORAL ASSES, V3, P123 FELDMAN J, 1995, TRANSITION TIME LETS FLANNERY KB, IN PRESS J BEHAV ED HART C, 1997, SPR S AUT SOC IOW DE HART C, 1993, PARENTS GUIDE AUTISM Kazdin A. 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A., 1996, BREAKING SPEECH BARR RYAN L, 1990, MIDS C COMM DIS MEMP Ryndak DL, 1999, J ASSOC PERS SEVERE, V24, P5, DOI 10.2511/rpsd.24.1.5 SAINATO D, 1983, ASSISTING BEHAV HAND Simon EW, 1996, J AUTISM DEV DISORD, V26, P9, DOI 10.1007/BF02276232 Sparrow S, 1984, VINELAND ADAPTIVE BE Stutsman R., 1948, MERRILLPALMER SCALE TUSTIN RD, 1995, J APPL BEHAV ANAL, V28, P91, DOI 10.1901/jaba.1995.28-91 VOLKMAR FR, 1986, J AM ACAD CHILD PSY, V25, P190, DOI 10.1016/S0002-7138(09)60226-0 Volkmar FR, 1996, J AUTISM DEV DISORD, V26, P155, DOI 10.1007/BF02172003 Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 NR 24 TC 23 Z9 24 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 2000 VL 38 IS 2 BP 131 EP 137 DI 10.1352/0047-6765(2000)038<0131:EOUAPC>2.0.CO;2 PG 7 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 306VG UT WOS:000086617300005 PM 10804703 ER PT J AU Lightdale, JR Hayer, C Duer, A Lind-White, C Siegel, B Elliott, GR Heyman, MB AF Lightdale, JR Hayer, C Duer, A Lind-White, C Siegel, B Elliott, GR Heyman, MB TI Analysis of formal language testing following an open-label trial of secretin in children with autism SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Childrens Hosp, Boston, MA 02115 USA. Univ Calif San Francisco, San Francisco, CA 94143 USA. NR 0 TC 1 Z9 1 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2000 VL 47 IS 4 SU S MA 169 BP 29A EP 29A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 298TM UT WOS:000086155300170 ER PT J AU Roseman, BD Schneider, E Crimmins, D Bostwick, H Visintainer, P Dong, S Accardo, P AF Roseman, BD Schneider, E Crimmins, D Bostwick, H Visintainer, P Dong, S Accardo, P TI The use of secretion to treat autism: a pilot study SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 New York Med Coll, Valhalla, NY 10595 USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2000 VL 47 IS 4 SU S MA 2747 BP 465A EP 465A PN 2 PG 1 WC Pediatrics SC Pediatrics GA 298TM UT WOS:000086155302746 ER PT J AU Takahaslu, M Mason, W AF Takahaslu, M Mason, W TI Pervasive development disorder resembling autism occurring after recovery from Kawasaki syndrome: A report of 3 cases. SO PEDIATRIC RESEARCH LA English DT Meeting Abstract C1 Childrens Hosp Los Angeles, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU INT PEDIATRIC RESEARCH FOUNDATION, INC PI BALTIMORE PA 351 WEST CAMDEN ST, BALTIMORE, MD 21201-2436 USA SN 0031-3998 J9 PEDIATR RES JI Pediatr. Res. PD APR PY 2000 VL 47 IS 4 MA 33 BP 554 EP 554 PN 1 PG 1 WC Pediatrics SC Pediatrics GA 298QQ UT WOS:000086151000058 ER PT J AU Perlman, L AF Perlman, L TI Adults with Asperger disorder misdiagnosed as schizophrenic SO PROFESSIONAL PSYCHOLOGY-RESEARCH AND PRACTICE LA English DT Article ID CHILDREN; AUTISM AB Psychologists have a prominent role in the diagnosis and treatment of developmental disorders. With the inclusion of Asperger disorder in the DSM-IV (Diagnostic and Statistical Manual of Mental Disorders, 4th ed.; American Psychiatric Association, 1994), there is an explosion of interest in mild autistic disorders. This syndrome, which is characterized by problems in interpersonal relatedness, empathic communication, and imagination, has only recently become known in this country. Practicing psychologists may encounter adult psychiatric patients who have erroneously been diagnosed as having chronic schizophrenia when a careful examination and history would reveal that they have lifelong deficit conditions within the autistic spectrum. Opportunities are available for psychologists to contribute to the proper diagnosis and treatment of these individuals. Some case illustrations and suggestions for the role of psychologists in providing more appropriate treatment of these individuals are provided. C1 Maimonides Med Ctr, Dev Ctr, Behav Management Serv, Brooklyn, NY 11219 USA. RP Perlman, L (reprint author), 684 Broadway,Suite 9E, New York, NY 10012 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H., 1991, AUTISM ASPERGER SYND, P37, DOI 10.1017/CBO9780511526770.002 BOWMAN EP, 1988, BRIT J PSYCHIAT, V152, P377, DOI 10.1192/bjp.152.3.377 COX AD, 1991, ARCH DIS CHILD, V66, P259 Dewey M, 1991, AUTISM ASPERGER SYND, P184, DOI 10.1017/CBO9780511526770.006 Frith U., 1991, AUTISM ASPERGER SYND, P1, DOI 10.1017/CBO9780511526770.001 GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 Grandin T., 1995, THINKING PICTURES GREEN J, 1990, DEV MED CHILD NEUROL, V32, P743 Kanner L, 1943, NERV CHILD, V2, P217 KERBESHIAN J, 1990, BRIT J PSYCHIAT, V156, P721, DOI 10.1192/bjp.156.5.721 Sinclair J., 1992, HIGH FUNCTIONING IND, P294 SZATMARI P, 1990, J AM ACAD CHILD PSY, V29, P130, DOI 10.1097/00004583-199001000-00021 SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 TANTAM D, 1988, J CHILD PSYCHOL PSYC, V29, P245, DOI 10.1111/j.1469-7610.1988.tb00713.x Tantam D., 1991, AUTISM ASPERGER SYND, P147, DOI 10.1017/CBO9780511526770.005 Wing L., 1992, HIGH FUNCTIONING IND, P129 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1981, PSYCHOL MED, V11, P115 Wing Lorna, 1988, DIAGNOSIS ASSESSMENT, P91 NR 20 TC 7 Z9 7 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0735-7028 J9 PROF PSYCHOL-RES PR JI Prof. Psychol.-Res. Pract. PD APR PY 2000 VL 31 IS 2 BP 221 EP 225 DI 10.1037/0735-7028.31.2.221 PG 5 WC Psychology, Multidisciplinary SC Psychology GA 368YN UT WOS:000090145200016 ER PT J AU Kobayashi, R AF Kobayashi, R TI Affective communication of infants with autistic spectrum disorder and internal representation of their mothers SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE affective communication; approach-avoidance motivational conflict; autistic spectrum disorder; internal representation; relationship disturbance ID ATTACHMENT; CHILDREN AB We have been examining the developmental process of affective communication in infants with autistic spectrum disorders from the viewpoint of relationship disturbance through our developmental and psychopathological studies on autism. In particular, the role of internal representation of the mother in the process of development of affective communication is discussed through the presentation of two cases diagnosed as autistic spectrum disorder in early infancy. In these cases, we postulate approach-avoidance motivational conflict as the primary factor impeding development of affective communication, focusing therapeutic intervention on this perspective. As a result, attachment behavior was remarkably improved in the children, but affective communication with their mothers was not readily improved. Taking up the mothers' own internal representation in mother-infant psychotherapy, in particular, the mothers' problems in attachment behavior with their own mothers in infancy precipitated transition in the mothers' internal representation of their children, leading to active evolution in mother-child interaction and development in affective communication between mother and child. In this context, the basis and significance of internal representation of both parties being determinants in the quality of mother-child communication are discussed. C1 Tokai Univ, Sch Hlth Sci, Dept Social Work, Kanagawa 2591193, Japan. RP Kobayashi, R (reprint author), Tokai Univ, Sch Hlth Sci, Dept Social Work, Kanagawa 2591193, Japan. CR BARONCOHEN S, 1988, J AUTISM DEV DISORD, V18, P379, DOI 10.1007/BF02212194 BEMPORAD JR, 1979, J AUTISM DEV DISORD, V9, P179, DOI 10.1007/BF01531533 Dawson G, 1989, AUTISM NATURE DIAGNO Dissanayake C, 1996, J CHILD PSYCHOL PSYC, V37, P149, DOI 10.1111/j.1469-7610.1996.tb01386.x Frith U., 1989, AUTISM EXPLAINING EN Hobson R. Peter, 1989, AUTISM NATURE DIAGNO, P22 HOBSON RP, 1992, HIGH FUNCTIONING IND, P157 Kanner L, 1943, NERV CHILD, V2, P217 KOBAYASHI R, 1995, JPN J CHILD ADOLESC, V36, P205 Kobayashi R, 1996, J AUTISM DEV DISORD, V26, P661, DOI 10.1007/BF02172355 Kobayashi R, 1999, PSYCHIAT CLIN NEUROS, V53, P549, DOI 10.1046/j.1440-1819.1999.00604.x Kobayashi R, 1998, PSYCHIAT CLIN NEUROS, V52, P611 KOBAYASHI R, 1993, JPN J NEUROPSYCHOPH, V15, P773 KUJIRAOKA T, 1997, SOME FEATURES PRIMIT LEBOVICI S, 1983, NOURRISON MERE PSYCH MAIN M, 1985, MONOGR SOC RES CHILD, V50, P66, DOI 10.2307/3333827 Mundy P., 1989, DEV PSYCHOPATHOL, V1, P173, DOI 10.1017/S0954579400000365 Newson J., 1978, ACTION GESTURE SYMBO, P31 RICHER JM, 1992, 5 C WORLD ASS INF ME RICHER JM, 1993, EARLY CHILD DEV CARE, V96, P7, DOI 10.1080/0300443930960102 ROGERS SJ, 1991, J AM ACAD CHILD PSY, V30, P483, DOI 10.1097/00004583-199105000-00021 Sameroff A. J., 1989, RELATIONSHIP DISTURB SHAPIRO T, 1987, J AM ACAD CHILD PSY, V26, P480, DOI 10.1097/00004583-198707000-00003 SIGMAN M, 1989, J AM ACAD CHILD PSY, V28, P74, DOI 10.1097/00004583-198901000-00014 SIGMAN M, 1984, J AUTISM DEV DISORD, V14, P231, DOI 10.1007/BF02409576 Stern D., 1985, INTERPERSONAL WORLD SZATMARI P, 1992, J AUTISM DEV DISORD, V22, P583, DOI 10.1007/BF01046329 Werner H., 1948, COMP PSYCHOL MENTAL Williams D., 1992, NOBODY NOWHERE NR 29 TC 2 Z9 2 PU BLACKWELL SCIENCE ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 1323-1316 J9 PSYCHIAT CLIN NEUROS JI Psychiatry Clin. Neurosci. PD APR PY 2000 VL 54 IS 2 BP 235 EP 243 DI 10.1046/j.1440-1819.2000.00664.x PG 9 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 301AR UT WOS:000086286400018 PM 10803821 ER PT J AU Page, T Coleman, M AF Page, T Coleman, M TI Purine metabolism abnormalities in a hyperuricosuric subclass of autism SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE LA English DT Article DE autism; hyperuricosuria; purine metabolism; uric acid AB A subclass of patients with classic infantile autism have uric acid excretion which is >2 S.D.s above the normal mean. These hyperuricosuric autistic individuals may comprise approx. 20% of the autistic population. In order to determine the metabolic basis for urate overexcretion in these patients, de novo purine synthesis was measured in the cultured skin fibroblasts of these patients by quantification of the radiolabeled purine compounds produced by incubation with radiolabeled sodium formate. For comparison, de novo purine synthesis in normal controls, in normouricosuric autistic patients, and cells from patients with other disorders in which excessive uric acid excretion is seen was also measured. These experiments showed that de novo purine synthesis is increased approx. 4-fold in the hyperuricosuric autistic patients. This increase was less than that found in other hyperuricosuric disorders. No unusual radiolabeled compounds (such as adenylosuccinate) were detected in these experiments, and no gross deficiencies of radiolabeled nucleotides were seen. However, the ratio of adenine to guanine nucleotides produced by de novo synthesis was found to be lower in the cells of the hyperuricosuric autistic patients than in the normal controls or the cells from patients with other disorders. These results indicate that the hyperuricosuric subclass of autistic patients have increased de novo purine synthesis, and that the increase is approximately that expected for the degree of urate overexcretion when compared to other hyperuricosuric disorders. No particular enzyme defect was suggested by either gross deficiency of a radiolabeled compound or the appearance of an unusual radiolabeled compound, and no potentially neurotoxic metabolites were seen. Although an enzyme defect responsible for the accelerated purine synthesis was not identified, the abnormal ratio of adenine to guanine nucleotides suggests a defect in purine nucleotide interconversion, (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. Georgetown Univ, Sch Med, Dept Med, Washington, DC 20008 USA. RP Page, T (reprint author), Univ Calif San Diego, Sch Med, Dept Neurosci, 9500 Gilman Dr, La Jolla, CA 92093 USA. 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Biophys. Acta-Mol. Basis Dis. PD MAR 17 PY 2000 VL 1500 IS 3 BP 291 EP 296 DI 10.1016/S0925-4439(99)00113-1 PG 6 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 293NY UT WOS:000085860100004 PM 10699370 ER PT J AU Salerno, C Siems, WG Crifo, C AF Salerno, C Siems, WG Crifo, C TI Succinylpurinemic autism: increased sensitivity of defective adenylosuccinate lyase towards 4-hydroxy-2-nonenal SO BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE LA English DT Article DE adenylosuccinate lyase; 4-hydroxy-2-nonenal; psychomotor retardation; lipid peroxidation; inherited diseases ID LIPID-PEROXIDATION PRODUCT; ISOLATED RAT HEPATOCYTES; ACTIVE-SITE; 2-<(4-BROMO-2,3-DIOXOBUTYL)THIO>ADENOSINE 5'-MONOPHOSPHATE; SMALL-INTESTINE; DEFICIENCY; LIVER; IDENTIFICATION; GLUCOSE-6-PHOSPHATE-DEHYDROGENASE; ACCUMULATION AB We studied the effect of trans-4-hydroxy-2-nonenal on the wild-type human adenylosuccinate lyase and on the enzyme from a patient compound-heterozygous for two missense mutations (P75A/D397Y; McKusick 103050.0003/103050.0004). Both the enzymes were inhibited by 10-50 mu M trans-4-hydroxy-2-nonenal in a concentration-dependent manner by means of a mixed-type co-operative mechanism. A significantly stronger inhibition was noticed in the presence of the defective enzyme. Nonanal and trans-2,3-nonenal inhibited the enzymes to a less extent and at about 10-times higher concentrations. Hydroxylamine reversed the inhibition by ti ans-4-hydroxy-2-nonenal, trans-2,3-nonenal or nonanal in the case of the wild type enzyme, but it was ineffective to reverse the inhibition by trans-4-hydroxy-2-nonenal on the defective enzyme. Dithiothreitol slightly decreased the inhibition exerted by transs-4-hydroxy-2-nonenal on both the wild-type and the defective adenylosuccinate lyase, while it did not produce practically any change in the presence of trans-2,3-nonenal or nonanal. (C) 2000 Published by Elsevier Science B.V. All rights reserved. C1 Univ Rome La Sapienza, Dept Biochem Sci, I-00185 Rome, Italy. Univ Rome La Sapienza, Clin Biochem Lab, I-00185 Rome, Italy. Herzog Julius Hosp Rheumatol & Orthoped, D-38655 Bad Harzburg, Germany. RP Salerno, C (reprint author), Univ Rome La Sapienza, Dept Biochem Sci, Piazzale Aldo Moro 5, I-00185 Rome, Italy. 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Biophys. Acta-Mol. Basis Dis. PD MAR 17 PY 2000 VL 1500 IS 3 BP 335 EP 341 DI 10.1016/S0925-4439(99)00117-9 PG 7 WC Biochemistry & Molecular Biology; Biophysics; Cell Biology SC Biochemistry & Molecular Biology; Biophysics; Cell Biology GA 293NY UT WOS:000085860100009 PM 10699375 ER PT J AU De Gaulejac, F Roge, B AF De Gaulejac, F Roge, B TI Object permanence and familiarity in autistic children. SO A N A E-APPROCHE NEUROPSYCHOLOGIQUE DES APPRENTISSAGES CHEZ L ENFANT LA French DT Article DE autism; child; object performance; familiarity; novelty AB The problem of relationships between autistic children and object has suggested a lot of researches since several decades, most of them been centrered on the description of specific behaviours related to objects or on the presence of object permanence. In this case, the examination of the conflicting results shows that the problem has yet a important theoretical and an epistemological interest that requires an detailed investigation of the cognitive relationships between infant and object. The aim of the present study is to analyse an autistic characteristic of the object permanence: the familiarity with the test-objects. This taking into account of the infant's subjectivity, and not only of the physical characteristics of the object, leads the observer to move off centre with regard to his own experience of the world of objects. C1 Univ Toulouse 2, CERPP, F-31058 Toulouse, France. CR Adrien J. 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Enfant PD MAR PY 2000 VL 12 IS 1 BP 21 EP 26 PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 356AQ UT WOS:000089421100005 ER PT J AU Sandman, CA Hetrick, W Taylor, DV Marion, SD Touchette, P Barron, JL Martinezzi, V Steinberg, RM AF Sandman, CA Hetrick, W Taylor, DV Marion, SD Touchette, P Barron, JL Martinezzi, V Steinberg, RM TI Long-term effects of naltrexone on self-injurious behavior SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID MENTALLY-RETARDED CLIENTS; OPIOID DEPENDENCE; SENSORY NEURONS; DOUBLE-BLIND; MORPHINE; NALOXONE; TOLERANCE; RECEPTORS; AUTISM; SYSTEM AB A subgroup of self-injuring patients responds positively to the opiate-blocking agent naltrexone in acute, double-blind studies. In this study we examined the effects of naltrexone after acute treatment and the long-term effects of naltrexone on SIE. Rates of SIE were collected from pretreatment baseline; a second baseline a year after the acute trial; and a subsequent 12-month double-blind, placebo-controlled treatment. A subgroup of patients decreased SIE for a year without treatment after acute exposure to naltrexone. Five participants who decreased SIE by 70% after acute treatment increased SIE to the long-term treatment with naltrexone. In contrast, those for whom SIE increased over the one-year treatment hiatus decreased their SIE after the first long-term treatment. Discussion of these complex effects considered the role of background opioid levels, dosing, and treatment regimen of naltrexone and other factors limiting receptor adaptation among patients who exhibit SIE. C1 Univ Calif Irvine, Irvine, CA 92717 USA. Indiana Univ, Bloomington, IN 47405 USA. Fairview Dev Ctr, Costa Mesa, CA USA. RP Sandman, CA (reprint author), 2501 Harbor Blvd 5A, Costa Mesa, CA 92626 USA. 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J. Ment. Retard. PD MAR PY 2000 VL 105 IS 2 BP 103 EP 117 DI 10.1352/0895-8017(2000)105<0103:LEONOS>2.0.CO;2 PG 15 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 295MU UT WOS:000085972200003 PM 10755174 ER PT J AU Mudford, OC Cross, BA Breen, S Cullen, C Reeves, D Gould, J Douglas, J AF Mudford, OC Cross, BA Breen, S Cullen, C Reeves, D Gould, J Douglas, J TI Auditory integration training for children with autism: No behavioral benefits detected. SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article AB Auditory integration training and a control treatment were provided for 16 children with autism in a crossover experimental design. Measures, blind to treatment order, included parent and teacher ratings of behavior, direct observational recordings, IQ, language, and social/adaptive tests. Significant differences tended to show that the control condition was superior on parent-rated measures of hyperactivity and on direct observational measures of ear-occlusion. No differences were detected on teacher-rated measures. Children's IQs and language comprehension did not increase, but adaptive/social behavior scores and expressive language quotients decreased. The majority of parents (56%) were unable to report in retrospect when their child had received auditory integration training. No individual child was identified as benefiting clinically or educationally from the treatment. C1 Univ Keele, Keele ST5 5BG, Staffs, England. Univ Manchester, Manchester, Lancs, England. Ctr Social & Commun Disorders, Bromley, England. RP Mudford, OC (reprint author), Univ Keele, Keele ST5 5BG, Staffs, England. 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PD MAR PY 2000 VL 105 IS 2 BP 118 EP 129 DI 10.1352/0895-8017(2000)105<0118:AITFCW>2.0.CO;2 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 295MU UT WOS:000085972200004 PM 10755175 ER PT J AU Skuse, DH AF Skuse, DH TI Behavioural phenotypes: what do they teach us? SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID TURNER-SYNDROME; CHROMOSOME; DELETIONS; ISSUES; AUTISM C1 Inst Child Hlth, Behav Sci Unit, London WC1N 1EH, England. RP Skuse, DH (reprint author), Inst Child Hlth, Behav Sci Unit, 30 Guilford St, London WC1N 1EH, England. CR Achenbach T. 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Dis. Child. PD MAR PY 2000 VL 82 IS 3 BP 222 EP 225 DI 10.1136/adc.82.3.222 PG 4 WC Pediatrics SC Pediatrics GA 291CN UT WOS:000085716300013 PM 10685925 ER PT J AU Pillion, JP Rawool, VW Naidu, S AF Pillion, JP Rawool, VW Naidu, S TI Auditory brainstem responses in Rett syndrome: Effects of hyperventilation, seizures, and tympanometric variables SO AUDIOLOGY LA English DT Article; Proceedings Paper CT 21st Midwinter Meeting of the Association-for-Research-in-Otolaryngology CY FEB 15-19, 1998 CL ST PETERSBURG, FLORIDA SP Assoc Res Otolaryngol DE auditory brainstem response; hyperventilation; middle ear; Rett syndrome; seizures; tympanometry ID EVOKED-POTENTIALS; AUTISM AB This study examined the effects of tympanometric variables, stage of disease, hyperventilation, and seizures on the auditory brainstem response (ABR) in Rett syndrome (RS). Thirty-four female children with RS ranging in age from 2 years, 3 months to 15 years, 7 months participated in the study. ABRs and tympanograms were recorded from all of the subjects. When the ABR peaks were identifiable, interpeak latency intervals (IPLIs) for I-III, III-V, and I-V were computed for each waveform. The peaks (I, III, and V) and IPLIs were characterized as abnormal if either the peaks were absent or the latencies were greater than 2 SD from the normative data (obtained on female children). Analyses revealed significant prolongation of wave I latencies in Rett children with abnormal tympanograms. ABR wave III latencies were significantly affected by the presence of seizures and hyperventilation. The Pearson chi-square statistic revealed significant differences in the rate of wave III and V abnormalities due to the presence and degree of hyperventilation and the presence of seizures. Wave I abnormalities were also observed in the presence of normal middle ear function, suggesting the presence of sensorineural hearing impairment in some RS children. Clinical implications of these findings are discussed. C1 Kennedy Krieger Inst, Dept Audiol, Baltimore, MD 21205 USA. Bloomsburg Univ Penn, Dept Speech Pathol & Audiol, Bloomsburg, PA 17815 USA. RP Pillion, JP (reprint author), Kennedy Krieger Inst, Dept Audiol, 707 N Broadway, Baltimore, MD 21205 USA. CR ADLER G, 1991, EUR ARCH PSY CLIN N, V240, P367, DOI 10.1007/BF02279768 American Speech-Language-Hearing Association, 1997, GUID AUD SCREEN Amir RE, 1999, NAT GENET, V23, P185 BADER GG, 1989, BRAIN DEV-JPN, V11, P102 Blake R, 1991, LANG SPEECH HEAR SER, V22, P111 BUDDEN S, 1990, DEV MED CHILD NEUROL, V32, P51 CHAN YW, 1990, ELECTROEN CLIN NEURO, V77, P119, DOI 10.1016/0168-5597(90)90025-9 Clarke A, 1996, J MED GENET, V33, P693, DOI 10.1136/jmg.33.8.693 FEAGANS L, 1986, OTITIS MEDIA CHILD D, P192 Flexer C., 1990, LANG SPEECH HEAR SER, V21, P177 GLAZE DG, 1985, ANN NEUROL, V18, P417 GREEN JB, 1982, NEUROLOGY, V32, P85 HAGBERG B, 1992, BRAIN DEV, V14, P5 HAGBERG B, 1986, AM J MED GENET, V24, P47 HAGBERG B, 1983, ANN NEUROL, V14, P471, DOI 10.1002/ana.410140412 Hood L.J., 1986, AUDITORY EVOKED POTE KALMANCHEY R, 1990, BRAIN DEV-JPN, V12, P73 KIMURA K, 1992, BRAIN DEV S, V12, pS37 Lenn N J, 1986, Am J Med Genet Suppl, V1, P153 Nicholas S, 1999, J Am Acad Audiol, V10, P436 NOMURA Y, 1984, BRAIN DEV-JPN, V6, P475 OLSSON B, 1990, BRAIN DEV-JPN, V12, P11 PELSON RO, 1987, BRAIN DEV-JPN, V9, P514 PERCY AK, 1985, BRAIN DEV-JPN, V7, P300 PERCY AK, 1993, J CHILD NEUROL, V8, P659 Rawool VW, 1996, SCAND AUDIOL, V25, P239, DOI 10.3109/01050399609074961 REISS AL, 1993, ANN NEUROL, V34, P227, DOI 10.1002/ana.410340220 REIVICH RS, 1972, J SPEECH HEAR RES, V15, P93 RETT A, 1992, BRAIN DEV S, V14, P141 ROLANDO S, 1985, BRAIN DEV-JPN, V7, P290 SANDERS JW, 1974, ARCH OTOLARYNGOL, V100, P283 SAUNDERS KJ, 1995, DEV MED CHILD NEUROL, V37, P496 SCHULTZ RJ, 1993, AM J DIS CHILD, V147, P633 SILVA PA, 1982, J LEARN DISABIL, V15, P417 SNYDERMAN NL, 1982, ANN OTO RHINOL LARYN, V91, P597 Stach B A, 1994, J Am Acad Audiol, V5, P226 STOCKARD JJ, 1980, ELECTROEN CLIN NEURO, V56, P167 TETZCHNER S, 1996, DEV MED CHILD NEUROL, V38, P212 TREVATHAN E, 1988, J CHILD NEUROL S, V3, P6 VERMA NP, 1987, ELECTROEN CLIN NEURO, V67, P327, DOI 10.1016/0013-4694(87)90118-0 WU XR, 1988, PEDIATR NEUROL, V4, P126, DOI 10.1016/0887-8994(88)90056-2 ZOGHBI HY, 1985, NEW ENGL J MED, V313, P921, DOI 10.1056/NEJM198510103131504 NR 42 TC 4 Z9 4 PU DECKER PERIODICALS INC PI HAMILTON PA 4 HUGHSON STREET SOUTH PO BOX 620, LCD 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0020-6091 J9 AUDIOLOGY JI Audiology PD MAR-APR PY 2000 VL 39 IS 2 BP 80 EP 87 PG 8 WC Otorhinolaryngology SC Otorhinolaryngology GA 320DY UT WOS:000087387600003 PM 10882046 ER PT J AU Elia, M Ferri, R Musumeci, SA Del Gracco, S Bottitta, M Scuderi, C Miano, G Panerai, S Bertrand, T Grubar, JC AF Elia, M Ferri, R Musumeci, SA Del Gracco, S Bottitta, M Scuderi, C Miano, G Panerai, S Bertrand, T Grubar, JC TI Sleep in subjects with autistic disorder: a neurophysiological and psychological study SO BRAIN & DEVELOPMENT LA English DT Article DE sleep; autistic disorder; rapid eye movements; twitches; psychoeducational profile-revised test; Childhood Autism Rating Scale ID BUTOCTAMIDE HYDROGEN SUCCINATE; REM-SLEEP; BEHAVIOR; WAKING AB Polysomnography (EOG, EEG, EMG) was carried out in 17 male children and adolescents with autistic disorder, in seven patients with mental retardation and fragile X syndrome, and in five age- and sex-matched normal male subjects. Density of rapid eye movements was not significantly different in the three groups of subjects; however, some sleep parameters such as time in bed, sleep period lime, and total sleep time were significantly lower in subjects with autistic disorder than in normal controls; moreover, patients with autistic disorder showed values of sleep period time, first REM latency and percent (Cc) sleep stage 1 lower than those of patients with fragile X syndrome with mental retardation. Density of muscle twitches was significantly higher in patients with autistic disorder than in normal controls. In contrast only minor differences were observed between patients with autistic disorder and those with fragile X syndrome with mental retardation. Furthermore, some psychoeducational profile-revised items such as perception and eye-hand coordination, showed significant correlation with some sleep parameters (time in bed, sleep latency, stage shifts, first REM latency and wakefulness after sleep onset). Childhood Autism Rating Scale (CARS) scores to visual response and non-verbal communication showed significant correlation with some tonic steep parameters, such as sleep period time, wakefulness after sleep onset, and total sleep time. Relating to people and activity level items were found to be significantly correlated with rapid eye movement density. Our results suggest the existence of a sleep pattern in autistic patients different from that observed in subjects with mental retardation and from that of normal controls. In addition, these findings indicate that sleep parameters in these patients are correlated with some psychological indices generally used for the diagnosis of autistic disorder; for this reason, polysomnographies might be useful in the comprehension of the neurophysiological mechanisms underlying this condition. (C) 2000 Elsevier Science B.V. All rights reserved. C1 IRCCS, Oasi Inst Res Mental Retardat & Brain Aging, Dept Neurol, I-94018 Troina, Italy. IRCCS, Oasi Inst Res Mental Retardat & Brain Aging, Sleep Res Ctr, I-94018 Troina, Italy. IRCCS, Oasi Inst Res Mental Retardat & Brain Aging, Dept Psychol, I-94018 Troina, Italy. Univ C De Gaulle, Dept Carrieres Sociales, IUT B, Tourcoing, France. RP Elia, M (reprint author), IRCCS, Oasi Inst Res Mental Retardat & Brain Aging, Dept Neurol, Via Conte Ruggero 73, I-94018 Troina, Italy. RI Ferri, Raffaele/B-5439-2013 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CASTALDO V, 1974, BIOL PSYCHIAT, V9, P231 CASTALDO V, 1973, J MENT DEFIC RES, V17, P231 COOK EH, 1990, SYNAPSE, V6, P292, DOI 10.1002/syn.890060309 DELONG R, 1994, DEV MED CHILD NEUROL, V36, P674 FEINBERG I, 1969, ELECTROEN CLIN NEURO, V27, P128, DOI 10.1016/0013-4694(69)90165-5 GEISLER P, 1987, ELECTROEN CLIN NEURO, V67, P499, DOI 10.1016/0013-4694(87)90051-4 GIGLI GL, 1995, PSYCHOPHARMACOLOGY, V117, P438, DOI 10.1007/BF02246216 GIGLI GL, 1987, SLEEP, V10, P563 Grubar J C, 1983, Rev Electroencephalogr Neurophysiol Clin, V13, P107, DOI 10.1016/S0370-4475(83)80068-9 HARTMAN EL, 1976, MECH SLEEP HASHIMOTO T, 1981, BRAIN DEV-JPN, V3, P31 HAURI P, 1971, ARCH GEN PSYCHIAT, V25, P56 Jackson J., 1932, SELECTED WRITINGS J KOHYAMA J, 1994, BRAIN DEV-JPN, V16, P81, DOI 10.1016/0387-7604(94)90040-X LAPIERRE O, 1992, NEUROLOGY, V42, P1371 MCGRATH MJ, 1978, PSYCHOL BULL, V85, P24, DOI 10.1037/0033-2909.85.1.24 MIRMIRAN M, 1982, BRAIN RES, V233, P287, DOI 10.1016/0006-8993(82)91203-3 Musumeci SA, 1995, DEV BRAIN DYSFUNCT, V8, P218 Ornitz E., 1988, BRAIN DYSFUNCT, V1, P309 ORNITZ EM, 1969, ELECTROEN CLIN NEURO, V26, P167, DOI 10.1016/0013-4694(69)90207-7 PETREQUA.O, 1966, J NEUROL SCI, V3, P608, DOI 10.1016/0022-510X(66)90049-9 Petre-Quadens O, 1969, Acta Neurol Psychiatr Belg, V69, P769 PETREQUADENS O, 1980, TOTUS HOMO, V12, P14 Rechtschaffen A., 1968, NIH PUBLICATION, P204 Richter A, 1999, NEUROSCIENCE, V89, P461, DOI 10.1016/S0306-4522(98)00321-2 SAKAI K, 1984, SLEEP MECH EXPT BR S, V8, P3 Schopler E., 1990, INDIVIDUALIZED ASSES, VI SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SEGAWA M, 1993, HEREDITARY PROGR DYS SEGAWA M, 1990, BRAIN DEV-JPN, V12, P55 Siegel S., 1956, NONPARAMETRIC STAT B SPREUX F, 1982, CAHIERS PSYCHOL COGN, V2, P327 Stock G, 1982, SLEEP CLIN EXPT ASPE, P1 TACHIBANA N, 1991, BIOL PSYCHIAT, V30, P4, DOI 10.1016/0006-3223(91)90065-T TANGUAY PE, 1976, J AUTISM CHILD SCHIZ, V6, P275, DOI 10.1007/BF01543468 YOUNG JG, 1982, J AUTISM DEV DISORD, V12, P147, DOI 10.1007/BF01531305 NR 37 TC 75 Z9 77 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0387-7604 J9 BRAIN DEV-JPN JI Brain Dev. PD MAR PY 2000 VL 22 IS 2 BP 88 EP 92 DI 10.1016/S0387-7604(99)00119-9 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 302DB UT WOS:000086349200003 PM 10722958 ER PT J AU Rossi, PG Posar, A Parmeggiani, A AF Rossi, PG Posar, A Parmeggiani, A TI Epilepsy in adolescents and young adults with autistic disorder SO BRAIN & DEVELOPMENT LA English DT Article DE epilepsy; adolescence; autistic disorder; pervasive developmental disorders; mental retardation; EEG paroxysmal abnormalities ID PSYCHIATRIC-DISORDERS; MENTAL-RETARDATION; INFANTILE-AUTISM; FOLLOW-UP; CHILDREN; PUBERTY AB Since the first description by Kanner (1943) the association between autistic disorder (AD) and epilepsy has been observed in 4-42% of patients. Some authors reported that seizures prevailed in adolescence but a systematic investigation has never been undertaken. We examined retrospectively 60 patients divided into two groups (with and without epilepsy and EEG paroxysmal abnormalities) with AD unrelated to a congenital or acquired encephalopathy (mean age 17 years 2 months). The aim was to investigate epilepsy, EEG paroxysmal abnormalities and possible etiological factors. The prevalence of epilepsy was 38.3%, much higher than that in a normal population of a similar age (6.6 parts per thousand), The prevalence of EEG paroxysmal abnormalities without epilepsy was 6.7%, higher than that in a population of adolescents and adults with psychiatric pathologies (2.6%). Seizure onset was after age 12 years in 66.7% of cases. The most common type of epilepsy was partial in 65.2% and four patients (17.4%) had a benign childhood epilepsy with centro-temporal spikes. Al the last observation 44.4% of patients had been seizure-free for 2 years or more. There were no organic factors influencing the development of epilepsy but familial and personal antecedents, mental retardation and CT scan/MRI data may suggest an early brain dysfunction responsible for AD and epilepsy. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Univ Bologna, Inst Neurol, Dept Child Neurol & Psychiat, I-40123 Bologna, Italy. RP Rossi, PG (reprint author), Univ Bologna, Inst Neurol, Dept Child Neurol & Psychiat, Via Ugo Foscolo 7, I-40123 Bologna, Italy. 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PD MAR PY 2000 VL 22 IS 2 BP 102 EP 106 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 302DB UT WOS:000086349200006 ER PT J AU Bauminger, N Kasari, C AF Bauminger, N Kasari, C TI Loneliness and friendship in high-functioning children with autism SO CHILD DEVELOPMENT LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; MENTAL-RETARDATION; EXECUTIVE FUNCTION; INFANTILE-AUTISM; SEX-DIFFERENCES; MIND; SCHOOL; COMMUNICATION; ADOLESCENCE AB Loneliness and friendship were examined in 22 high-functioning children with autism and 19 typically developing children equated with the autistic children for IQ, CA, gender, mother's education, and ethnicity. Children between the ages of 8 and 14 were asked to report on both their understanding and feelings of loneliness and the quality of their friendship. Compared to typically developing children, children with autism were both lonelier and had less complete understandings of loneliness. Although all children with autism reported having at least one friend, the quality of their friendships was poorer in terms of companionship, security, and help. Fewer associations were found between loneliness and friendship for the autistic than for the non-autistic children, suggesting less understanding of the relation between loneliness and friendship. Implications of these results are discussed for conceptualizing the social deficits in autism. C1 Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. Univ Calif Los Angeles, Los Angeles, CA USA. RP Bauminger, N (reprint author), Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. CR ALGINA J, 1978, PSYCHOL BULL, V85, P133 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asher S. 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S, 1973, LONELINESS EXPERIENC Weiss RS, 1974, DOING OTHERS WILLIAMS GA, 1992, AM J MENT RETARD, V96, P373 WING L, 1981, PSYCHIAT RES, V5, P129, DOI 10.1016/0165-1781(81)90043-3 World Health Organization, 1990, INT CLASS DIS, V10th Yirmiya N, 1996, J CHILD PSYCHOL PSYC, V37, P1003, DOI 10.1111/j.1469-7610.1996.tb01497.x NR 57 TC 191 Z9 193 PU BLACKWELL PUBLISHERS PI MALDEN PA 350 MAIN STREET, STE 6, MALDEN, MA 02148 USA SN 0009-3920 J9 CHILD DEV JI Child Dev. PD MAR-APR PY 2000 VL 71 IS 2 BP 447 EP 456 DI 10.1111/1467-8624.00156 PG 10 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 307ZJ UT WOS:000086683800014 PM 10834476 ER PT J AU Leekam, SR Lopez, B Moore, C AF Leekam, SR Lopez, B Moore, C TI Attention and joint attention in preschool children with autism SO DEVELOPMENTAL PSYCHOLOGY LA English DT Article; Proceedings Paper CT 15th Biennial Meeting of the International-Society-for-the-Study-of-Behavioral-Development CY JUL, 1998 CL BERN, SWITZERLAND SP Int Soc Study Behav Dev ID VISUAL-ATTENTION; INFANTS; INFORMATION; DEFICITS; TARGETS; ORIGINS; STIMULI; PEOPLE; SHIFTS AB Three experiments examined the role of attention in explaining dyadic (child-adult) and triadic (child-adult-object) joint attention difficulties in autism. Experiments 1 and 2 investigated children's ability to orient to an adult's attention bid and to follow the direction of a human or nonhuman cue. Experiment 3 tested ability to disengage and shift attention to objects. Results showed autism-specific difficulties at both dyadic and triadic levels. Children with autism were less responsive than developmentally delayed controls in orienting to attention bids and in following a human head-turn cue yet had no difficulty in shifting attention and were faster overall in orienting to targets. Results suggest a specific developmental delay in which children with autism rely on the presence of objects in the visual field to guide action. The relation between this problem and autistic children's difficulties with human communicative signals is discussed. C1 Univ Canterbury, Dept Psychol, Canterbury, Kent, England. Dalhousie Univ, Dept Psychol, Halifax, NS, Canada. RP Leekam, SR (reprint author), Univ Durham, Sci Labs, Dept Psychol, South Rd, Durham DH1 3LE, England. 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Psychol. PD MAR PY 2000 VL 36 IS 2 BP 261 EP 273 DI 10.1037/0012-1649.36.2.261 PG 13 WC Psychology, Developmental SC Psychology GA 324TD UT WOS:000087636700012 PM 10749083 ER PT J AU [Anonymous] AF [Anonymous] TI Repligen initiates largest-ever study in autism SO DRUG NEWS & PERSPECTIVES LA English DT News Item NR 0 TC 0 Z9 0 PU PROUS SCIENCE, SA PI BARCELONA PA PO BOX 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 0214-0934 J9 DRUG NEWS PERSPECT JI Drug News Perspect. PD MAR PY 2000 VL 13 IS 2 BP 116 EP 116 PG 1 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 322WR UT WOS:000087532700021 ER PT J AU Zakian, A Malvy, J Desombre, H Roux, S Lenoir, P AF Zakian, A Malvy, J Desombre, H Roux, S Lenoir, P TI Early signs of autism: a new study of family home movies SO ENCEPHALE-REVUE DE PSYCHIATRIE CLINIQUE BIOLOGIQUE ET THERAPEUTIQUE LA French DT Article DE autism; child; early diagnosis; family home video ID PERVASIVE DEVELOPMENTAL DISORDERS; EARLY RECOGNITION; YOUNG-CHILDREN; RELIABILITY; SYMPTOMS AB Since the initial individualization of infantile autism by Kanner, subsequent work has attempted to define the age at wich disorders appear, their symptomatology and their specificity. Initially, retrospective studies based on questionnaires and interviews with parents were conducted in order to determine the age of at which the first signs appeared. Combined with interviews, clinical observations have provided incontestable aid for describing the early signs of autism. The study of home movies taken by parents before their infant's disorders were recognized has led to a new approach to the initials signs of autism. Our study is a continuation of work in our Child Psychiatry Unit under way since 1984. The aim of this work is the symptomatological and comparative analysis of home movies of 14 autistic and 10 normal infants, during the first two years of their life. Each film was scored for the 0-8, 9-17 and 18-24 month periods. Based on the use of the Infant Behavioral Summarized Evaluation (IBSE), this study confirms prior data and also shows the emergence of very early disorders, perceptible within the first few months even by blind evaluators : a docile baby, showing no overt manifestations, not seeking contact, with an absence of pre-language. 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Psychiatr. Clin. Biol. Ther. PD MAR-APR PY 2000 VL 26 IS 2 BP 38 EP 44 PG 7 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 319FP UT WOS:000087331100007 PM 10858914 ER PT J AU Bonde, E AF Bonde, E TI Comorbidity and subgroups in childhood autism SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE social subgroups; childhood autism ID ATTENTIONAL DEFICITS; CHILDREN; DISORDERS; CLASSIFICATION; QUESTIONNAIRE; VALIDITY; MOTOR AB The objective of this study was to identify clinical subgroups in children with childhood autism and to examine comorbidity in each subgroup. The study was based on medical records of 30 inpatients referred to a specialist ward for children with pervasive developmental disorders. Eighteen consecutive patients with an IQ above 50 and fulfilling research criteria for childhood autism were grouped in accordance with the Wing's social subgroups of autism (aloof, passive, and active but odd). Comorbidity, in terms of deficits in attention, motor control, visuo-motor and visuo-spatial function, as well as epilepsy, was described in each of the three groups. The aloof and passive groups produced a pure autistic triad of deficits, while the active but odd group was characterized by strong comorbidity. RP Bonde, E (reprint author), Hojtoftevej 20, DK-8240 Risskov, Denmark. 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Child Adolesc. Psych. PD MAR PY 2000 VL 9 IS 1 BP 7 EP 10 PG 4 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 305WD UT WOS:000086562800002 PM 10795850 ER PT J AU Lingarde, B Jonsson, SAT Luts, A Brun, A AF Lingarde, B Jonsson, SAT Luts, A Brun, A TI Cerebellar abnormalities in mental illness. A study on Purkinje cell density in schizophrenic men SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE schizophrenia; autism; cerebellum; vermis; Purkinje cell density; hippocampal abnormalities ID CEREBRAL BLOOD-FLOW; AUTISM; INVOLVEMENT; HIPPOCAMPUS; DISORDERS; ATROPHY AB The linear Purkinje cell density in the cerebellar vermis was investigated in a small cohort of adult onset schizophrenic men with well-documented hippocampal abnormalities. There were no differences in comparison with age-matched controls. This negative finding indicates that vermian abnormalities undoubtedly seen in some schizophrenic patients may constitute a subsyndrome, possibly related to autistic disorders in which cerebellar abnormalities are well corroborated. C1 Univ Lund Hosp, Dept Clin Neurosci, Div Psychiat, S-22185 Lund, Sweden. Univ Lund Hosp, Dept Pathol, S-22185 Lund, Sweden. RP Jonsson, SAT (reprint author), Univ Lund Hosp, Dept Clin Neurosci, Div Psychiat, S-22185 Lund, Sweden. 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Child Adolesc. Psych. PD MAR PY 2000 VL 9 IS 1 BP 21 EP 25 PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 305WD UT WOS:000086562800004 PM 10795852 ER PT J AU Mao, R Jalal, SM Snow, K Michels, VV Szabo, SM Babovic-Vuksanovic, D AF Mao, R Jalal, SM Snow, K Michels, VV Szabo, SM Babovic-Vuksanovic, D TI Characteristics of two cases with dup(15)(q11.2-q12): one of maternal and one of paternal origin SO GENETICS IN MEDICINE LA English DT Article DE PWS/AS critical region; duplication; clinical features ID SYNDROME CHROMOSOME REGION; PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; DEVELOPMENTAL DELAY; ANGELMAN-SYNDROME; PRADER-WILLI; 15Q11-Q13; PATIENT; AUTISM AB Purpose: The phenotype correlations for interstitial duplications that include the Prader-Willi/Angelman syndrome critical region are not well established. We describe two such duplication cases, one of which was of maternal origin and the other was paternal. Methods: High resolution G-banding, fluorescence in situ hybridization (FISH) for SNRP-N and D15S10 were used for cytogenetic analysis. Southern blot analyses based on parent of origin specific DNA methylation at D15S63 (PW71) locus were utilized for detection of methylated and unmethylated fragments. Results: The duplication was established by the FISH analysis. The molecular pattern suggested a maternal origin of the duplication in patient 1 and a paternal origin in patient 2. Patient 1 (2 years old) had developmental and speech delays with pervasive developmental disorder or mild autism, strabismus, and normal growth parameters with seizures. Patient 2 (16 years old) had global developmental delay, verbal IQ of 94, depression, obesity, food-seeking behavior, and significant behavioral problems that included self-injurious tendencies. Neither patient had significant dysmorphic features or abnormalities of internal organs. 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Med. PD MAR-APR PY 2000 VL 2 IS 2 BP 131 EP 135 DI 10.1097/00125817-200003000-00003 PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 409PP UT WOS:000167392300003 PM 11397326 ER PT J AU Ivry, R AF Ivry, R TI Exploring the role of the cerebellum in sensory anticipation and timing: Commentary on Tesche and Karhu SO HUMAN BRAIN MAPPING LA English DT Article DE cerebellum; temporal processing; sensory expectancy; cognition; neuroimaging ID DEFICIT HYPERACTIVITY DISORDER; INFANTILE-AUTISM; MOTOR CONTROL; ACQUISITION AB The past decade has witnessed a paradigm shift concerning the study of the cerebellum. Results from various studies employing a variety of methodologies suggest that the functional role of this structure is not limited to motor control. The article by Tesche and Karhu appearing in this issue, provides strong evidence that the cerebellum in humans is activated in anticipation of somatosensory events, even when these events do not require overt responses. 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EM mscory@mscc.huji.ac.il CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BILU Y, 1993, CULT MED PSYCHIAT, V17, P197, DOI 10.1007/BF01379326 LOCKYER L, 1970, BRIT J SOC CLIN PSYC, V9, P152 Lord C., 1994, PRESCHOOL ED PROGRAM, P87 MESIBOV GB, 1994, CURR I AUT, P195 MISHORI E, 1992, AUTISM COMMUNICATION Schopler E., 1995, LEARNING COGNITION A, P243 Schopler E., 1997, HDB AUTISM PERVASIVE, P767 NR 8 TC 0 Z9 0 PU M E SHARPE INC PI ARMONK PA 80 BUSINESS PARK DR, ARMONK, NY 10504 USA SN 0020-7411 J9 INT J MENT HEALTH JI Int. J. Ment. 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PD MAR PY 2000 VL 29 IS 1 BP 144 EP 145 PG 2 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 281YR UT WOS:000085189500014 ER PT J AU Rapoport, M van Reekum, R Mayberg, H AF Rapoport, M van Reekum, R Mayberg, H TI The role of the cerebellum in cognition and behavior: A selective review SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Review ID ALZHEIMERS-DISEASE; CHRONIC-SCHIZOPHRENIA; GLUCOSE-METABOLISM; ATROPHY; DEMENTIA; DISORDER; AUTISM; VERMIS; ABNORMALITIES; DYSFUNCTION AB The cerebellum has traditionally been seen primarily to coordinate voluntary movement, but evidence is accumulating that it may play a role in cognition and behavior as well. This is a selective review of studies assessing potential cognitive deficits and personality changes associated with cerebellar disease. Preliminary studies of the role of the cerebellum in schizophrenia, dementia, and other psychiatric disorders are also discussed. 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Neuropsychiatr. Clin. Neurosci. PD SPR PY 2000 VL 12 IS 2 BP 193 EP 198 DI 10.1176/appi.neuropsych.12.2.193 PG 6 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 314UH UT WOS:000087075600003 PM 11001597 ER PT J AU Stathis, SL Cowley, DM Broe, D AF Stathis, SL Cowley, DM Broe, D TI Autism and adenylosuccinase deficiency SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter C1 Mater Misericordiae Hosp, S Brisbane, Australia. RP Stathis, SL (reprint author), Mater Misericordiae Hosp, S Brisbane, Australia. 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PD MAR PY 2000 VL 39 IS 3 BP 274 EP 275 DI 10.1097/00004583-200003000-00007 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 288TP UT WOS:000085580800007 PM 10714045 ER PT J AU Stevens, MC Fein, DA Dunn, M Allen, D Waterhouse, LH Feinstein, C Rapin, I AF Stevens, MC Fein, DA Dunn, M Allen, D Waterhouse, LH Feinstein, C Rapin, I TI Subgroups of children with autism by cluster analysis: A longitudinal examination SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; subtype; subgroup; cluster; IQ ID ASPERGER-SYNDROME; FAMILY HISTORY; FOLLOW-UP; DISORDERS; CLASSIFICATION; INDIVIDUALS; STABILITY; SUBTYPES; AGE AB Objective: A hierarchical cluster analysis was conducted using a sample of 138 school-age children with autism. The objective was to examine (1) the characteristics of resulting subgroups, (2) the relationship of these subgroups to subgroups of the same children determined at preschool age, and (3) preschool variables that best predicted school-age functioning. Method: Ninety-five cases were analyzed. Results: Findings support the presence of 2 subgroups marked by different levels of social, language, and nonverbal ability, with the higher group showing essentially normal cognitive and behavioral scores. The relationship of high- and low-functioning subgroup membership to levels of functioning at preschool age was highly significant. Conclusions: School-age functioning was strongly predicted by preschool cognitive functioning but was not strongly predicted by preschool social abnormality or severity of autistic symptoms. The differential outcome of the 2 groups shows that high IQ is necessary but not sufficient for optimal outcome in the presence of severe language impairment. 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PD MAR PY 2000 VL 39 IS 3 BP 346 EP 352 DI 10.1097/00004583-200003000-00017 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 288TP UT WOS:000085580800017 PM 10714055 ER PT J AU Marks, SU Schrader, C Longaker, T Levine, M AF Marks, SU Schrader, C Longaker, T Levine, M TI Portraits of three adolescent students with Asperger's syndrome: Personal stories and how they can inform practice SO JOURNAL OF THE ASSOCIATION FOR PERSONS WITH SEVERE HANDICAPS LA English DT Article DE Asperger's syndrome; autism; autism spectrum disorder; case studies; adolescent students ID SCHOOL-STUDENTS; EPIDEMIOLOGY; DISABILITIES; IMPAIRMENTS; MEMBERSHIP; MIDDLE AB This article presents three portraits of adolescent students with Asperger's syndrome. These portraits include descriptive details about these students as young children, their schooling experiences, their interests, and their social life experiences. To construct these portraits, we conducted a series of focus groups with professionals who provide direct services to these students. We also conducted interviews with the students and parents. The purpose of these three portraits is to serve as a starting point for those in the field to further examine possible solutions for better meeting the needs of these students. The role of these portraits (or personal stories) in helping to inform critical areas of need and important directions for meeting the needs of adolescent students with Asperger's syndrome conclude our article. C1 SRI Int, Menlo Park, CA 94025 USA. RP Marks, SU (reprint author), SRI Int, 333 Ravenswood Ave, Menlo Park, CA 94025 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H., 1991, AUTISM ASPERGER SYND, P37, DOI 10.1017/CBO9780511526770.002 Attwood T., 1998, ASPERGERS SYNDROME G Baker MJ, 1998, J ASSOC PERS SEVERE, V23, P300, DOI 10.2511/rpsd.23.4.300 BARBER C, 1996, BRIT J SPECIAL ED, V23, P19, DOI 10.1111/j.1467-8578.1996.tb00938.x Bogdan R. C., 1992, QUALITATIVE RES ED I Cumine V., 1998, ASPERGER SYNDROME PR Dewey M, 1991, AUTISM ASPERGER SYND, P184, DOI 10.1017/CBO9780511526770.006 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Ferguson P. 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K., 1989, CASE STUDY RES DESIG NR 41 TC 7 Z9 7 PU ASSN PERS SEVERE HANDICAP PI BALTIMORE PA 29 W SUSQUEHANNA AVE STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 J ASSOC PERS SEVERE JI J. Assoc. Pers. Sev. Handicap PD SPR PY 2000 VL 25 IS 1 BP 3 EP 17 DI 10.2511/rpsd.25.1.3 PG 15 WC Rehabilitation SC Rehabilitation GA 317HH UT WOS:000087219600001 ER PT J AU Hwang, B Hughes, C AF Hwang, B Hughes, C TI Increasing early social-communicative skills of preverbal preschool children with autism through social interactive training SO JOURNAL OF THE ASSOCIATION FOR PERSONS WITH SEVERE HANDICAPS LA English DT Article DE autism; preschool children; social-communicative skills; social interactive training ID YOUNG-CHILDREN; BEHAVIOR; IMITATION AB We evaluated the effects of a social interactive training program on early social-communicative skills (i.e., eve contact, joint attention, motor imitation) of three preverbal preschool children with autism. Training was conducted in the children's classroom during naturally occurring daily activities. Findings indicated that implementation of social interactive training components (i.e., contingent imitation, use of naturally occurring reinforcement, expectant look, environmental arrangement) was associated with increases in target behaviors across participants. In addition, generalization of eye contact and motor imitation behavior were found across an additional setting and different interactive partners, although joint attention rarely generalized Social validation measures provided by 30 raters indicated that perceived positive changes in performance had occurred in child behaviors and that training procedures M ere considered acceptable. Results are discussed in terms of implications for research and practice. C1 Ewha Womans Univ, Dept Special Educ, Seodaemun Gu, Seoul 120750, South Korea. Vanderbilt Univ, Nashville, TN 37240 USA. RP Hwang, B (reprint author), Ewha Womans Univ, Dept Special Educ, Seodaemun Gu, 11-1 Daehyun Dong, Seoul 120750, South Korea. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baker MJ, 1998, J ASSOC PERS SEVERE, V23, P300, DOI 10.2511/rpsd.23.4.300 CHARLOP MH, 1991, J APPL BEHAV ANAL, V24, P747, DOI 10.1901/jaba.1991.24-747 COHEN J, 1960, EDUC PSYCHOL MEAS, V20, P37, DOI 10.1177/001316446002000104 CRONIN P, 1990, UNPUB ENV RATING SCA DATTILO J, 1991, J APPL BEHAV ANAL, V24, P369, DOI 10.1901/jaba.1991.24-369 Dawson G., 1990, DEV PSYCHOPATHOL, V2, P151, DOI 10.1017/S0954579400000675 Guralnick MJ, 1996, CHILD DEV, V67, P471 Hedrick D. L., 1984, SEQUENCED INVENTORY Hepting NH, 1996, J EARLY INTERVENTION, V20, P249 HORNER RD, 1978, J APPL BEHAV ANAL, V11, P189, DOI 10.1901/jaba.1978.11-189 Hwang B, 1995, EDUC TRAIN MENT RET, V30, P336 Kazdin A. E., 1982, SINGLE CASE RES DESI Klinger LG, 1992, CAUSES EFFECTS COMMU, VI, P157 Koegel L. 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Handicap PD SPR PY 2000 VL 25 IS 1 BP 18 EP 28 DI 10.2511/rpsd.25.1.18 PG 11 WC Rehabilitation SC Rehabilitation GA 317HH UT WOS:000087219600002 ER PT J AU Prince, TA Leung, AKC AF Prince, TA Leung, AKC TI Children with autism: Diagnosis and intervention to meet their needs, 2nd edition SO JOURNAL OF THE ROYAL SOCIETY FOR THE PROMOTION OF HEALTH LA English DT Book Review CR Trevarthen C., 1998, CHILDREN AUTISM DIAG NR 1 TC 0 Z9 0 PU ROYAL SOC OF HEALTH PI LONDON PA 38A ST, GEORGES DR, LONDON SW1V 4BH, ENGLAND SN 1466-4240 J9 J R SOC PROMO HEALTH JI J. R. Soc. Promot. Health PD MAR PY 2000 VL 120 IS 1 BP 57 EP 58 DI 10.1177/146642400012000130 PG 2 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 312BB UT WOS:000086921900030 ER PT J AU Bass, MP Menold, MR Wolpert, CM Donnelly, SL Ravan, SA Hauser, ER Maddox, LO Vance, JM Abramson, RK Wright, HH Gilbert, JR Cuccaro, ML DeLong, GR Pericak-Vance, MA AF Bass, MP Menold, MR Wolpert, CM Donnelly, SL Ravan, SA Hauser, ER Maddox, LO Vance, JM Abramson, RK Wright, HH Gilbert, JR Cuccaro, ML DeLong, GR Pericak-Vance, MA TI Genetic studies in autistic disorder and chromosome 15 SO NEUROGENETICS LA English DT Article DE autistic disorder; chromosome 15q11-q13; linkage; increased recombination; gamma-aminobutyric acid(A) ID PRADER-WILLI-SYNDROME; DINUCLEOTIDE REPEAT POLYMORPHISM; SISTER-CHROMATID EXCHANGE; RECEPTOR SUBUNIT BETA-3; AFFECTED RELATIVE PAIRS; MENTAL-RETARDATION; INV DUP(15); LINKAGE STRATEGIES; ANGELMAN SYNDROME; INFANTILE-AUTISM AB Autistic disorder (AD) is a developmental disorder affecting social interactions, communication, and behavior. AD is a disease of complex genetic architecture, It is postulated that several genes contribute to the underlying etiology of AD. Chromosome 15 is of particular interest due to numerous reports of AD in the presence of chromosomal abnormalities, located mainly in the 15q11-q13 region. There are also a number of plausible candidate genes in this area, including the gamma-aminobutyric acid(A) (GABA(A)) receptor gene complex, Ne have undertaken a study of this region of chromosome 15 in a data set of 63 multiplex families (with 2 or more AD affected individuals per family). We found evidence in support of linkage to the 15q11-q13 region, as,well as evidence of increased recombination in this region, These findings provide further support for the involvement of chromosome 15q1l-q13 in the genetic etiology of AD. C1 Duke Univ, Med Ctr, Ctr Human Genet, Dept Med, Durham, NC 27710 USA. Univ S Carolina, WS Hall Psychiat Inst, Columbia, SC 29208 USA. 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This study examines serotonergic and noradrenergic markers in a study group of 13 males, post-pubertal, caucasian autistic patients (age 112-18 y; I.Q. > 55) and 13 matched volunteers. [H-3]-paroxetine binding Kd values were significantly higher in patients with autism than in healthy volunteers. Plasma concentrations of tryptophan, the precursor of 5-HT, were significantly lower in autistic patients than in healthy volunteers. There were no significant differences between autistic and normal children in the serum concentrations of 5-HT, or the 24-hr urinary excretion of 5-hydroxy-indoleacetic acid (5-HIAA), adrenaline, noradrenaline, and dopamine. There were no significant differences in [H-3]-rauwolscine binding Bmax or Kd values, or in the serum concentrations of tyrosine, the precursor of noradrenaline, between both study groups. There were highly significant positive correlations between age and 24-hr urinary excretion of 5-HIAA and serum tryptophan. The results suggest that: 1) serotonergic disturbances, such as defects in the 5-HT transporter system and lowered plasma tryptophan, may play a role in the pathophysiology of autism; 2) autism is not associated with alterations in the noradrenergic system; and 3) the metabolism of serotonin in humans undergoes significant changes between the ages of 12 and 18 years. [Neuropsychopharmacology 22:275-283, 2000] (C) 2000 American College of Neuropsychopharmacology. Published by Elsevier Science Inc. C1 Univ Antwerp, Ctr Child & Adolescent Psychiat, AZ Middelheim, B-2020 Antwerp, Belgium. CRC MH, Antwerp, Belgium. Univ Antwerp, Dept Med Biochem, Wilrijk, Belgium. Univ Antwerp, Dept Math & Computerized Sci, Wilrijk, Belgium. Univ Antwerp, Dept Clin Biochem, AZ Middelheim, B-2020 Antwerp, Belgium. Univ Antwerp Hosp, Dept Hematol, Edegem, Belgium. Vanderbilt Univ, Dept Psychiat, Nashville, TN USA. IRCCS, Ist Fatebenefratelli, Brescia, Italy. 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Two approaches were compared. In one approach, the participants observed two models engaging in cooperative play, before taking the place of one of the models while the play episode just observed was repeated. The second approach was identical to the first except that the participants were now required to verbally describe the modeled play episode before taking the place of one of the models. During training, modeled play episodes varied across play topics, and the criterion for mastery was first trial learning of novel play episodes. A nonconcurrent multiple baseline design across participants was applied. The results showed that the participants failed to acquire cooperative play until the verbal description was included in the training procedure. Following training with verbal description, all participants: a) could initiate episodes and sustain episodes initiated by their play partner; b) were able to take turns in episodes that were considerably longer than the episodes practiced during training; c) varied their play within and between play episodes; and, d) transferred those skills across play partners, settings, and time. (C) 2000 Elsevier Science Ltd. All rights reserved. C1 Akershus Cent Hosp, Sentralsykehuset & Akershus, Barneavdelingen, Seksjon Habilitering, N-1474 Nordbyhagen, Norway. Akershus Coll, Nordbyhagen, Norway. RP Jahr, E (reprint author), Akershus Cent Hosp, Sentralsykehuset & Akershus, Barneavdelingen, Seksjon Habilitering, POB 42, N-1474 Nordbyhagen, Norway. EM erik.jahr@online.no CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARLOW DH, 1988, SINGLE CASE EXPT DES BROWN WH, 1994, RES DEV DISABIL, V15, P99, DOI 10.1016/0891-4222(94)90016-7 BRYANT SE, 1995, PSYCHOL REC, V45, P495 BURGOON JK, 1995, J EXP SOC PSYCHOL, V31, P287, DOI 10.1006/jesp.1995.1014 Charlop M. H., 1994, AUTISM CHILDREN ADUL, P213 CHASE PN, 1992, UNDERSTANDING VERBAL, P181 DECKER PJ, 1982, PERS PSYCHOL, V35, P323, DOI 10.1111/j.1744-6570.1982.tb02198.x DUCHARME JM, 1992, J APPL BEHAV ANAL, V25, P166 DUNCAN CP, 1958, J EXP PSYCHOL, V55, P63, DOI 10.1037/h0047506 ELLIS HC, 1975, MEM COGNITION, V3, P226, DOI 10.3758/BF03212902 FERSTER CB, 1961, CHILD DEV, V32, P437, DOI 10.1111/j.1467-8624.1961.tb05042.x GOLDSTEIN H, 1989, J APPL BEHAV ANAL, V22, P245, DOI 10.1901/jaba.1989.22-245 Guerin B., 1994, ANAL SOCIAL BEHAV BE Hake D. F., 1978, HDB APPL BEHAV ANAL, P208 HARRIS SL, 1994, AUTISM CHILDREN ADUL, P127 Horner R. H., 1982, J ASS SEVERELY HANDI, V7, P7 HUGHES C, 1995, J APPL BEHAV ANAL, V28, P201, DOI 10.1901/jaba.1995.28-201 HUGHES C, 1992, AM J MENT RETARD, V97, P302 JOYCE JH, 1990, J EXP ANAL BEHAV, V54, P251, DOI 10.1901/jeab.1990.54-251 KAZDIN AE, 1994, BEHAV MODIFICATION A KOEGEL RL, 1994, CURR I AUT, P81 KOEGEL RL, 1972, J APP BEHAV ANAL, V18, P187 Kohler F. W., 1990, J EARLY INTERVENTION, V14, P327 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 Lord C., 1993, PRESCHOOL ISSUES AUT, P61 Lovaas O. I., 1981, TEACHING DEV DISABLE Lovaas O. 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R., 1988, GEN STUDENTS SEVERE, P15 NR 44 TC 28 Z9 29 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD MAR-APR PY 2000 VL 21 IS 2 BP 151 EP 169 DI 10.1016/S0891-4222(00)00031-7 PG 19 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 312GD UT WOS:000086934100006 PM 10817421 ER PT J AU MacLean, JE Teshima, IE Szatmari, P Nowaczyk, MJM AF MacLean, JE Teshima, IE Szatmari, P Nowaczyk, MJM TI Ring chromosome 22 and autism: Report and review SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE ring chromosome 22; 2-3 toe syndactyly; autism ID PERVASIVE DEVELOPMENTAL DISORDERS; PHENOTYPIC CORRELATIONS; PATIENT; NEUROFIBROMATOSIS; MENINGIOMAS; KARYOTYPE; TWINS AB Ring chromosome 22 has been described in over 50 cases. A characteristic phenotype has not been fully delineated; however, long face, thick eyebrows, 2-3 toe syndactyly, mental retardation, adequate somatic growth and the absence of major malformations are noted in many cases. An 11-year-old boy with ring chromosome 22 and 46,XY,r(22)(p11.31-q13.31-q13.33) karyotype presented with global developmental delay, autistic disorder, and dolichocephaly, apparently low-set and large ears, midface hypoplasia, and 2-3 toe syndactyly. This is the second report of a ring chromosome 22 with autistic disorder. There appears to be an association between abnormalities of chromosome 22, including r(22), and autistic disorder; however, this occurrence may be a result of the association of autistic disorder with mental retardation rather than specifically due to r(22). The physical findings in this case also suggest that ring chromosome 22 causes a subtle but distinct phenotype which has previously been proposed. (C) 2000 Wiley-Liss, Inc. C1 McMaster Univ, Med Ctr, Dept Pathol & Mol Med, Hamilton, ON L8S 4J9, Canada. Hmailton Hlth Sci Corp, Hamilton, ON, Canada. Hosp Sick Children, Dept Pediat Lab Med, Div Clin Genet, Toronto, ON M5G 1X8, Canada. Univ Toronto, Toronto, ON, Canada. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. McMaster Univ, Dept Pediat, Hamilton, ON, Canada. RP Nowaczyk, MJM (reprint author), McMaster Univ, Med Ctr, Dept Pathol & Mol Med, Room 3N16,1200 Main St W, Hamilton, ON L8S 4J9, Canada. CR ARINAMI T, 1986, J MED GENET, V23, P178, DOI 10.1136/jmg.23.2.178 Assumpcao FB, 1998, J AUTISM DEV DISORD, V28, P253 BAILEY A, 1995, PSYCHOL MED, V25, P63 Carratala F, 1998, DEV MED CHILD NEUROL, V40, P492 CHRISTODOULOU J, 1990, AM J MED GENET, V37, P422, DOI 10.1002/ajmg.1320370324 COULTERMACKIE MB, 1995, J MED GENET, V32, P787, DOI 10.1136/jmg.32.10.787 CRUSI A, 1986, ANN GENET-PARIS, V29, P253 DALLAPICCOLA B, 1977, ACTA GENET MED GEMEL, V26, P287 DUNCAN AMV, 1987, CANCER GENET CYTOGEN, V25, P169, DOI 10.1016/0165-4608(87)90173-7 FRYNS JP, 1979, HUM GENET, V47, P213, DOI 10.1007/BF00273205 FUNDERBURK SJ, 1979, CLIN GENET, V16, P305 Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 GUSTAVSON KH, 1986, CLIN GENET, V29, P337 HUNTER AGW, 1977, CLIN GENET, V12, P239 Joyce CA, 1996, J MED GENET, V33, P986, DOI 10.1136/jmg.33.12.986 KehrerSawatzki H, 1997, HUM GENET, V100, P67, DOI 10.1007/s004390050467 KOSZTOLANYI G, 1987, HUM GENET, V75, P174, DOI 10.1007/BF00591082 LASSEN C, 1987, ANN PEDIATR-PARIS, V34, P451 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 LINDENBA.RH, 1973, J MED GENET, V10, P85, DOI 10.1136/jmg.10.1.85 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Marie S, 1999, HUM MUTAT, V13, P197, DOI 10.1002/(SICI)1098-1004(1999)13:3<197::AID-HUMU3>3.0.CO;2-D MITELMAN F., 1995, INT SYSTEM HUMAN CYT PALMER CG, 1977, J MED GENET, V14, P54, DOI 10.1136/jmg.14.1.54 PETRELLA R, 1993, AM J MED GENET, V47, P184, DOI 10.1002/ajmg.1320470211 RITTER CL, 1990, AM J MED GENET, V35, P14, DOI 10.1002/ajmg.1320350104 Rubio A, 1997, BRAIN PATHOL, V7, P1027, DOI 10.1111/j.1750-3639.1997.tb00902.x SEVERIEN C, 1991, KLIN PADIATR, V203, P467, DOI 10.1055/s-2007-1025476 Sovner R, 1996, J INTELL DISABIL RES, V40, P82, DOI 10.1111/j.1365-2788.1996.tb00607.x STOLL C, 1983, HUM GENET, V63, P294 Szatmari P, 1996, AM J MED GENET, V67, P354, DOI 10.1002/(SICI)1096-8628(19960726)67:4<354::AID-AJMG7>3.0.CO;2-M TAALMAN RDFM, 1987, CLIN GENET, V32, P81 TOMMERUP N, 1992, CLIN GENET, V42, P171 TURNER FW, 1962, CANCER RES, V22, P49 WATANABE H, 1988, CLIN GENET, V34, P206 NR 35 TC 22 Z9 22 PU WILEY-LISS PI NEW YORK PA DIV JOHN WILEY & SONS INC, 605 THIRD AVE, NEW YORK, NY 10158-0012 USA SN 0148-7299 J9 AM J MED GENET JI Am. 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PD FEB 28 PY 2000 VL 90 IS 5 BP 382 EP 385 DI 10.1002/(SICI)1096-8628(20000228)90:5<382::AID-AJMG7>3.0.CO;2-T PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 281NC UT WOS:000085166300007 PM 10706359 ER PT J AU Ogilvie, CM Moore, J Daker, M Palferman, S Docherty, Z AF Ogilvie, CM Moore, J Daker, M Palferman, S Docherty, Z CA IMGSAC TI Chromosome 22q11 deletions are not found in autistic patients identified using strict diagnostic criteria SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autism; 22q11 deletion; velocardiofacial syndrome; DiGeorge syndrome ID CARDIO-FACIAL SYNDROME; VELOCARDIOFACIAL-SYNDROME; DIGEORGE-SYNDROME; CHILDREN; ADULTS; REGION AB A group of 103 subjects with a strict diagnosis of autism were tested for deletion of band q11.2 on the long arm of chromosome 22, No deletions were found, indicating that when a patient has been diagnosed with autism using strict and consistent criteria, in the absence of other indications, it is unlikely that this individual will have a 22q11 deletion. Testing for 22q11 deletions is therefore unlikely to be necessary in these patients, Am. J. Med, Genet. (Neuropsychiatr. Genet,) 98:15-17, 2000, (C) 2000 Wiley-Liss, Inc. C1 Guys & St Thomas Hosp, Dept Cytogenet, Div Med & Mol Genet, London SE1 9RT, England. Inst Psychiat, MRC, Child Psychiat Unit, London, England. RP Ogilvie, CM (reprint author), Guys & St Thomas Hosp, Dept Cytogenet, Div Med & Mol Genet, 5th 7th & 8th Floors,Guys Tower,St Thomas St, London SE1 9RT, England. EM c.ogilvie@umds.ac.uk RI Monaco, Anthony/A-4495-2010; Bolton, Patrick/E-8501-2010; Bailey, Anthony/J-2860-2014 OI Monaco, Anthony/0000-0001-7480-3197; Bolton, Patrick/0000-0002-5270-6262; Bailey, Anthony/0000-0003-4257-972X CR Bassett AS, 1998, AM J MED GENET, V81, P328, DOI 10.1002/(SICI)1096-8628(19980710)81:4<328::AID-AJMG10>3.0.CO;2-N BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x BURD L, 1988, CLIN GENET, V33, P356 GOLDBERG R, 1993, AM J MED GENET, V45, P313, DOI 10.1002/ajmg.1320450307 GOLDINGKUSHNER KJ, 1985, J CRAN GENET DEV BIO, V5, P259 Gothelf D, 1997, AM J MED GENET, V72, P455 Bailey A, 1998, HUM MOL GENET, V7, P571 Karayiorgou Maria, 1995, Proceedings of the National Academy of Sciences of the United States of America, V92, P7612, DOI 10.1073/pnas.92.17.7612 Kozma C, 1998, AM J MED GENET, V81, P269, DOI 10.1002/(SICI)1096-8628(19980508)81:3<269::AID-AJMG12>3.0.CO;2-D Lachman HM, 1997, AM J MED GENET, V74, P121, DOI 10.1002/(SICI)1096-8628(19970418)74:2<121::AID-AJMG2>3.0.CO;2-X LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Rineer S, 1998, AM J MED GENET, V81, P428, DOI 10.1002/(SICI)1096-8628(19980907)81:5<428::AID-AJMG12>3.0.CO;2-E RITVO ER, 1990, AM J PSYCHIAT, V147, P1614 RUTTER M, 1993, NATURE NURTURE PSYCH, P269, DOI 10.1037/10131-013 Ryan AK, 1997, J MED GENET, V34, P798, DOI 10.1136/jmg.34.10.798 SHPRINTZEN RJ, 1992, AM J MED GENET, V42, P141, DOI 10.1002/ajmg.1320420131 Stewart HS, 1997, CLIN DYSMORPHOL, V6, P165 Swillen A, 1997, J MED GENET, V34, P453, DOI 10.1136/jmg.34.6.453 WENGER SL, 1988, J MED GENET, V25, P263, DOI 10.1136/jmg.25.4.263 WILSON DI, 1993, ARCH DIS CHILD, V68, P187 WILSON DI, 1993, J MED GENET, V30, P852, DOI 10.1136/jmg.30.10.852 WILSON IG, 1994, AM J HUM GENET S, V55, pA975 Zori RT, 1998, AM J MED GENET, V77, P8, DOI 10.1002/(SICI)1096-8628(19980428)77:1<8::AID-AJMG2>3.0.CO;2-O NR 23 TC 15 Z9 15 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET JI Am. J. Med. Genet. PD FEB 7 PY 2000 VL 96 IS 1 BP 15 EP 17 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 276TM UT WOS:000084893500005 PM 10686546 ER PT J AU Martin, ER Menold, MM Wolpert, CM Bass, MP Donnelly, SL Ravan, SA Zimmerman, A Gilbert, JR Vance, JM Maddox, LO Wright, HH Abramson, RK DeLong, GR Cuccaro, ML Pericak-Vance, MA AF Martin, ER Menold, MM Wolpert, CM Bass, MP Donnelly, SL Ravan, SA Zimmerman, A Gilbert, JR Vance, JM Maddox, LO Wright, HH Abramson, RK DeLong, GR Cuccaro, ML Pericak-Vance, MA TI Analysis of linkage disequilibrium in gamma-aminobutyric acid receptor subunit genes in autistic disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS LA English DT Article DE autistic disorder; gamma-aminobutyric acid receptor; linkage disequilibrium; Transmission/Disequilibrium Test (TDT) ID GENETICALLY COMPLEX TRAITS; DINUCLEOTIDE REPEAT POLYMORPHISM; AFFECTED RELATIVE PAIRS; INFANTILE-AUTISM; CHROMOSOME; REGION; DUPLICATION; STRATEGIES; 15Q11-13; INDIVIDUALS AB Autistic disorder (AD) is a neurodevelopmental disorder characterized by abnormalities in behavior, communication, and social interactions and functioning. Recently, Cook et al. reported significant linkage disequilibrium with an AD susceptibility locus and a marker, GABRB3 155CA-2, in the gamma-aminobutyric acid(A) (GABA(A)) receptor ps-subunit gene on chromosome 15q11-q13, This linkage disequilibrium was detected using a multiallelic version of the transmission/disequilibrium test (TDT) in a sample of nuclear families having at least one child with autistic disorder. In an attempt to replicate this finding we tested for linkage disequilibrium with this marker, as well as with three additional markers in and around the GABA(A) receptor beta(3)-subunit gene, in an independent, clinically comparable set of AD families. Unlike Cook et al,, we failed to detect significant linkage disequilibrium between GABRB3 155CA-2 and AD in our sample. We did, however, find suggestive evidence for linkage disequilibrium with a marker, GABRB3, approximately 60 kb beyond the 3' end of beta 3-subunit gene. This finding lends support for previous reports implicating the involvement of genes in this region with AD. Am, J, Med. Genet, (Neuropsychiatr. Genet,) 96:43-48, 2000 (C) 2000 Wiley-Liss, Inc. C1 Duke Univ, Med Ctr, Ctr Human Genet, Durham, NC 27710 USA. Duke Univ, Med Ctr, Div Neurol, Durham, NC 27710 USA. Univ S Carolina, WS Hall Psychiat Inst, Columbia, SC 29208 USA. Johns Hopkins Univ, Med Ctr, Dept Neurol, Baltimore, MD 21218 USA. RP Martin, ER (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Box 3468, Durham, NC 27710 USA. 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During our attempts to study the fragile sites in more detail we were unable to reproduce the fragile sites found several years earlier. The potential relationship between the fragile sites and the neuropsychiatric disorders in these patients is discussed. Am. J, Med, Genet. (Neuropsychiatr. Genet.) 96:69-73, 2000, (C) 2000 Wiley-Liss, Inc. C1 Univ N Dakota, Sch Med & Hlth Sci, Dept Neurosci, Grand Forks, ND 58202 USA. Univ N Dakota, Sch Med & Hlth Sci, Dept Pediat, Grand Forks, ND 58202 USA. Univ N Dakota, Sch Med & Hlth Sci, N Dakota Fetal Alcohol Syndrome Ctr, Grand Forks, ND 58202 USA. Univ N Dakota, Sch Med & Hlth Sci, Child Evaluat & Treatment Program, Grand Forks, ND 58202 USA. Univ N Dakota, Sch Med & Hlth Sci, Dept Pathol, Grand Forks, ND 58202 USA. RP Burd, L (reprint author), Univ N Dakota, Sch Med & Hlth Sci, Dept Neurosci, 1300 S Columbia Rd, Grand Forks, ND 58202 USA. 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Linkage/association between 5-HTT gene promoter alleles and autistic disorder was assessed using the transmission/disequilibrium test (TDT) and the haplotype-based haplotype relative risk (HHRR), Both the Italian and the American samples, either singly or combined, displayed no evidence of linkage/association between 5-HTT gene promoter alleles and autistic disorder. Our findings do not support prominent contributions of 5-HTT gene variants to the pathogenesis of idiopathic infantile autism. Heterogeneity in pathogenetic mechanisms underlying the disease may require that linkage/association studies be targeted toward patient subgroups isolated on the basis of specific biochemical markers, such as serotonin (5-HT) blood levels. Am. J, Med. Genet. (Neuropsychiatr. Genet,) 96:123-127, 2000, (C) 2000 Wiley-Liss, Inc. C1 Liberia Univ Campus Biomed, Dept Physiol & Neurosci, Neurosci Lab, I-00155 Rome, Italy. Univ Naples 2, Dept Child Neuropsychiat, Naples, Italy. 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PD FEB 7 PY 2000 VL 96 IS 1 BP 123 EP 127 DI 10.1002/(SICI)1096-8628(20000207)96:1<123::AID-AJMG24>3.0.CO;2-N PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 276TM UT WOS:000084893500024 PM 10686565 ER PT J AU Goldberg, D AF Goldberg, D TI MMR, autism, and Adam SO BRITISH MEDICAL JOURNAL LA English DT Editorial Material NR 0 TC 2 Z9 2 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-8138 J9 BRIT MED J JI Br. Med. J. PD FEB 5 PY 2000 VL 320 IS 7231 BP 389 EP 389 DI 10.1136/bmj.320.7231.389 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 282HC UT WOS:000085211400076 ER PT J AU Volkmar, FR Klin, A Schultz, RT Rubin, E Bronen, R AF Volkmar, FR Klin, A Schultz, RT Rubin, E Bronen, R TI Asperger's disorder SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID AUTISM C1 Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. 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PD FEB PY 2000 VL 34 IS 1 BP 181 EP 182 DI 10.1080/000486700380 PG 2 WC Psychiatry SC Psychiatry GA 286RW UT WOS:000085460200036 ER PT J AU Gershon, ES AF Gershon, ES TI Bipolar illness and schizophrenia as oligogenic diseases: Implications for the future SO BIOLOGICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Janssen CNS Summit on Psychiatric Genetics CY FEB 09, 1999 CL TEMPE, ARIZONA DE bipolar illness; schizophrenia; genetics; common disease; oligogenic; genetic counseling ID MANIC-DEPRESSIVE ILLNESS; COMPLEX TRAITS; LINKAGE; SUSCEPTIBILITY; MARKERS; GENE; STRATEGIES; DISORDER; GENOME; LOCI AB As with most complex inheritance diseases, there are err this time no identified susceptibility genes for schizophrenia, bipolar manic-depressive illness, major depression, childhood autism, and other inherited brain disorders whose manifestations are primarily behavioral. Nonetheless, progress has occurred. Genetic epidemiologic research, based on reliable phenotypic definitions, has demonstrated the heritability of many of these disorders. Genetic linkages and associations have been reported and replicated, although there have been inconsistencies between studies, apparently due to the low statistical power of the samples studied to detect small effects genes. Nonreplications of early linkage reports in manic-depressive illness ill the 1980s occurred when new cases developed in the same large families in which the linkage was originally reported and the newly ill pet-sons had the wrong genetic markers ir I the linkage region. This appears to have resulted from applying inappropriate analytic assumptions of single-gene dominant inheritance of a rare gene, which implied that new cases must arise from the same ancestral gene within the pedigree. When new cases arose in family members not sharing that chromosomal region, the initial linkage report was proved invalid. Under oligogenic inheritance, oil the other hand, susceptibility genes are expected to be common, and have a substantial probability of being brought into the pedigree by persons marrying in. Nonspecific psychopathology genes may exist, shared by schizophrenia and biopolar illness, diagnoses which do not co-aggregate in families. The discovery of susceptibility mutations may be expected. Biol Psychiatry 2000; 47:240-244 (C) 2000 Society of Biological Psychiatry. C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. RP Gershon, ES (reprint author), Univ Chicago, Dept Psychiat, 5841 S Maryland Ave,MC3077, Chicago, IL 60637 USA. 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Psychiatry PD FEB 1 PY 2000 VL 47 IS 3 BP 240 EP 244 DI 10.1016/S0006-3223(99)00299-1 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 282AW UT WOS:000085194500009 PM 10682221 ER PT J AU Jambaque, I Chiron, C Dumas, C Mumford, J Dulac, O AF Jambaque, I Chiron, C Dumas, C Mumford, J Dulac, O TI Mental and behavioural outcome of infantile epilepsy treated by vigabatrin in tuberous sclerosis patients SO EPILEPSY RESEARCH LA English DT Article DE tuberous sclerosis; vigabatrin; infantile spasms; cognitive functions; autism ID CHILDREN; SPASMS; CARBAMAZEPINE; MONOTHERAPY; POPULATION; SEIZURES; MEMORY; WEST AB Vigabatrin (VGB) has demonstrated high efficacy in infantile spasms (IS) due to tuberous sclerosis. Our first objective was to evaluate the cognitive long term effect outcome of children whose refractory spasms definitely disappeared when VGB was given as an add on drug. Our second objective was to determine the response of generalized epilepsy (infantile spasms) compared to partial epilepsy on cognitive impairment. A non selected series of 13 children underwent psychometric and behavioural evaluation before VGB initiation at a mean of 3 years on VGB treatment. Eight of them could perform detailed neuropsychological tests at follow-up. Seven had infantile spasms (Group I), they all were spasm free before 2 years of age and five remained with rare partial seizures (mean age, 5.5 years). Six others had partial epilepsy without spasms (Group II) and five remained with rare seizures (mean age, 7.5 years). Patients of Group I experienced dramatic changes. Developmental quotient (DQ) significantly rose in six out of seven by ten to more than 45 points (P = 0.03) and autistic behaviour disappeared in five out of the six who presented with. The four tested children had normal verbal level after 5 years and could integrate at school but they remained with marked visuospatial disabilities. By contrast, patients of Group II remained with an unchanged DQ of about 60 so that both groups had similar DQ levels on follow-up. The cessation of spasms with VGB is therefore associated with significant improvement of cognition and behaviour in children with tuberous sclerosis. Controlling secondary generalization induced by infantile spasms seems to be a key factor for mental development. (C) 2000 Elsevier Science B.V. All rights reserved. C1 Hosp St Vincent de Paul, Dept Pediat Neurol, F-75674 Paris 14, France. INSERM, U29, Paris, France. Univ Paris 05, Paris, France. Hoechst Marion Roussel, Paris, France. RP Chiron, C (reprint author), Hosp St Vincent de Paul, Dept Pediat Neurol, 82 Ave Denfert Rochereau, F-75674 Paris 14, France. 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PD FEB PY 2000 VL 38 IS 2-3 BP 151 EP 160 DI 10.1016/S0920-1211(99)00082-0 PG 10 WC Clinical Neurology SC Neurosciences & Neurology GA 273PU UT WOS:000084716700007 PM 10642043 ER PT J AU Gordon, D AF Gordon, D TI Early negative results not the last word on secretin/autism story SO GASTROENTEROLOGY LA English DT News Item NR 0 TC 0 Z9 0 PU W B SAUNDERS CO PI PHILADELPHIA PA INDEPENDENCE SQUARE WEST CURTIS CENTER, STE 300, PHILADELPHIA, PA 19106-3399 USA SN 0016-5085 J9 GASTROENTEROLOGY JI Gastroenterology PD FEB PY 2000 VL 118 IS 2 BP 250 EP 250 DI 10.1016/S0016-5085(00)70202-2 PG 1 WC Gastroenterology & Hepatology SC Gastroenterology & Hepatology GA 277MT UT WOS:000084937900003 PM 10691370 ER PT J AU Rutter, M AF Rutter, M TI Genetic studies of autism: From the 1970s into the millennium SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article; Proceedings Paper CT 9th Biennial Conference of the International-Society-for-Research-in-Child-and-Adolescent-Psychopatholo gy CY JUL 16-20, 1999 CL BARCELONA, SPAIN SP Int Soc Res Child & Adolescent Psychopathol DE autism; quantitative genetics; molecular genetics; functional genomics; clinical practice ID SIB-PAIR ANALYSIS; FAMILY HISTORY; QUANTITATIVE TRAITS; INFANTILE-AUTISM; PSYCHIATRIC-DISORDERS; PARENTS; INDIVIDUALS; CHILDREN; TWIN; ASSOCIATION AB Reviewers in the 1960s and early 1970s were skeptical about any substantial role for genetic factors in the etiology of autism. A realization that the 2% rate of autism in siblings las estimated at that time) was far above the general population base rate, and that this suggested a possible high genetic liability, led to the first small-scale twin study of autism. The replicated evidence from both twin and family studies undertaken in the 1970s and 1980s indicated both strong genetic influences and the likelihood that they applied to a phenotype that was much broader than the traditional diagnostic category of autism. Medical and chromosomal findings also indicated genetic heterogeneity. Advances in molecular genetics led to genome-wide scans of affected relative pair samples with a positive log of the odds to base 10 score for a location on chromosome 7. The major remaining research challenges and the likely clinical benefits that should derive from genetic research are considered in relation to both current knowledge and that anticipated to emerge from research over the next decade. 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Abnorm. Child Psychol. PD FEB PY 2000 VL 28 IS 1 BP 3 EP 14 DI 10.1023/A:1005113900068 PG 12 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 299RV UT WOS:000086212400002 PM 10772346 ER PT J AU Renner, P Klinger, LG Klinger, MR AF Renner, P Klinger, LG Klinger, MR TI Implicit and explicit memory in autism: Is autism an amnesic disorder? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE memory; autism; and amnesia ID EXECUTIVE FUNCTION; INFANTILE-AUTISM; FREE-RECALL; CHILDREN; INDIVIDUALS; PERFORMANCE; HIPPOCAMPUS; SIMILARITY; COMPLETION; DEFICITS AB Medial temporal lobe amnesic disorder is characterized by an impairment in explicit memory (e.g., remembering a shopping list) and intact implicit memory (e.g., a woman seems familiar although you cannot remember having met her before). This study examined whether children with high-functioning autism have this same dissociation between explicit and implicit memory abilities. Children with autism and normal development participated in three memory tasks: one implicit task (perceptual identification) and two explicit tasks (recognition and recall). Children with autism showed intact implicit and explicit memory abilities. However, they did not show the typical pat tern of recalling more items from both the beginning and end of a list and instead only recalled items from the end of the list. These results do not support the theory that high-functioning autism is a type of medial temporal lobe amnesia. However, these findings suggest that persons with autism use different organizational strategies during encoding or retrieval of items from memory. C1 Univ Alabama, Dept Psychol, Tuscaloosa, AL 35401 USA. Univ Alabama, Dept Psychol, Tuscaloosa, AL 35487 USA. RP Klinger, LG (reprint author), Univ Alabama, Dept Psychol, Tuscaloosa, AL 35401 USA. 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Autism Dev. Disord. PD FEB PY 2000 VL 30 IS 1 BP 3 EP 14 DI 10.1023/A:1005487009889 PG 12 WC Psychology, Developmental SC Psychology GA 305ND UT WOS:000086546000002 PM 10819116 ER PT J AU Millward, C Powell, S Messer, D Jordan, R AF Millward, C Powell, S Messer, D Jordan, R TI Recall for self and other in autism: Children's memory for events experienced by themselves and their peers SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE memory processing; self; other; autism; personal episodic memory ID AUTONOETIC CONSCIOUSNESS; EPISODIC MEMORY; INDIVIDUALS; RECOGNITION AB Research on memory processing suggests that memory for events that an individual experiences should be superior to that for similar events that someone else experiences (e.g., Baker-Ward et al., 1990). However, such predictions may not be applicable to individuals with autism. There are already suggestions that individuals with autism have specific difficulties in remembering (Boucher & Lewis, 1989). In addition, they are known to have more general difficulties involving processes related to the "self." If children with autism have difficulties in encoding information about themselves this could result in a deficit in personal episodic memory. The studies reported here compare memory for personally experienced events with that of memory for events experienced by a peer. An adaption of a method devised by Boucher and Lewis has been employed to assess recall. Two separate studies were conducted to investigate whether children with autism are impaired at recalling personal events. Two groups of children took part in Study 1, a group of children with autism and a control group of typical children matched for verbal mental age. 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PD FEB PY 2000 VL 30 IS 1 BP 15 EP 28 DI 10.1023/A:1005455926727 PG 14 WC Psychology, Developmental SC Psychology GA 305ND UT WOS:000086546000003 PM 10819117 ER PT J AU Kraijer, D AF Kraijer, D TI Review of adaptive behavior studies in mentally retarded persons with autism/pervasive developmental disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE autism; social development; mental retardation; Vineland Behavior Scales ID DOWN-SYNDROME; AUTISM; CHILDREN; ADOLESCENTS; SCALES AB A review is presented of the investigations carried out concerning the adaptive behavior of persons with the dual disability of mental retardation and autism/PDD. A close correspondence is found between the results obtained by means of a Dutch set of scales, the SRZ, SGZ, and SMZ, and those obtained by means of the Vineland Adaptive Behavior Scales. Compared with matched nonautistic persons, the performance of dually disabled persons is found to be particularly poor in the domain Social Skills/Socialization and somewhat less poor in the domain Communication. Performance of the two categories does not differ in the domains Self Help/Daily Living Skills and Gross Motor Skills/Motor Skills. As a net result, persons of the dually disabled category are found to obtain comparatively low total scores for social competency, the SRZ-Total/Adaptive Behavior Composite. In addition, autistic mentally retarded persons are found to display more maladaptive behavior. For comparative studies in the mental retardation field the use of level of Self Help/Daily Living Skills and, to a lesser extent, level of Gross Motor Skills/Motor Skills are recommended as suitable matching variables. C1 Stichting Hendr Boeijen, NL-9400 RA Assen, Netherlands. RP Kraijer, D (reprint author), Stichting Hendr Boeijen, POB 30014, NL-9400 RA Assen, Netherlands. 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