FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Walker, DR Thompson, A Zwaigenbaum, L Goldberg, J Bryson, SE Mahoney, WJ Strawbridge, CP Szatmari, P AF Walker, DR Thompson, A Zwaigenbaum, L Goldberg, J Bryson, SE Mahoney, WJ Strawbridge, CP Szatmari, P TI Specifying PDD-NOS: A comparison of PDD-NOS, Asperger syndrome, and autism SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE pervasive developmental disorder-not otherwise specified; autism; pervasive developmental disorder; Asperger syndrome ID PERVASIVE DEVELOPMENTAL DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PRESCHOOL-CHILDREN; DSM-IV; SPECTRUM DISORDERS; BEHAVIOR CHECKLIST; FIELD TRIAL; CLASSIFICATION; INDIVIDUALS; DIAGNOSIS AB Objective: To describe the clinical characteristics of children given a diagnosis of pervasive developmental disorder-not otherwise specified (PDD-NOS) by expert clinicians and to compare these to the clinical characteristics of children given a diagnosis of autism and Asperger syndrome (AS). Method: Two hundred sixteen children with autism, 33 with AS, and 21 with PDD-NOS were compared on measures of level of functioning (communication, daily living and social skills, 10, and age of acquisition of language) and on various symptoms of autism (impaired communication and reciprocal social interaction and a preference for repetitive and stereotyped activities). Results: In terms of level of functioning measures, the PDD-NOS children had scores that were between those of the children with autism and those of the children with AS. In contrast, the PDD-NOS group had fewer autistic symptoms, especially repetitive stereotyped behaviors, than both the autism and AS groups (chi(2) = 11.06, p = .004). Children with PDD-NOS could be placed into one of three subgroups: a high-functioning group (24%) who resembled AS but had transient language delay or mild cognitive impairment; a subgroup resembling autism (24%) but who had late age of onset or too severe cognitive delays or were too young to potentially meet the full diagnostic criteria for autism; and a group (52%) not fulfilling the criteria for autism because of fewer stereotyped and repetitive behaviors. Conclusions: With some revision to current diagnostic criteria, a more homogenous atypical group with significant impairments in social-communication but fewer repetitive behaviors can be differentiated from the more nonspecific PDD-NOS group. This differentiation may lead to better reliability in diagnosis and to further progress in studies of etiology. J. Am. Acad. Child Adolesc. Psychiatry, 2004;43(2):172-180. Key Words: pervasive developmental disorder-not otherwise specified, autism, pervasive developmental disorder, Asperger syndrome. C1 McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. McMaster Univ, Dept Pediat, Hamilton, ON L8S 4L8, Canada. Dalhousie Univ, Dept Pediat, Halifax, NS, Canada. Dalhousie Univ, Dept Psychol, Halifax, NS, Canada. RP Szatmari, P (reprint author), Hamilton Hlt Sci, Chedoke Site,Patterson Bldg 207, Hamilton, ON L8N 3Z5, Canada. 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Am. Acad. Child Adolesc. Psychiatr. PD FEB PY 2004 VL 43 IS 2 BP 172 EP 180 DI 10.1097/01.chi.0000101375.03068.db PG 9 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 765NH UT WOS:000188289500012 PM 14726723 ER PT J AU Seeman, C AF Seeman, C TI Songs of the gorilla nation: My journey through autism. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Lib, Toledo, OH USA. RP Seeman, C (reprint author), Univ Toledo Lib, Toledo, OH USA. CR Prince-Hughes Dawn, 2004, SONGS GORILLA NATION NR 1 TC 0 Z9 0 PU BOWKER MAGAZINE GROUP CAHNERS MAGAZINE DIVISION PI NEW YORK PA 249 W 17TH ST, NEW YORK, NY 10011 USA SN 0363-0277 J9 LIBR J JI Libr. J. PD FEB 1 PY 2004 VL 129 IS 2 BP 111 EP 111 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 768BC UT WOS:000188507500193 ER PT J AU Buxbaum, JD Silverman, J Keddache, M Smith, CJ Hollander, E Ramoz, N Reichert, JG AF Buxbaum, JD Silverman, J Keddache, M Smith, CJ Hollander, E Ramoz, N Reichert, JG TI Linkage analysis for autism in a subset families with obsessive-compulsive behaviors: Evidence for an autism susceptibility gene on chromosome 1 and further support for susceptibility genes on chromosome 6 and 19 SO MOLECULAR PSYCHIATRY LA English DT Article DE autistic disorder; OCD; repetitive behaviors ID SINGLE-LOCUS APPROXIMATIONS; MULTIPLEX FAMILIES; OLIGOGENIC TRAITS; GENOMEWIDE SCREEN; LOD SCORES; DISORDER; TWIN; HETEROGENEITY; HISTORY; PAIRS AB Although there is considerable evidence for a strong genetic component to idiopathic autism, several genome-wide screens for susceptibility genes have been carried out with limited concordance of linked loci, reflecting numerous genes of weak effect and/or sample heterogeneity. In the current study, linkage analysis was carried out in a sample of 62 autism-affected relative pairs with more severe obsessive - compulsive behaviors, selected from a larger (n = 115) set of autism-affected relative pairs as a means of reducing sample heterogeneity. Obsessive - compulsive behaviors were assessed using the Autism Diagnostic Interview-Revised (ADI-R). In the sample with more severe obsessive - compulsive behaviors, multipoint NPL scores above 2 were observed on chromosomes 1, 4, 5, 6, 10, 11 and 19, with the strongest evidence for linkage on chromosome 1 at the marker D1S1656, where the multipoint NPL score was 3.06, and the two-point NPL score was 3.21. In follow-up analyses, analyzing the subset of families ( n = 35) where the patients had the most severe obsessive compulsive behaviors generated a multipoint NPL score of 2.76, and a two-point NPL score of 2.79, indicating that the bulk of evidence for linkage was derived from the families most severely affected with obsessive - compulsive behaviors. The data suggest that there is an autism susceptibility gene on chromosome 1 and provide further support for the presence of autism susceptibility genes on chromosomes 6 and 19. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Neurobiol, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY 10029 USA. RP Buxbaum, JD (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, Lab Mol Neuropsychiat, 1 Gustave L Levy Pl,Box 1668, New York, NY 10029 USA. 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PD FEB PY 2004 VL 9 IS 2 BP 144 EP 150 DI 10.1038/sj.mp.4001465 PG 7 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 774GN UT WOS:000188971600006 PM 14699429 ER PT J AU Ylisaukko-oja, T Nieminen-von Wendt, T Kempas, E Sarenius, S Varilo, T von Wendt, L Peltonen, L Jarvela, I AF Ylisaukko-oja, T Nieminen-von Wendt, T Kempas, E Sarenius, S Varilo, T von Wendt, L Peltonen, L Jarvela, I TI Genome-wide scan for loci of Asperger syndrome SO MOLECULAR PSYCHIATRY LA English DT Article DE Asperger syndrome; autism; schizophrenia; bipolar disorder; genome-wide scan; linkage analysis ID PERVASIVE DEVELOPMENTAL DISORDERS; MAJOR SUSCEPTIBILITY LOCUS; AUTISM-SPECTRUM DISORDERS; LINKAGE ANALYSIS; BIPOLAR-DISORDER; FAMILY HISTORY; TOTAL POPULATION; CHROMOSOME 7Q; SCREEN; SCHIZOPHRENIA AB Asperger syndrome ( AS), characterised by inadequate social interaction, lack of empathy and a dependence of routines and rituals, is classified as belonging to the autism spectrum disorders (DSM-IV and ICD-10). Although the prevalence of AS has been estimated to range from 0.3 up to 48.4 per 10 000, the phenotype still remains relatively unrecognised by clinicians. Several reports, including the original description by Hans Asperger (1944), have suggested that AS has a strong genetic component. Here, we have performed a genome- wide scan on Finnish families ascertained for AS with a strictly defined phenotype. In the initial scan, Z(max)>1.5 was observed on nine chromosomal regions, 1q21 - 22, 3p14 - 24, 3q25 - 27, 4p14, 4q32, 6p25, 6q16, 13q31 - 33 and 18p11. In the fine mapping stage, the highest two-point LOD scores were observed on chromosomes 1q21 - 22 (D1S484, Z(max dom) = 3.58), 3p14 - 24 (D3S2432, Z(max dom) = 2.50) and 13q31 - 33 (D13S793, Z(max dom) = 1.59). The loci on 1q21 - 22 and 3p14 - 24 overlap with previously published autism susceptibility loci, and the loci on 1q21 - 22 and 13q31 - 33 overlap with the reported schizophrenia susceptibility loci. 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PD FEB PY 2004 VL 9 IS 2 BP 161 EP 168 DI 10.1038/sj.mp.4001385 PG 8 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 774GN UT WOS:000188971600008 PM 14966474 ER PT J AU Turic, D Langley, K Mills, S Stephens, M Lawson, D Govan, C Williams, N Van den Bree, M Craddock, N Kent, L Owen, M O'Donovan, M Thapar, A AF Turic, D Langley, K Mills, S Stephens, M Lawson, D Govan, C Williams, N Van den Bree, M Craddock, N Kent, L Owen, M O'Donovan, M Thapar, A TI Follow-up of genetic linkage findings on chromosome 16p13: evidence of association of N-methyl-D aspartate glutamate receptor 2A gene polymorphism with ADHD SO MOLECULAR PSYCHIATRY LA English DT Article DE NMDA2A; attention deficit hyperactivity disorder; genetics ID DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DOPAMINE TRANSPORTER; MICE LACKING; SCHIZOPHRENIA; SUBUNIT; AUTISM AB Attention deficit hyperactivity disorder (ADHD) is a childhood onset disorder, for which there is good evidence that genetic factors contribute to the aetiology. Recently reported linkage findings suggested evidence of a susceptibility locus on chromosome 16p13 ( maximum LOD score of 4.2, P = 5 x 10(-6)). The GRIN2A (glutamate receptor, ionotropic, N-methyl D-aspartate 2A) gene that encodes the N-methyl D-aspartate receptor subunit 2A ( NMDA2A) maps to this region of linkage. As this is also a good functional candidate gene for ADHD, we undertook family-based association analysis in a sample of 238 families. We found significant evidence of association with a GRIN2A exon 5 polymorphism (chi(2) = 5.7, P = 0.01). Our data suggest that genetic variation in GRIN2A may confer increased risk for ADHD and that this, at least in part, might be responsible for the linkage result on 16p reported by Smalley et al. We conclude that replication is required and that further work examining for association of GRIN2A polymorphisms with ADHD is warranted. C1 Univ Wales Coll Med, Dept Psychol Med, Cardiff CF14 4XN, S Glam, Wales. 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Psychiatr. PD FEB PY 2004 VL 9 IS 2 BP 169 EP 173 DI 10.1038/sj.mp.4001387 PG 5 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 774GN UT WOS:000188971600009 PM 14966475 ER PT J AU Mostofsky, SH Bunoski, R Morton, SM Goldberg, MC Bastian, AJ AF Mostofsky, SH Bunoski, R Morton, SM Goldberg, MC Bastian, AJ TI Children with autism adapt normally during a catching task requiring the cerebellum SO NEUROCASE LA English DT Article ID PARKINSONS-DISEASE; LESIONS; ATTENTION AB The cerebellum, which has been found to be abnormal in histopathological studies of autism, is important for motor adaptation. We studied controls and children with high functioning autism (HFA) performing a catching adaptation test that is known to be impaired following cerebellar damage. Results showed no differences in adaptation rates or after-effects for HFA subjects versus controls. The findings indicate normal motor adaptation in HFA, suggesting normal or compensated cerebellar function for this task. C1 Kennedy Krieger Inst, Dept Dev Cognit Neurol, Baltimore, MD 21205 USA. Washington Univ, St Louis, MO 63130 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21218 USA. Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21218 USA. RP Mostofsky, SH (reprint author), Kennedy Krieger Inst, Dept Dev Cognit Neurol, 707 N Broadway, Baltimore, MD 21205 USA. EM mostofsky@kennedykrieger.org CR Bailey A, 1998, BRAIN, V121, P889, DOI 10.1093/brain/121.5.889 Bauman M. 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To compare ages at first measles-mumps-rubella (MMR) vaccination between children with autism and children who did not have autism in the total population and in selected subgroups, including children with regression in development. Methods. A case-control study was conducted in metropolitan Atlanta. Case children ( N = 624) were identified from multiple sources and matched to control children ( N = 1824) on age, gender, and school. Vaccination data were abstracted from immunization forms required for school entry. Records of children who were born in Georgia were linked to Georgia birth certificates for information on maternal and birth factors. Conditional logistic regression was used to estimate odds ratios (ORs). Results. The overall distribution of ages at MMR vaccination among children with autism was similar to that of matched control children; most case (70.5%) and control children (67.5%) were vaccinated between 12 and 17 months of age. Similar proportions of case and control children had been vaccinated before 18 or before 24 months. No significant associations for either of these age cutoffs were found for specific case subgroups, including those with evidence of developmental regression. More case (93.4%) than control children (90.6%) were vaccinated before 36 months ( OR: 1.49; 95% confidence interval: 1.04 - 2.14 in the total sample; OR: 1.23; 95% confidence interval: 0.64 - 2.36 in the birth certificate sample). This association was strongest in the 3- to 5-year age group. Conclusions. Similar proportions of case and control children were vaccinated by the recommended age or shortly after (ie, before 18 months) and before the age by which atypical development is usually recognized in children with autism ( ie, 24 months). Vaccination before 36 months was more common among case children than control children, especially among children 3 to 5 years of age, likely reflecting immunization requirements for enrollment in early intervention programs. C1 Ctr Dis Control & Prevent, Natl Immunizat Program, Atlanta, GA 30333 USA. Battelle Mem Inst, Ctr Publ Hlth Res & Evaluat, Atlanta, GA USA. CDC, Natl Ctr Birth Defects & Dev Disabil, Atlanta, GA 30333 USA. RP DeStefano, F (reprint author), Ctr Dis Control & Prevent, Natl Immunizat Program, E-61,1600 Clifton Rd NE, Atlanta, GA 30333 USA. 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RP Keenan, M (reprint author), Univ Ulster, Sch Psychol, Coleraine BT52 1SA, Londonderry, North Ireland. EM mickeykeenan@bigfoot.com CR *CAL DEP ED DEV SE, 1997, BEST PRACT DES DEL E Chiesa M., 1994, RADICAL BEHAV PHILOS Cooper J., 1987, APPL BEHAV ANAL DESROCHERS M, 2002, FUNCTIONAL ASSESSMEN Grant L, 1994, PRINCIPLES BEHAV ANA GROSS R, 1995, THEMES ISSUES DEBATE Guerin B, 1994, ANAL SOCIAL BEHAV Holth P, 2001, BEHAV PHILOS, V29, P203 Johnston J. 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Department of Health and Human Services, 1999, MENT HLTH REP SURG G Watts A., 1966, BOOK TABOO KNOWING W WYATT WJ, 1990, AM PSYCHOL, V45, P1181 NR 27 TC 1 Z9 1 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 FEB PY 2004 VL 17 IS 2 BP 72 EP 75 PG 4 WC Psychology, Multidisciplinary SC Psychology GA 777LT UT WOS:000189180400014 ER PT J AU Myers, K Goulet, M Rusche, J Boismenu, R Davis, M AF Myers, K Goulet, M Rusche, J Boismenu, R Davis, M TI Inhibition of fear potentiated startle in rats following peripheral administration of secretin SO PSYCHOPHARMACOLOGY LA English DT Article DE amygdala; anxiety; autism; memory; fear-potentiated startle ID VASOACTIVE-INTESTINAL-PEPTIDE; CONDITIONED FEAR; BRAIN; AUTISM; AMYGDALA; EXPRESSION; RECEPTOR; GENE; DIAZEPAM; LOCALIZATION AB Rationale. Previous results indicate that peripheral administration of secretin leads to robust Fos protein expression in the central nucleus of the rat amygdala. The implications of this observation on rat brain function, if any, remain unclear. Objectives. We examined the effect of systemic secretin administration on the expression of fear-potentiated startle in rats, a behavioral response known to require an intact, functional central nucleus of the amygdala. Methods. Rats were trained to associate a neutral light conditioned stimulus (CS) with footshock, a fear-inducing unconditioned stimulus (US). Twenty-four hours later, rats were administered secretin or vehicle and were tested immediately for their startle response to a loud noise in the presence or absence of the light. Results. Within a dose range relevant to its clinical use in autistic children, secretin dose-dependently decreased the magnitude of fear-potentiated startle in rats. Conclusions. This investigation provides additional evidence that systemically administered secretin can influence a neural network implicated in the acquisition and expression of emotional behaviors, including fear and anxiety. C1 Emory Univ, Dept Psychol, Atlanta, GA 30322 USA. Emory Univ, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA. Emory Univ, Ctr Behav Neurosci, Atlanta, GA 30322 USA. Repligen Corp, Waltham, MA 02453 USA. RP Davis, M (reprint author), Emory Univ, Dept Psychol, Atlanta, GA 30322 USA. 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A possibly under-diagnosed heterogeneous neurocutaneous syndrome SO REVISTA DE NEUROLOGIA LA Spanish DT Article DE achromic nevus; dysmorphic traits; Hypomelanosis of Ito; incontinentia pigmenti achromians neurocutaneous syndrome; psychomotor retardation ID INCONTINENTIA PIGMENTI ACHROMIANS; INVOLVEMENT; AUTISM; EEG AB Introduction. Hypomelanosis of Ito (HI) or incontinentia pigmenti achromians is a multisystemic neurocutaneous disorder that is associated to neurological complications in a high percentage of patients. Aims. The purpose of this study is to review the most significant features in a series of 14 patients with HI. Patients and methods. We conducted a retrospective study in which the following data were analysed: age, sex, familial and personal history, clinical features and complementary explorations that were carried out. We report the cases of nine females and five males aged between 4 months and 14 years. Results. All the patients presented neurological anomalies, including psychomotor or mental retardation in 11 (associated to autistic behaviour in two of them), neuroradiological anomalies in seven, microcephalus in three and epileptic seizures in two. Other significant complications were musculoskeletal and ocular anomalies (each of which were present in nine patients), dental disorders in six, coarse facies and dysmorphic ears in four patients, hypoacusis in five and congenital heart disease in two. The following were also observed, but as isolated events: choanal atresia, cleft palate, segmental dilatation of the colon, cryptorchidism, inguinal hernia, low height, vesicoureteral reflux and premature pubarche. Conclusions. There is no biological marker that identifies HI and a number of clinical, forms only appear in the skin in a very mild form, which means they sometimes going unnoticed or are not considered to be important enough to establish a diagnosis. This entity may, therefore, be more frequent than we think and its prevalence is perhaps underestimated. C1 Hosp Clin Univ, Dept Pediat, Serv Neuropediat, E-15706 Santiago De Compostela, Spain. Hosp Clin Univ, Serv Dermatol, E-15706 Santiago De Compostela, Spain. RP Eiris-Punal, J (reprint author), Hosp Clin Univ, Dept Pediat, Serv Neuropediat, Choupana S-N, E-15706 Santiago De Compostela, Spain. 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Neurologia PD FEB 1 PY 2004 VL 38 IS 3 BP 223 EP 228 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 778KZ UT WOS:000189241900004 PM 14963848 ER PT J AU Sheitman, BB Knable, MB Jarskog, LF Chakos, M Boyce, LH Early, J Lieberman, JA AF Sheitman, BB Knable, MB Jarskog, LF Chakos, M Boyce, LH Early, J Lieberman, JA TI Secretin for refractory schizophrenia SO SCHIZOPHRENIA RESEARCH LA English DT Article DE secretin; schizophrenia; autism ID PLACEBO-CONTROLLED TRIAL; PORCINE SECRETIN; DOUBLE-BLIND; AUTISM; CHOLECYSTOKININ; HYPOCRETINS; CHILDREN; CORTEX AB In preliminary uncontrolled studies, intravenous injection of the gastrointestinal peptide secretin produced improvements in the symptoms of autism. Because of the phenotypic overlap between autism and some aspects of schizophrenia, we performed a pilot study of secretin for treatment refractory schizophrenia. Twenty-two patients were randomized to a single intravenous dose of porcine secretin or placebo. Patients were evaluated with the Positive and Negative Symptom Scale for Schizophrenia (PANSS) and the Clinical Global Impression Scale (CGI) at baseline, 2 days after secretin infusion and weekly for 4 weeks. There were no statistically significant differences between drug- and placebo-treated patients with repeated measures analysis of variance (ANOVA). However, several patients treated with secretin experienced clinically meaningful, but transient, reductions in symptoms and a greater percentage of patients treated with secretin were rated as improved with the CGI. Further study of brain hypocretins and molecules affecting this system are warranted in schizophrenia. (C) 2003 Elsevier Science B.V. All rights reserved. C1 Dorothea Dix Hosp, Raleigh, NC 27699 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. Stanley Med Res Inst, Bethesda, MD USA. Univ N Carolina, Dept Neurol, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Pharm, Chapel Hill, NC 27599 USA. RP Sheitman, BB (reprint author), Dorothea Dix Hosp, 3601 Mail Serv Ctr, Raleigh, NC 27699 USA. EM brian.sheitman@ncmail.net CR Bachus SE, 1997, J PSYCHIATR RES, V31, P233, DOI 10.1016/S0022-3956(96)00041-6 Coniglio SJ, 2001, J PEDIATR-US, V138, P649, DOI 10.1067/mpd.2001.112474 De Lecea L, 1998, P NATL ACAD SCI USA, V95, P322, DOI 10.1073/pnas.95.1.322 Dunn-Geier J, 2000, DEV MED CHILD NEUROL, V42, P796 Elliott GR, 2001, PEDIATRICS, V108, pE90, DOI 10.1542/peds.108.5.e90 GABRIEL SM, 1996, BIOL PSYCHIAT, V39, P79 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Lahti RA, 1998, J NEURAL TRANSM, V105, P507, DOI 10.1007/s007020050074 MOROJI T, 1982, ARCH GEN PSYCHIAT, V39, P485 NAIR NPV, 1983, PSYCHOPHARMACOL BULL, V19, P134 Owley T, 2001, J AM ACAD CHILD PSY, V40, P1293, DOI 10.1097/00004583-200111000-00009 Roberts W, 2001, PEDIATRICS, V107, part. no., DOI 10.1542/peds.107.5.e71 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Siegel JM, 1999, CELL, V98, P409, DOI 10.1016/S0092-8674(00)81969-8 Tooney PA, 2001, BIOL PSYCHIAT, V49, P523, DOI 10.1016/S0006-3223(00)01068-4 Zachrisson O, 1999, NEUROREPORT, V10, P3265, DOI 10.1097/00001756-199911080-00003 NR 16 TC 18 Z9 18 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD FEB 1 PY 2004 VL 66 IS 2-3 BP 177 EP 181 DI 10.1016/S0920-9964(03)00068-9 PG 5 WC Psychiatry SC Psychiatry GA 763FJ UT WOS:000188064000012 PM 15061251 ER PT J AU Alamy, SS Jarskog, LF Sheitman, BB Lieberman, JA AF Alamy, SS Jarskog, LF Sheitman, BB Lieberman, JA TI Secretin in a patient with treatment-resistant schizophrenia and prominent autistic features SO SCHIZOPHRENIA RESEARCH LA English DT Article DE secretin; schizophrenia; autism; treatment-resistant; neurodevelopment ID PERVASIVE DEVELOPMENTAL DISORDER; APOPTOTIC REGULATION; DENSITY; CORTEX; BRAIN; MRI AB Secretin, a gastrointestinal (GI) peptide, may offer therapeutic benefit in autism. Autistic features can also be present in schizophrenia and a recent study suggested a role for adjunctive secretin in treatment-resistant schizophrenia. The current report describes one patient with undifferentiated schizophrenia and prominent autistic features who received a single dose of secretin and demonstrated substantial yet transient improvement. The case illustrates the potential role of secretin as a novel adjunctive treatment strategy in schizophrenic patients with autistic features. (C) 2003 Elsevier B.V. All rights reserved. C1 Univ N Carolina, Sch Med, Dept Psychiat, Chapel Hill, NC 27599 USA. Univ N Carolina, Sch Med, UNC Schizophrenia Res Ctr, Chapel Hill, NC 27599 USA. Dorothea Dix Hosp, Raleigh, NC USA. RP Jarskog, LF (reprint author), Univ N Carolina, Sch Med, Dept Psychiat, CB 7160, Chapel Hill, NC 27599 USA. EM jarskog@med.unc.edu CR Benes FM, 2001, NEUROPSYCHOPHARMACOL, V25, P1, DOI 10.1016/S0893-133X(01)00225-1 CAMPBELL M, 1995, COMPREHENSIVE TXB PS, P2277 Carpenter WT, 1995, COMPREHENSIVE TXB PS, P889 Chez MG, 2000, J AUTISM DEV DISORD, V30, P87, DOI 10.1023/A:1005443119324 De Lecea L, 1998, P NATL ACAD SCI USA, V95, P322, DOI 10.1073/pnas.95.1.322 Fatemi SH, 2001, SYNAPSE, V42, P281, DOI 10.1002/syn.10002 Glantz LA, 2000, ARCH GEN PSYCHIAT, V57, P65, DOI 10.1001/archpsyc.57.1.65 HORROBIN DF, 1980, BIOMEDICINE, V32, P54 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 Jarskog LF, 2000, BIOL PSYCHIAT, V48, P641, DOI 10.1016/S0006-3223(00)00988-4 Kanner L, 1943, NERV CHILD, V2, P217 Kemper TL, 1998, J NEUROPATH EXP NEUR, V57, P645, DOI 10.1097/00005072-199807000-00001 Kern JK, 2002, J AUTISM DEV DISORD, V32, P153, DOI 10.1023/A:1015441428154 Lord C, 2000, NEURON, V28, P355, DOI 10.1016/S0896-6273(00)00115-X McCarley RW, 1999, BIOL PSYCHIAT, V45, P1099, DOI 10.1016/S0006-3223(99)00018-9 Nozaki S, 2002, BIOCHEM BIOPH RES CO, V292, P133, DOI 10.1006/bbrc.2002.6640 PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Raymond GV, 1996, ACTA NEUROPATHOL, V91, P117 Rivto E. R., 1986, AM J PSYCHIAT, V143, P862 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 SELEMON LD, 1995, ARCH GEN PSYCHIAT, V52, P805 SHEITMAN BB, 2003, IN PRESS SCHIZOPHR R, V66, P177 Whiteley P, 2002, EXPERT OPINION THERA, V6, P175, DOI 10.1517/14728222.6.2.17512223079 Wright IC, 1999, SCHIZOPHR RES, V35, P1, DOI 10.1016/S0920-9964(98)00094-2 NR 24 TC 13 Z9 13 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0920-9964 J9 SCHIZOPHR RES JI Schizophr. Res. PD FEB 1 PY 2004 VL 66 IS 2-3 BP 183 EP 186 DI 10.1016/j.schres.2003.07.003 PG 4 WC Psychiatry SC Psychiatry GA 763FJ UT WOS:000188064000013 PM 15061252 ER PT J AU Kamer, A Zohar, AH Youngmann, R Diamond, GW Inbar, D Senecky, Y AF Kamer, A Zohar, AH Youngmann, R Diamond, GW Inbar, D Senecky, Y TI A prevalence estimate of pervasive developmental disorder among Immigrants to Israel and Israeli natives - A file review study SO SOCIAL PSYCHIATRY AND PSYCHIATRIC EPIDEMIOLOGY LA English DT Article DE PDD; autism; immigration; prevalence rate; risk factor ID BRITISH NATIONWIDE SURVEY; CHILD MENTAL-HEALTH; INFANTILE-AUTISM; FRENCH; CALIFORNIA; POPULATION; PAIRS; RISK AB developmental disorder (PDD) have risen in the West over the last 10 years. There is argument over the etiology of this change in rates. Social and cultural processes including migration have been hypothesized. Israel, as a country of ongoing immigration with a national registry of children diagnosed with PDD, offers an opportunity to compare rates of PDD among immigrants from developing countries and native Israelis. Method A Social Security national registry of 1,004 children diagnosed with PDD was reviewed and rates were calculated using data extracted from the Israel National Bureau of Statistics. Of all Jewish children that were born in the years 1983-1997 and who are currently living in Israel, we defined four groups: (1) native Israelis of non-Ethiopian extraction (N = 1,198,300), (2) native Israelis of Ethiopian extraction (N = 15,600), (3) immigrants of non-Ethiopian extraction (N = 110,300) and (4) children born in Ethiopia (N = 11,800). A further breakdown of groups 1 and 3 by well-characterized ethnic or geographical origins was not possible. Results The rate of PDD was significantly elevated in native Israelis as compared to all immigrant children. Among immigrants, the rate of PDD in Ethiopian-born children was lower than that of those born in other countries. The rate of PDD in immigrant Ethiopian children was much lower than in native Israeli children of Ethiopian extraction. Conclusions Birth in Israel, an industrialized country, is a marker for an environmental risk factor for PDD. This may indicate that gestation, birth or infancy in industrialized countries exposes children to environmental insults that increase the risk for contracting PDD. C1 Ruppin Acad Ctr, Psychol Behav Sci, IL-40250 Emek Hefer, Israel. Tel Aviv Univ, Sackler Sch Med, IL-69978 Tel Aviv, Israel. Tel Aviv Univ, Schneider Childrens Med Ctr, IL-69978 Tel Aviv, Israel. RP Kamer, A (reprint author), Ruppin Acad Ctr, Psychol Behav Sci, IL-40250 Emek Hefer, Israel. EM adaz@ruppin.ac.il CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Charman T, 2002, EUR CHILD ADOLES PSY, V11, P249, DOI 10.1007/s00787-002-0297-8 CIALDELLA P, 1989, J CHILD PSYCHOL PSYC, V30, P165, DOI 10.1111/j.1469-7610.1989.tb00775.x Croen LA, 2002, J AUTISM DEV DISORD, V32, P217, DOI 10.1023/A:1015405914950 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Croonenberghs J, 2002, NEUROPSYCHOBIOLOGY, V45, P1, DOI 10.1159/000048665 Davidovitch M, 2001, ISRAEL MED ASSOC J, V3, P188 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Fombonne E, 2002, AUTISM, V6, P149, DOI 10.1177/1362361302006002002 Fombonne E, 1997, J AM ACAD CHILD PSY, V36, P1561, DOI 10.1016/S0890-8567(09)66566-7 Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 FOMBONNE E, 1992, SOC PSYCH PSYCH EPID, V27, P203, DOI 10.1007/BF00789007 Fombonne E, 2003, INT REV PSYCHIATR, V15, P158, DOI 10.1080/0954026021000046119 GILLBERG C, 1995, J INTELL DISABIL RES, V39, P141 GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 GILLMAN MW, 1999, CIRCULATION, V99, P6 GOODMAN R, 1995, BRIT J PSYCHIAT, V167, P362, DOI 10.1192/bjp.167.3.362 Greenberg DA, 2001, AM J HUM GENET, V69, P1062, DOI 10.1086/324191 Jones MB, 2002, AM J MED GENET, V114, P558, DOI 10.1002/ajmg.10513 Kaplan S., 1998, ETHIOPIAN IMMIGRANTS Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Mandell DS, 2002, J AM ACAD CHILD PSY, V41, P1447, DOI 10.1097/01.CHI.0000024863.60748.53 McGuffin P, 2001, SCIENCE, V291, P1232, DOI 10.1126/science.1057264 SENECKY Y, 2002, ANN C AUT SHAAR ZED STROMLAND K, 1994, DEV MED CHILD NEUROL, V36, P351 YEARGINALLSOPP M, 2003, JAMA-J AM MED ASSOC, V289, P87 Youngmann Rafi, 2002, Harefuah, V141, P10 1997, ISRAEL NATL BUREAU S NR 28 TC 11 Z9 11 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 0933-7954 J9 SOC PSYCH PSYCH EPID JI Soc. Psychiatry Psychiatr. Epidemiol. PD FEB PY 2004 VL 39 IS 2 BP 141 EP 145 DI 10.1007/s00127-004-0696-x PG 5 WC Psychiatry SC Psychiatry GA 775RJ UT WOS:000189072200008 PM 15052396 ER PT J AU Bolte, S Poustka, F AF Bolte, S Poustka, F TI The German form of the Autism Diagnostic Observation Schedule (ADOS): first results on reliability and validity SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE autism; diagnostics; pervasive development disorders; observation scale; reliability; validity ID PERVASIVE DEVELOPMENTAL DISORDERS; INTERRATER RELIABILITY; INTERVIEW; INDIVIDUALS; BEHAVIOR AB Objective: To examine the psychometric properties of the German version of the Autism Diagnostic Observation Schedule (ADOS). Methods: Interrater and retest reliability, internal consistency, convergent and diagnostic validity were determined in a total sample of 137 subjects with autism, 23 with atypical autism or pervasive developmental disorder not otherwise specified, 16 with Asperger-syndrome and 13 with other psychiatric disorders. Results: Interrater and retest reliability on the level of diagnosis (kappa(w) = 1.00 and .62 and raw-scores (r(u) = .84 and .79) were good. Likewise, the internal consistency of the algorithm scale communication and social interaction of modules 1 to 4 was fair (r(u) = .78 to .89). The categorical convergence for autism between the ADOS and the Autism Diagnostic Interview-Revised (ADI-R) reached 79% (kappa = .23), with their corresponding subscales correlating moderately (r(tc) = .31 to .45). The concordance of the ADOS judgment and the clinical consensus diagnosis was 77% (kappa(w) = .37), with a sensitivity of the ADOS of 90.4% and a specificity of 48.1% regarding the discrimination of autism and other autistic disorders. Conclusions: The ADOS is a reliable and sufficiently sensitive diagnostic tool in the assessment of autistic disorders. For ICD-10/DSM-IV classification and to ensure a high specificity of diagnosis additional information concerning repetitive, stereotyped behavior and early development (e.g. taken from the ADI-R) has to be collected. C1 Univ Frankfurt Klinikum, Klin Psychiat & Psychotherapie Kindes & Jugendalt, D-60528 Frankfurt, Germany. RP Bolte, S (reprint author), Univ Frankfurt Klinikum, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, D-60528 Frankfurt, Germany. EM Boelte@em.uni-frankfurt.de CR Bolte S, 2002, CHILD PSYCHIAT HUM D, V33, P165, DOI 10.1023/A:1020734325815 Bolte S, 2000, DIAGNOSTICA, V46, P149, DOI 10.1026//0012-1924.46.3.149 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Howlin P., 1998, AUTISM PERVASIVE DEV, P209 Klin A, 2000, J AUTISM DEV DISORD, V30, P163, DOI 10.1023/A:1005415823867 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2002, CHILD ADOL PSYCH CL, P636 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C., 2001, AUTISM DIAGNOSTIC OB Bolte S, 2001, Z KINDER JUG-PSYCH, V29, P221, DOI 10.1024//1422-4917.29.3.221 Pilowsky T, 1998, J AUTISM DEV DISORD, V28, P143, DOI 10.1023/A:1026092632466 Poustka F, 1996, PSYCHOPATHOLOGY, V29, P145 Ruhl D, 2004, DIAGNOSTISCHE BEOBAC Rutter M., 2003, SOCIAL COMMUNICATION Schmotzer G, 1993, AUTISMUS DIAGNOSTISC NR 16 TC 29 Z9 29 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD FEB PY 2004 VL 32 IS 1 BP 45 EP 50 DI 10.1024/1422-4917.32.1.45 PG 6 WC Psychiatry SC Psychiatry GA 772NU UT WOS:000188848800006 PM 14992047 ER PT J AU Busari, JO Weggelaar, NM AF Busari, JO Weggelaar, NM TI How to investigate and manage the child who is slow to speak SO BRITISH MEDICAL JOURNAL LA English DT Review ID LANGUAGE; DISORDERS AB Delay in speech and language development is the most common developmental disorder in children aged 3 to 16 years. The prevalence of this disorder ranges from 1% to 32% in the normal population and is influenced by factors such as the age of the child at presentation and the test method used in diagnosis.(1-2) A high rate of comorbidity (up to 50%) is known to exist between psychiatric disorders such as autism and disorders of speech and language development.(3) Despite the prevalence and reported risks of comorbidity, however, about 60% of cases of speech and language delay tend to resolve spontaneously in children aged under 3 years.(1) Children who are slow to speak form a particular category of patients with speech and language developmental disorders and often present clinicians with a dilemma-whether to conduct further investigations or just wait and see. This is because a delay in speaking could be either a normal (and temporary) stage in the child's development or the initial symptom of a psychiatric, neurological, or behavioural problem. As a result, the timely diagnosis, choice of therapy, and an individualised approach to the child with a speech and language delay become imperative as these interventions may prevent subsequent psychological or psychiatric problems later in life. We provide here an update of the current literature on speech and language development in children. Using a real patient encounter, we illustrate how a child with a delay in language development is presented to the clinician. We also propose a guideline that can be used to investigate and manage children with speech or language delays. C1 Boven IJ Hosp, Dept Paediat, NL-1030 BD Amsterdam, Netherlands. Univ Amsterdam, Acad Med Ctr, Emma Childrens Hosp, NL-1105 AZ Amsterdam, Netherlands. RP Busari, JO (reprint author), Boven IJ Hosp, Dept Paediat, Statenjachtstr 1, NL-1030 BD Amsterdam, Netherlands. EM Ojay33@hotmail.com CR Beitchman JH, 1998, J AM ACAD CHILD PSY, V37, P1117 BERMAN S, 1996, PEDIAT DECISION MAKI, P40 CANTWEL DP, 1991, PSYCHIAT DEV DISORDE Chevrie-Muller C, 2000, Acta Otorhinolaryngol Belg, V54, P419 COPLAN J, 1990, PEDIATRICS, V86, P963 Cronin VS, 2002, J CHILD LANG, V29, P189, DOI 10.1017/S0305000901004998 CROSLEY CJ, 1999, PEDIAT NEUROLOGY PRI, P568 FENSON L, 1994, MONOGR SOC RES CHILD, V59, pR5 GILLBERG C, 1998, DIS NERVOUS SYSTEM C, P850 LAW J, 1998, HLTH TECHNOL ASSESS, V2 Toppelberg CO, 2000, J AM ACAD CHILD PSY, V39, P143, DOI 10.1097/00004583-200002000-00011 Wetherby AM, 2002, J SPEECH LANG HEAR R, V45, P1202, DOI 10.1044/1092-4388(2002/097) NR 12 TC 6 Z9 8 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD JAN 31 PY 2004 VL 328 IS 7434 BP 272 EP 276 DI 10.1136/bmj.328.7434.272 PG 5 WC Medicine, General & Internal SC General & Internal Medicine GA 771LC UT WOS:000188786000024 PM 14751899 ER PT J AU Cosgrove, PVF AF Cosgrove, PVF TI Diagnosis of autism - Use of autistic spectrum shows undisciplined thinking SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 Bristol Prior Clin, Bath BA2 5YD, Avon, England. RP Cosgrove, PVF (reprint author), Bristol Prior Clin, Bath BA2 5YD, Avon, England. EM bristolpriorityclinic@btopenworld.com CR Baird G, 2003, BRIT MED J, V327, P488, DOI 10.1136/bmj.327.7413.488 NR 1 TC 0 Z9 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD JAN 24 PY 2004 VL 328 IS 7433 BP 226 EP 226 DI 10.1136/bmj.328.7433.226-b PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 769LU UT WOS:000188652200028 PM 14739198 ER PT J AU McClure, L Mamdani, H McCaughey, R AF McClure, L Mamdani, H McCaughey, R TI Diagnosis of autism - Adequate funding is needed for assessment services SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 Vale Leven Hosp, Acorn Ctr, Alexandria G83 0UA, Scotland. RP McClure, L (reprint author), Vale Leven Hosp, Acorn Ctr, Alexandria G83 0UA, Scotland. EM imcclure@vol.scot.nhs.uk CR Baird G, 2003, BRIT MED J, V327, P488, DOI 10.1136/bmj.327.7413.488 Le Couteur A. S., 2003, NATL AUTISM PLAN CHI *PUBL HLTH I SCOTL, 2001, AUT SPECTR DIS ASS R NR 3 TC 0 Z9 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD JAN 24 PY 2004 VL 328 IS 7433 BP 226 EP 226 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 769LU UT WOS:000188652200026 ER PT J AU Timimi, S AF Timimi, S TI Diagnosis of autism - Current epidemic has social context SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 Ash Villa, Sleaford NG34 8QA, Lincs, England. RP Timimi, S (reprint author), Ash Villa, Sleaford NG34 8QA, Lincs, England. EM stimimi@talk21.com CR Baird G, 2003, BRIT MED J, V327, P488, DOI 10.1136/bmj.327.7413.488 Timimi S., 2002, PATHOLOGICAL CHILD P NR 2 TC 0 Z9 0 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD JAN 24 PY 2004 VL 328 IS 7433 BP 226 EP 226 DI 10.1136/bmj.328.7433.226-a PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 769LU UT WOS:000188652200027 PM 14739199 ER PT J AU Yazbak, FE AF Yazbak, FE TI Autism seems to be increasing worldwide, if not in London SO BRITISH MEDICAL JOURNAL LA English DT Letter C1 TL Autism Res, Falmouth, MA 02540 USA. RP Yazbak, FE (reprint author), TL Autism Res, 70 Viewcrest Dr, Falmouth, MA 02540 USA. EM TLAutStudy@aol.com CR California Department of Developmental Services, 2003, AUT SPECTR DIS CHANG MAYOR S, 2003, BRIT MED J, V327, P248, DOI 10.1136/bmj.327.7409.248 RAMADAN G, 2002, ARAB NEWS 0809 2003, INVERNESS COURI 1205 NR 4 TC 6 Z9 7 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0959-535X J9 BRIT MED J JI Br. Med. J. PD JAN 24 PY 2004 VL 328 IS 7433 BP 226 EP 227 DI 10.1136/bmj.328.7433.226-c PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 769LU UT WOS:000188652200029 PM 14739196 ER PT J AU Singh, VK Rivas, WH AF Singh, VK Rivas, WH TI Prevalence of serum antibodies to caudate nucleus in autistic children SO NEUROSCIENCE LETTERS LA English DT Article DE autism; autoimmunity; caudate nucleus; antibodies; neurobiology AB Autism may involve autoimmunity to brain. We studied regional distribution of antibodies to rat caudate nucleus, cerebral cortex, cerebellum, brain stem and hippocampus. The study included 30 normal and 68 autistic children. Antibodies were assayed by immunoblotting. Autistic children, but not normal children, had antibodies to caudate nucleus (49% positive sera), cerebral cortex (18% positive sera) and cerebellum (9% positive sera). Brain stem and hippocampus were negative. Antibodies to caudate nucleus were directed towards three proteins having 160, 115 and 49 kD molecular weights. Since a significant number of autistic children had antibodies to caudate nucleus, we propose that an autoimmune reaction to this brain region may cause neurological impairments in autistic children. Thus, the caudate nucleus might be involved in the neurobiology of autism. (C) 2003 Elsevier Ireland Ltd. All rights reserved. C1 Utah State Univ, Dept Biol, Logan, UT 84322 USA. RP Singh, VK (reprint author), Utah State Univ, Dept Biol, Biotechnol Ctr Bldg,4700 Old Main Hill, Logan, UT 84322 USA. 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RP Perry, EK (reprint author), Newcastle Gen Hosp, Dev Clin Brain Ageing, MRC Bldg,Westgate Rd, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England. 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genetic; association; HOXA1; HOXB1 ID LINKAGE-DISEQUILIBRIUM; SEROTONIN TRANSPORTER; SUSCEPTIBILITY GENE; FAMILY HISTORY; GENOMIC SCREEN; DISORDER; HOXA1; HOXB1; TWIN; TRANSMISSION AB Two recent studies have reported conflicting findings of association of a variant in the HOXA1 gene and autism. To try to resolve the conflict in findings, we conducted an association study in 78 Irish families of the reported DNA variants. We did not find statistically significant association between the variants and autism. Similarly there was no evidence of preferential transmission of variants from parent of either sex to affected offspring. We also report negative findings for HOXB1 variants. We conclude that the HOXA1/B1 are unlikely to be the susceptibility genes for autism in our sample. (C) 2003 Wiley-Liss, Inc. C1 Univ Dublin Trinity Coll, Smurfit Inst Genet, Dept Genet, Dublin 2, Ireland. RP Gallagher, L (reprint author), Univ Dublin Trinity Coll, Smurfit Inst Genet, Dept Genet, Dublin 2, Ireland. 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J. Med. Genet. B PD JAN 1 PY 2004 VL 124B IS 1 BP 64 EP 67 DI 10.1002/ajmg.b.20094 PG 4 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 777PE UT WOS:000189186100014 PM 14681917 ER PT J AU Greenberg, JS Seltzer, MM Krauss, MW Chou, RJA Hong, J AF Greenberg, JS Seltzer, MM Krauss, MW Chou, RJA Hong, J TI The effect of quality of the relationship between mothers and adult children with schizophrenia, autism, or Down syndrome on maternal well-being: The mediating role of optimism SO AMERICAN JOURNAL OF ORTHOPSYCHIATRY LA English DT Article ID GENERALIZED OUTCOME EXPECTANCIES; SERIOUS MENTAL-ILLNESS; LATER-LIFE; RETARDATION; GRATIFICATIONS; EXPERIENCE; APPRAISAL; DAUGHTERS; BEHAVIOR; FAMILIES AB This article investigates the effects of the quality of the relationship between maternal caregivers and their adult child with disabilities on maternal well-being and whether this effect is mediated by dispositional optimism. Mothers caring for an adult child with Down syndrome (n = 126), schizophrenia (n = 292), or autism (n = 102) were surveyed. Mothers of adults with schizophrenia and autism had better psychological well-being when the mother/adult child relationship was positive, but this effect was mediated totally or partially by optimism. For all 3 groups, optimism was related to better mental and physical health. The findings highlight the importance of dispositional optimism, a psychological resource that has been virtually ignored in studies of family caregivers of adults with disabilities. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. Univ Wisconsin, Sch Social Work, Madison, WI 53705 USA. Brandeis Univ, Heller Sch, Waltham, MA 02254 USA. RP Greenberg, JS (reprint author), Univ Wisconsin, Waisman Ctr, 1500 Highland Ave,Room 555, Madison, WI 53705 USA. CR BARON RM, 1986, J PERS SOC PSYCHOL, V51, P1173, DOI 10.1037/0022-3514.51.6.1173 Bengtson V. 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PD JAN PY 2004 VL 74 IS 1 BP 14 EP 25 DI 10.1037/0002-9432.74.1.14 PG 12 WC Psychiatry; Social Work SC Psychiatry; Social Work GA 842OL UT WOS:000223013600003 PM 14769105 ER PT J AU Blaxill, MF AF Blaxill, MF TI Concerns continue over mercury and autism SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE LA English DT Letter CR California Department of Developmental Services, 2003, AUT SPECTR DIS CHANG California Department of Developmental Services, 1999, CHANG POP PERS AUT P Geier MR, 2003, EXP BIOL MED, V228, P660 HOLMES AS, 2004, INT J TOXICOL, V111, P277 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Stehr-Green P, 2003, AM J PREV MED, V25, P101, DOI 10.1016/S0749-3797(03)00113-2 Stratton K., 2001, IMMUNIZATION SAFETY NR 7 TC 6 Z9 7 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0749-3797 J9 AM J PREV MED JI Am. J. Prev. Med. PD JAN PY 2004 VL 26 IS 1 BP 91 EP 91 DI 10.1016/j.amepre.2003.10.019 PG 1 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA 760DZ UT WOS:000187797500014 PM 14700719 ER PT J AU Stehr-Green, P AF Stehr-Green, P TI Concerns continue over mercury and autism - Reply SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE LA English DT Letter C1 Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA. RP Stehr-Green, P (reprint author), Univ Washington, Dept Epidemiol, Seattle, WA 98195 USA. CR BLAXILL M, 2001, THIMEROSAL CONTAININ MORGENSTERN H, 1982, AM J PUBLIC HEALTH, V72, P1336, DOI 10.2105/AJPH.72.12.1336 Stehr-Green P, 2003, AM J PREV MED, V25, P101, DOI 10.1016/S0749-3797(03)00113-2 NR 3 TC 0 Z9 0 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0749-3797 J9 AM J PREV MED JI Am. J. Prev. Med. PD JAN PY 2004 VL 26 IS 1 BP 91 EP 92 DI 10.1016/j.amepre.2003.10.019 PG 2 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA 760DZ UT WOS:000187797500015 ER PT J AU Krausz, C Quintana-Murci, L Forti, G AF Krausz, C Quintana-Murci, L Forti, G TI Y chromosome polymorphisms in medicine SO ANNALS OF MEDICINE LA English DT Review DE medicine; polymorphisms; reproductive medicine; spermatogenesis; Y chromosome; Y haplogroups ID SPONTANEOUSLY HYPERTENSIVE RAT; HUMAN PROSTATE-CANCER; BLOOD-PRESSURE; MALE-INFERTILITY; DNA HAPLOTYPES; EXPRESSION ANALYSIS; GENERAL-POPULATION; TURNER-SYNDROME; CANDIDATE GENE; LONG ARM AB Ninety-five percent of the length of the human Y chromosome is inherited as a single block in linkage from father to male offspring as a haploid entity. Thus, the Y chromosome represents an invaluable record of all mutations that have occurred along male lineages throughout evolution. For this reason, Y chromosomal DNA variation has been mainly used for investigations on human evolution and for forensic purposes or paternity analysis. Recently, Y chromosomal polymorphisms have been applied in molecular medicine from the perspective of male-specific (spermatogenic failure, testis and prostate cancer) and prevalently male-associated (hypertension, autism) diseases. The absence of recombination on the MSY (male-specific Y) region means that polymorphisms, located in this region, are in tight association with potential functional variations associated with Y-linked phenotypes. Thus, an indirect way to explore if Y chromosome genes are involved in the etiology of a specific disease is the definition of Y chromosome haplo-groups in patients versus disease-free and/or the general population. Data on patients with reduced sperm count and prostate cancer indicate that the 'at risk Y haplogroup' may be different in different populations. The situation is rather contradictory for other male-specific or male-associated diseases and further multicenter - possibly multiethnic - studies are needed. C1 Univ Florence, Dept Clin Physiopathol, Androl Unit, I-50139 Florence, Italy. Inst Pasteur, CNRS, URA1961, Paris, France. Inst Pasteur, Unit Mol Prevent & Therapy Human Dis, Paris, France. RP Krausz, C (reprint author), Univ Florence, Dept Clin Physiopathol, Androl Unit, Viale Pieraccini 6, I-50139 Florence, Italy. 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PY 2004 VL 56 SU 8 BP S94 EP S94 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100324 ER PT J AU Cortell, R Bukelis, I Gray, RM Cox, C Tierney, E Stanard, P Kau, ASM Kaufmann, WE AF Cortell, R Bukelis, I Gray, RM Cox, C Tierney, E Stanard, P Kau, ASM Kaufmann, WE TI Autism spectrum disorder in boys with Fragile X: Serial evaluation SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 1 Z9 1 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S104 EP S104 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100360 ER PT J AU Kagawa, K Chugani, DC Behen, M Chandana, SR Juhasz, C Muzik, O Chugani, HT AF Kagawa, K Chugani, DC Behen, M Chandana, SR Juhasz, C Muzik, O Chugani, HT TI Altered brain growth in children with tuberous sclerosis complex and autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S93 EP S94 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100323 ER PT J AU Nabi, R Serajee, FJ Zhong, H Huq, AHMM AF Nabi, R Serajee, FJ Zhong, H Huq, AHMM TI Association analyses of 50 candidate genes for autism from 7q21-36 region SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S100 EP S101 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100348 ER PT J AU Nabi, R Serajeel, FJ Zhong, H Huq, AHMM AF Nabi, R Serajeel, FJ Zhong, H Huq, AHMM TI Distribution and heritability of phenotypic traits in autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S105 EP S105 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100364 ER PT J AU Nabi, R Serajee, FJ Zhong, H Huq, AHMM AF Nabi, R Serajee, FJ Zhong, H Huq, AHMM TI Serotonin neurotransmitter system in autism: Association with HTR4, HTR6, and TDO2 SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S99 EP S100 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100344 ER PT J AU Nabi, R Serajee, FJ Zhong, H Huq, AHMM AF Nabi, R Serajee, FJ Zhong, H Huq, AHMM TI Genetics of phosphatidylinositol signaling in autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S103 EP S103 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100356 ER PT J AU Serajee, FJ Nabi, R Zhong, H Huq, AHMM AF Serajee, FJ Nabi, R Zhong, H Huq, AHMM TI Association of chromosome 15 GABA(A) receptor subunit genes with autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S103 EP S103 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100357 ER PT J AU Serajee, FJ Nabi, R Zhong, H Huq, AHMM AF Serajee, FJ Nabi, R Zhong, H Huq, AHMM TI Association of reelin gene polymorphisms with autism SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S99 EP S99 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100342 ER PT J AU Serajee, FJ Nabi, R Zhong, H Huq, AHMM AF Serajee, FJ Nabi, R Zhong, H Huq, AHMM TI Immunogenetic studies in autism: Association with IL4R and ICAM5 genes SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S101 EP S101 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100349 ER PT J AU Spence, SJ Caplan, R Sullivan, AEN Qui, SK Gotham, KO Lord, CE AF Spence, SJ Caplan, R Sullivan, AEN Qui, SK Gotham, KO Lord, CE TI Relationship of epilepsy and IQ in autism spectrum disorders and non-spectrum developmental delay SO ANNALS OF NEUROLOGY LA English DT Meeting Abstract CT 33rd Annual Meeting of the Child-Neurology-Society CY OCT 13-16, 2004 CL Toronto, CANADA SP Child Neurol Soc NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PY 2004 VL 56 SU 8 BP S125 EP S126 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 852ND UT WOS:000223761100439 ER PT J AU Veenstra-VanderWeele, J Christian, SL Cook, EH AF Veenstra-VanderWeele, J Christian, SL Cook, EH TI Autism as a paradigmatic complex genetic disorder SO ANNUAL REVIEW OF GENOMICS AND HUMAN GENETICS LA English DT Review DE autism; chromosomal abnormalities; epigenetic; linkage; association ID SEROTONIN TRANSPORTER GENE; PERVASIVE DEVELOPMENTAL DISORDERS; CPG-BINDING PROTEIN-2; FRAGILE-X-SYNDROME; LINKAGE-DISEQUILIBRIUM; RETT-SYNDROME; PROMOTER VARIANTS; GENOMEWIDE SCREEN; SPECTRUM DISORDERS; ALLELIC VARIANTS AB Autism is one of the most heritable complex disorders, with compelling evidence for genetic factors and little or no support for environmental influence. The estimated prevalence of autism has increased since molecular genetic studies began, owing to loosening of diagnostic criteria and, more importantly, to more complete ascertainment strategies. This has led to a reduction in the sibling relative risk, but strong heritability estimates remain. It is essential to recognize that genetics is the only current approach to understanding the pathophysiology of autism in which there is not the usual concern about whether one is studying a consequence rather than a cause. There are hundreds, if not thousands, of patients with autism spectrum disorder with documented single-gene mutations or chromosomal abnormalities. Autism may be one of the most complex, yet strongly genetic, disorders in which chromosomal disorders, relatively rare highly penetrant mutations, and multiplicative effects of common variants all have support in different cases and families. The field of complex genetics is replete with many researchers and reviewers who want to promote their overly focused interest in one method at the exclusion of others. However, it is essential that the restricted interests of patients with autism not be reflected in overly restrictive genetic approaches if we are to better understand the genetics of autism in the most expeditious and thorough manner. C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. RP Veenstra-VanderWeele, J (reprint author), Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. 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Rev. Genomics Hum. Genet. PY 2004 VL 5 BP 379 EP 405 DI 10.1146/annurev.genom5.061903.180050 PG 27 WC Genetics & Heredity SC Genetics & Heredity GA 861KO UT WOS:000224415600015 PM 15485354 ER PT J AU Insel, TR Fernald, RD AF Insel, TR Fernald, RD TI How the brain processes social information: Searching for the social brain SO ANNUAL REVIEW OF NEUROSCIENCE LA English DT Review DE imprinting; vomeronasal; oxytocin; parental care; affiliation ID QUANTITATIVE BEHAVIORAL OBSERVATIONS; GONADOTROPIN-RELEASING-HORMONE; VOLES MICROTUS-OCHROGASTER; ACCESSORY OLFACTORY-BULB; MEDIAL PREOPTIC AREA; PAIR-BOND FORMATION; DARK-REARED CHICKS; MATERNAL-BEHAVIOR; LACTATING RATS; PRAIRIE VOLE AB Because information about gender, kin, and social status are essential for reproduction and survival, it seems likely that specialized neural mechanisms have evolved to process social information. This review describes recent studies of four aspects of social information processing: (a) perception of social signals via the vomeronasal system, (b) formation of social memory via long-term filial imprinting and short-term recognition, (c) motivation for parental behavior and pair bonding, and (d) the neural consequences of social experience. Results from these studies and some recent functional imaging studies in human subjects begin to define the circuitry of a "social brain." Such neurodevelopmental disorders as autism and schizophrenia are characterized by abnormal social cognition and corresponding deficits in social behavior; thus social neuroscience offers an important opportunity for translational research with an impact on public health. C1 NIMH, Bethesda, MD 20892 USA. Stanford Univ, Program Neurosci, Stanford, CA 94305 USA. RP Insel, TR (reprint author), NIMH, Bethesda, MD 20892 USA. 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Rev. Neurosci. PY 2004 VL 27 BP 697 EP 722 DI 10.1146/annurev.neuro.27.070203.144148 PG 26 WC Neurosciences SC Neurosciences & Neurology GA 845MH UT WOS:000223246300025 PM 15217348 ER PT J AU Davis, BW Nattrass, K O'Brien, S Patronek, G MacCollin, M AF Davis, BW Nattrass, K O'Brien, S Patronek, G MacCollin, M TI Assistance dog placement in the pediatric population: Benefits, risks, and recommendations for future application SO ANTHROZOOS LA English DT Review DE autism; familial support; human-animal bond; pediatric disability; service dog; social support ID SERVICE DOGS; GUIDE DOGS; PEOPLE; DISABILITIES; IMPAIRMENTS; OWNERSHIP; MOBILITY AB Assistance animals have long been recognized for their value in enhancing the lives of adults with disabilities by increasing the physical independence, confidence, and social lives of their handlers. Recently, this concept has been applied to the growing population of children with physical disabilities and developmental impairments, though the benefits and risks of these placements have not been thoroughly assessed. Our study used interviews to evaluate the outcome of placing assistance dogs in the pediatric population, looking specifically at the unique advantages and disadvantages of this application of the human-animal bond. We administered a structured interview assessing risks and benefits of assistance dog relationships to 17 families with a child under 18 years who graduated from a single provider (NEADS) over a five-year time period. Benefits were found in 88% of families, and were overwhelmingly social and cognitive, with additional physical and medical benefits for the pediatric client. However, risks, including behavioral, financial, and time/cost issues were significant, becoming a burden in 53% of families. Perhaps more than with adult placements, we found that it was of prime importance to understand the assistance animal in the context of the family, rather than just in relation to the individual with a disability. It is hoped that results of this and future studies will enhance the welfare of both client and assistance animal, as well as the overall success of this unique human-animal relationship. (c) 2004 International Societyfor Anthrozoology C1 Tufts Univ, Sch Vet Med, Ctr Anim & Publ Policy, Medford, MA 02155 USA. Tufts Univ, Ctr Children, Medford, MA 02155 USA. RP MacCollin, M (reprint author), Massachusetts Gen Hosp E, Bldg 149,13th St, Charlestown, MA 02129 USA. 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EM kristell@psy.uq.edu.au NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2004 VL 56 SU S BP 17 EP 17 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 893MM UT WOS:000226723400051 ER PT J AU Nicoll, N AF Nicoll, N TI A preliminary evaluation of the Autism Diagnostic Observation Schedule-Generic in an Australian clinical setting SO AUSTRALIAN JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract EM nprnic@ozemail.com.au NR 0 TC 0 Z9 0 PU AUSTRALIAN PSYCHOLOGICAL SOC PI CARLTON PA 1 GRATTAN STREET, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-9530 J9 AUST J PSYCHOL JI Aust. J. Psychol. PY 2004 VL 56 SU S BP 24 EP 25 PG 2 WC Psychology, Multidisciplinary SC Psychology GA 893MM UT WOS:000226723400072 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 erratic body movement maintained by visual stimulation - Incorporating conjugate, reinforcement into a paired-stimulus preference assessment SO BEHAVIOR MODIFICATION LA English DT Article DE automatic reinforcement; conjugate reinforcement; noncontingent reinforcement; stimulus preference assessment; visual stimulation ID ABERRANT BEHAVIOR; DEVELOPMENTAL-DISABILITIES; AUTOMATIC REINFORCEMENT AB A concurrent-operants design was used to analyze the repetitive behavior of observing reflective surfaces while simultaneously engaging in erratic gross-motor body movements (EBMs) exhibited by a young boy diagnosed with autism. The assessment involved an evaluation of preference for controlled (i.e., the participant controlled the visual activity on a TV screen) versus uncontrolled (i.e., the participant viewed a previously recorded tape from the controlled condition) TV footage of his EBMs. The analysis indicated that both observing and EBMs were maintained by the direct correspondence between the body movements and the visual stimulation they produced when controlled by the participant. Thus, the EBMs appeared to be maintained on a conjugate schedule of reinforcement. C1 Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. Western Michigan Univ, Kalamazoo, MI 49008 USA. Marcus Inst, Atlanta, GA USA. Univ Nevada, Reno, NV 89557 USA. RP Carr, JE (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Kalamazoo Ave, Kalamazoo, MI 49008 USA. 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Modificat. PD JAN PY 2004 VL 28 IS 1 BP 118 EP 132 DI 10.1177/0145445503259260 PG 15 WC Psychology, Clinical SC Psychology GA 752LZ UT WOS:000187163500005 PM 14710709 ER PT J AU Silva, JA Leong, GB Ferrari, MM AF Silva, JA Leong, GB Ferrari, MM TI A neuropsychiatric developmental model of serial homicidal behavior SO BEHAVIORAL SCIENCES & THE LAW LA English DT Article ID ASPERGERS-SYNDROME; SEXUAL HOMICIDE; MIND; ADULTS; AUTISM; VIOLENCE; DISORDERS; JUVENILE; CHILDREN AB Serial sexual homicide has been the object of intensive study from forensic psychiatric, criminological, developmental, and sociological perspectives. In contradistinction to these approaches, neuropsychiatric concepts and methods have received relatively little attention in this area. In this article we adopt a neuropsychiatric developmental perspective and undertake a review of the psychiatric literature on violence and autism spectrum disorders. Our analysis of this literature suggests the presence of an association between autism spectrum psychopathology and serial homicidal behavior. Recommendations for further research to help clarify the nature of this association are briefly discussed. Copyright (C) 2004 John Wiley Sons, Ltd. C1 Univ Washington, Dept Psychiat, Tacoma, WA USA. Western State Hosp, Ctr Forens Serv, Tacoma, WA USA. Kaiser Permanente Med Grp, Div Child & Adolescent Psychiat, Santa Clara, CA USA. Stanford Univ, Dept Psychiat & Behav Sci, Stanford, CA 94305 USA. RP Silva, JA (reprint author), POB 20928, San Jose, CA 95160 USA. 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Law PY 2004 VL 22 IS 6 BP 787 EP 799 DI 10.1002/bsl.620 PG 13 WC Psychology, Applied; Law SC Psychology; Government & Law GA 884RC UT WOS:000226102600004 PM 15568202 ER PT J AU Attwood, T AF Attwood, T TI Cognitive behaviour therapy for children and adults with Asperger's syndrome SO BEHAVIOUR CHANGE LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; OBSESSIVE-COMPULSIVE DISORDER; HIGH-FUNCTIONING ADULTS; EXECUTIVE FUNCTIONS; FAMILY-HISTORY; AUTISM; MIND; ADOLESCENT AB Asperger's syndrome is a relatively newly diagnosed developmental disorder within the autistic spectrum. Children and adults with Asperger's syndrome have an intellectual ability within the normal range but due to their unusual profile of cognitive, social and emotional abilities are vulnerable to the development of a secondary mood disorder. This paper provides an explanation of the abilities associated with Asperger's syndrome, and modifications to cognitive behaviour therapy (CBT) for this very unusual client group. In particular, the paper emphasises the importance of affective education for this clinical population and describes a new strategy used in cognitive restructuring, namely, the emotional toolbox. The paper concludes with a brief description of a current evaluation study of the effectiveness of CBT to treat anxiety and anger in children who have Asperger's syndrome. However, the strategies described in this paper can also be used with adults with Asperger's syndrome and applied to other clinical populations. C1 Griffith Univ, Nathan, Qld 4111, Australia. RP Attwood, T (reprint author), Aspergers Syndrome Clin, POB 224, Petrie, Qld 4502, Australia. 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Change PY 2004 VL 21 IS 3 BP 147 EP 161 DI 10.1375/bech.21.3.147.55995 PG 15 WC Psychology, Clinical SC Psychology GA 886XR UT WOS:000226266900001 ER PT J AU Rodier, PM AF Rodier, PM TI 2003 Warkany lecture: Autism as a birth defect SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY LA English DT Editorial Material DE autism; birth defect; developmental disorder; autism spectrum disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; FETAL VALPROATE SYNDROME; SPECTRUM DISORDERS; MOBIUS SEQUENCE; SUSCEPTIBILITY GENE; ALLELIC VARIANTS; CHILDREN; THALIDOMIDE; ANOMALIES; EMBRYOPATHY 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, Box 668,601 Elmwood Ave, Rochester, NY 14642 USA. 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PD JAN PY 2004 VL 70 IS 1 BP 1 EP 6 DI 10.1002/bdra.10152 PG 6 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA 769FW UT WOS:000188616700001 PM 14745888 ER PT J AU Smeeth, L Cook, C Fombonne, PE Heavey, L Rodrigues, LC Smith, PG Hall, AJ AF Smeeth, Liam Cook, Claire Fombonne, Professor Eric Heavey, Lisa Rodrigues, Laura C. Smith, Peter G. Hall, Andrew J. TI Rate of first recorded diagnosis of autism and other pervasive developmental disorders in United Kingdom general practice, 1988 to 2001 SO BMC MEDICINE LA English DT Article AB Background: There has been concern that the incidence of autism and other pervasive developmental disorders (PDDs) is increasing. Previous studies have been smaller, restricted to autism (excluding other pervasive developmental disorders such as Asperger's syndrome), included boys only, or have not been based on a national sample. We investigated time trends in the rates of diagnosis of pervasive developmental disorders. Methods: We analysed the rates of first diagnosis of pervasive developmental disorders among people registered with a practice contributing to the United Kingdom General Practice Research Database during the period 1988 to 2001. We included 1410 cases from over 14 million person-years of observation. The main outcome measures were rates of diagnosis of pervasive developmental disorders by year of diagnosis, year of birth, gender and geographical region. Results: The rate increased progressively from 0.40/10,000 person-years (95% CI 0.30 to 0.54) in 1991 to 2.98/10,000 (95% CI 2.56 to 3.47) in 2001. A similar change occurred in the age standardised incidence ratios, from 35 (95% CI: 26-47) in 1991 to 365 (95% CI: 314-425) in 2001. The temporal increase was not limited to children born during specific years nor to children diagnosed in a specific time period. The rate of diagnosis of PDDs other than autism rose from zero for the period 1988-1992 to 1.06/10,000 person-years in 2001. The rate of diagnosis of autism also increased but to a lesser extent. There was marked geographical variation in rates, with standardised incidence ratios varying from 66 for Wales to 141 for the South East of England. Conclusions: Better ascertainment of diagnosis is likely to have contributed to the observed temporal increase in rates of diagnosis of PDD, but we cannot exclude a real increase. C1 [Smeeth, Liam] London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, London WC1E 7HT, England. [Cook, Claire; Rodrigues, Laura C.; Smith, Peter G.; Hall, Andrew J.] London Sch Hyg & Trop Med, Dept Infect & Trop Dis, London WC1E 7HT, England. [Fombonne, Professor Eric] McGill Univ, Dept Psychiat, Montreal, PQ, Canada. [Heavey, Lisa] Kings Coll London, Inst Psychiat, London WC2R 2LS, England. RP Smeeth, L (reprint author), London Sch Hyg & Trop Med, Dept Epidemiol & Populat Hlth, Keppel St, London WC1E 7HT, England. EM liam.smeeth@lshtm.ac.uk; claire.cook@lshtm.ac.uk; eric.fombonne@staff.mcgill.ca; l.reidy@shu.ac.uk; laura.rodrigues@lshtm.ac.uk; peter.smith@lshtm.ac.uk; andy.hall@lshtm.ac.uk RI Research Datalink, Clinical Practice/H-2477-2013 FU Medical Research Council FX The study was funded by the Medical Research Council. LS is supported by a Medical Research Council Clinician Scientist Fellowship. 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DEVELOPMENT LA English DT Article DE pervasive developmental disorders; somatic; behaviour ID FEEDING PROBLEMS; NORMAL-CHILDREN; AUTISM; INDOLYL-3-ACRYLOYLGLYCINE; IDENTIFICATION; URINE AB Objectives To ascertain the frequency of parental reporting of selected variables related to development, behaviour and physiology in subgroups diagnosed with pervasive developmental disorders (PDDs) and identify any significant intragroup differences. Design Retrospective cross-sectional analysis of records of patients (n = 512) held on a computerized database with a chronological age between 3 and 11 years resident in the UK/Republic of Ireland and with a formal diagnosis of autism, Asperger syndrome (AS) or autism spectrum disorder (ASD). Methods Non-parametric analysis (P > 0.01) of the frequency of specific variables for PDD subgroups reported by parents/primary caregiver. Variables included timing of symptom onset, presence of skills acquired prior to symptom onset, indications of regression and regression events, current language, history of viral infections, history of ear problems, achievement of continence, current skin complaints, current bowel habits and adverse events at parturition. Results Preliminary results showed general agreement with the principle diagnostic differences between the PDD subgroups with patients diagnosed with AS showing an increased frequency of skills acquired before symptom onset (two- to three-word phrase speech, toileting skills) and a decreased frequency of regression in acquired skills when compared with other PDD subgroups. Developmental milestones such as the achievement of bowel and bladder continence were also more frequently reported for the AS group. Infantile feeding problems defined as vomiting, reflux, colic and failure to feed were more frequently reported for the AS group as was a reported history of the bacterial skin infection impetigo. Results are discussed with reference to relationships between behavioural and somatic factors in PDD. C1 Univ Sunderland, Sch Hlth Nat & Social Sci, Autism Res Unit, Sunderland SR1 3SD, England. RP Whiteley, P (reprint author), Univ Sunderland, Sch Hlth Nat & Social Sci, Autism Res Unit, Sunderland SR1 3SD, England. 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PD JAN PY 2004 VL 30 IS 1 BP 5 EP 11 DI 10.1111/j.1365-2214.2004.00380.x PG 7 WC Psychology, Developmental; Pediatrics SC Psychology; Pediatrics GA 753RR UT WOS:000187244800002 PM 14678306 ER PT J AU Carpenter, EM Frankel, F Marina, M Duan, N Smalley, SL AF Carpenter, EM Frankel, F Marina, M Duan, N Smalley, SL TI Internet treatment delivery of parent-adole scent conflict training for families with an ADHD teen: A feasibility study SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Article DE Internet; treatment; parent-adolescent conflict; attention-deficit/hyperactivity disorder; web-based; parent training ID DEFICIT HYPERACTIVITY DISORDER; MENTAL-HEALTH; ADOLESCENTS; CHILDREN; PROGRAM; EDUCATION; BEHAVIOR; BENEFITS; STRESS; AUTISM AB The present study examines the feasibility of Internet delivery of a Parent-Adolescent Conflict Training (PACT) program to families with an ADHD teen. The goals of the project are to ascertain the willingness of families to participate in this web-based study, identify relevant issues related to confidentiality of Internet data collection, and determine participant satisfaction with this treatment approach. Six families participated and four were compliant with the Internet participation requirements. A series of single subject linear regressions revealed that all but one participant maintained a steady login rate over time. Treatment compliance results are promising. Participants gave high ratings to the security of the website and Satisfaction Scale scores were also above neutral. (C) 2004 by The Haworth Press, Inc. All rights reserved. C1 Univ Calif Los Angeles, Parenting & Childrens Friendship Program, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, NPI, Cttr Neurobehav Genet, Los Angeles, CA 90024 USA. 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Behav. Ther. PY 2004 VL 26 IS 3 BP 1 EP 20 DI 10.1300/J019v26n03_01 PG 20 WC Psychology, Clinical; Family Studies SC Psychology; Family Studies GA 861FX UT WOS:000224402600001 ER PT J AU Luiselli, JK Ricciardi, JN Schmidt, S Tarr, M AF Luiselli, JK Ricciardi, JN Schmidt, S Tarr, M TI Brief functional analysis and intervention evaluation for treatment of saliva-play SO CHILD & FAMILY BEHAVIOR THERAPY LA English DT Article DE functional analysis; stereotypy; automatic reinforcement; autism; male age 6 ID CHILDREN; SUCKING AB We conducted a brief (8 days) functional analysis to identify sources of control over persistent saliva-play displayed by a 6-year old child with autism in a school setting. The functional analysis suggested that saliva-play was maintained by automatic reinforcement, leading to an intervention evaluation (3 days) that compared two methods of providing alternative sensory consequences. 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RP Darling, RB (reprint author), Indiana Univ Penn, Dept Sociol, 102 McElhaney Hall, Indiana, PA 15705 USA. CR DARLING RB, 2004, DISABILITY SOCIETY, V18 Gill Carol J., 1997, J VOCATIONAL REHABIL, V9, P39 Harris S. L., 2003, SIBLINGS CHILDREN AU Oliver M., 1996, UNDERSTANDING DISABI Seligman M, 1997, ORDINARY FAMILIES SP NR 5 TC 0 Z9 0 PU HAWORTH PRESS INC PI BINGHAMTON PA 10 ALICE ST, BINGHAMTON, NY 13904-1580 USA SN 0731-7107 J9 CHILD FAM BEHAV THER JI Child Fam. Behav. Ther. PY 2004 VL 26 IS 2 BP 55 EP 60 DI 10.1300/J019v26n02_04 PG 6 WC Psychology, Clinical; Family Studies SC Psychology; Family Studies GA 828II UT WOS:000221966600004 ER PT J AU Suchankova, J Soukupova, K Tesarova, E Bosakova, Z Coufal, P AF Suchankova, J Soukupova, K Tesarova, E Bosakova, Z Coufal, P TI Separation and quantification of enkephalin and vasopressin related peptides in reversed-phase capillary liquid chromatography SO CHROMATOGRAPHIA LA English DT Article; Proceedings Paper CT 5th Balaton Symposium on High-Performance Separation Methods CY SEP 03-05, 2003 CL Siofok, HUNGARY SP Hungarian Soc Separat Sci DE capillary liquid chromatography; enkephalin and vasopressin related peptides; separation and quantification ID ZONE ELECTROPHORESIS; OPIOID-PEPTIDES; PROTEINS; ANALOGS; SELECTIVITIES; FLUORESCENCE; PROTEOMICS; PH AB A method for determination of some biologically active penta- and nona-peptides under isocratic conditions in capillary liquid chromatography was developed. Separation system consisting of XTerra C18 stationary phase and mobile phase composed of a mixture of acetonitrile with 0.1% trifluoroacetic acid (TFA) and water with 0.1% TFA in the ratios 75/25 (v/v) and 85/15 (v/v) was suitable not only for a good resolution of enkephalin and vasopressin related peptides, respectively, but it also enabled separation of the respective biopeptides from other constituents of human urine. Calibration curves for the studied peptides were linear in the measured concentration range from 1.00 to 1.57x10(-2) mg mL(-1). The limit of detection and limit of quantification were in the range of units of mug mL(-1) and tens of mug mL(-1), respectively; slightly higher values were obtained for nonapeptides. Determination of certain biologically active peptides in urine can serve in future as a tool for diagnosis of various diseases, e.g. autism. C1 Charles Univ, Dept Analyt Chem, Fac Sci, CR-12840 Prague 2, Czech Republic. Charles Univ, Fac Sci, Dept Phys & Macromol Chem, CR-12840 Prague 2, Czech Republic. RP Suchankova, J (reprint author), Charles Univ, Dept Analyt Chem, Fac Sci, Albertov 2030, CR-12840 Prague 2, Czech Republic. 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Mt Sinai Sch Med, Seaver & New York Autism Ctr Excellence, New York, NY USA. Univ So Calif, Keck Sch Med, Los Angeles, CA 90089 USA. RP Hollander, E (reprint author), Mt Sinai Sch Med, Dept Psychiat, New York, NY USA. NR 0 TC 3 Z9 3 PU M B L COMMUNICATIONS, INC PI NEW YORK PA 333 HUDSON ST, 7TH FLOOR, NEW YORK, NY 10013 USA SN 1092-8529 J9 CNS SPECTRUMS JI CNS Spectr. PD JAN PY 2004 VL 9 IS 1 BP 20 EP 21 PG 2 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895UY UT WOS:000226890500002 ER PT J AU Scahill, L Lord, C AF Scahill, L Lord, C TI Subject selection and characterization in clinical trials in children with autism SO CNS SPECTRUMS LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDER; ABERRANT BEHAVIOR CHECKLIST; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; SPECTRUM DISORDERS; PORCINE SECRETIN; FOLLOW-UP; ADI-R; MULTISITE; COMMUNITY AB The goal of psychopharmacologic research in autism is to provide guidance to clinicians and families on the risks and benefits of specific interventions. Careful subject selection and subject characterization in clinical trials are necessary for replication, to inform clinicians about the sample, and to elucidate the type of patients who might benefit from the treatment. At minimum, subject characterization includes demographic information, diagnosis (autism, Asperger's syndrome, or pervasive developmental disorder-not otherwise specified), intellectual functioning, adaptive functioning, symptom severity, general behavioral profile, health status, pertinent clinical laboratory measures, height, weight, current treatments, and educational placements. Subject selection, sample size, and choice of the primary outcome measure are closely interrelated and linked to the study hypothesis. The magnitude of expected improvement on. the primary outcome measure, which can be expressed by effect size, has direct implications for sample size. Large sample sizes are required to detect small effect sizes. To facilitate interpretation of study results, research reports should provide descriptive characteristics of the sample as well as the mean change and standard deviation on the primary outcome measure data to permit calculation of the effect size. C1 Yale Univ, Study Ctr, New Haven, CT 06520 USA. Yale Univ, Dept Nursing, New Haven, CT 06520 USA. Yale Univ, Dept Child Psychiat, New Haven, CT 06520 USA. Univ Michigan, Dept Psychol, Ann Arbor, MI 48109 USA. Univ Michigan, Dept Psychiat, Ann Arbor, MI 48109 USA. RP Scahill, L (reprint author), Yale Univ, Study Ctr, POB 207900, New Haven, CT 06520 USA. EM lawrence.scahill@yale.edu CR AMAM MG, 2003, CNS SPECTRUMS, V9, P36 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Arnold LE, 2000, J AUTISM DEV DISORD, V30, P99, DOI 10.1023/A:1005451304303 Begg C, 1996, JAMA-J AM MED ASSOC, V276, P637, DOI 10.1001/jama.276.8.637 Borenstein M, 2001, POWER AND PRECISION Brown EC, 2002, RES DEV DISABIL, V23, P45, DOI 10.1016/S0891-4222(01)00091-9 Cohen J., 1988, STAT POWER ANAL BEHA, V2nd Constantino JN, 2002, SOCIAL RESPONSIVENES Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 DUNN LM, 1997, PEADBODY PICTURE VOC Elliott C. 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PD JAN PY 2004 VL 9 IS 1 BP 22 EP 32 PG 11 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895UY UT WOS:000226890500003 PM 14999173 ER PT J AU Aman, MG Novotny, S Samango-Sprouse, C Lecavalier, L Leonard, E Gadow, KD King, BH Pearson, DA Gernsbacher, MA Chez, M AF Aman, MG Novotny, S Samango-Sprouse, C Lecavalier, L Leonard, E Gadow, KD King, BH Pearson, DA Gernsbacher, MA Chez, M TI Outcome measures for clinical drug trials in autism SO CNS SPECTRUMS LA English DT Review ID OBSESSIVE-COMPULSIVE SCALE; RECIPROCAL SOCIAL-BEHAVIOR; PLACEBO-CONTROLLED TRIAL; RATING-SCALE; MENTAL-RETARDATION; CHILDHOOD AUTISM; DEVELOPMENTAL-DISABILITIES; STEREOTYPED BEHAVIOR; INFANTILE-AUTISM; DOUBLE-BLIND AB This paper identifies instruments and measures that may be appropriate for randomized clinical trials in participants with autism spectrum disorders (ASDs). The Clinical Global Impressions scale was recommended for all randomized clinical trials. At this point, however, there is no "perfect" choice of outcome measure for core features of autism, although we will discuss five measures of potential utility. Several communication instruments are recommended, based in part on suitability across the age range. In trials where the intention is to alter core features of ASDs, adaptive behavior scales are also worthy of consideration. Several "behavior complexes" common to ASDs are identified, and instruments are recommended for assessment of these. Given the prevalence of cognitive impairment in ASDs, it is important to assess any cognitive effects, although cognitive data from ASD randomized clinical trials, thus far, are minimal. Guidance from trials in related pharmacologic areas and behavioral pharmacology may be helpful. We recommend routine elicitation of side effects, height and weight, vital signs, and (in the case of antipsychotics) extrapyramidal side-effects assessment. It is often appropriate to include laboratory tests and assessments for continence and sleep pattern. C1 Ohio State Univ, Nisonger Ctr, Dept Psychol, Columbus, OH 43210 USA. Ohio State Univ, Nisonger Ctr, Dept Psychiat, Columbus, OH 43210 USA. Univ Med & Dent New Jersey, Dept Psychiat, Newark, NJ 07103 USA. George Washington Univ, Dept Pediat, Washington, DC 20052 USA. Ohio State Univ, Dept Psychol, Columbus, OH 43210 USA. Harvard Univ, Sch Med, Dept Psychiat, Cambridge, MA 02138 USA. SUNY Stony Brook, Dept Psychiat, Stony Brook, NY USA. Dartmouth Coll Sch Med, Dept Psychiat, Hanover, NH USA. Univ Texas, Sch Med, Dept Psychiat & Behav Sci, Houston, TX USA. Univ Wisconsin, Dept Psychiat & Behav Sci Psychol, Madison, WI USA. Rush Med Sch, Chicago Med Sch, Chicago, IL USA. RP Aman, MG (reprint author), Ohio State Univ, Nisonger Ctr, Dept Psychol, 175 McCampbell Hall,1581 Dodd Dr, Columbus, OH 43210 USA. 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T., 1997, EXPRESSIVE VOCABULAR Zelazo PR, 1997, INFANT YOUNG CHILD, V10, P1 NR 75 TC 31 Z9 31 PU M B L COMMUNICATIONS, INC PI NEW YORK PA 333 HUDSON ST, 7TH FLOOR, NEW YORK, NY 10013 USA SN 1092-8529 J9 CNS SPECTRUMS JI CNS Spectr. PD JAN PY 2004 VL 9 IS 1 BP 36 EP 47 PG 12 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895UY UT WOS:000226890500004 PM 14999174 ER PT J AU Hollander, E Phillips, A King, BH Guthrie, D Aman, MG Law, P Owley, T Robinson, R AF Hollander, E Phillips, A King, BH Guthrie, D Aman, MG Law, P Owley, T Robinson, R TI Impact of recent findings on study design of future autism clinical trials SO CNS SPECTRUMS LA English DT Review ID PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; RATING-SCALE; CHILDREN; SECRETIN; DISORDERS AB There are specific challenges to studying the design of pharmacologic trials in child/adolescent and adult autism, such as subject stratification and parallel versus crossover designs. This article describes how optimal study design is influenced by subject selection and outcome measures chosen. Lessons teamed in study design from the Research Units on Pediatric Psychopharmacology Autism Network trial with risperidone, Seaver Center trials with fluoxetine and valproate, Dartmouth trials with amantadine, and National Institutes of Health secretin trials are highlighted. The Internet System for Assessing Autistic Children system for managing multicenter clinical trials in autism and statistical issues in autism research are also described. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Seaver & New York Autism Ctr Excellence, New York, NY 10029 USA. Dartmouth Coll Sch Med, Dept Psychiat, Hanover, NH USA. Univ Calif Los Angeles, Dept Psychiat & Behav Sci, Los Angeles, CA USA. Ohio Univ, Nisonger Ctr, Columbus, OH 45701 USA. Johns Hopkins Univ, Baltimore, MD USA. Univ Illinois, Chicago, IL 60680 USA. 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PD JAN PY 2004 VL 9 IS 1 BP 49 EP 56 PG 8 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895UY UT WOS:000226890500005 PM 14999175 ER PT J AU Anderson, GM Zimmerman, AW Akshoomoff, N Chugani, DC AF Anderson, GM Zimmerman, AW Akshoomoff, N Chugani, DC TI Autism clinical trials: Biological and medical issues in patient selection and treatment response SO CNS SPECTRUMS LA English DT Review ID POSITRON-EMISSION-TOMOGRAPHY; BRAIN-SEROTONIN SYNTHESIS; INFANTILE-AUTISM; SPECTRUM DISORDERS; CORPUS-CALLOSUM; CHILDREN; ABNORMALITIES; INDIVIDUALS; MRI; CEREBELLUM AB Biomedical measures are critical in the initial patient-screening and -selection phases of a clinical trial in autism and related disorders. These measures can also play an important role in the assessment and characterization of response and can provide an opportunity to study underlying etiologic and pathophysiologic processes. Thus, biomedical measures, including clinical laboratory analyses, metabolic screening, and chromosomal analysis, are used to screen for potential safety-related problems, to decrease biological and genetic heterogeneity, and to define subgroups. Neurobiological measures can be examined as possible predictors, modifiers or surrogates of therapeutic response, and adverse effects. Neurobiological research measures can also be used to study mechanisms and extent of drug action and to perform baseline and longitudinal investigations of possible pathophysiologic alterations. The potential utility and desirability of specific measures are considered and the general approach to choosing measures for incorporation is discussed. C1 Yale Univ, Sch Med, Dept Child Psychiat, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dept Lab Med, New Haven, CT 06520 USA. Johns Hopkins Univ, Sch Med, Dept Neurol & Psychiat, Baltimore, MD USA. Johns Hopkins Univ, Sch Med, Kennedy Krieger Inst, Baltimore, MD USA. Childrens Hosp, Res Ctr, San Diego, CA USA. Univ Calif San Diego, Sch Med, Dept Psychiat, La Jolla, CA USA. Wayne State Univ, Dept Pediat, Detroit, MI USA. Wayne State Univ, Dept Radiol, Detroit, MI USA. RP Anderson, GM (reprint author), Yale Child Study Ctr, 230 S Frontage Rd, New Haven, CT 06510 USA. 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PD JAN PY 2004 VL 9 IS 1 BP 57 EP 64 PG 10 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895UY UT WOS:000226890500006 PM 14999176 ER PT J AU Vitiello, B Wagner, A AF Vitiello, B Wagner, A TI Government initiatives in autism clinical trials SO CNS SPECTRUMS LA English DT Review ID RISPERIDONE AB Randomized clinical trials remain the most valid method of testing the efficacy and safety of treatments. While efforts to elucidate the genetic and neurodevelopmental bases of autism are underway, clinicians and families are in need of scientifically valid information on how to best treat patients with autism. The effectiveness of many interventions currently used in communities has not been adequately tested. Given the high public health relevance of autism treatment research and the low interest of the pharmaceutical industry in autism, the role of the National Institutes of Health in supporting this research is paramount. Among recently launched initiatives in autism clinical trials, there are the Research Units on Pediatric Psychopharmacology Autism Network and the network of centers for Studies to Advance Autism Research and Treatment. These and other government activities in the area of autism clinical trials are here briefly reviewed. C1 Natl Inst Mental Hlth, Div Serv & Intervent Res, Bethesda, MD 20892 USA. RP Vitiello, B (reprint author), Natl Inst Mental Hlth, Div Serv & Intervent Res, Room 7147,6001 Execut Blvd,MSC 9633, Bethesda, MD 20892 USA. EM bvitiell@mail.nih.gov CR *FDA OFF ORPH PROD, FOOD DRUG ADM Fombonne E, 2003, JAMA-J AM MED ASSOC, V289, P87, DOI 10.1001/jama.289.1.87 McDougle CJ, 2000, CHILD ADOL PSYCH CL, V9, P201 *NAT I HLTH, 2002, AUT RES CTR EXC STAA *NAT I MENT HLTH, 2001, MH02002 RUPP PI NIH *NAT I MENT HLTH, 2001, RES WORKSH MENT HLTH *NAT I MENT HLTH, 2002, RES WORKSH RES PSYCH McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Rumsey JM, 2000, J AUTISM DEV DISORD, V30, P369, DOI 10.1023/A:1005595303185 *RUPP AUT NETW, METH CHILDR AD PERV Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 NR 11 TC 3 Z9 3 PU M B L COMMUNICATIONS, INC PI NEW YORK PA 333 HUDSON ST, 7TH FLOOR, NEW YORK, NY 10013 USA SN 1092-8529 J9 CNS SPECTRUMS JI CNS Spectr. PD JAN PY 2004 VL 9 IS 1 BP 66 EP 70 PG 5 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895UY UT WOS:000226890500007 PM 14999177 ER PT S AU Lanyi, CS Tilinger, A AF Lanyi, CS Tilinger, A BE Miesenberger, K Klaus, J Zagler, W Burger, D TI Multimedia and virtual reality in the rehabilitation of autistic children SO COMPUTERS HELPING PEOPLE WITH SPECIAL NEEDS: PROCEEDINGS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 9th International Conference on Computers Helping People with Special Needs CY JUL 07-09, 2004 CL Paris, FRANCE AB At present autism is beyond recovery, thus the only way that autistic children can adapt themselves to grown-up life is rehabilitation. As the application of computers becomes more and more general in teaching healthy children so does it in teaching children with learning disabilities. Thence a multimedia and virtual reality software package was designed for the rehabilitation of autistic children. This paper presents the developed programs and the results of their usability test. C1 Univ Veszprem, Dept Image Proc & Neurocomp, H-8200 Veszprem, Hungary. RP Lanyi, CS (reprint author), Univ Veszprem, Dept Image Proc & Neurocomp, Egyetem U10, H-8200 Veszprem, Hungary. EM tilinger@vision.vein.hu CR Charitos D., 2000, 3 INT C DIS VIRT REA, P147 COBB SV, 1998, 2 EUR C DIS VIRT REA Cromby JJ, 1996, J INTELL DISABIL RES, V40, P489, DOI 10.1111/j.1365-2788.1996.tb00659.x Frith U., 1989, AUTISM EXPLAINING EN Neale H. R., 2000, 3 INT C DIS VIRT REA, P265 PANTELIDIS VS, 1993, ED TECHNOLOGY 0423 Strickland D., 1997, VIRTUAL REALITY NEUR, P81 STRICKLAND D, 1995, 3 C INT AUT FRANC NI, P119 TAKACS I, 2000, NEPSZAVA 2000 NR 9 TC 6 Z9 6 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-22334-7 J9 LECT NOTES COMPUT SC PY 2004 VL 3118 BP 22 EP 28 PG 7 WC Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Rehabilitation SC Computer Science; Rehabilitation GA BAK50 UT WOS:000222635100004 ER PT S AU Trehin, T AF Trehin, T BE Miesenberger, K Klaus, J Zagler, W Burger, D TI Computer use for people with learning difficulties: Basic needs SO COMPUTERS HELPING PEOPLE WITH SPECIAL NEEDS: PROCEEDINGS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 9th International Conference on Computers Helping People with Special Needs CY JUL 07-09, 2004 CL Paris, FRANCE ID AUTISM AB My main area of interest and competences is autism, and in that domain quite a few research programs have been proposed over these years. However many of the needs for educational programs that I will develop here are applicable to learning difficulties in general. The main idea being that such program development should start from the needs of the people with disabilities rather than from the available technology. The case of programs for people with autism will illustrate some of the specific needs that should be satisfied. 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The individual with autism who participated in this research has a combination of difficulties (degree of 76 percent of disability and unable to learn to read and write) and abilities (being able to follow single verbal instructions). Positive results are expounded together with considerations about the desirable features of future products that would overcome the mere training process and also be useful for the final and real task in any working environment where bar codes are present. This paper also provides a preview of what work this group will face in the future in order to progress in the development of this more general and standard aid. C1 Univ Valencia, Inst Robot, Autism & Learning Difficulties Grp, Valencia 46071, Spain. Diagnost & Intervent Ctr, Valladolid, Spain. RP Herrera, G (reprint author), Univ Valencia, Inst Robot, Autism & Learning Difficulties Grp, POB 2085, Valencia 46071, Spain. EM Gerardo.Herrera@uv.es; Gabriel.Labajo@terra.es CR TREATMENT ED AUTISTI ELECT PRODUCT CARD G NR 2 TC 0 Z9 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-22334-7 J9 LECT NOTES COMPUT SC PY 2004 VL 3118 BP 976 EP 982 PG 7 WC Computer Science, Interdisciplinary Applications; Computer Science, Theory & Methods; Rehabilitation SC Computer Science; Rehabilitation GA BAK50 UT WOS:000222635100143 ER PT J AU Kennedy, RC Byers, VS Marchalonis, JJ AF Kennedy, RC Byers, VS Marchalonis, JJ TI Measles virus infection and vaccination: Potential role in chronic illness and associated adverse events SO CRITICAL REVIEWS IN IMMUNOLOGY LA English DT Review DE cytokines; T cells; autism; antibodies ID SUBACUTE SCLEROSING-PANENCEPHALITIS; INFLAMMATORY-BOWEL-DISEASE; INFLUENZAE TYPE-B; HUMAN-IMMUNODEFICIENCY-VIRUS; POLYMERASE-CHAIN-REACTION; MUMPS-RUBELLA VACCINATION; LIVE ATTENUATED MEASLES; CENTRAL-NERVOUS-SYSTEM; DEFECTIVE INTERFERING PARTICLES; IMMUNOGOLD ELECTRON-MICROSCOPY AB Over the last decade, a number of concerns have arisen related to safety issues that have had an adverse effect on the public's trust, particularly among parents whose children are the primary recipient of the vaccine. Historically, the live attenuated measles virus (MV) vaccine and the combination multivalent measles, mumps, and rubella (MMR) vaccine have had a major impact on the health of children worldwide and have been extremely successful at preventing infectious diseases associated with three childhood viral pathogens. In this report, we describe MV infection, replication, pathogenesis, and immunization. MV is a viral pathogen that exhibits a number of complex processes that can effect its replication, pathogenesis, and the induction of an effective antiviral immune response. We describe the published literature as it relates to MV infection and immunization and report adverse events in an attempt to provide a balanced discussion and an historical perspective of the MMR vaccine and autism. C1 Univ Arizona, Coll Med, Dept Microbiol & Immunol, Tucson, AZ 85724 USA. Texas Tech Univ, Hlth Sci Ctr, Dept Microbiol, Lubbock, TX 79430 USA. 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Rev. Immunol. PY 2004 VL 24 IS 2 BP 129 EP 156 DI 10.1615/CritRevImmunol.v24.i2.30 PG 28 WC Immunology SC Immunology GA 856LP UT WOS:000224047000003 PM 15581394 ER PT J AU Dogrukol-Ak, D Tore, F Tuncel, N AF Dogrukol-Ak, D Tore, F Tuncel, N TI Passage of VIP/PACAP/secretin family across the blood-brain barrier: Therapeutic effects SO CURRENT PHARMACEUTICAL DESIGN LA English DT Review ID VASOACTIVE-INTESTINAL-PEPTIDE; CYCLASE-ACTIVATING POLYPEPTIDE; GLUCAGON-LIKE PEPTIDE-1; GASTRIC-INHIBITORY POLYPEPTIDE; HORMONE-RELEASING HORMONE; ALPHA-AMINOISOBUTYRIC-ACID; RECEPTOR MESSENGER-RNA; SLEEP-INDUCING PEPTIDE; ISCHEMIA-INDUCED DEATH; CENTRAL-NERVOUS-SYSTEM AB In recent years, VIP/PACAP/secretin family has special interest. Family members are vasoactive intestinal peptide (VIP), pituitary adenylate cyclase-activating polypeptide (PACAP), secretin, glucagon, glucagon like peptide-1 (GLP(1)), GLP(2), gastric inhibitory peptide (GIP), growth hormone releasing hormone (GHRH or GRF), and peptide histidine methionine (PHM). Most of the family members present both in central nervous system (CNS) and ill various peripheral tissues. The family members that are released into blood from periphery, especially gut, circulate the brain and they can cross the blood brain barrier. Oil the other hand, some of the members of this family that present in the brain, call cross from brain to blood and reach the peripheral tat-gets. VIP, secretin, GLP(1), and PACAP 27 are transported into the brain by transmembrane diffusion, a non-saturable mechanism. However, uptake of PACAP 38 into the brain is saturable mechanism. While there is no report for the passage of GIP, GLP(2) and PHM, there is only one report that shows, glucagon and GHRH can cross the BBB. The passage of VIP/PACAP/secretin family members opens up new horizon for understanding of CNS effects of peripherally administrated peptides. There is much hope that those peptides may prove to be useful in the treatment of serious neurological diseases such as Alzheimer's disease, amyotropic lateral sclerosis, Parkinson's disease, AIDS related neuropathy, diabetic neuropathy, autism, stroke and nerve injury. Their benefits ill various pathophysiologic conditions undoubtly motivate the development of a novel drug design for future therapeutics. C1 Anadolu Univ, Fac Pharm, Dept Analyt Chem, TR-26470 Eskisehir, Turkey. Abant Izzet Baysal Univ, Fac Med, Dept Physiol, TR-14280 Bolu, Turkey. Osmangazi Univ, Fac Med, Dept Physiol, TR-26480 Eskisehir, Turkey. RP Dogrukol-Ak, D (reprint author), Anadolu Univ, Fac Pharm, Dept Analyt Chem, TR-26470 Eskisehir, Turkey. 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Pharm. Design PY 2004 VL 10 IS 12 BP 1325 EP 1340 DI 10.2174/1381612043384934 PG 16 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 815UB UT WOS:000221066100004 PM 15134484 ER PT J AU Harvard, C Malenfant, P Koochek, M Holden, JJA Lewis, MES Rajcan-Separovic, E AF Harvard, C Malenfant, P Koochek, M Holden, JJA Lewis, MES Rajcan-Separovic, E TI Multiple microdeletions in a patient with intellectual disability and autism spectrum disorder detected using a 1 Mb CGH array SO CYTOGENETIC AND GENOME RESEARCH LA English DT Meeting Abstract CT 16th European Colloquium on Animal Cytogenetics and Gene Mapping (16th ECACGM) CY JUL 06-09, 2004 CL Jouy en Josas, FRANCE SP Natl Inst Agron Res C1 Univ British Columbia, Dept Pathol, Vancouver, BC, Canada. Univ British Columbia, Dept Med Genet, Vancouver, BC, Canada. Queens Univ, Dept Psychiat & Physiol, Kingston, ON, Canada. NR 0 TC 0 Z9 0 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 1424-8581 J9 CYTOGENET GENOME RES JI Cytogenet. Genome Res. PY 2004 VL 106 IS 1 MA 15 BP 129 EP 129 PG 1 WC Cell Biology; Genetics & Heredity SC Cell Biology; Genetics & Heredity GA 859DU UT WOS:000224243600109 ER PT J AU Wahlberg, T Magliano, JP AF Wahlberg, T Magliano, JP TI The ability of high function individuals with autism to comprehend written discourse SO DISCOURSE PROCESSES LA English DT Article ID DOMAIN-RELATED INFORMATION; NORMAL-CHILDREN; ASPERGER-SYNDROME; CENTRAL COHERENCE; INFANTILE-AUTISM; LANGUAGE; MIND; ADULTS; TEXT; KNOWLEDGE AB This study assessed whether high functioning readers with autism are capable of drawing on prior knowledge during reading. Readers with autism and matched normal readers read ambiguous texts that described well-known historical events. The presence of an informative or noninformative title and primer texts that explicitly described the referenced events were manipulated. Story recall was collected. The results indicated that readers with autism were able to take advantage of cues to background knowledge to activate and associate the referenced event at a general level, but were not able to use that knowledge to interpret and remember specific information. These results suggest that difficulties in discourse understanding that are experienced by high functioning individuals with autism may stem from a difficulty in making use of relevant background knowledge to interpret ambiguities in language. C1 No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. RP Magliano, JP (reprint author), No Illinois Univ, Dept Psychol, De Kalb, IL 60115 USA. 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SO DRUG SAFETY LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; MUMPS-RUBELLA VACCINATION; SUBACUTE SCLEROSING PANENCEPHALITIS; POLYMERASE-CHAIN-REACTION; VIRUS GENOME SEQUENCE; MEASLES-VIRUS; CROHNS-DISEASE; EPIDEMIOLOGIC EVIDENCE; ASEPTIC-MENINGITIS; NO EVIDENCE AB It has been suggested that vaccination with the measles-mumps-rubella (MMR) vaccine causes autism. The wide-scale use of the MMR vaccine has been reported to coincide with the apparent increase in the incidence of autism. Case reports have described children who developed signs of both developmental regression and gastrointestinal symptoms shortly after MMR vaccination. A review of the literature revealed no convincing scientific evidence to support a causal relationship between the use of MMR vaccines and autism. No primate models exist to support the hypothesis. The biological plausibility remains questionable and there is a sound body of epidemiologcal evidence to refute the hypothesis. 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PY 2004 VL 27 IS 12 BP 831 EP 840 DI 10.2165/00002018-200427120-00001 PG 10 WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology GA 860XX UT WOS:000224378700001 PM 15366972 ER PT J AU Wood, L Martinez, C AF Wood, L Martinez, C TI The general, practice research database - Role in pharmacovigilance SO DRUG SAFETY LA English DT Article ID SIGNAL GENERATION; PUBLIC-HEALTH; RISK; PHARMACOEPIDEMIOLOGY; MEASLES; AUTISM; MUMPS; WOMEN; UK AB The General Practice Research Database (GPRD) is the world's largest computerised database of anonymised longitudinal clinical records from primary care. The database already has an international reputation in the field of drug safety signal evaluation where the results of GPRD-based pharmacoepidemiological studies have been used to inform regulatory pharmacovigilance decision making., The characteristics and richness of the data are such that the GPRD is likely to prove a key data resource for the proactive pharmacovigilance anticipated in risk management and pharmacovigilance plans. An update of recent developments to the database and new data available from it - including spontaneously recorded suspected adverse drug reactions - is presented in the article, with a description of how the data can be used to support a variety of pharmacovigilance applications. The possibility of using the GPRD in signal detection and assessment of the impact of pharmacovigilance activities in the future is also discussed. C1 GPRD Div, Med & Healthcare Prod Regulatory Agcy, London SW8 5NQ, England. RP Wood, L (reprint author), GPRD Div, Med & Healthcare Prod Regulatory Agcy, Room 15-103 Market Towers,1 9 Elms Lane,Vauxhall, London SW8 5NQ, England. 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PY 2004 VL 27 IS 12 BP 871 EP 881 DI 10.2165/00002018-200427120-00004 PG 11 WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology GA 860XX UT WOS:000224378700004 PM 15366975 ER PT J AU Valdes, ARVR AF Valdes, ARVR TI Autism and paediatric vaccines SO DRUG SAFETY LA English DT Meeting Abstract CT 4th Annual Meeting of the International-Society-of-Pharmacovigilance (ISoP) CY OCT 06-08, 2004 CL Dublin, IRELAND SP Int Soc Pharmacovigilance C1 Finlay Inst, Havana, Cuba. NR 0 TC 0 Z9 0 PU ADIS INTERNATIONAL LTD PI AUCKLAND PA 41 CENTORIAN DR, PRIVATE BAG 65901, MAIRANGI BAY, AUCKLAND 10, NEW ZEALAND SN 0114-5916 J9 DRUG SAFETY JI Drug Saf. PY 2004 VL 27 IS 12 BP 958 EP 958 PG 1 WC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology SC Public, Environmental & Occupational Health; Pharmacology & Pharmacy; Toxicology GA 860XX UT WOS:000224378700119 ER PT J AU Yasuhara, A Yoshida, Y Hori, A AF Yasuhara, A Yoshida, Y Hori, A TI Analysis of the convulsive seizure wave in children with autism. SO EPILEPSIA LA English DT Meeting Abstract CT 35th Annual Meeting of the Japan-Epilepsy-Society CY SEP 27-28, 2001 CL Tokyo, JAPAN SP Japan Epilepsy Soc C1 Kansai Med Univ, Kohri Univ, Dept Pediat, Neyagawa, Osaka, Japan. NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING INC PI MALDEN PA 350 MAIN ST, MALDEN, MA 02148 USA SN 0013-9580 J9 EPILEPSIA JI Epilepsia PY 2004 VL 45 SU 8 BP 65 EP 65 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 880YN UT WOS:000225826600032 ER PT J AU Kadesjo, B Janols, LO Korkman, M Mickelsson, K Strand, G Trillingsgaard, A Gillberg, C AF Kadesjo, B Janols, LO Korkman, M Mickelsson, K Strand, G Trillingsgaard, A Gillberg, C TI The FTF (Five to Fifteen): the development of a parent questionnaire for the assessment of ADHD and comorbid conditions SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE FTF; ADHD; questionnaire; comorbidity; rating scale; childhood; adolescence ID DISORDERS; STRENGTHS; AUTISM AB This paper describes the development of a new parent questionnaire ("Five to Fifteen", or the FTF) for elicitation of symptoms and problems typical of ADHD and its comorbidities. The FTF comprises 181 statements related to behavioural or developmental problems that can be endorsed as either "does not apply" (0), applies sometimes or to some extent" (1), "definitely applies" (2), plus a number of open-ended questions including some about the child's strengths. The items are arranged into eight different domains (memory, learning, language, executive functions, motor skills, perception, social skills, and emotional/behavioural problems), most of which can be subdivided into subdomains. For each domain, a mean score ranging from 0-2 can be calculated. A representative sample (n = 1350) of the total population of 6-15-year-old children was targeted. Parents of 63% of these completed a questionnaire and returned it to the researchers. Boys showed significantly more problems than did girls across domains and age. Younger children had more problems than pre-adolescents and adolescents (except in the domains of social skills and emotional/behavioural problems). Executive dysfunction was common, and 5.3% of all children in the population had clear problems suggesting a diagnosis of ADHD according to parent report. The paper provides means, medians, and 90(th) and 95(th) centiles for individual items as well as for the eight domains. The Discussion centres on whether or not the FTF can (or should) be used in school-aged children for the identification of children at risk for ADHD or other early childhood onset neuropsychiatric disorder. C1 Gothenburg Univ, Dept Child & Adolescent Psychiat, S-41119 Gothenburg, Sweden. Univ London, St Georges Hosp, Sch Med, London, England. Uppsala Univ, Dept Neurosci Child & Adolescent Psychiat, S-78185 Uppsala, Sweden. Univ Turku, Abo Akad, Inst Psychol, Turku, Finland. ADHD Ctr, Helsinki 00250, Finland. Ulleval Univ Sykehus HF, Nasjonalt Kompetansesenter AD HD Tourettes Syndro, N-0407 Oslo, Norway. Aarhus Univ Hosp, Psychiat Hosp Children & Adolescents, DK-8240 Risskov, Denmark. 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PY 2004 VL 8 IS 6 BP 327 EP 332 DI 10.1016/j.ejpn.2004.08.005 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 875KS UT WOS:000225419700008 PM 15542389 ER PT J AU Carminati, GG Constantin, N Legay, Y Tschopp, B Zid, L Hermet, A Thibault, P Gorianz, P Schaya, M Levental, M Carrell, C Ritter, S AF Carminati, GG Constantin, N Legay, Y Tschopp, B Zid, L Hermet, A Thibault, P Gorianz, P Schaya, M Levental, M Carrell, C Ritter, S TI Evolution of 2 persons with severe disability over a period of 3 years: "Sonar Group" underwater music therapy SO EUROPEAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT International Conference on Training and Researcb in Group Therapy CY SEP 19-20, 2003 CL Geneva, SWITZERLAND SP World Psychiat Assoc, O M I E Fdn HO Univ Hosp Geneva DE learning disability; autism; group therapy; aquatic environment; underwater music ID INFANTILE-AUTISM; RATING-SCALE AB Autism is a neurobehavioral disorder including anomalies of the sensorial and cognitive functions, verbal and non-verbal communication, affectivity and social relationships. This brief report describes the evolution of four autistic persons participating to the "Sonar Group": this therapeutic approach consists in exposing autistic persons to a situation recalling the immersion of the foetus in the amniotic fluid in order to offer to the persons a relaxing environment. Each autistic person was evaluated with ABC (Aberrant Behavior Checklist) for behavior and with CARS (Childhood Autism Rating Scale) for autistic features before the beginning of the Sonar one year and 3 years later. C1 Univ Hosp Geneva, Dept Psychiat, Geneva, Switzerland. DIAE, Serv Cantonal Eco Toxicol, ECOTOX, Geneva, Switzerland. RP Carminati, GG (reprint author), Univ Hosp Geneva, Dept Psychiat, Geneva, Switzerland. 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PD JAN-MAR PY 2004 VL 69 IS 1 BP 161 EP 168 DI 10.1016/j.evopsy.2003.11.003 PG 8 WC Psychiatry SC Psychiatry GA 810DR UT WOS:000220685500014 ER PT J AU Roman, GC Rogers, SJ AF Roman, GC Rogers, SJ TI Donepezil: a clinical review of current and emerging indications SO EXPERT OPINION ON PHARMACOTHERAPY LA English DT Review DE aphasia; Alzheimer's disease; autism; cholinesterase inhibitors; cholinergic transmission; dementia; donepezil; drowsiness; Down's syndrome; head injury; Lewy body; memory; migraine; opioid drowsiness; Parkinson's disease; schizophrenia; seizures; stroke; tardive dyskinesia; vascular dementia ID MILD COGNITIVE IMPAIRMENT; PLACEBO-CONTROLLED TRIAL; CEREBRAL BLOOD-FLOW; PROGRESSIVE SUPRANUCLEAR PALSY; SEVERE ALZHEIMERS-DISEASE; TRAUMATIC BRAIN INJURY; HUMAN BASAL FOREBRAIN; LEWY BODY DEMENTIA; VASCULAR DEMENTIA; DOUBLE-BLIND AB This article reviews the piperidine derivative, donepezil hydrochloride (E2020, Aricept(R)), a reversible central acetylcholinesterase inhibitor currently approved for treatment of mild-to-moderate Alzheimer's disease. Donepezil is well absorbed orally, unaffected by food or by time of administration; it reaches therapeutic levels in doses of 5-10 mg/day and peak plasma concentrations are obtained 3-4 h after oral administration. A single bedtime dose is recommended due to the long elimination half-life of the drug (70 h). Donepezil does not cause liver toxicity or significant drug interactions and is relatively well-tolerated. Initial side effects include nausea, vomiting, diarrhoea, insomnia, muscle cramps, fatigue, anorexia and syncope. Caution is advised in patients with bradycardia. Long-term use of donepezil in AD has been found to delay nursing-home placement and to result in caregiver respite. Donepezil also slows deterioration of cognition and global function in patients with moderate-to-severe AD, with improvement of abnormal behaviours. in addition to AD, donepezil demonstrates significant improvement in cognition, global function and activities of daily living in comparison with placebo-treated patients with vascular dementia and has potential therapeutic benefit for other neurological conditions. C1 Univ Texas, Hlth Sci Ctr, Coll Pharm, San Antonio, TX 78229 USA. Audie L Murphy Mem Vet Adm Med Ctr, San Antonio, TX 78284 USA. RP Roman, GC (reprint author), Univ Texas, Hlth Sci Ctr, Coll Pharm, 7703 Floyd Curl Dr,Mail Code 7883, San Antonio, TX 78229 USA. 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PD JAN-MAR PY 2004 VL 19 IS 1 BP 7 EP 8 PG 2 WC Neurosciences SC Neurosciences & Neurology GA 828WK UT WOS:000222004200001 ER PT J AU Brambilla, P Hardan, AY di Nemi, SU Caverzasi, E Soares, JC Perez, J Barale, F AF Brambilla, P Hardan, AY di Nemi, SU Caverzasi, E Soares, JC Perez, J Barale, F TI The functional neuroanatomy of autism SO FUNCTIONAL NEUROLOGY LA English DT Article DE brain imaging; fMRI; MRS; neuroimaging; PET; SPECT ID CEREBRAL-BLOOD-FLOW; MAGNETIC-RESONANCE; ASPERGER-SYNDROME; CHILDHOOD AUTISM; FACIAL EXPRESSIONS; NEURAL MECHANISMS; CORTICAL ACTIVITY; FACE RECOGNITION; HUMAN BRAIN; MIND AB Autism is a neurodevelopmental syndrome characterized by impaired social and executive functions. Functional magnetic resonance imaging (fMRI) is a non-invasive technique that allows investigation of the neural networks underlying cognitive impairments in autism. In this article, brain imaging studies investigating the functional brain anatomy of autism are reviewed. Face recognition, theory of mind and executive functions have all been explored in functional neuroimaging studies involving autistic patients. The available literature suggests an involvement of abnormal functional mechanisms in face recognition, mentalization and executive functions in adults with high-functioning autism or Asperger's syndrome, possibly due to brain maturation abnormalities, and resulting in dysfunctional reciprocal cortico-subcortical connections. Future functional neuroimaging research should investigate subgroups of autistic children and adolescents longitudinally and attempt to integrate genetic, cognitive and empirical approaches. Such studies will be instrumental in furthering understanding of the pathophysiology of autism and in exploring the importance of dimensional measures of the broader phenotype currently defined as autism. C1 IRCCS S Giovanni Dio Fatebenefratelli, Biol Psychiat Unit, Brescia, Italy. 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Neurol. PD JAN-MAR PY 2004 VL 19 IS 1 BP 9 EP 17 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 828WK UT WOS:000222004200002 PM 15212111 ER PT J AU Moog, U Engelen, JJM Weber, BW Van Gelderen, M Steyaert, J Baas, F Sijstermans, HMJ Fryns, JP AF Moog, U Engelen, JJM Weber, BW Van Gelderen, M Steyaert, J Baas, F Sijstermans, HMJ Fryns, JP TI Hereditary motor and sensory neuropathy (HMSN) IA, developmental delay and autism related disorder in a boy with duplication (17)(p11.2p12) SO GENETIC COUNSELING LA English DT Article DE Charcot-Marie-Tooth type 1; HMSN IA; duplication (17)(p11.2); duplication (17)(p11.2p12) ID TOOTH DISEASE TYPE-1A; 17P P11.2)>; TANDEM DUPLICATION; 17P11.2; CHROMOSOME-17; MECHANISM; GENE; DNA; 1A AB We present a 6-year-old boy with moderate developmental delay, gait disturbance, autism related disorder and mild dysmorphic features. He was seen for evaluation of his retardation since the age of 2.8 years. At first sight, a cytogenetic analysis showed a normal 46,XY karyotype. Neurological examination at the age of 5.5 years revealed a motor and sensory polyneuropathy. A quantitative Southern blot with probes PMP22 and VAW409 specific for Charcot-Marie-Tooth type I (CMTI) disclosed a duplication which confirmed the diagnosis HMSN Ia. Subsequently, GTG banded metaphases were re-evaluated and a small duplication 17p was seen on retrospect. Additional FISH with probe LSISMS (Vysis) specific for the Smith-Magenis region at 17p11.2 again showed a duplication. Both parents had a normal karyotype and the duplication test for CMTI showed normal results for both of them. The boy had a de novo 46,XY,dup(17)(p11.2p12) karyotype. The present observation confirms previous findings of mild psychomotor delay, neurobehavioural features and minor craniofacial anomalies as the major phenotypic features of dup(17)(p11.2) and dup(17)(p11.2p12); in cases of duplications comprising the PMP22 locus HMSN1 is associated. A recognizable facial phenotype emerges characterized by a broad forehead, hypertelorism, downslant of palpebral fissures, smooth philtrum, thin upper lip and ear anomalies. C1 Univ Hosp Maastricht, Dept Clin Genet, NL-6202 AZ Maastricht, Netherlands. Univ Hosp Maastricht, Dept Neurol, NL-6202 AZ Maastricht, Netherlands. Univ Hosp Maastricht, Dept Child Psychiat, NL-6202 AZ Maastricht, Netherlands. Maastricht Univ, Res Inst Growth & Dev, Maastricht, Netherlands. Acad Med Ctr, Neurogenet Lab, Amsterdam, Netherlands. Atrium Med Ctr, Dept Paediat, Heerlen, Netherlands. Katholieke Univ Leuven, Univ Hosp Gasthuisberg, Ctr Human Genet, Louvain, Belgium. RP Moog, U (reprint author), Univ Hosp Maastricht, Dept Clin Genet, POB 5800, NL-6202 AZ Maastricht, Netherlands. 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Couns. PY 2004 VL 15 IS 1 BP 73 EP 80 PG 8 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medical Ethics; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Medical Ethics; Research & Experimental Medicine GA 806YS UT WOS:000220469800011 PM 15083703 ER PT J AU Lukusa, T Vermeesch, JR Holvoet, M Fryns, JP Devriendt, K AF Lukusa, T Vermeesch, JR Holvoet, M Fryns, JP Devriendt, K TI Deletion 2q37.3 and autism: Molecular cytogenetic mapping of the candidate region for autistic disorder SO GENETIC COUNSELING LA English DT Article DE autism; deletion 2q37.3; molecular cytogenctic mapping ID ALBRIGHT HEREDITARY OSTEODYSTROPHY; CRYPTIC TRANSLOCATION; MEDICAL CONDITIONS; CHROMOSOME 7Q; GENE; LINKAGE; COMPLEX; TWIN; DELINEATION; IMPAIRMENT AB Deletion 2q37.3 and autism: molecular cytogenetic mapping of the candidate region for autistic disorder. Fine mapping of deletion regions in autistic patients represents a valuable screening tool for identifying candidate genes for autism. A number of studies have ascertained associations between autism and terminal 2q deletion with the breakpoint within 2q37. Here we describe a 12-year-old female patient with terminal 2q37.3 cryptic deletion and autistic behaviour. Her clinical features included hypotonia and feeding difficulties during infancy, coarse face with notably prominent forehead, prominent eyebrows, broad flat nasal bridge and round cheeks, small hands and feet with bilateral brachymetaphalangism, proximal implantation of the thumbs and short toenails, mild mental retardation and autistic behaviour. Recorded autistic features included early lack of eye contact and, during infancy, little social interactions, propensity to be stereotypically busy and to get anxious. In order to more closely delineate the linkage region for autism within 2q37, the findings in this patient were combined to those in 2 previously reported siblings with a well documented 2q37.3 deletion, but without autistic disorder. The exact size of the deleted segment was determined by mapping the deleted region in each group with a series of specific BAC clones linearly ordered on the 2q37 region. The deletion in the autistic patient appeared to be larger [breakpoint flanked by more centromeric clones RP11-680O16 (236.9 Mb) and 201F21 (237.4 Mb)] than in the non autistic siblings [more telomeric clones RP11-205L13 (237.8 Mb) and 346I14 (238.2 Mb), revealing a distance of maximum 1.3 Mb between the breakpoints. Accordingly, the extent of the candidate region for susceptibility genes for autism on distal 2q is reduced to maximum 1.3 Mb. Comparison with another well documented autistic patient from the literature results in the same conclusion. 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Couns. PY 2004 VL 15 IS 3 BP 293 EP 301 PG 9 WC Biotechnology & Applied Microbiology; Genetics & Heredity; Medical Ethics; Medicine, Research & Experimental SC Biotechnology & Applied Microbiology; Genetics & Heredity; Medical Ethics; Research & Experimental Medicine GA 860KO UT WOS:000224342700001 PM 15517821 ER PT J AU Acosta, MT Arcos-Burgos, M Muenke, M AF Acosta, MT Arcos-Burgos, M Muenke, M TI Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype? SO GENETICS IN MEDICINE LA English DT Review DE attention-deficit/hyperactivity disorder; autism; schizophrenia; epistasis; pleiotropy ID DEFICIT-HYPERACTIVITY DISORDER; DOPAMINE-D4 RECEPTOR GENE; CATECHOL-O-METHYLTRANSFERASE; SMITH-MAGENIS-SYNDROME; SUBSTANCE USE DISORDERS; DUPLICATION POLYMORPHISM UPSTREAM; HAPLOTYPE RELATIVE RISK; III REPEAT POLYMORPHISM; 22Q11 DELETION SYNDROME; TRAUMATIC BRAIN INJURY AB Complex genetic traits refer to those phenotypes not fitting patterns of Mendelian segregation and/or assortment but exhibiting a preferential familial clustering that cannot be explained by cultural or environmental causes. Attention-deficit/hyperactivity disorder (ADHD) is the most common neurodevelopmental disorder of childhood and probably the most controversial. ADHD has been considered a complex genetic trait based upon the absence of a clear-cut boundary between affected and unaffected status. Furthermore, its high comorbidity with other disorders strongly suggests complex epistatic or pleiotropic effects acting in common with the environmental influences. This implies that the same gene or genes is or are associated with different and concurrently occurring phenotypes. In this study, we will review clinical and epidemiological aspects related to the ADHD phenotype, which are considered either as categorical or continuous traits. We also will discuss genetic models underlying the complexity of this behavioral phenotype and the probable role of epistatic interactions between major genes contributing to the ADHD phenotype. C1 Childrens Natl Med Ctr, Dept Neurol, Washington, DC 20010 USA. NHGRI, Med Genet Branch, NIH, Dept Hlth & Human Serv, Bethesda, MD 20892 USA. RP Acosta, MT (reprint author), Childrens Natl Med Ctr, Dept Neurol, 111 Michigan Ave NW, Washington, DC 20010 USA. 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Med. PD JAN-FEB PY 2004 VL 6 IS 1 BP 1 EP 15 DI 10.1097/01.GIM.0000110413.07490.OB PG 15 WC Genetics & Heredity SC Genetics & Heredity GA 764PU UT WOS:000188215900001 PM 14726804 ER PT J AU Mayer, JD Goleman, D Barrett, C Gutstein, S Boyatzis, R Goldberg, E Jung, A Book, H Goffee, R Gergen, D Harman, S Lalich, J George, W Thomas, MT Bartz, C Takeuchi, H Stone, L Heifetz, R AF Mayer, JD Goleman, D Barrett, C Gutstein, S Boyatzis, R Goldberg, E Jung, A Book, H Goffee, R Gergen, D Harman, S Lalich, J George, W Thomas, MT Bartz, C Takeuchi, H Stone, L Heifetz, R TI Leading by feel SO HARVARD BUSINESS REVIEW LA English DT Article AB Like it or not, leaders need to manage the mood of their organizations. The most gifted leaders accomplish that by using a mysterious blend of psychological abilities known as emotional intelligence. Them are self-aware and empathetic. They can read and regulate their own emotions while intuitively grasping how others feel and gauging their organization's emotional state. But where does emotional intelligence come from, and how do leaders learn to use it? in this article, 18 leaders and scholars (including business executives, leadership researchers, psychologists, an autism expert, and a symphony conductor) explore the nature and management of emotional intelligence-its sources, uses, and abuses. Their responses varied, but Some common themes emerged: the importance of consciously-and conscientiously-honing one's skills,the double-edged nature of self-awareness, and the danger of letting any one emotional intelligence skill dominate. Among their observations: Psychology professor John Mayer, who codeveloped the concept of emotional intelligence, warns managers not to be confused by popular definitions of the term, which suggest that if you have a certain set of personality traits then you automatically possess emotional intelligence. Neuropsychologist Elkhonon Goldberg agrees with professors Daniel Goleman and Robert Goffee that emotional intelligence can be learned-but only by people who already show an aptitude for it. Cult expert Janja Lalich points out that leaders can use their emotional intelligence skills for ill in the same way they can for good. "Sometimes the only difference is [the leader's] intent," she says. And business leaders Carol Bartz, William George, Sidney Harman, and Andrea Jung (of Autodesk, Medtronic, Harman International, and Avon respectively) describe situations in which emotional intelligence traits such as self-awareness and empathy have helped them and their companies perform at a higher level. C1 Univ New Hampshire, Durham, NH 03824 USA. RP Mayer, JD (reprint author), Univ New Hampshire, Durham, NH 03824 USA. EM jack.mayer@unh.edu; gutstein@connections.center.com; reb2@cwru.edu; egneurocog@aol.com; hbwork@netsurf.net; rgoffee@london.edu; sharman@harman.com; jlalich@csuchico.edu; carol.bartz@autodesk.com; linda@lindastone.net; ronald_heifetz@harvard.edu NR 0 TC 6 Z9 6 PU HARVARD BUSINESS SCHOOL PUBLISHING CORPORATION PI WATERTOWN PA 300 NORTH BEACON STREET, WATERTOWN, MA 02472 USA SN 0017-8012 J9 HARVARD BUS REV JI Harv. Bus. Rev. PD JAN PY 2004 VL 82 IS 1 BP 27 EP + PG 12 WC Business; Management SC Business & Economics GA 758CQ UT WOS:000187615300007 ER PT J AU Bartlett, CW Flax, JF Logue, MW Smith, BJ Vieland, VJ Tallal, P Brzustowicz, LM AF Bartlett, CW Flax, JF Logue, MW Smith, BJ Vieland, VJ Tallal, P Brzustowicz, LM TI Examination of potential overlap in autism and language loci on chromosomes 2, 7, and 13 in two independent samples ascertained for specific language impairment SO HUMAN HEREDITY LA English DT Article DE autism; language impairment; multiple data sets; heterogeneity; linkage analysis ID PEDIGREE DISEQUILIBRIUM TEST; SUSCEPTIBILITY GENE; POSTERIOR PROBABILITY; 1ST-DEGREE RELATIVES; QUANTITATIVE TRAIT; GENOMEWIDE SCREEN; LINKAGE ANALYSIS; GENOMIC SCREEN; LOD SCORES; FOLLOW-UP AB Specific language impairment is a neurodevelopmental disorder characterized by impairments essentially restricted to the domain of language and language learning skills. This contrasts with autism, which is a pervasive developmental disorder defined by multiple impairments in language, social reciprocity, narrow interests and/or repetitive behaviors. Genetic linkage studies and family data suggest that the two disorders may have genetic components in common. Two samples, from Canada and the US, selected for specific language impairment were genotyped at loci where such common genes are likely to reside. Significant evidence for linkage was previously observed at chromosome 13q21 in our Canadian sample (HLOD 3.56) and was confirmed in our US sample ( HLOD 2.61). Using the posterior probability of linkage (PPL) to combine evidence for linkage across the two samples yielded a PPL over 92%. Two additional loci on chromosome 2 and 7 showed weak evidence for linkage. However, a marker in the cystic fibrosis transmembrane conductance regulator (7q31) showed evidence for association to SLI, confirming results from another group (O'Brien et al. 2003). Our results indicate that using samples selected for components of the autism phenotype may be a useful adjunct to autism genetics. Copyright (C) 2004 S. Karger AG, Basel. C1 Rutgers State Univ, Ctr Mol & Behav Neurosci, Newark, NJ 07102 USA. Univ Iowa, Coll Med, Dept Psychiat, Iowa City, IA 52242 USA. Rutgers State Univ, Dept Genet, Newark, NJ 07102 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Psychiat, Newark, NJ 07103 USA. Univ Iowa, Coll Publ Hlth, Program Publ Hlth Genet, Iowa City, IA USA. RP Bartlett, CW (reprint author), Rutgers State Univ, Dept Genet, Nelson Biol Labs, Room B314,604 Allison Rd, Piscataway, NJ 08854 USA. 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We now report 13 novel and two recurrent mutations of ARX, and one nucleotide change of uncertain significance in 20 genotypic males from 16 families. Most had XLAG, but two had hydranencephaly and abnormal genitalia, and three males from one family had Proud syndrome or ACC with abnormal genitalia. We obtained detailed clinical information on all 29 affected males, including the nine previously reported subjects. Premature termination mutations consisting of large deletions, frameshifts, nonsense mutations, and splice site mutations in exons 1 to 4 caused XLAG or hydranencephaly with abnormal genitalia. Nonconservative missense mutations within the homeobox caused less severe XLAG, while conservative substitution in the homeodomain caused Proud syndrome. A nonconservative missense mutation near the C-terminal aristaless domain caused unusually severe XLAG with microcephaly and mild cerebellar hypoplasia. 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Rhode Isl Hosp, Dept Pediat, Providence, RI USA. Univ Michigan, Teratol Unit, Dept Pediat, Ann Arbor, MI 48109 USA. Univ Michigan, Teratol Unit, Dept Pathol, Ann Arbor, MI 48109 USA. Univ Michigan, Teratol Unit, Dept Obstet, Ann Arbor, MI 48109 USA. CHU Angers, Serv Genet Med, Angers, France. NW London Hosp NHS Trust, Kennedy Galton Ctr, NW Thames Reg Genet Serv, London, England. Univ Oklahoma, Hlth Sci Ctr, HA Chapman Inst Med Genet, Tulsa, OK 74136 USA. Childrens Hosp Philadelphia, Div Human Genet & Mol Biol, Philadelphia, PA 19104 USA. Univ Penn, Philadelphia, PA 19104 USA. Osped Gen Zona Valduce, Congregaz Suore Infermiere Addolorata, Div Patol Neonatale, Como, Italy. Univ Pisa, INPE Ist Neuropsichiatria & Psicopedagogia Evolut, IRCCS, Pisa, Italy. Natl Inst Neurosci, Natl Ctr Neurol & Psychiat, Tokyo, Japan. Inova Fairfax Hosp Children, Div Genet, Falls Church, VA USA. Johns Hopkins Univ, Sch Med, Baltimore, MD USA. Tottori Univ, Sch Med, Yonago, Tottori 683, Japan. 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Mutat. PY 2004 VL 23 IS 2 BP 147 EP 159 DI 10.1002/humu.10310 PG 13 WC Genetics & Heredity SC Genetics & Heredity GA 770GX UT WOS:000188715800007 PM 14722918 ER PT J AU Camaioni, L Perucchini, P Bellagamba, F Colonnesi, C AF Camaioni, L Perucchini, P Bellagamba, F Colonnesi, C TI The role of declarative pointing in developing a theory of mind SO INFANCY LA English DT Article; Proceedings Paper CT 17th Biennial Meeting of the International-Society-for-the-Study-of-Behavioural-Development CY AUG, 2002 CL OTTAWA, CANADA SP Int Soc Study Behav Dev ID INTENDED ACTS; INFANTS; AUTISM; 18-MONTH-OLDS; CHILDREN AB It has been suggested that the child's capacity to represent and influence another person's attentional state about an object or event in triadic interactions (declarative communication) is an early manifestation of social understanding in the second year of life. This study tested the following predictions: First, in typically developing children declarative pointing emerges later than imperative pointing. Second, the capacity to use declarative pointing is linked to the understanding of other's intentions (i.e., to the capacity to reproduce other's intended acts after seeing failed attempts to perform these acts). The study was conducted in 2 phases. In the first phase, the parents of 133 typically developing infants completed the Questionnaire on Pointing Gesture, which allowed the identification of babies able to use pointing in familiar contexts. Of these children, 40 participated in the experiment and were tested on 2 tasks: a new task designed to elicit production and comprehension of imperative and declarative pointing, and a modified version of Meltzoff's (1995) task designed to assess understanding of others' intentions. Tasks were administered to each participant in 2 sessions carried out at 3-month intervals. Children were 12 months old on average at the 1st session and 15 months old on average at the 2nd session. Results showed that children produced and understood declarative pointing later than imperative pointing. Furthermore, production of declarative pointing was clearly linked to understanding of others' intentions. No relation was found between production and comprehension of imperative pointing and intention understanding. Implications from the association between declarative pointing and inferring other's intentions are discussed. C1 Univ Roma Tre, Dept Educ Sci, I-00185 Rome, Italy. Univ Roma La Sapienza, Dept Dev & Social Psychol, Rome, Italy. RP Perucchini, P (reprint author), Univ Roma Tre, Dept Educ Sci, Via Castro Pretorio 20, I-00185 Rome, Italy. 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Considered as a syndrome-complex of chromosomal (genetic) origin with multiple neurodevelopmental and neuropsychological manifestations it will be a very long time before a complete understanding of this condition emerges based upon molecular, genetic, and neurobiological principles. The construct of Down syndrome (DS) as a developmental disorder is, by itself, incomplete and most unsatisfactory based upon emerging biological concepts. However discussions of DS as a developmental disorder characterized primarily by developmental delay, does permit highly complex biological events to be easily conceptualized in terms of the whole child. Our current models of child development and the interventions designed to support neuromaturation in young children with DS will require further integration with emerging genetic, neurobiological, neuropsychological, and pharmacological paradigms. A cogent framework for successful pharmacological treatment of certain aspects of cognitive and behavioral dysfunction is beginning to emerge. At the same tine, a growing number of untested, nutrition- and development-based therapies are continually offered to the families of young children. The need for well-designed studies to measure the effects of early, focused clinical intervention of any kind is obvious. Our ability to competently serve young children with DS will advance once a commitment to clinical trials is recognized and acted upon. C1 Johns Hopkins Univ, Sch Med, Dept Pediat, Baltimore, MD 21205 USA. Kennedy Krieger Inst, Div Neurol & Dev Med, Baltimore, MD USA. RP Capone, GT (reprint author), Johns Hopkins Univ, Sch Med, Dept Pediat, 725 Rutland Ave, Baltimore, MD 21205 USA. 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NR 0 TC 1 Z9 1 PU TRANSACTION PERIOD CONSORTIUM PI PISCATAWAY PA RUTGERS UNIV, DEPT 8010, 35 BERRUE CIRCLE, PISCATAWAY, NJ 08854-8042 USA SN 1053-881X J9 INTEGR PHYS BEH SCI JI Integr. Physiol. Behav. Sci. PD JAN-MAR PY 2004 VL 39 IS 1 BP 70 EP 71 PG 2 WC Psychology, Biological; Neurosciences SC Psychology; Neurosciences & Neurology GA 848DY UT WOS:000223448800057 ER PT J AU Mingroni, MA AF Mingroni, MA TI The secular rise in IQ: Giving heterosis a closer look SO INTELLIGENCE LA English DT Article DE heterosis; IQ; intelligence ID HEAD CIRCUMFERENCE; YOUNG-ADULTS; AUTISM; ASTHMA; PREVALENCE; INCREASE; HEIGHT; FAMILY; TWINS; INTELLIGENCE AB Although most discussions today start from the assumption that the secular rise in IQ must be environmental in origin, three reasons warrant giving the genetic phenomenon heterosis a closer look as a potential cause. 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To examine this issue, we compared the test performance of 33 savant and 26 nonsavant autistic subjects using the Wechsler Intelligence Scales-Revised for children or adults (WISC-R/WAIS-R). Data analysis revealed inconsistent results with rather negligible differences concerning the compound of cognitive capacities. However, savant and nonsavant individuals with autism exhibited a significant mean difference on the subscale Digit Span. This finding may indicate less impaired Is working memory and executive function in autistic savants or rote memory and low-level processing being core savant skills. Several limitations of the study are discussed. (C) 2004 Published by Elsevier Inc. C1 Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. RP Bolte, S (reprint author), Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, D-60528 Frankfurt, Germany. 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The work presented in this paper is part of the Aurora project, rooted in assistive technology and robot-human interaction research. Our primary aim is to study if robots can potentially be used as therapeutically or educationally useful 'toys'. In this paper we outline the aims of the project that this study belongs to, as well as the specific qualitative contextual perspective that is being used. We then provide an in-depth evaluation, in part using Conversation Analysis (CA), of segments of trials where three children with autism interacted with a robot as well as an adult. We focus our analysis primarily on joint attention which plays a fundamental role in human development and social understanding. Joint attention skills of children with autism have been studied extensively in autism research and therefore this behaviour provides a relevant focus for our study. In the setting used, joint attention emerges from natural and spontaneous interactions between a child and an adult. We present the data in the form of transcripts and photo stills. The examples were selected from extensive video footage for illustrative purposes, i.e. demonstrating how children with autism can respond to the changing behaviour of their co-participant, i.e. the experimenter. Furthermore, our data shows that the robot provides a salient object, or mediator for joint attention. The paper concludes with a discussion of implications of this work in the context of further studies with robots and children with autism within the Aurora project, as well as the potential contribution of robots to research into the nature of autism. C1 [Robins, Ben; Dautenhahn, Kerstin] Univ Hertfordshire, Adapt Syst Res Grp, Hatfield AL10 9AB, Herts, England. [Dickerson, Paul; Stribling, Penny] Univ Surrey, Sch Psychol & Counselling, Guildford GU2 5XH, Surrey, England. RP Robins, B (reprint author), Univ Hertfordshire, Adapt Syst Res Grp, Coll Lane, Hatfield AL10 9AB, Herts, England. 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Stud. PY 2004 VL 5 IS 2 BP 161 EP 198 DI 10.1075/is.5.2.02rob PG 38 WC Communication; Linguistics SC Communication; Linguistics GA V26KM UT WOS:000208544500001 ER PT J AU Meyer, JA Hobson, RP AF Meyer, Jessica A. Hobson, R. Peter TI Orientation in relation to self and other The case of autism SO INTERACTION STUDIES LA English DT Article DE autism; self; imitation; intersubjectivity AB With the aim of studying foundations for self-other relations and understanding, we conducted an experimental investigation of a specific aspect of imitation in children with autism: the propensity to copy self-other orientation. We hypothesised that children with autism would show limitations in identifying with the stance of another person. We tested 16 children with autism and 16 non-autistic children with learning difficulties, matched on both chronological and verbal mental age, for their propensity to imitate the self- or other-orientated aspects of another person's actions. All participants were attentive to the demonstrator and copied her actions, but the children with autism were significantly less likely to imitate those aspects of her actions that involved movement in relation to her own vis-a-vis the child's body. There were a number of children with autism who copied the identical geometric orientation of objects acted-upon. These results suggest that children with autism have a diminished propensity to identify with other people, and point to the importance of this mechanism for shaping self-other relations and flexible thinking. C1 [Meyer, Jessica A.] Tavistock Clin, London NW3 5BA, England. UCL, Inst Child Hlth, London NW3 5BA, England. RP Meyer, JA (reprint author), Tavistock Clin, 120 Belsize Lane, London NW3 5BA, England. 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Stud. PY 2004 VL 5 IS 2 BP 221 EP 244 DI 10.1075/is.5.2.04mey PG 24 WC Communication; Linguistics SC Communication; Linguistics GA V26KM UT WOS:000208544500003 ER PT J AU Laws, G Bishop, D AF Laws, G Bishop, D TI Pragmatic language impairment and social deficits in Williams syndrome: a comparison with Down's syndrome and specific language impairment SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Article DE Down's syndrome; pragmatics; specific language impairment; Williams syndrome ID CHILDRENS COMMUNICATION CHECKLIST; YOUNG-CHILDREN; AUTISM; SKILLS; INDIVIDUALS; DISORDERS; MIND; DIFFICULTIES; ADOLESCENTS; ABILITIES AB Background: The social communication strength of individuals with Williams syndrome described by some researchers contrasts with the picture of social difficulties painted by others. Aims: To study the pragmatic aspects of language, social relationships and unusual interests in a group of children and adults with Williams syndrome, and to compare them with a group of children and adults with Down's syndrome, children with specific language impairment, and a group of typically developing children. Methods & Procedures: Parents or teachers completed the Children's Communication Checklist or a modified version of it with wording appropriate for adults. Study groups consisted of 19 children and young adults with Williams syndrome, 24 with Down's syndrome, 17 children with specific language impairment and 32 typically developing children. Outcomes & Results: Checklist ratings for the group with Williams syndrome indicated significant levels of pragmatic language impairment, and difficulties with social relationships. Together with evidence of unusual or restricted interests, the results suggested deficits across all three domains covered by the checklist. 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Univ Kentucky, Lexington, KY USA. Primary Care Phys, Baton Rouge, LA USA. RP Blaxill, MF (reprint author), Safe Minds, Cambridge, MA USA. CR Croen LA, 2003, J AUTISM DEV DISORD, V33, P227, DOI 10.1023/A:1022964132203 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 GRANDJEAN P, 1995, NEUROTOXICOLOGY, V16, P27 Hightower JM, 2003, ENVIRON HEALTH PERSP, V111, P604, DOI 10.1289/ehp.5837 Hu LW, 2003, T AM NUCL SOC, V89, P681 National Academy of Sciences, 2000, TOX EFF METH NR 6 TC 0 Z9 0 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1091-5818 J9 INT J TOXICOL JI Int. J. Toxicol. 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Since mercury is potentially a risk factor for autoimmunity, we conducted a study of mercury-induced antinuclear and antilaminin antibodies in autistic and normal children who had been pre-administered with thimerosal-containing vaccines. Laboratory analysis by different immunoassays showed that the serum level of these two autoimmune markers did not significantly differ between autistic and normal children. This finding suggests that the mercury as in thimerosal-containing vaccines is likely not related to autoimmune phenomenon in autism. Copyright (C) 2004 National Science Council, ROC and S. Karger AG, Basel. C1 Utah State Univ, Dept Biol, Logan, UT 84322 USA. RP Singh, VK (reprint author), Utah State Univ, Dept Biol, Biotechnol Ctr Bldg,UMC 4700, Logan, UT 84322 USA. 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Fifty-one patients who suffered from the above-mentioned early-onset neurological impairments were admitted to our burn center during a 4-year period. The average TBSA burned was 8.9% yet resulted in prolonged hospitalizations. This study describes our burn center's experience in treating patients admitted with early-onset neurological impairments. C1 New York Presbyterian Hosp, New York Weill Cornell Med Ctr, William Randolph Hearst Burn Ctr, New York, NY 10021 USA. RP Alden, NE (reprint author), New York Presbyterian Hosp, New York Weill Cornell Med Ctr, William Randolph Hearst Burn Ctr, Room L706,525 E 68th St, New York, NY 10021 USA. 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PD JAN-FEB PY 2004 VL 25 IS 1 BP 107 EP 111 DI 10.1097/01.BCR.0000105099.60083.F5 PG 5 WC Emergency Medicine; Rehabilitation; Surgery SC Emergency Medicine; Rehabilitation; Surgery GA 770ZL UT WOS:000188761200015 PM 14726747 ER PT J AU Volkmar, FR Lord, C Bailey, A Schultz, RT Klin, A AF Volkmar, FR Lord, C Bailey, A Schultz, RT Klin, A TI Autism and pervasive developmental disorders SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Review DE autistic disorder; Asperger's disorder; genetics; neuroimaging; neuropsychology ID PLACEBO-CONTROLLED TRIAL; FUSIFORM FACE AREA; INTENSIVE BEHAVIORAL INTERVENTION; POSTERIOR-FOSSA STRUCTURES; HIGH-FUNCTIONING CHILDREN; WEAK CENTRAL COHERENCE; 6-YEAR FOLLOW-UP; ASPERGER-SYNDROME; YOUNG-CHILDREN; MAGNETIC-RESONANCE AB The quantity and quality of research into autism and related conditions have increased dramatically in recent years. Consequently we selectively review key accomplishments and highlight directions for future research. More consistent approaches to diagnosis and more rigorous assessment methods have significantly advanced research, although the boundaries of the 'broader phenotype' remain to be defined and the validity of Asperger's disorder as a discrete syndrome remains controversial. Recent epidemiological studies have shown that Autism Spectrum Disorders are common, but there continues to be debate about the causes of the increase in the frequency with which autism is diagnosed. Psychological research has helped to develop new developmental models for the disorder and there have also been significant advances in the molecular genetics of autism and understanding of the underlying neurobiological processes. Areas important for future research include the study of autism as it first develops, i.e., in infants and very young children, and of specific processes (psychological and neurobiological) which underlie the disorder. 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Psychiatry PD JAN PY 2004 VL 45 IS 1 BP 172 EP 173 DI 10.1111/j.1469-7610.2004.t01-3-00211.x PG 2 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 825WA UT WOS:000221788100011 ER PT J AU McElroy, SL AF McElroy, SL TI Diagnosing and treating comorbid (complicated) bipolar disorder SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT National Summit Meeting of the Bipolar Care Options Initiative CY SEP 04-06, 2003 CL Washington, DC ID OBSESSIVE-COMPULSIVE DISORDER; BORDERLINE PERSONALITY-DISORDER; PLACEBO-CONTROLLED TRIAL; RANDOMIZED CONTROLLED-TRIAL; HOSPITALIZED AGGRESSIVE-CHILDREN; POSTTRAUMATIC-STRESS-DISORDER; BLIND CONTROLLED TRIAL; BINGE-EATING DISORDER; LITHIUM-CARBONATE; DIVALPROEX SODIUM AB Comorbidity is the rule, not the exception, in bipolar disorder. The most common mental disorders that co-occur with bipolar disorder in community studies include anxiety, substance use, and conduct disorders. Disorders of eating, sexual behavior, attention-deficit/hyperactivity, and impulse control, as well as autism spectrum disorders and Tourette's disorder, co-occur with bipolar disorder in clinical samples. The most common general medical comorbidities are migraine, thyroid illness, obesity, type II diabetes, and cardiovascular disease. Bipolarity is a marker for comorbidity, and comorbid disorders, especially multiple conditions occurring when a patient is young, may be a marker for bipolarity. Relatively few controlled clinical studies have examined the treatment of bipolar disorder in the context of comorbid conditions (i.e., complicated or comorbid bipolar disorder). However, the first step in treating any type of complicated bipolar disorder-stabilizing a patient's mood-may be associated with improving the comorbid disorder. Standard mood stabilizers, atypical antipsychotics, and nonantimanic antiepileptic agents are emerging as potentially useful treatments for several of the disorders that frequently co-occur with bipolar disorder, and therefore may be useful treatments for comorbid bipolar disorder. C1 Univ Cincinnati, Coll Med, Dept Psychiat, Cincinnati, OH 45267 USA. RP McElroy, SL (reprint author), Univ Cincinnati, Coll Med, Dept Psychiat, 231 Albert Sabin Way,ML559, Cincinnati, OH 45267 USA. 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Clin. Psychiatry PY 2004 VL 65 SU 15 BP 35 EP 44 PG 10 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 879QN UT WOS:000225732400009 PM 15554795 ER PT J AU Cohen, SA Fitzgerald, BJ Khan, SRF Khan, A AF Cohen, SA Fitzgerald, BJ Khan, SRF Khan, A TI The effect of a switch to ziprasidone in an adult population with autistic disorder: Chart review of naturalistic, open-label treatment SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Review ID MENTAL-RETARDATION; RISPERIDONE; CHILDREN; WEIGHT AB Background: The present investigation retrospectively assessed the effect of an open-label switch to ziprasidone from other atypical antipsychotics on behavior, weight, and lipid levels in an adult Population with autistic disorder. Method: We conducted a chart review of 10 adults (mean +/- SD age = 43.8 +/- 6.0 years) with DSM-IV autistic disorder who were switched from other atypical antipsychotics to ziprasidone, primarily due to weight gain, but other reasons included hypercholesterolemia, maladaptive behaviors, drowsiness. and depression. They had been treated with ziprasidone for at least 6 months. Our review focused on frequency of maladaptive behaviors, weight, and lipid levels. Results: The mean SD daily dose of ziprasidone was 128 +/- 41 m.g. and all 10 patients continued with this same treatment after completion of the 6-month trial. Seven patients were found to have an improvement or no change in their maladaptive behavior. Eight patients (80%) lost weight (mean change = -13.1 +/- 7.0 lb [-5.9 +/- 3.2 kg]), 4 (80%) of 5 patients had a decrease in total cholesterol level, and 3 (60%) of 5 had a decrease in triglyceride levels. Data on lipid levels were available for 5 of the 10 patients. Behavioral activation was not noted in this population. There were no significant adverse effects associated with ziprasidone. Conclusion: In adults with autism, a switch to ziprasidone from other atypical antipsychotics appears to have the potential for maintaining beneficial effect on behavior while improving major health indices including weight and lipid levels. C1 Fircrest Seattle, Seattle, WA USA. NW Clin Res Ctr, Bellevue, WA USA. Duke Univ, Med Ctr, Dept Psychiat & Behav Sci, Durham, NC USA. RP Cohen, SA (reprint author), 1315 1st Ave N, Seattle, WA 98109 USA. EM sacohenmd@msn.com CR Campbell M, 1997, J AM ACAD CHILD PSY, V36, P835, DOI 10.1097/00004583-199706000-00022 Cohen S, 2003, J CLIN PSYCHIAT, V64, P60 Cohen S, 2001, J CLIN PSYCHIAT, V62, P114 Kaye NS, 2003, J CLIN PSYCHOPHARM, V23, P206, DOI 10.1097/00004714-200304000-00015 Lott RS, 1996, PSYCHOPHARMACOL BULL, V32, P721 McDougle CJ, 2002, J AM ACAD CHILD PSY, V41, P921, DOI 10.1097/00004583-200208000-00010 MCDOUGLE CJ, 2000, J AUTISM DEV DISORD, V30, P425 McDougle CJ, 1998, ARCH GEN PSYCHIAT, V55, P633, DOI 10.1001/archpsyc.55.7.633 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 SCHAIN RJ, 1961, J PEDIATR-US, V58, P315, DOI 10.1016/S0022-3476(61)80261-8 Weiden P J, 2001, J Psychiatr Pract, V7, P145, DOI 10.1097/00131746-200103000-00009 2003, MED EC, P1559 NR 12 TC 29 Z9 30 PU PHYSICIANS POSTGRADUATE PRESS PI MEMPHIS PA P O BOX 240008, MEMPHIS, TN 38124 USA SN 0160-6689 J9 J CLIN PSYCHIAT JI J. Clin. Psychiatry PD JAN PY 2004 VL 65 IS 1 BP 110 EP 113 PG 4 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 831JE UT WOS:000222189900018 PM 14744179 ER PT J AU Valdovinos, MG Zarcone, JR Hellings, JA Kim, G Schroeder, SR AF Valdovinos, MG Zarcone, JR Hellings, JA Kim, G Schroeder, SR TI Using the Diagnostic Assessment of the Severely Handicapped-II (DASH-II) to measure the therapeutic effects of risperidone SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE intellectual disabilities; medication; monitoring; problem behaviour ID ABERRANT BEHAVIOR CHECKLIST; PERVASIVE DEVELOPMENTAL DISORDER; DOUBLE-BLIND CROSSOVER; MULTIPLE MEASURES; AUTISM; VALIDITY; DISABILITIES; SUBSCALE; CHILDREN; ADULTS AB Background Within the scope of a double-blind, placebo-controlled, crossover medication study, the Diagnostic Assessment of the Severely Handicapped-II (DASH-II) was evaluated as a measurement for determining the effectiveness of the medication risperidone in treating the problem behaviour of 21 people with intellectual disabilities (ID). Method Participants' caregivers completed the DASH-II during the placebo/baseline phase of the study and the maintenance phase of the study, and completed the Aberrant Behavior Checklist - Community (ABC-C) weekly throughout the entire study. The results obtained using the DASH-II were compared to those obtained using the ABC-C, an instrument shown to be well correlated with the DASH-II. Results Results suggest that while the DASH-II and the ABC-C were well correlated during the placebo/baseline phase of the current study, they were not well correlated at completion of the 6-month maintenance phase of the medication trial. Conclusion The DASH-II, while appropriate for assisting in the diagnosis of psychopathology in people with ID, does not appear to monitor changes in problem behaviour as a result of risperidone use as well as the ABC-C. Differences in the frequency of problem behaviour that each measure evaluated and the applicability of using the DASH-II to measure medication effects on problem behaviour are discussed. C1 Vanderbilt Univ, Peabody Coll, John F Kennedy Ctr, Nashville, TN 37203 USA. Univ Kansas, Med Ctr, Lawrence, KS 66045 USA. RP Valdovinos, MG (reprint author), Vanderbilt Univ, Peabody Coll, John F Kennedy Ctr, Box 74, Nashville, TN 37203 USA. RI Valdovinos, Maria/F-5721-2014 CR AMAN MG, 1995, AM J MENT RETARD, V100, P283 AMAN MG, 1985, AM J MENT DEF, V89, P492 Horrigan JP, 1997, J AUTISM DEV DISORD, V27, P313, DOI 10.1023/A:1025854532079 Hurley A. 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Intell. Disabil. Res. PD JAN PY 2004 VL 48 BP 53 EP 59 DI 10.1111/j.1365-2788.2004.00583.x PN 1 PG 7 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 753YH UT WOS:000187275600008 PM 14675232 ER PT J AU Lopez-Rangel, E Vallance, H Palaty, J Mickelson, E Hrynchak, M Separovic, E MacLeod, PM Arbour, L Clarke, L Lewis, MES AF Lopez-Rangel, E Vallance, H Palaty, J Mickelson, E Hrynchak, M Separovic, E MacLeod, PM Arbour, L Clarke, L Lewis, MES TI Expansion of the 22q13 deletion phenotype in four patients with autism spectrum disorder SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Western Regional Meeting of the American-Federation-for-Medical-Research CY JAN 28-31, 2004 CL CARMEL, CALIFORNIA SP Amer Federat Med Res C1 Univ British Columbia, Sunnyhill Ctr Children, Vancouver, BC V5Z 1M9, Canada. NR 0 TC 0 Z9 0 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 2004 VL 52 IS 1 BP S100 EP S100 PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 765ER UT WOS:000188254600145 ER PT J AU Nowicki, ST Jacquemont, S Li, L Nguyen, DV Gregg, JP Hagerman, RJ Hagerman, PJ AF Nowicki, ST Jacquemont, S Li, L Nguyen, DV Gregg, JP Hagerman, RJ Hagerman, PJ TI An approach to identify epistatic genes involved in the development of autism spectrum disorder in patients with fragile X syndrome SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract CT Western Regional Meeting of the American-Federation-for-Medical-Research CY JAN 28-31, 2004 CL CARMEL, CALIFORNIA SP Amer Federat Med Res C1 Univ Calif Davis, Sch Med, MIND Inst, Davis, CA 95616 USA. Univ Calif Davis, Sch Med, Dept Pediat, Davis, CA 95616 USA. Univ Calif Davis, Sch Med, Dept Pathol, Davis, CA 95616 USA. Univ Calif Davis, Sch Med, Dept Biol Chem, Davis, CA 95616 USA. Univ Calif Davis, Dept Appl Sci, Div Biostat, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 1081-5589 J9 J INVEST MED JI J. Invest. Med. PD JAN PY 2004 VL 52 IS 1 BP S101 EP S101 PG 1 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 765ER UT WOS:000188254600147 ER PT J AU Greig, TC Bryson, GJ Bell, MD AF Greig, TC Bryson, GJ Bell, MD TI Theory of mind performance in schizophrenia: Diagnostic, symptom, and neuropsychological correlates SO JOURNAL OF NERVOUS AND MENTAL DISEASE LA English DT Article ID NEGATIVE SYNDROME SCALE; PEOPLE; IMPAIRMENTS; BEHAVIOR; AUTISM AB The purpose of this study was to explore the relationship between Theory of Mind (ToM) performance and schizophrenia subtype, symptom, and neuropsychological variables. One hundred twenty-eight stable outpatients with schizophrenia or schizoaffective disorder were assessed during the intake phase of a vocational and cognitive rehabilitation study. Results indicate that ToM performance differed significantly by schizophrenia diagnosis, with people diagnosed with disorganized schizophrenia performing the most poorly. Theory of Mind performance was also significantly correlated with measures of thought disorder and verbal memory. Regression analysis revealed that thought disorder and verbal memory measures explained 30% of the variance in ToM scores. Findings suggest that there is theory of mind variance in the schizophrenia population and theory of mind is strongly related to thought disorder, verbal memory, and cognitive disorganization. Contrary to previous reports, ToM was not related to measures of paranoia. C1 Yale Univ, Sch Med, Dept Psychiat, CMHC, New Haven, CT 06519 USA. VA Connecticut Healthcare Syst, West Haven, CT USA. RP Greig, TC (reprint author), Yale Univ, Sch Med, Dept Psychiat, CMHC, 5th Floor,34 Floor St, New Haven, CT 06519 USA. 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Nerv. Ment. Dis. PD JAN PY 2004 VL 192 IS 1 BP 12 EP 18 DI 10.1097/01.nmd.0000105995.67947.fc PG 7 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 764GU UT WOS:000188199800002 PM 14718771 ER PT J AU Sokol, DK Edwards-Brown, M AF Sokol, DK Edwards-Brown, M TI Neuroimaging in autistic spectrum disorder (ASD) SO JOURNAL OF NEUROIMAGING LA English DT Review DE autism; autisic spectrum disorder; neuroimaging; review; children ID MAGNETIC-RESONANCE SPECTROSCOPY; POSITRON-EMISSION-TOMOGRAPHY; POSTERIOR-FOSSA STRUCTURES; EARLY INFANTILE-AUTISM; CEREBRAL-BLOOD-FLOW; CHILDHOOD AUTISM; CORPUS-CALLOSUM; ASPERGER-SYNDROME; CEREBELLAR ABNORMALITIES; DEVELOPMENTAL DISORDERS AB Autistic spectrum disorder (ASD) is a lifelong developmental disorder characterized by impairment in socialization and communication. Neuroimaging research has shown abnormalities in the frontal lobes, limbic systems, and cerebella of individuals with ASD. Recently, abnormal developmental trajectories of brain growth have been reported, with increases in brain volume (in both gray and white matter) seen in younger rather than older individuals with this disorder. Despite 30 years of research, a reliable marker for ASD has not been identified. Therefore, routine neuroimaging for individuals with ASD is not recommended. C1 Indiana Univ, Sch Med, Dept Neurol, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Radiol, Indianapolis, IN 46202 USA. RP Sokol, DK (reprint author), Indiana Univ, Sch Med, Dept Neurol, 702 Barnhill Dr,RI 1757, Indianapolis, IN 46202 USA. 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Neuroimaging PD JAN PY 2004 VL 14 IS 1 BP 8 EP 15 DI 10.1177/1051228403258145 PG 8 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 876CZ UT WOS:000225474800001 PM 14748203 ER PT J AU Stavrakaki, C Antochi, R Emery, PC AF Stavrakaki, C Antochi, R Emery, PC TI Olanzapine in the treatment of pervasive developmental disorders: a case series analysis SO JOURNAL OF PSYCHIATRY & NEUROSCIENCE LA English DT Article DE antipsychotic agents; child development disorders, pervasive; dopamine; serotonin ID OPEN-LABEL; ATYPICAL ANTIPSYCHOTICS; DOUBLE-BLIND; CHILDREN; SCHIZOPHRENIA; ADOLESCENTS; EFFICACY; AUTISM; ADULTS AB Controlling the symptoms that are characteristic of patients with pervasive developmental disorders is often challenging. We report on the safety and efficacy of olanzapine in the treatment of 7 patients with pervasive developmental disorders. The patients were all male and ranged in age from 8 to 52 years. They received olanzapine doses of 5-10 mg/d along with their various other drug regimens. Patients were monitored and evaluated for a mean duration of 17.7 (range 12-26) months while on olanzapine therapy. Very few side effects were observed during treatment. All patients showed clinically significant improvement on the Clinical Global Impressions scale, as well as an improved score as measured by the Global Assessment of Functioning scale. Our observations support the use of long-term olanzapine therapy for symptom control in patients with pervasive developmental disorders. C1 Childrens Hosp Eastern Ontario, Child & Family Psychiatr Unit, Ottawa, ON K1L 8M3, Canada. Univ Ottawa, Dept Psychiat, Ottawa, ON K1L 8M3, Canada. Univ Ottawa, Sch Psychol, Ottawa, ON, Canada. RP Stavrakaki, C (reprint author), Childrens Hosp Eastern Ontario, Child & Family Psychiatr Unit, 311 McArthur Ave,Suite 200, Ottawa, ON K1L 8M3, Canada. 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Psychiatry Neurosci. PD JAN PY 2004 VL 29 IS 1 BP 57 EP 60 PG 4 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 803PZ UT WOS:000220244300007 PM 14719051 ER PT J AU Persico, AM Stodgell, C D'Agruma, L Zelante, L Militerni, R Bravaccio, C Trillo, S Montecchi, F Schneider, C Melmed, R Elia, M Palermo, M Pascucci, T Puglisi-Allegra, S Reichelt, KL Muscarella, L Guarnieri, V Conciatori, M Rodier, P AF Persico, AM Stodgell, C D'Agruma, L Zelante, L Militerni, R Bravaccio, C Trillo, S Montecchi, F Schneider, C Melmed, R Elia, M Palermo, M Pascucci, T Puglisi-Allegra, S Reichelt, KL Muscarella, L Guarnieri, V Conciatori, M Rodier, P TI The HOXA1 G allele may be associated with dysmorphism in autism SO JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 UCBM, Lab Mol Psychiat & Neurogenet, Rome, Italy. Univ Rochester, Sch Med, Rochester, NY USA. IRCCS Casa Sollievo dalla Sofferenza, San Giovanni Rotondo, FG, Italy. Univ Naples, I-80138 Naples, Italy. IRCCS Osp Bambino Gesu, Rome, Italy. SARC, Phoenix, AZ USA. IRCCS Oasi Maria SS, Troina, EN, Italy. Assoc Anni Verdi, Rome, Italy. Univ Roma La Sapienza, Dept Psychol, Rome, Italy. Univ Oslo, Rikshosp, Dept Pediat Res, N-0316 Oslo, Norway. RI Stodgell, Christopher/A-1161-2007 NR 0 TC 0 Z9 0 PU HOGREFE & HUBER PUBLISHERS PI GOTTINGEN PA ROHNSWEG 25, D-37085 GOTTINGEN, GERMANY SN 0269-8803 J9 J PSYCHOPHYSIOL JI J. Psychophysiol. PY 2004 VL 18 IS 1 BP 47 EP 47 PG 1 WC Psychology, Biological; Neurosciences SC Psychology; Neurosciences & Neurology GA 828QT UT WOS:000221988500036 ER PT J AU Kephart, B AF Kephart, B TI The ride together: A brother and sister's memoir of autism in the family. SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Book Review CR KARASIK P, 2003, RIDE TOGETHER BROTHE NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0890-8567 J9 J AM ACAD CHILD PSY JI J. Am. Acad. Child Adolesc. Psychiatr. PD JAN PY 2004 VL 43 IS 1 BP 112 EP 112 DI 10.1097/01.chi.0000096621.64367.f3 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 759EB UT WOS:000187724400020 ER PT J AU Probst, P Hillig, S AF Probst, P Hillig, S TI Computer-assisted training of purchasing skills: A single case study of a 15-year-old boy with early infantile autism SO KINDHEIT UND ENTWICKLUNG LA German DT Article DE early infantile autism; computer-assisted training; rehabilitation; purchasing skills; single case study ID CHILDREN; INSTRUCTION; RATIONALE AB The aim of the present exploratory single case study is to examine the effectiveness of computer-assisted training of purchasing skills in a 15-year-old boy with early infantile autism. The purchasing behavior was systematically observed under baseline, training, and post-training conditions. The systematic observation of the training process included variables of trainee's learning and tutor's teaching behavior. Video-based behavioral observations are analyzed by the partial time sampling and the event sampling method. The results indicate that the purchasing skills of the autistic adolescent improved significantly during the training. The training process is characterized by high fluctuations between attentive and distracted behaviors in the autistic student as well as intensive teaching activities on the part of the tutor. The findings support the assumption that daily living skills such as shopping behavior in autistic persons can be significantly improved by means of computer-based interventions. C1 Univ Hamburg, Psychol Inst 2, D-20146 Hamburg, Germany. RP Probst, P (reprint author), Univ Hamburg, Psychol Inst 2, Von Melle Pk 5, D-20146 Hamburg, Germany. 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Entwickl. PY 2004 VL 13 IS 2 BP 122 EP 128 DI 10.1026/0942-5403.13.2.122 PG 7 WC Psychology, Developmental SC Psychology GA 817OQ UT WOS:000221187200006 ER PT S AU Peterson, D Galitsky, B AF Peterson, D Galitsky, B BE Negoita, MG Howlett, RJ Jain, LC TI Handling default rules by autistic reasoning SO KNOWLEDGE-BASED INTELLIGENT INFORMATION AND ENGINEERING SYSTEMS, PT 3, PROCEEDINGS SE LECTURE NOTES IN ARTIFICIAL INTELLIGENCE LA English DT Article; Proceedings Paper CT 8th International Conference on Knowledge-Based Intelligent Information and Engineering Systems CY SEP, 2004 CL Wellington, NEW ZEALAND SP Royal Soc New Zealand, IPENZ, New Zealand Trade & Enterprise, Telecom, Allied Telesyn, Positively Wellington Business HO Wellington Inst Technol AB We employ the formalism of default logic to model the phenomena of autistic reasoning. Our main finding is that while people with autism may be able to process single default rules, they have a characteristic difficulty in cases where two default rules conflict. Even though default reasoning was intended to simulate the reasoning of typical human subjects, it turns out that following the operational semantics of default reasoning in a literal way leads to the peculiarities of autistic behavior observed in the literature. C1 Univ London, Inst Educ, London WC1E 7HU, England. Univ London Birkbeck Coll, Sch Comp Sci & Informat Syst, London WC1E 7HX, England. RP Peterson, D (reprint author), Univ London, Inst Educ, 20 Bedford Way, London WC1E 7HU, England. EM d.peterson@ioe.ac.uk; galitsky@dcs.bbk.ac.uk CR Antoniou G., 1997, NONMONOTONIC REASONI Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bochman A., 2001, LOGICAL THEORY NONMO Bratman M., 1987, INTENTION PLANS PRAC BREWKA G, 1995, CSLI LECT NOTES, V73 GALITSKY B, 2003, FLAIRS GALITSKY B, 1908, ADV KNOWLEDGE INT Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x Peterson D., 2000, AUTISM, V4, P391, DOI 10.1177/1362361300004004005 Russel J., 1997, AUTISM EXECUTIVE DIS NR 10 TC 2 Z9 2 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-23205-2 J9 LECT NOTES ARTIF INT PY 2004 VL 3215 BP 314 EP 320 PG 7 WC Computer Science, Artificial Intelligence; Computer Science, Information Systems SC Computer Science GA BBB77 UT WOS:000224585500042 ER PT J AU Dhossche, DM Stanfill, S AF Dhossche, DM Stanfill, S TI Could ECT be effective in autism? SO MEDICAL HYPOTHESES LA English DT Article ID LANDAU-KLEFFNER-SYNDROME; PERIODIC CATATONIA; ASPERGERS-SYNDROME; INFANTILE-AUTISM; REGRESSION; DISORDERS; CHROMOSOME-15; 15Q11-Q13; SEIZURES; LINKAGE AB Autism is increasingly diagnosed, but therapeutic options are limited in many children. ECT is considered as a safe, effective, and life-saving treatment in people of all ages who suffer from affective disorders, acute psychosis, and, in particular, catatonia. There are recent speculations that certain types of autism may be the earliest expression of catatonia and that both disorders have identical risk factors. Therefore, ECT may improve autism and, if started early enough, may prevent further development of autistic symptoms in some children. The use of ECT in autism has never been systematically assessed. There have been two large ECT studies in children in the 1940s. Autism was not assessed in these studies because the autistic syndrome was just then being recognized as a separate entity. Findings from these studies add little to the hypothesis that ECT may be effective in autistic children, but attest to the safety and feasibility of ECT in children. Another limitation is the use of older ECT techniques. What may well be the greatest deterrent to use ECT in autism is widespread anti- ECT sentiment not only among the public but within the medical community as well. All child specialists - psychiatrists, neurologists, psychologists, and developmental pediatricians - should independently review the feasibility, potential, and risk of using ECT in autism. Unless anti-ECT prejudice can be overcome, it is unlikely that any ECT trial in autism is forthcoming. Research areas that may support the hypothesis that ECT is effective in autism should be pursued. First, any link between autism and catatonia should be further explored in clinical and biochemical studies. A GABA theory of autism and catatonia may be pivotal. Second, the rote of abnormal GABA(A) receptor subunit genes in autism and catatonia should be further assessed. Candidate loci for autism and catatonia have been found on the long arm of chromosome 15 where three GABA(A) receptor subunits genes are located. The GABA(A) receptor beta 3 subunit gene (GABRB3) was the Leading candidate gene for a subgroup of autism in two independent studies. Third, a novel genetic mouse model of autism should be tested. Mutant mice with a targeted deletion of the GABRB3 gene have a complete deficit of the beta 3 subunit of the GABA(A) receptor. This knockout mouse model seems promising to study developmental effects of altered GABA(A) receptor function as it relates to certain developmental disorders including autism. (C) 2004 Elsevier Ltd. ALL rights reserved. C1 Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, Jackson, MS 39216 USA. RP Dhossche, DM (reprint author), Univ Mississippi, Med Ctr, Dept Psychiat & Human Behav, 2500 N State St, Jackson, MS 39216 USA. 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Hypotheses PY 2004 VL 63 IS 3 BP 371 EP 376 DI 10.1016/j.mehy.2004.03.023 PG 6 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 848SH UT WOS:000223486900001 PM 15288351 ER PT J AU Wahl, RUR AF Wahl, RUR TI Could oxytocin administration during labor contribute to autism and related behavioral disorders? - A look at the literature SO MEDICAL HYPOTHESES LA English DT Article ID NEONATAL HYPERBILIRUBINEMIA; PITOCIN INDUCTION; SOCIAL DEFICITS; RECEPTOR; BRAIN; DESENSITIZATION; BILIRUBIN; INFUSION; PATHOGENESIS; VASOPRESSIN AB This literature review summarizes recent potential evidence, most of which is at the molecular/ mechanistic level., in support of Hollander's hypothesis that excess oxytocin (OT), possibly through OT administration at birth, could contribute to the development of autistic spectrum disorders and related syndromes by proposed down regulation of the OT receptor (OTR). In this review, recent molecular evidence for OTR internalization by excess OT is related to OT's reported effects on animal social behavior, favoring social bondage, notably in sheep, votes, rats and especially mice. Adding indications for OT's capability of crossing the maternal placenta and OT's possibility of crossing an underdeveloped or stressed infantile blood brain barrier at birth, a causal connection between OT excess and behavioral disorders such as autism can be supported from a molecular perspective. Possible strategies such as a thorough statistical analysis of numerous birth records as well as molecular studies such as radiotracing using labeled OT are proposed to test this hypothesis. (C) 2004 Elsevier Ltd. All rights reserved. C1 Initiat Mol Studies Autism, Teaneck, NJ 07666 USA. RP Wahl, RUR (reprint author), Initiat Mol Studies Autism, 516 North St, Teaneck, NJ 07666 USA. 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Hypotheses PY 2004 VL 63 IS 3 BP 456 EP 460 DI 10.1016/j.mehy.2004.03.008 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 848SH UT WOS:000223486900018 PM 15288368 ER PT J AU Yun, AJ Bazar, KA Lee, PY AF Yun, AJ Bazar, KA Lee, PY TI Pineal attrition, loss of cognitive plasticity, and onset of puberty during the teen years: is it a modern maladaptation exposed by evolutionary displacement? SO MEDICAL HYPOTHESES LA English DT Review ID LONG-TERM POTENTIATION; SONG CONTROL-SYSTEM; CONGENITAL ADRENAL-HYPERPLASIA; HIPPOCAMPAL SYNAPTIC PLASTICITY; SEROTONIN REUPTAKE INHIBITORS; EYE-MOVEMENT SLEEP; SERUM MELATONIN; CRITICAL PERIOD; MENSTRUAL-CYCLE; MALE RATS AB Cognitive plasticity, a developmental trait that promotes acquisition of complex skills such as language or playing musical instruments, diminishes substantially during puberty. The loss of plasticity has been attributed to surge of sex steroids during adolescence, but the phenomenon remains poorly understood. We hypothesize that pineal involution during puberty may contribute to plasticity decay. The pineal gland produces melatonin, the level of which declines dramatically during onset of puberty. Emerging evidence suggest that melatonin may modulate cognitive plasticity, independent of the effects of sex steroids, and low sex steroids and high melatonin may be simultaneously required to maintain cognitive plasticity. Potential mechanisms by which melatonin may modulate plasticity are examined within the steep and hippocampal. long-term potentiation frameworks. Implications for psychiatric conditions that involve sleep disorders and learning dysfunctions such as schizophrenia and autism are discussed, and the potential adaptive roles of postprandial and postcoital steep are explored. From the Darwinian perspective, development and reproductive maturity may represent distinct phases that require tailored cognitive strategies to maximize fitness. While cognitive flexibility and susceptibility to new skills may be paramount during development, reduced cognitive flexibility and increased cognitive determinism may enable more efficient responses to stimuli during adulthood. Thus, cognitive plasticity and cognitive determinism may represent trade-off adaptations and different dimensions of intelligence. The decline of plasticity and emergence of puberty during the second decade may be relics of prehistoric times when the human lifespan was short and the environment was relatively simple and static. Today, when the environment is more complex and dynamic, and humans are living far longer, the early obsolescence of plasticity during puberty may represent a Darwinian inefficiency exposed by evolutionary displacement. Regulation of plasticity may be a systemic phenomenon, as exemplified by the association of learning disability with allergic conditions, a form of immune plasticity dysfunction. Ramifications for other plastic functions that decline during puberty such as wound heating and hyaline cartilage regeneration are explored. Like the plasticity of immunity and cognition, the plasticity of hyaline cartilage during youth may enable hosts to respond to ecologic opportunities and generate the optimally adapted adult phenotype. Pineal involution may represent a potential target for therapeutic extension or restoration of plasticity after puberty. Extending plasticity may have far-reaching consequences for human evolution. (C) 2004 Elsevier Ltd. All rights reserved. C1 Stanford Univ, Palo Alto, CA 94301 USA. San Mateo Med Ctr, Dept Dermatol, San Mateo, CA 94403 USA. RP Bazar, KA (reprint author), Stanford Univ, 4700 Univ Ave, Palo Alto, CA 94301 USA. 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Hypotheses PY 2004 VL 63 IS 6 BP 939 EP 950 DI 10.1016/j.mehy.2004.07.027 PG 12 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 871JV UT WOS:000225128500004 PM 15504560 ER PT J AU Ijichi, S Ijichi, N AF Ijichi, S Ijichi, N TI The prenatal autistic imprinting hypothesis: developmental maladaptation to the environmental changes between womb and the social world SO MEDICAL HYPOTHESES LA English DT Article ID SPECTRUM DISORDERS; GENETIC INFLUENCES; BRAIN; MRI; NEUROPATHOLOGY; INTELLIGENCE; PREVALENCE; BEHAVIOR; MEMORY; LIFE AB Although the importance of biological and genetic aspects of the etiology is well recognized, the pathological process of autism still remains to be elucidated. In contrast to a qualitative dichotomy concept, a dimensional perspective that places the autistic traits as quantitative extremes can easily explain the diversity and subtlety of the clinical features. In a dimensional (quantitative continuum) condition, no single qualitative process can distinguish the extremes from normal variations. In addition, the traditional view, which regards autism as a hyporeproductive disease with a strong genetic contribution, cannot interpret the recent worldwide prevalence of autism. From a novel viewpoint, we have proposed 'the prenatal autistic imprinting hypothesis' in which autism is regarded as an inevitable consequence of human social evolution in both past and future. Postulated primary phenotypes are closely associated with the autistic savant skills and the autistic adherent temperament, and might increase the chance of specific prenatal experiences, named 'autistic imprinting'. An earlier prenatal brain growth and an earlier establishment of a type of consciousness may be critical for the imprinting process. A postnatal autistic social maladaptation may be a mere outcome of the putative intrauterine behavioral adaptation in individuals with the primary phenotypes. Both an autistic manner of thinking, which is referred to as 'visual thinking', and the prenatal early development of visual cortical. architectures may play a key rote in the autistic imprinting process. (C) 2003 Elsevier Ltd. All rights reserved. C1 EGT, Kagoshima 8961411, Japan. RP Ijichi, S (reprint author), EGT, 8-3 Nagahama, Kagoshima 8961411, Japan. 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Hypotheses PY 2004 VL 62 IS 2 BP 188 EP 194 DI 10.1016/S0306-9877(03)00310-4 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 779KE UT WOS:000189293200007 PM 14962624 ER PT J AU Kane, RC AF Kane, RC TI A possible association between fetal/neonatal exposure to radiofrequency electromagnetic radiation and the increased incidence of Autism Spectrum Disorders (ASD) SO MEDICAL HYPOTHESES LA English DT Article ID RAT-BRAIN CELLS; MICROWAVE EXPOSURE; HUMAN-LYMPHOCYTES; SINGLE-STRAND; IN-VITRO; DNA; FIELDS; IRRADIATION; DAMAGE; BREAKS AB Recently disclosed epidemiological data indicate a dramatic increase in the incidence of autism spectrum disorders. Previously, the incidence of autism has been reported as 4-5 per 10,000 children. The most recent evidence indicates an increased incidence of about 1 per 500 children. However, the etiology of autism is yet to be determined. The recently disclosed data suggest a possible correlation between autism incidence and a previously unconsidered environmental toxin. It is generally accepted in the scientific community that radiofrequency (RF) radiation is a biologically active substance. It is also readily acknowledged that human exposures to RF radiation have become pervasive during the past 20 years, whereas such exposures were uncommon prior to that time. It is suggested that fetal or neo-natal exposures to RF radiation may be associated with an increased incidence of autism. (C) 2003 Elsevier Ltd. All rights reserved. C1 Associated Bioelectromagnet Technol, Blanchardville, WI 53516 USA. RP Kane, RC (reprint author), Associated Bioelectromagnet Technol, POB 113, Blanchardville, WI 53516 USA. 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Hypotheses PY 2004 VL 62 IS 2 BP 195 EP 197 DI 10.1016/S0306/9877(03)00309-8 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 779KE UT WOS:000189293200008 PM 14962625 ER PT J AU Blaxill, MF Redwood, L Bernard, S AF Blaxill, MF Redwood, L Bernard, S TI Thimerosal and autism? A plausible hypothesis that should not be dismissed SO MEDICAL HYPOTHESES LA English DT Article ID ET-AL. 2002; CHANGING PREVALENCE; SPECTRUM DISORDERS; MINAMATA DISEASE; METHYLMERCURY; MERCURY; EXPOSURE; CHILDREN; BRAIN; EPIDEMIOLOGY AB The autism-mercury hypothesis first described by Bernard et al. has generated much interest and controversy. The Institute of Medicine (IOM) reviewed the connection between mercury-containing vaccines and neurodevelopmental disorders, including autism. They concluded that the hypothesis was biologically plausible but that there was insufficient evidence to accept or reject a causal connection and recommended a comprehensive research program. Without citing new experimental evidence, a number of observers have offered opinions on the subject, some of which reject the IOM's conclusions. In a recent review, Nelson and Bauman argue that a link between the preservative thimerosal, the source of the mercury in childhood vaccines, is improbable. In their defense of thimerosal, these authors take a narrow view of the original hypothesis, provide no new evidence, and rely on selective citations and flawed reasoning. We provide evidence here to refute the Nelson and Bauman critique and to defend the autism-mercury hypothesis. (C) 2004 Elsevier Ltd. All rights reserved. C1 Sensible Action Ending Mercury Induced Neurol Diso, PH Cranford, NJ 07016 USA. RP Blaxill, MF (reprint author), 22 Fayerweather St, Cambridge, MA 02138 USA. 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Hypotheses PY 2004 VL 62 IS 5 BP 788 EP 794 DI 10.1016/j.mehy.2003.11.033 PG 7 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 820HA UT WOS:000221376900027 PM 15082108 ER PT J AU Clark-Taylor, T Clark-Taylor, BE AF Clark-Taylor, T Clark-Taylor, BE TI Is autism a disorder of fatty acid metabolism? Possible dysfunction of mitochondrial beta-oxidation by long chain acyl-CoA dehydrogenase SO MEDICAL HYPOTHESES LA English DT Article ID INFANTILE-AUTISM; DEFICIENCY; CHILDREN; GENE; PHOSPHORYLATION; INHIBITION; COENZYME; PLASMA; NEUROTOXICITY; FIBROBLASTS AB Long chain acyl-CoA dehydrogenase (LCAD) has recently been shown to be the mitochondrial enzyme responsible for the beta-oxidation of branched chain and unsaturated fatty acids [Biochim. Biophys. Acta 1393 (1998) 35; Biochim. Biophys. Acta 1485 (2000) 121]. Whilst disorders of short, medium and very long chain acyl dehydrogenases are known, there is no known disorder of LCAD deficiency in humans. Experimental LCAD deficiency in mice shows an acyl-carnitine profile with prominent elevations of unsaturated fatty acid metabolites C14:1 and C14:2 [Hum. Mol. Genet. 10 (2001) 2069]. A child with autism whose acyl-carnitine profile also shows these abnormalities is presented, and it is hypothesized that the child may have LCAD deficiency. Additional metabolic abnormalities seen in this patient include alterations of TCA energy production, ammonia detoxification, reduced synthesis of omega-3 DHA, and abnormal cholesterol metabolism. These metabolic changes are also seen as secondary abnormalities in dysfunction of fatty acid beta-oxidation, and have also been reported in autism. It is hypothesized that LCAD deficiency may be a cause of autism. Similarities between metabolic disturbances in autism, and those of disorders of fatty acid beta-oxidation are discussed. (C) 2004 Elsevier Ltd. All rights reserved. RP Clark-Taylor, T (reprint author), POB 1524, Canberra, ACT, Australia. 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Remodeling of existing neurons induced by such factors has been observed throughout the brain, and includes alterations in dendritic field dimensions, synaptogenesis, and synaptic morphology. The brain loci affected by these plastic neuronal changes are dependent on the type of experience and learning. Increased neurogenesis in the hippocampal dentate gyrus is a well-documented response to environmental complexity ("enrichment") and learning. Exposure to challenging experiences and (earning opportunities also alters existing glial cells (i.e., astrocytes and oligodendrocytes), and up-regulates gliogenesis, in the cerebral cortex and cerebellum. Such glial plasticity often parallels neuronal remodeling in both time and place, and this enhanced morphological synergism may be important for optimizing the functional interaction between glial cells and neurons. Aberrant structural plasticity of nonneuronal elements is a contributing factor, as is aberrant neuron plasticity, to neurological and developmental disorders such as epilepsy, autism, and mental retardation (i.e., fragile X syndrome). Some of these nonneuronal pathologies include abnormal cerebral and cerebellar white matter and myelin-related proteins in autism, abnormal myelin basic protein in fragile X syndrome (FXS); and abnormal astrocytes in autism, FXS, and epilepsy. A number of recent studies demonstrate the possibility of using environmental and experiential intervention to reduce or ameliorate some of the neuronal and nonneuronal abnormalities, as well as behavioral deficits, present in these neurological and developmental disorders. (C) 2004 Wiley-Liss, Inc. C1 Univ Illinois, Beckman Inst, Neurotech Grp, Urbana, IL 61801 USA. Univ Illinois, Beckman Inst, Dept Psychol, Urbana, IL 61801 USA. Univ Illinois, Beckman Inst, Dept Psychiat, Urbana, IL 61801 USA. Univ Illinois, Beckman Inst, Dept Cell & Struct Biol, Urbana, IL 61801 USA. RP Greenough, WT (reprint author), Univ Illinois, Beckman Inst, Neurotech Grp, 405 N Mathews, Urbana, IL 61801 USA. 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Conversely, rearing animals in larger, more complex environments results in enhanced brain structure and function, including increased brain weight, dendritic branching, neurogenesis, gene expression, and improved learning and memory. Moreover, in animal models of CNS insult (e-g., gene deletion), a more complex environment has attenuated or prevented the sequelae of the insult. Of relevance is the prevention of seizures and attenuation of their neuropathological sequelae as a consequence of exposure to a more complex environment. Relatively little attention, however, has been given to the issue of sensitive periods associated with such effects, the relative importance of social versus inanimate stimulation, or the unique contribution of exercise. Our studies have examined the effects of environmental complexity on the development of the restricted, repetitive behavior commonly observed in individuals with autism. In this model, a more complex environment substantially attenuates the development of the spontaneous and persistent stereotypies observed in deer mice reared in standard laboratory cages. Our findings support a sensitive period for such effects and suggest that early enrichment may have persistent neuroprotective effects after the animal is returned to a standard cage environment, Attenuation or prevention of repetitive behavior by environmental complexity was associated with increased neuronal metabolic activity, increased dendritic spine density, and elevated neurotrophin (BDNF) levels in brain regions that are part of cortical-basal ganglia circuitry. These effects were not observed in limbic areas such as the hippocampus. (C) 2004 Wiley-Liss, Inc. C1 Univ Florida, Dept Psychiat, McKnight Brain Inst, Gainesville, FL 32601 USA. RP Lewis, MH (reprint author), Univ Florida, Dept Psychiat, McKnight Brain Inst, 100 S Newell Dr, Gainesville, FL 32601 USA. 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Understanding the critical periods of vulnerability of the developing nervous system to seizure-induced changes may provide insights into parallel or divergent processes in the development of autism. In experimental rodent models, the consequences of seizures are dependent on age, etiology, seizure duration, and frequency. Recurring seizures in immature rats result in long-term adverse effects on learning and memory. These behavioral changes are paralleled by changes in brain connectivity, changes in excitatory neurotransmitter receptor distribution, and decreased neurogenesis. These changes occur in the absence of cell loss. Although impaired cognitive function and brain changes have been well-documented following early-onset seizures, the mechanisms of seizure-induced dysfunction remain unclear. (C) 2004 Wiley-Liss, Inc. C1 Dartmouth Coll, Hitchcock Med Ctr, Ctr Neurosci, Sect Neurol,Med Sch, Lebanon, NH 03756 USA. RP Holmes, GL (reprint author), Dartmouth Coll, Hitchcock Med Ctr, Ctr Neurosci, Sect Neurol,Med Sch, 1 Med Ctr Dr, Lebanon, NH 03756 USA. 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The increased use of retrospective measures such as head circumference along with a surge of MRI studies of toddlers with autism, have opened whole new area of research and discovery. Recent studies have now shown that abnormal brain overgrowth occurs during the first 2 years of life in children with autism. By 2-4 years of age, the most deviant overgrowth is in cerebral, cerebellar, and limbic structures that underlie higher-order cognitive, social, emotional, and language functions. Excessive growth is followed by abnormally slow or arrested growth. Deviant brain growth in autism occurs at the very time when the formation of cerebral circuitry is at its most exuberant and vulnerable stage, and it may signal disruption of this process of circuit formation. The resulting aberrant connectivity and dysfunction may lead to the development of autistic behaviors. To discover the causes, neural substrates, early-warning signs and effective treatments of autism, future research should focus on elucidating the neurobiological defects that underlie brain growth abnormalities in autism that appear during these critical first years of life. (C) 2004 Wiley-Liss, Inc. C1 Childrens Hosp, Res Ctr, Ctr Autism Res, La Jolla, CA USA. Univ Calif San Diego, Sch Med, Dept Neurosci, La Jolla, CA 92093 USA. RP Courchesne, E (reprint author), Ctr Autism Res, 8110 La Jolla Shores Dr, La Jolla, CA 92037 USA. 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PY 2004 VL 10 IS 2 BP 106 EP 111 DI 10.1002/mrdd.20020 PG 6 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100006 PM 15362165 ER PT J AU Chugani, DC AF Chugani, DC TI Serotonin in autism and pediatric epilepsies SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE serotonin; autism; epilepsy; tryptophan; cortical development; kynurenine ID WHOLE-BLOOD SEROTONIN; HUMAN AUDITORY-CORTEX; METHYL-L-TRYPTOPHAN; TEMPORAL-LOBE EPILEPSY; QUINOLINIC ACID; MONOAMINE-OXIDASE; MINICOLUMNAR PATHOLOGY; INTRACTABLE EPILEPSY; SOMATOSENSORY CORTEX; CORTICAL DEVELOPMENT AB Serotonergic abnormalities have been reported in both autism and epilepsy. This association may provide insights into underlying mechanisms of these disorders because serotonin plays an important neurotrophic role during brain development-and there is evidence for abnormal cortical development in both autism and some forms of epilepsy. This review explores the hypothesis that an early disturbance in the serotonin system affects cortical development and the development of thalamocortical innervation, and is a potential mechanism, common to autism and pediatric epilepsies associated with cortical dysplasia. An argument is made that cortical malformation leads to abnormalities of thalamocortical connectivity, and that serotonin plays a critical role in this process. Finally, a role for altered metabolism of the serotonin precursur, tryptophan, in both epilepsy and autism is discussed, (C) 2004 Wiley-Liss, Inc. C1 Childrens Hosp Michigan, PET Ctr, Dept Pediat, Detroit, MI 48201 USA. Childrens Hosp Michigan, PET Ctr, Dept Radiol, Detroit, MI 48201 USA. Wayne State Univ, Sch Med, Detroit, MI USA. RP Chugani, DC (reprint author), Childrens Hosp Michigan, PET Ctr, Dept Pediat, 3901 Beaubien Blvd, Detroit, MI 48201 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 2 BP 112 EP 116 DI 10.1002/mrdd.20021 PG 5 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100007 PM 15362166 ER PT J AU Shouse, MN Scordato, JC Farber, PR AF Shouse, MN Scordato, JC Farber, PR TI Sleep and arousal mechanisms in expeirjmental epilepsy: Epileptic components of NREM and antiepileptic components of REM sleep SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE sleep; epilepsy; animal models; cats; amygdala kindling; penicillin epilepsy ID AMYGDALA-KINDLED KITTENS; SEIZURES; AUTISM AB Neural generators related to different sleep components have different effects on seizure discharge. These sleep-related systems can provoke seizure discharge propagation during nonrapid eye movement (NREM) sleep and can suppress propagation during REM sleep. Experimental manipulations of discrete physiological components were conducted in feline epilepsy models, mostly in the systemic penicillin epilepsy model of primary generalized epilepsy and the amygdala kindling model of the localization-related seizure disorder, temporal lobe epilepsy. The sleep-wake state distribution of seizures was quantified before and after discrete lesions, Systemic and localized drug administration, and/or photic stimulation, as well as in relation to microdialysis of norepinephrine. We found that (1) neural generators of synchronous EEG oscillations-including tonic background slow waves and phasic "arousal" events (sleep EEG transients such as sleep spindles and k-complexes)-combine to promote electrographic seizure propagation during NREM and drowsiness, and antigravity muscle tone permits seizure-related movement; (2) neural generators of asynchronous neuronal discharge patterns reduce electrographic seizures during alert waking and REM sleep, and skeletal motor paralysis blocks seizure-related movement during REM; (3) there are a number of similarities between amygdala-kindled kittens and children with Landau-Kleffner Syndrome (LKS) that suggest a link among seizures, sleep disorders, and behavioral abnormalities/regression. Published 2004 Wiley-Liss, Inc. C1 VA Greater Los Angeles Hlth Care Syst, Sleep Disturbance Res, Los Angeles, CA USA. Univ Calif Los Angeles, Sch Med, Dept Neurobiol, Los Angeles, CA USA. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 2 BP 117 EP 121 DI 10.1002/mrdd.20022 PG 5 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100008 PM 15362167 ER PT J AU Malow, BA AF Malow, BA TI Steep disorders, epilepsy, autism SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; sleep; epilepsy; polysomnography; REM sleep; melatonin ID EYE-MOVEMENT SLEEP; WAKE RHYTHM; BEHAVIOR DISORDER; REM-SLEEP; CHILDREN; MELATONIN; APNEA; SEROTONIN; PATTERNS; ADULTS AB The purpose of this review article is to describe the clinical data linking autism with sleep and epilepsy and to discuss the impact of treating sleep disorders in children with autism either with or without coexisting epileptic seizures. Studies are presented to support the view that sleep is abnormal in individuals with autistic spectrum disorders, Epilepsy and sleep have reciprocal relationships, with sleep facilitating seizures and seizures adversely affecting sleep architecture. The hypothesis put forth is that identifying and treating sleep disorders, which are potentially caused by or contributed to by autism, may impact favorably on seizure control and on daytime behavior. The article concludes with some practical suggestions for the evaluation and treatment of sleep disorders in this population of children with autism. (C) 2004 Wiley-Liss, Inc. C1 Vanderbilt Univ, Sch Med, Vanderbilt Sleep Disorders Ctr, Nashville, TN 37212 USA. RP Malow, BA (reprint author), Dept Neurol, 2100 Pierce Ave, Nashville, TN 37212 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 2 BP 122 EP 125 DI 10.1002/mrdd.20023 PG 4 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100009 PM 15362168 ER PT J AU Bolton, PF AF Bolton, PF TI Neuroepileptic correlates of autistic symptomatology in tuberous sclerosis SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; epilepsy; tuberous sclerosis; brain; temporal lobes ID INFANTILE SPASMS; GENETIC DISORDER; ATYPICAL AUTISM; COMPLEX; TSC2; EPILEPSY; FACE; SEVERITY; INDIVIDUALS; ASSOCIATION AB Tuberous sclerosis is a genetic condition that is strongly associated with the development of an autism spectrum disorder. However, there is marked variability in expression, and only a subset of children with tuberous sclerosis develop autism spectrum disorder. Clarification of the mechanisms that underlie the association and variability in expression will potentially throw light on the biological processes involved in the etiology of idiopathic forms of autism spectrum disorder. Current evidence indicates that the likelihood of a child with tuberous sclerosis developing an autism spectrum disorder is greater if the child has a mutation in the TSC2 gene, although autism can and does develop in children with TSC1 mutations. The likelihood is also greater if the child has early-onset infantile spasms that are difficult to control, especially if there is an epileptiform focus in the temporal lobes. The emerging evidence is consistent with the notion that early onset electrophysiological disturbances within the temporal lobes (and perhaps other locations) has a deleterious effect on the development and establishment of key social cognitive representations concerned with processing social information, perhaps especially from faces. However, alternative mechanisms to account for the findings cannot yet be ruled out. Future research will have to employ prospective longitudinal designs and treatment trials to clarify the processes involved. (C) 2004 Wiley-Liss, Inc. C1 Kings Coll London, Inst Psychiat, Dept Child Psychiat, London SE5 8AF, England. Kings Coll London, Inst Psychiat, Ctr Social Genet & Dev Psychiat, London SE5 8AF, England. RP Bolton, PF (reprint author), Kings Coll London, Inst Psychiat, Dept Child Psychiat, Denmark Hill,Box P043, London SE5 8AF, England. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 2 BP 126 EP 131 DI 10.1002/mrdd.20024 PG 6 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100010 PM 15362169 ER PT J AU Tharp, BR AF Tharp, BR TI Epileptic encephalopathies and their relationship to developmental disorders: Do spikes cause autism? SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE pervasive developmental disorder; autism; seizures; interictal EEG; spike and wave; multiple subpial transaction ID FOCAL INTERICTAL SPIKES; CAT CUNEATE NUCLEUS; EEG DISCHARGES; COGNITIVE IMPAIRMENT; REACTION-TIME; CHILDREN; REGRESSION; ELECTROENCEPHALOGRAM; PERCEPTION; SEIZURES AB Epileptic encephalopathies are progressive clinical and electroencephalographic syndromes where deterioration is thought to be caused by frequent seizures and abundant EEG epileptiform activity. Seizures occur in approximately 10-15% of children with pervasive developmental disorders (PDD) and 8-10% have epileptiform EEG abnormalities without seizures. Thirty percent of children with PDD have regression of social behavior and language at 2-3 years of age. Some authors speculate that the regression is caused by epileptiform activity even in the absence of overt clinical seizures ("autism with epileptic regression") and suggest that elimination of the epileptiform activity, either medically or surgically, should lead to improvement in behavior. This review examines the data showing that interictal epileptiform discharges are associated with transient clinical dysfunction and discusses the implications of these observations for autistic behavioral abnormalities. The results of resective surgery, vagal nerve stimulation, and multiple subpial transaction on children with autism and epileptiform EEG abnormalities are also discussed. I conclude that there is no evidence that interictal discharges per se cause (or contribute to) the complex behavioral phenotype of autism. There is no justification to support the use of anticonvulsant medication or surgery in children with PDD without seizures; that is, there is no evidence that treatment to eliminate EEG spikes will have a therapeutic effect on the behavioral abnormalities of PDD and autism. (C) 2004 Wiley-Liss, Inc. C1 Univ Calif Davis, MIND Inst, Dept Neurol, Sacramento, CA 95817 USA. Univ Calif Davis, MIND Inst, Dept Pediat, Sacramento, CA 95817 USA. RP Tharp, BR (reprint author), Univ Calif Davis, MIND Inst, Dept Neurol, 2825 50th St, Sacramento, CA 95817 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 2 BP 132 EP 134 DI 10.1002/mrdd.20025 PG 3 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100011 PM 15362170 ER PT J AU Tuchman, R AF Tuchman, R TI AEDs and psychotropic drugs in children with autism and epilepsy SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; epilepsy; treatment; AEDs; psychotropics ID PERVASIVE DEVELOPMENTAL DISORDER; TECHNOLOGY-ASSESSMENT SUBCOMMITTEE; QUALITY STANDARDS SUBCOMMITTEE; DOUBLE-BLIND; SPECTRUM DISORDERS; ANTIEPILEPTIC DRUGS; BIPOLAR DISORDERS; EPILEPTIFORM EEG; AMERICAN ACADEMY; CONTROLLED TRIAL AB The efficacy of antiepileptic drugs (AEDs) and psychotropic medications in children with autism is limited to the treatment of seizures or to specific behaviors such as irritability, impulsivity, hyperactivity, repetitive behaviors, or aggression. The reliability and value of the available data-to determine the efficacy of these medications in autism-are limited by lack of controlled clinical trials, the small number of subjects, the heterogeneity of the population studied, and the brief duration of most drug trials. Indeed, few controlled clinical trials using AEDs in autism, with or without seizures, have been conducted. Because some AEDs also have a positive effect on mood, the benefits that children with autism sometimes obtain from these medications may not be due to the treatment of the abnormal electrical activity or the seizures per se but to an effect on common neuronal systems responsible for both behavior and epilepsy. The relationship between epilepsy and autism, and specifically the effects that abnormal electrical activity may have on the developing brain, may provide some valuable insights into the type of studies that are needed to help us understand the pathophysiology of autism. (C) 2004 Wiley-Liss, Inc. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 2 BP 135 EP 138 DI 10.1002/mrdd.20026 PG 4 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100012 PM 15362171 ER PT J AU Rogers, SJ AF Rogers, SJ TI Developmental regression in autism spectrum disorders SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE developmental regression; language; social/attachment behaviors ID CHILDHOOD DISINTEGRATIVE DISORDER; INFANTILE-AUTISM; SYMPTOM ONSET; SPEECH LOSS; CHILDREN; AGE; SETBACK AB The occurrence of developmental regression in autism is one of the more puzzling features of this disorder. Although several studies have documented the validity of parental reports of regression using home videos, accumulating data suggest that most children who demonstrate regression also demonstrated previous, subtle, developmental differences. Counter to clinical intuition, the earlier development of social, language, and attachment behaviors followed by regression does not seem to support later recovery of skills or better developmental outcomes compared to children who never had speech or typical social responsivity. In fact, this regressive group may have somewhat greater developmental impairment than the nonregressive group, though the two groups do not appear to present different behavioral phenotypes, Although autism is not the only condition in which regression occurs, it appears to be the most frequent condition. Other disorders that demonstrate an early regression with no known etiology include total blindness from birth and childhood disintegrative disorder, both of which demonstrate behavioral relations to autism. In addition, two biological conditions with known etiologies also involve regression with some behaviors resembling autism behavioral phenotype: Rett syndrome (a genetic disorder; see Glaze, this issue) and Landau-Kleffner syndrome (see McVicar and Shinnar, this issue), which involves a seizure disorder. (C) 2004 Wiley-Liss, Inc. C1 Univ Calif Davis, Med Ctr, MIND Inst, Sacramento, CA 95817 USA. RP Rogers, SJ (reprint author), Univ Calif Davis, Med Ctr, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. 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PY 2004 VL 10 IS 2 BP 139 EP 143 DI 10.1002/mrdd.20027 PG 5 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100013 PM 15362172 ER PT J AU McVicar, KA Shinnar, S AF McVicar, KA Shinnar, S TI Landau-Kleffner syndrome, electrical status epilepticus in slow wave sleep, and language regression in children SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE Landau-Kleffner syndrome; electrical status epilepticus in slow wave sleep; language regression; autism; epilepsy ID PERVASIVE DEVELOPMENTAL DISORDER; BENIGN ROLANDIC EPILEPSY; ACQUIRED APHASIA; CLINICAL CHARACTERISTICS; CONVULSIVE DISORDER; CORTICOSTEROID-THERAPY; AUTISTIC REGRESSION; DYSPHASIC CHILDREN; CHILDHOOD; EEG AB The Landau-Kleffner syndrome (LKS) and electrical status epilepticus in slow wave sleep (ESES) are rare childhood-onset epileptic encephalopathies in which loss of language skills occurs in the context of an epileptiform EEG activated in sleep. Although in LKS the loss of function is limited to language, in ESES there is a wider spectrum of cognitive impairment. The two syndromes are distinct but have some overlap. The relationship between the epileptiform EEG abnormalities and the loss of cognitive function remains controversial, even in LKS which is the most widely accepted as an acquired epileptic aphasia. Language regression also occurs in younger children, frequently in the context of a more global autistic regression. Many of these children have epileptiform EEGs. The term autistic regression with epileptiform EEG has been proposed for these children. Whether these children are part of an extended LKS spectrum is very controversial, because there are differences in age of onset, clinical phenotype, and EEG findings. An understanding of the available data on clinical characteristics, EEG findings, pathology, prognosis, and treatment of these syndromes is essential for further progress in this area. (C) 2004 Wiley-Liss, Inc. C1 Montefiore Med Ctr, Albert Einstein Coll Med, Comprehens Epilepsy Management Ctr, Bronx, NY 10467 USA. Montefiore Med Ctr, Albert Einstein Coll Med, Dept Neurol, Bronx, NY 10467 USA. Montefiore Med Ctr, Albert Einstein Coll Med, Dept Pediat, Bronx, NY 10467 USA. RP Shinnar, S (reprint author), Montefiore Med Ctr, Albert Einstein Coll Med, Comprehens Epilepsy Management Ctr, 111 E 210th St, Bronx, NY 10467 USA. 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The discovery of the genetic cause of RTT, mutations in the MECP2 gene, a transcriptional repressor, has promoted the early diagnosis of RTT and development of mouse models. The phenotype of one mouse model includes features such as regression and abnormal behavioral and social interactions. The timing of the period of regression in RTT-during ages 1 to 2 years-parallels the period of intense synaptic development. The effects of the MECP2 mutation also increases concomitantly with peak synaptogenesis. Neuropathological findings in Rett include the selective reduction of dendritric spines in the pyramidal cells of RTT brains, this feature has also been reported in autism. Studies have observed that MIECP influences the expression of brain-derived neurotrophic factor and thus may influence synaptic plasticity. Abnormalities in synapse maintenance and modulation may contribute to regression in RTT and autism. Studies of the clinical aspects of the regression period and of the mouse model may be useful in understanding the pathophysiology of RTT and other neurodevelopmental disorders such as autism. A recent study observed abnormal expression of MeCP2 in RTT and other neurodevelopmental disorders such as autism. Although the genetic background and certain clinical features differ in RTT and autism, a similar mechanism involving MeCP2 regulation and expression may contribute to regression. (C) 2004 Wiley-Liss, Inc. C1 Baylor Coll Med, Blue Bird Circle Rett Ctr, Houston, TX 77030 USA. RP Glaze, DG (reprint author), Baylor Coll Med, Blue Bird Circle Rett Ctr, 1 Baylor Pl,Room 319C, Houston, TX 77030 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 2 BP 154 EP 158 DI 10.1002/mrdd.20030 PG 5 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 857KL UT WOS:000224115100016 PM 15362175 ER PT J AU Camarata, SM Wertz, RT AF Camarata, SM Wertz, RT TI Treatment efficacy research: A window into genetic and neurodevelopmental correlates of developmental disabilities SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE treatment efficacy; developmental disabilities; autism; language disorder; genetics; neurological development ID CHILDREN AB This issue of MRDD research reviews is dedicated to treatment efficacy research. The treatment of MRDD conditions has long been a central question, but the clinical science of treatment efficacy has not yet been systematically applied to many MRDD typologies. The purpose of this paper is to provide an overview of this special issue and to provide a rationale for including treatment efficacy research as a tool for studying selected neurological development and genetic correlates of MRDD. Existing treatment efficacy paradigms should be applied systematically to relevant populations (and theoretical questions) and new, objectively tested paradigms should be developed in order to integrate ongoing discovery in MRDD. (C) 2004 Wiley-Liss, Inc. C1 Vanderbilt Univ, Sch Med, Dept Speech & Hearing Sci, Nashville, TN 37232 USA. Vanderbilt Univ, Sch Med, Kennedy Ctr Res Dev & Disabilities, Nashville, TN 37232 USA. Vet Adm Hosp, Nashville, TN USA. RP Camarata, SM (reprint author), Vanderbilt Univ, Sch Med, Dept Speech & Hearing Sci, 221 Kirkland Hall, Nashville, TN 37232 USA. 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PY 2004 VL 10 IS 3 BP 159 EP 161 DI 10.1002/mrdd.20033 PG 3 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 882GP UT WOS:000225927700001 PM 15611984 ER PT J AU Bruinsma, Y Koegel, RL Koegel, LK AF Bruinsma, Y Koegel, RL Koegel, LK TI Joint attention and children with autism: A review of the literature SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; joint attention; intentional communication ID LATER EXPRESSIVE VOCABULARY; NONVERBAL-COMMUNICATION; EARLY RECOGNITION; YOUNG-CHILDREN; LANGUAGE; INFANTS; ACQUISITION; PREDICTORS; 1-YEAR-OLD; BEHAVIOR AB Preverbal communication and joint attention have long been of interest to researchers and practitioners. Both attending to social partners and sharing attentional focus between objects or events and others precede the onset of a child's first lexicon. In addition, these prelinguistic acts also appear to have important implications with regard to learning to socialize. The construct of joint attention has been noted as an early developing area prior to the transition to symbolic communication. Thus, the importance of joint attention in typically developing children, and the lack thereof in children with autism, has interested researchers for use in diagnosis and intervention for autism. That is, joint attention has been gaining momentum as an area that not only helps characterize children with autism, but also as a prognostic indicator and a potential intervention goal. In this paper, the status of the literature about initiation of joint attention by young typically developing children and young children with autism was examined. 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PY 2004 VL 10 IS 3 BP 169 EP 175 DI 10.1002/mrdd.20036 PG 7 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 882GP UT WOS:000225927700003 PM 15611988 ER PT J AU Symons, FJ Thompson, A Rodriguez, MC AF Symons, FJ Thompson, A Rodriguez, MC TI Self-injurious behavior and the efficacy of Naltrexone treatment: A quantitative synthesis SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE self-injurious behavior; Naltrexone; efficacy; mental retardation ID MENTALLY-RETARDED ADULTS; SINGLE-SUBJECT RESEARCH; DOUBLE-BLIND; AUTISTIC-CHILDREN; DEVELOPMENTAL-DISABILITIES; NARCOTIC-ANTAGONISTS; FUNCTIONAL-ANALYSIS; OPIATE ANTAGONISTS; RETARDATION; PLACEBO AB People with mental retardation, autism, and related developmental disabilities who self-injure are treated with a wide array of behavioral techniques and psychotropic medications. Despite numerous reports documenting short-term and some long-term changes in self-injury assocated with the opiate antagonist naltrexone hydrochloride, no quantitative review of its efficacy has been reported. We conducted a quantitative synthesis of the peer-reviewed published literature from 1983 to 2003 documenting the use of naltrexone for the treatment of self-injurious behavior (SIB). Individual-level results were analyzed given subject and study characteristics. A sample of 27 research articles involving 86 subjects with self-injury was reviewed. Eighty percent of subjects were reported to improve relative to baseline (i.e., SIB reduced) during naltrexone administration and 47% of subjects SIB was reduced by 50% or greater. In studies reporting dose levels in milligrams, males were more likely than females to respond. No significant relations were found between treatment outcomes and autism status or form of self-injury. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 3 BP 193 EP 200 DI 10.1002/mrdd.20031 PG 8 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 882GP UT WOS:000225927700006 PM 15611982 ER PT J AU Gillum, H Camarata, S AF Gillum, H Camarata, S TI Importance of treatment efficacy research on language comprehension in MR/DD research SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE treatment efficacy research; language; language intervention; language disorders; receptive language disorder; language comprehension; autism ID IMPAIRED CHILDREN; PROCESSING ABILITIES; DISORDERED CHILDREN; RECEPTIVE LANGUAGE; SPEECH-PERCEPTION; LATE TALKERS; FOLLOW-UP; ACQUISITION; INTERVENTION; COMMUNICATION AB The purpose of this review is to discuss the importance of treatment efficacy research in language comprehension in MR/DD populations. Although receptive language deficit is an integral part of most MR/DD typologies, there have been relatively few studies evaluating the effectiveness or efficacy of treatment for this condition. Recently, there has been increased attention placed on auditory processing in children with disabilities, an aspect of cognition related to receptive language, but there have also been few studies investigating the effectiveness or efficacy of training designed to improve auditory processing. In addition to arguing that additional studies in this area are needed, the review includes several theoretical frameworks for addressing the treatment of receptive language deficits in MR/DD. (C) 2004 Wiley-Liss, Inc. C1 Vanderbilt Univ, Dept Speech & Hearing Sci, Sch Med, Nashville, TN 37232 USA. Vanderbilt Univ, Sch Med, John F Kennedy Ctr Res Dev & Disabilities, Nashville, TN 37232 USA. 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A model of genetic association for treatment studies SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE genetic association; language; language intervention; language disorders; genetic association and autism; treatment efficacy ID MULTIFACTOR-DIMENSIONALITY REDUCTION; SINGLE-NUCLEOTIDE POLYMORPHISMS; AUTISM SUSCEPTIBILITY GENE; ANGELMAN-SYNDROME GENE; LINKAGE-DISEQUILIBRIUM; DIAGNOSTIC INTERVIEW; ALZHEIMERS-DISEASE; CHROMOSOME 7Q; CROHNS-DISEASE; FAMILY HISTORY AB The purpose of this review is to provide a model for studying genetic association of response to intervention in child language disorders. in addition to a theoretical overview and review of different approaches to studying candidate genes, a specific methodology for completing this type of analysis is presented. 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PY 2004 VL 10 IS 4 BP 219 EP 220 DI 10.1002/mrdd.20037 PG 2 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 892VA UT WOS:000226676900001 PM 15666337 ER PT J AU Sigman, M Dijamco, A Gratier, M Rozga, A AF Sigman, M Dijamco, A Gratier, M Rozga, A TI Early detection of core deficits in autism SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; early detection; dyadic interactions; imitation; emotion discrimination; attachment security ID PERVASIVE DEVELOPMENTAL DISORDERS; FACIAL EXPRESSIONS; 7-MONTH-OLD INFANTS; JOINT ATTENTION; YOUNG-CHILDREN; EMOTIONAL EXPRESSIONS; INTERACTIONAL SYNCHRONY; INTERMODAL PERCEPTION; 5-MONTH-OLD INFANTS; ATTACHMENT BEHAVIOR AB The goal of this review of the research literature is to discuss approaches to the early detection of autism in infancy. Early detection would enable diagnoses to be made before 18 months of age rather than at 24-30 months, the age where diagnoses start to be made now. After summarizing the criteria for a deficit to be considered "core" to the disorder, the literature on research strategies used in early detection is examined. In order to guide the design of future studies, the review then turns to an overview of what is known about the processes of early social development in typically developing children that underlie the domains in which core deficits are manifested in young children with autism. The social domains covered in the review are those that show development in typically developing infants below 18 months of age: dyadic interaction and imitation; emotion discrimination; and attachment. The review concludes that all of these areas are worthy of investigation in young children, particularly those at higher risk of showing some of the core deficits of autism such as the infant siblings of children with autism. (C) 2004 Wiley-Liss, Inc. C1 Univ Calif Los Angeles, Los Angeles, CA 90095 USA. RP Sigman, M (reprint author), Univ Calif Los Angeles, Box 95175759,68-237 NPI, Los Angeles, CA 90095 USA. 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PY 2004 VL 10 IS 4 BP 221 EP 233 DI 10.1002/mrdd.20046 PG 13 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 892VA UT WOS:000226676900002 PM 15666338 ER PT J AU Seltzer, MM Shattuck, P Abbeduto, L Greenberg, JS AF Seltzer, MM Shattuck, P Abbeduto, L Greenberg, JS TI Trajectory of development in adolescents and adults with autism SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; adolescence; life course development ID RECEPTIVE LANGUAGE DISORDER; FOLLOW-UP; DOWN-SYNDROME; INFANTILE PSYCHOSIS; MENTAL-RETARDATION; ASPERGER-SYNDROME; YOUNG-ADULTS; SPECTRUM DISORDERS; CHILDHOOD AUTISM; FAMILY STRESS AB This article seeks to elucidate the trajectory of development in adolescents and adults with autism. Prospective, retrospective, and cross-sectional studies are reviewed to reveal the manifestation of and changes in the core symptoms of autism in adolescence and adulthood. Comparing children with adolescents and adults, modest degrees of symptom abatement and improvement in skills have been documented in multiple studies, as are increases in verbal and decreases in performance IQ. Nevertheless, most individuals do not attain normative outcomes in adulthood and continue to manifest significant degrees of symptomatology and dependency. However, a small sub-group (about 15%) has more favorable adult outcomes. (C) 2004 Wiley-Liss, Inc. C1 Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. RP Seltzer, MM (reprint author), Univ Wisconsin, Waisman Ctr, Madison, WI 53705 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 4 BP 234 EP 247 DI 10.1002/mrdd.20038 PG 14 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 892VA UT WOS:000226676900003 PM 15666341 ER PT J AU Crawley, JN AF Crawley, JN TI Designing mouse behavioral tasks relevant to autistic-like behaviors SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; mice; social interaction; ultrasonic vocalizatons; olfactory communication; reversal learning; social approach; anxiety ID ANXIETY-LIKE BEHAVIOR; OVEREXPRESSING TRANSGENIC MICE; FRAGILE-X-SYNDROME; SENSORIMOTOR GATING ABNORMALITIES; QUANTITATIVE TRAIT LOCUS; LEMLI-OPITZ-SYNDROME; ANIMAL-MODELS; KNOCKOUT MICE; CANDIDATE GENES; MUTANT MICE AB The importance of genetic factors in autism has prompted the development of mutant mouse models to advance our understanding of biological mechanisms underlying autistic behaviors. Mouse models of human neuropsychiatric diseases are designed to optimize (1) face validity, i.e., resemblance to the human symptoms; (2) construct validity, i.e., similarity to the underlying causes of the disease; and (3) predictive validity, i.e., expected responses to treatments that are effective in the human disease. There is a growing need for mouse behavioral tasks with all three types of validity for modeling the symptoms of autism. We are in the process of designing a set of tasks with face validity for the defining features of autism: deficits in appropriate reciprocal social interactions, deficits in verbal social communication, and high levels of ritualistic repetitive behaviors. Social approach is tested in an automated three-chambered apparatus that offers the subject a choice between a familiar environment, a novel environment, and a novel environment containing a stranger mouse. Preference for social novelty is tested in the same apparatus, with a choice between the start chamber, the chamber containing a familiar mouse, and the chamber containing a stranger mouse. Social communication is evaluated by measuring the ultrasonic distress vocalizations emitted by infant mouse pups and the parental response of retrieving the pup to the nest. Resistance to change in ritualistic repetitive behaviors is modeled by forcing a change in habit, including reversal of the spatial location of a reinforcer in a T-maze task and in the Morris water maze. Mouse behavioral tasks that may model additional features of autism are discussed, including tasks relevant to anxiety, seizures, sleep disturbances, and sensory hypersensitivity. Applications of these tests include (1) behavioral phenotyping of transgenic and knockout mice with mutations in genes relevant to autism, (2) characterization of mutant mice derived from random chemical mutagenesis, (3) DNA microarray analyses of genes in inbred strains of mice that differ in social interaction, social communication and resistance to change in habit, and (4) evaluation of proposed therapeutics for the treatment of autism. Published 2004 Wiley-Liss, Inc. C1 Univ N Carolina, Mouse Behav Phenotyping Lab, Neurodev Disorders Res Ctr, Chapel Hill, NC 27514 USA. NIMH, Lab Behav Neurosci, Intramural Res Program, Bethesda, MD USA. RP Crawley, JN (reprint author), Univ N Carolina, Mouse Behav Phenotyping Lab, Neurodev Disorders Res Ctr, Chapel Hill, NC 27514 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 4 BP 259 EP 271 DI 10.1002/mrdd PG 13 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 892VA UT WOS:000226676900005 PM 15666336 ER PT J AU Wassink, TH Brzustowicz, LM Bartlett, CW Szatmari, P AF Wassink, TH Brzustowicz, LM Bartlett, CW Szatmari, P TI The search for autism disease genes SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; linkage; genetics; cytogenetics; language; microarray ID SEROTONIN TRANSPORTER GENE; PERVASIVE DEVELOPMENTAL DISORDERS; COMPARATIVE GENOMIC HYBRIDIZATION; OBSESSIVE-COMPULSIVE BEHAVIORS; MAJOR SUSCEPTIBILITY LOCUS; RECEPTOR SUBUNIT GENES; LANGUAGE IMPAIRMENT; LINKAGE-DISEQUILIBRIUM; GENOMEWIDE SCREEN; POSTERIOR PROBABILITY AB Autism is a heritable disorder characterized by phenotypic and genetic complexity. This review begins by surveying current linkage, gene association, and cytogenetic studies performed with the goal of identifying autism disease susceptibility variants. Though numerous linkages and associations have been identified, they tend to diminish upon closer examination or attempted replication. The review therefore explores challenges to current methodologies presented by the complexities of autism that might underlie some of the current difficulties, and finishes by describing emerging phenotypic, statistical, and molecular investigational approaches that offer hope of overcoming those challenges. (C) 2004 Wiley-Liss, Inc. C1 Univ Iowa, Carver Coll Med, Dept Psychiat, Iowa City, IA 52242 USA. Rutgers State Univ, Ctr Mol & Behav Neurosci, Newark, NJ 07102 USA. Rutgers State Univ, Dept Genet, Newark, NJ 07102 USA. Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Psychiat, Newark, NJ 07103 USA. Univ Iowa, Ctr Stat Genet Res, Iowa City, IA USA. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. RP Wassink, TH (reprint author), Univ Iowa, Carver Coll Med, Dept Psychiat, Iowa City, IA 52242 USA. 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PY 2004 VL 10 IS 4 BP 272 EP 283 DI 10.1002/mrdd.20041 PG 12 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 892VA UT WOS:000226676900006 PM 15666342 ER PT J AU Dykens, EM Sutcliffe, JS Levitt, P AF Dykens, EM Sutcliffe, JS Levitt, P TI Autism and15q11-q13 disorders: Behavioral, genetic, and pathophyiological issues SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE 15q11-q13 disorders; Prader-Willi syndrome; interneuron pathogenesis; endophenotypes ID PRADER-WILLI-SYNDROME; LINKAGE-DISEQUILIBRIUM; ANGELMAN SYNDROME; INTERSTITIAL DUPLICATIONS; CHROMOSOME 15Q11-Q13; SPECTRUM DISORDERS; GENOMIC SCREEN; PROXIMAL 15Q; INTRACHROMOSOMAL TRIPLICATION; MOLECULAR CHARACTERIZATION AB New insights into biological factors that underlie autism may be gained by comparing autism to other neurodevelopmental disorders that have autistic features and relatively well-delineated genetic etiologies or neurobiological findings. This review moves beyond global diagnoses of autism and instead uses an endophenotypic approach to compare specific clusters of autistic symptomatology to features of chromosome 15q11-q13 disorders. Paternally or maternally derived deficiencies of 15q11-q13 result in Prader-Willi or Angelman syndromes, and we first use a global approach to review potential autism susceptibility genes in the 15q11-q13 region. We then use a more trait-based approach to suggest possible ties between specific phenotypic characteristics of autism and Prader-Willi syndrome, namely savant-like skills. We conclude with insights from pathophysiological studies that implicate altered development of specific neuron types and circuits in the cerebral cortex as part of the pathophysiological processes associated with autism and mental retardation. (C) 2004 Wiley-Liss, Inc. C1 Vanderbilt Kennedy Ctr Res Human Dev, Dept Psychol & Human Dev, Nashville, TN 37203 USA. Vanderbilt Kennedy Ctr Res Human Dev, Dept Physiol & Mol Biophys, Nashville, TN 37203 USA. Vanderbilt Kennedy Ctr Res Human Dev, Dept Pharmacol, Nashville, TN 37203 USA. RP Dykens, EM (reprint author), Vanderbilt Kennedy Ctr Res Human Dev, Dept Psychol & Human Dev, 230 Appleton Pl,Peabody Box 40, Nashville, TN 37203 USA. 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PY 2004 VL 10 IS 4 BP 284 EP 291 DI 10.1002/mrdd.20042 PG 8 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 892VA UT WOS:000226676900007 PM 15666333 ER PT J AU Lawler, CP Croen, LA Grether, JK Van de Water, J AF Lawler, CP Croen, LA Grether, JK Van de Water, J TI Identifying environmental contributions to autism: Provocative clues and false leads SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; epidemiology; prevalence; neurotoxicology; surveillance; toxicokinetics; environmental response genes; gene-environment interaction; genetic susceptibility; immunology; children's environmental health; epigenetics; exposure assessment ID CENTRAL-NERVOUS-SYSTEM; POLYCYCLIC AROMATIC-HYDROCARBONS; MENTAL-RETARDATION; NEURODEVELOPMENTAL DISORDERS; ALPHA-NAPHTHOFLAVONE; MULTIPLE-SCLEROSIS; CHILDRENS HEALTH; ANIMAL-MODELS; PREVALENCE; CYTOKINES AB The potential role of environmental factors in autism spectrum disorders (ASD) is an area of emerging interest within the public and scientific communities. The high degree of heritability of ASD suggests that environmental influences are likely to operate through their interaction with genetic susceptibility during vulnerable periods of development. Evaluation of the plausibility of specific neurotoxicants as etiological agents in ASD should be guided by toxicological principles, including dose-effect dependency and pharmacokinetic parameters. Clinical and epidemiological investigations require the use of sufficiently powered study designs with appropriate control groups and unbiased case ascertainment and exposure assessment. Although much of the existing data that have been used to implicate environmental agents in ASD are limited by methodological shortcomings, a number of efforts are underway that will allow more rigorous evaluation of the role of environmental exposures in the etiology and/or phenotypic expression of the disorder. Surveillance systems are now in place that will provide reliable prevalence estimates going forward in time. Anticipated discoveries in genetics, brain pathology, and the molecular/cellular basis of functional impairment in ASD are likely to provide new opportunities to explore environmental aspects of this disorder. (C) 2004 Wiley-Liss, Inc. C1 NIEHS, Div Extramural Res & Training, Res Triangle Pk, NC 27709 USA. Kaiser Permanente No California, Div Res, Oakland, CA USA. Calif Dept Hlth Serv, Environm Hlth Invest Branch, Oakland, CA USA. Univ Calif Davis, Dept Internal Med, Davis, CA 95616 USA. RP Lawler, CP (reprint author), NIEHS, Div Extramural Res & Training, POB 1123,MD EC 23, Res Triangle Pk, NC 27709 USA. 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PY 2004 VL 10 IS 4 BP 292 EP 302 DI 10.1002/mrdd.20043 PG 11 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 892VA UT WOS:000226676900008 PM 15666339 ER PT J AU Polleux, F Lauder, JM AF Polleux, F Lauder, JM TI Toward a developmental neurobiology of autism SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; development; cortex; mouse genetics; serotonin; dopamine; norepinephrine; glutamate; neurotransmitters; GABA; interneurons; patterning; gene expression; neuroligin; neuronal migration; dendrite; synaptogenesis ID SEROTONIN TRANSPORTER GENE; DOPAMINE-BETA-HYDROXYLASE; CORTICAL DENDRITIC GROWTH; LINKED MENTAL-RETARDATION; DEVELOPING HUMAN BRAIN; CEREBRAL-CORTEX; SPECTRUM DISORDERS; GENOMEWIDE SCREEN; LOCUS-COERULEUS; NEURODEVELOPMENTAL DISORDERS AB Autism is a complex, behaviorally defined, developmental brain disorder with an estimated prevalence of 1 in 1,000. It is now clear that autism is not a disease, but a syndrome with a strong genetic component. The etiology of autism is poorly defined both at the cellular and the molecular levels. Based on the fact that seizure activity is frequently associated with autism and that abnormal evoked potentials have been observed in autistic individuals in response to tasks that require attention, several investigators have recently proposed that autism might be caused by an imbalance between excitation and inhibition in key neural systems including the cortex. Despite considerable ongoing effort toward the identification of chromosome regions affected in autism and the characterization of many potential gene candidates, only a few genes have been reproducibly shown to display specific mutations that segregate with autism, likely because of the complex polygenic nature of this syndrome. Among those, several candidate genes have been shown to control the early patterning and/or the late synaptic maturation of specific neuronal subpopulations controlling the balance between excitation and inhibition in the developing cortex and cerebellum. In the present article, we review our current understanding of the developmental mechanisms patterning the balance between excitation and inhibition in the context of the neurobiology of autism. (C) 2004 Wiley-Liss, Inc. C1 Univ N Carolina, Sch Med, Dept Pharmacol, Ctr Neurosci, Chapel Hill, NC 27514 USA. Univ N Carolina, Sch Med, Dept Cell & Dev Biol, Chapel Hill, NC USA. RP Polleux, F (reprint author), Univ N Carolina, Sch Med, Dept Pharmacol, Ctr Neurosci, Chapel Hill, NC 27514 USA. 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In contrast, a growing body of empirical evidence supports the use of a few forms of theory-based and empirically validated treatment for some aspects of the core features of autism. These include behavioral/psychoeducational interventions and specific forms of medication treatment, which can produce significant improvements in communication, social interaction, and problem behaviors that both maintain over time and generalize across settings. While there is no doubt that treatment and educational services for persons with autism have improved over the past 6 decades, it also appears that significant issues remain with respect to (1) the routine application of validated treatments for the majority of cases with autism, (2) the resistance to even validated forms of treatment for a substantial minority of cases with autism, and (3) the extent to which validated treatments effectively treat the specific core features of autism that are most disabling for persons with autism and their families. (C) 2004 Wiley-Liss, Inc. C1 Univ N Carolina, STAART, Ctr Autism Res, Chapel Hill, NC 27514 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. RP Bodfish, JW (reprint author), Univ N Carolina, STAART, Ctr Autism Res, Chapel Hill, NC 27514 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2004 VL 10 IS 4 BP 318 EP 326 DI 10.1002/mrdd.20045 PG 9 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 892VA UT WOS:000226676900010 PM 15666340 ER PT J AU Klosinski, G Troje, AE AF Klosinski, G Troje, AE TI Kanner autism. Course of the disorder in the second and third decade in 18 patients regarding socially adaptive behavior. Results of a qualitative retrospective study SO NERVENARZT LA German DT Article DE Kanner autism; developmental factors; social adaptation ID FOLLOW-UP; CHILDREN; ADULTS AB The development of Kanner autism in 18 patients (mean age 28 years) in their second and third decade was explored and recorded With respect to factors affecting social competence in adulthood. To validate the diagnoses, we used the Childhood Autism Rating Scale (CARS). A version of the Vineland Adaptive Behavior Scales (VABS) was employed to assess social adaptation. On average,the individuals showed socially adaptive skills typical for healthy children at the age of 4 years and 3 months. Seventy-two percent of the autistic persons showed a characteristic pattern: they scored highest in daily living skills and lowest in social skills, especially in inter-personal relationships, where they performed at an average age equivalent of only 2 years and 7 months! Correlation analysis was conducted between developmental factors due to the disorder on the one hand and socially adaptive skills on the other. It showed,among other results,that positive developmental tendencies during adolescence are related to better social adaptation in adulthood (r=0.57). C1 Univ Tubingen, Abt Psychiat & Psychotherapie Kindes & Jugendalte, Poliklin, Tubingen, Germany. RP Klosinski, G (reprint author), Univ Tubingen, Abt Psychiat & Psychotherapie Kindes & Jugendalte, Poliklin, Tubingen, Germany. EM gunther.klosinski@med.uni-tuebingen.de CR BRYSON SE, 1997, HDB AUTISM PERVASIVE CANTWELL DP, 1978, AUTISM REAPPRAISAL C DeMyer M., 1979, PARENTS CHILDREN AUT DEMYER MK, 1973, J AUTISM CHILD SCHIZ, V3, P199, DOI 10.1007/BF01538281 GILLBERG C, 1987, J AUTISM DEV DISORD, V17, P273, DOI 10.1007/BF01495061 Gillberg C., 1992, BIOL AUTISTIC SYNDRO KOBAYASHI R, 1992, J AUTISM DEV DISORD, V22, P395, DOI 10.1007/BF01048242 LOCKYER L, 1969, BRIT J PSYCHIAT, V115, P865, DOI 10.1192/bjp.115.525.865 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x LOTTER V, 1974, J AUTISM CHILD SCHIZ, V4, P11, DOI 10.1007/BF02104997 LOVELAND KA, 1988, AM J MENT RETARD, V93, P84 MESIBOV GB, 1983, AUTISM ADOLESCENTS A PERRY A, 1990, J AUTISM DEV DISORD, V19, P41 Remschmidt H., 1992, PSYCHIAT ADOLESZENZ Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 RUMSEY JM, 1985, J AM ACAD CHILD PSY, V24, P465, DOI 10.1016/S0002-7138(09)60566-5 RUTTER M, 1970, SEMIN PSYCHIAT, V2, P435 RUTTER M, 1987, J AUTISM DEV DISORD, V17, P159, DOI 10.1007/BF01495054 RUTTER M, 1978, REAPPRAISAL CONCEPTS SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Sparrow S, 1984, VINELAND ADAPTIVE BE SZATMARI P, 1989, J AUTISM DEV DISORD, V19, P213, DOI 10.1007/BF02211842 TROJE AE, 2000, THESIS MED FAK TUBIN VOLKMAR FR, 1991, AM J PSYCHIAT, V148, P1705 VOLKMAR FR, 1987, J AM ACAD CHILD PSY, V26, P156, DOI 10.1097/00004583-198703000-00005 NR 25 TC 0 Z9 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0028-2804 J9 NERVENARZT JI Nervenarzt PD JAN PY 2004 VL 75 IS 1 BP 23 EP + DI 10.1007/s00115-003-1504-7 PG 6 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 775FW UT WOS:000189030900004 PM 14722658 ER PT J AU Pruter, C Kawohl, W Hoff, R AF Pruter, C Kawohl, W Hoff, R TI A case of schizophrenia simplex? SO NERVENARZT LA German DT Article DE schizophrenia simplex; classification; diagnosis AB In routine clinical work, the psychopathology of some patients makes distinct diagnosis more difficult for the psychiatrist. In schizophrenia, especially those patients with dominant autism,eccentric behaviour, and abnormalities of affect with no evidence of positive symptoms pose special diagnostic problems. We report a case with formal thought disorder, autism, altered interactional behaviour and disturbed emotional expression with no characteristic schizophrenic perception disorders, delusions, or other positive symptoms. With the help of this exemplary case, we discuss the diagnostic dilemma in careful use of diagnostic criteria in diagnosing schizophrenia in such cases. C1 Univ Klinikum, Klin Psychiat & Psychotherapie, Fak Med, Rhein Westfal TH Aachen, D-52074 Aachen, Germany. Univ Zurich, Psychiat Klin, Zurich, Switzerland. RP Pruter, C (reprint author), Univ Klinikum, Klin Psychiat & Psychotherapie, Fak Med, Rhein Westfal TH Aachen, Pauwelsstr 30, D-52074 Aachen, Germany. EM cprueter@ukaachen.de RI Hoff, Paul/A-1636-2008 CR BLACK DW, 1989, AM J PSYCHIAT, V146, P1267 BLEULER E, 1911, HDB PSYCHIAT, V4 BLEULER E, 1983, LEHRBUCH PSYCHIATRIE, V15, pS440 Diem O, 1903, ARCH PSYCHIAT NERVEN, V37, P111, DOI 10.1007/BF02227700 Dilling H, 1994, INT KLASSIFIKATION P DWORKIN RH, 1992, ACTA PSYCHIAT SCAND, V85, P61, DOI 10.1111/j.1600-0447.1992.tb01443.x KENDLER KS, 1994, AM J PSYCHIAT, V151, P27 KLOSTERKOTTER J, 1983, NERVENARZT, V54, P340 KRAEPLIN E, 1909, PSYCHIATRIE, V7 Maier W, 2001, NERVENARZT, V72, P167 PICK A, 1981, PRIMARE DEMENZ JUGEN PRIEBE S, 1989, PSYCHIAT PRAX, V16, P86 Rohricht F, 1998, PSYCHIAT PRAX, V25, P44 ROLLNIK JD, 2001, ERFOLGREICHE BEHANDL SASS H, 2000, PSYCHIAT PSYCHOTHERA, pS370 VONSASS H, 1996, DIAGNOSTICHES STAT M NR 16 TC 0 Z9 0 PU SPRINGER-VERLAG PI NEW YORK PA 175 FIFTH AVE, NEW YORK, NY 10010 USA SN 0028-2804 J9 NERVENARZT JI Nervenarzt PD JAN PY 2004 VL 75 IS 1 BP 63 EP 66 DI 10.1007/s00115-003-1590-6 PG 4 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 775FW UT WOS:000189030900010 PM 14722664 ER PT J AU Beyenburg, S Schmidt, D AF Beyenburg, S Schmidt, D TI Comorbidity and epilepsy SO NERVENHEILKUNDE LA German DT Article DE comorbidity; epilepsy; depression; reproductive and endocrine dysfunction; migraine; injuries; SUDEP ID SUDDEN UNEXPECTED DEATH; TEMPORAL-LOBE EPILEPSY; RISK-FACTORS; ATYPICAL ANTIPSYCHOTICS; ANTIEPILEPTIC DRUGS; UNEXPLAINED DEATH; MAJOR DEPRESSION; CO-MORBIDITY; SEIZURES; ADULTS AB Comorbidity is common in patients with epilepsy; particularly other neurological, psychiatric, and endocrine disorders as well as injuries and increased mortality may complicate the course of epilepsy. Comorbidity in epilepsy represents challenges for both diagnosis and treatment. Therapeutic strategies may need to be modified to avoid potential drug interactions. Depression in epilepsy is very common, particularly among patients with partial seizures of temporal lobe origin. Despite its high prevalence, depression remains often unrecognized and untreated in patients with epilepsy. Other psychiatric conditions such as psychosis, panic disorders, autism, and psychogenic non-epileptic seizures (PNES) are also frequently found in patients with epilepsy. Recent studies have shown that seizure outcome in PNES remains poor. The risk of migraine in epilepsy is also increased, in particular in individuals with head trauma, partial seizures, and a positive family history of migraine. Furthermore, reproductive endocrine disorders and sexual dysfunction are common among women and men with epilepsy. This may be attributable to epilepsy itself, effects of antiepileptic drugs on endocrine function, and/or psychosocial factors. Patients with seizure disorders are also at increased risk for injuries and death. Comorbidity of epilepsy and other conditions may be due to shared pathophysiological mechanisms, however, coincidence or selection bios cannot always be excluded. Unfortunately, iatrogenic factors may also contribute to the comorbidity in patients with epilepsy. C1 Ctr Hosp Luxembourg, Dept Neurosci, L-1210 Luxembourg, Luxembourg. Univ Klinikum Bonn, Klin Epileptol, Bonn, Germany. Arbeitsgrp Epilepsieforsch Berlin, Berlin, Germany. RP Beyenburg, S (reprint author), Ctr Hosp Luxembourg, Dept Neurosci, 4,Rue Barble, L-1210 Luxembourg, Luxembourg. 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The computational neuroscience division of NBRC is developing computational techniques to investigate speech production and their disorders in children, with special reference to autism. Stochastic Resonance approach is being used to enhance neuroimaging findings with application to brain tumour diagnosis and contrast accentuation during scanning. The National Facility of Functional Brain Imaging is being set up at NBRC to serve as India's first research venture on high-field MRI/fMRI/MRS/MRSI. Research work pursued in other institutions in the country is also briefly outlined, implying the presence of a vibrant research community. Efforts are also being undertaken to develop a National Neuroinformatics Initiative. C1 Natl Brain Res Ctr, Haryana 122050, India. RP Roy, PK (reprint author), Natl Brain Res Ctr, Haryana 122050, India. EM pkroy@nbrc.ac.in; nandini@nbrc.ac.in CR Bhaumik B, 2003, IETE J RES, V49, P87 BHAUMIK B, 2003, NEUROSCIENCE, V14, P211 Kumar MJ, 1996, IEEE T SYST MAN CY B, V26, P822, DOI 10.1109/3477.544296 PALIT S, 2003, P IND US S BRAIN RES RAJAN K, 1994, IEEE T NUCL SCI, V41, P1721, DOI 10.1109/23.317381 RAJU B, 2000, EXP BRAIN RES, V132, P149 ROY P, STOCHASTIC RESONANCE ROY P, 2002, LECT NOTES ARTIF INT, V2275, P191 Roy PK, 2002, IEEE T EVOLUT COMPUT, V6, P292, DOI 10.1109/TEVC.2002.1011542 SINGH L, 2003, P INT C THEOR NEUR N SINGH L, 2003, MUSIC MIND HLTH Singh NC, 2003, J ACOUST SOC AM, V114, P3394, DOI 10.1121/1.1624067 Turale N, 2003, MED BIOL ENG COMPUT, V41, P589, DOI 10.1007/BF02345322 Vaidya P, 2000, IEEE Trans Biomed Eng, V47, P701, DOI 10.1109/10.844215 NR 14 TC 0 Z9 0 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-23931-6 J9 LECT NOTES COMPUT SC PY 2004 VL 3316 BP 891 EP 897 PG 7 WC Computer Science, Artificial Intelligence; Computer Science, Theory & Methods SC Computer Science GA BBK50 UT WOS:000225878300136 ER PT J AU Bartzokis, G AF Bartzokis, G TI Quadratic trajectories of brain myelin content: unifying construct for neuropsychiatric disorders SO NEUROBIOLOGY OF AGING LA English DT Editorial Material DE brain development; aging; dementia; myelin; white matter; oligodendrocytes; Alzheimer; Parkinson; degeneration; amyloid; tau; alpha; synuclein; iron; cholesterol; free radicals; gender; head trauma; Lewy body; frontotemporal; FTD; ADHD; autism; learning disability; schizophrenia; addiction; impulse control; language; oscillations; processing speed; memory; medication; butyrylcholinesterase; evolution; brain; behavior; tauopathy; synucleinopathy; proteinopathy ID CENTRAL-NERVOUS-SYSTEM; WHITE-MATTER CHANGES; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; BUTYRYLCHOLINESTERASE K-VARIANT; CHILDHOOD-ONSET SCHIZOPHRENIA; AMYLOID PRECURSOR PROTEIN; MILD COGNITIVE IMPAIRMENT; PRIMARY VISUAL-CORTEX; NORMAL ADULT BRAIN; TOTAL GRAY-MATTER AB Myelin plays an essential but largely underappreciated role in human brain structure and function. The central challenge raised by the six commentaries is whether the developmental model of age-related cognitive decline and Alzheimer's disease (AD) (Bartzokis, 2003, this issue) is applicable to a wider range of neurodegenerative and neuropsychiatric disorders. The model's premise that the trajectory of myelin development and breakdown is essential to our very uniqueness as a species, directly addresses this issue. In its widest perspective, the model primarily delineates a myelin hypothesis of human brain evolution and normal development and is "secondarily" useful in conceptualizing a wide range of age-related neuropsychiatric diseases. The unique vulnerabilities of oligodendrocytes and the highly protracted and extensive developmental process of human brain myelination delineated in the model are directly pertinent to many uniquely human brain functions and neuropsychiatric diseases including late-life neurodegenerative disorders. This lifelong perspective classifies AD as a disorder likely to arise in old age after a normal trajectory of myelin development. Genetic and environmental factors causing deviations in the myelination trajectory at any point in the lifespan will contribute to differences in the manifestations of later-life degenerative diseases and/or be detected in epidemiologic studies as risk factors or risk mitigators (age, cholesterol, iron, gender, education, brain, trauma, etc.). Ultimately, these perturbations of the myelination process could result in divergent-appearing disorders, such as frontotemporal dementia, dementia pugilistica, AD, dementia with Lewy bodies, and Parkinson's disease, that nonetheless have overlapping neuropathologic and/or clinical manifestations. Furthermore, the model's developmental perspective suggests that dysregulation in the uniquely vulnerable myelination process also contributes to highly prevalent early-life psychiatric disorders such as autism, attention deficit, schizophrenia, addiction, as well as their striking male predominance. Eventually, the dysregulated myelination associated with such disorders may have a direct and predictable impact on the appearance and manifestations of the later-life dementias. By increasing the scientific focus on the process of myelination, this model may facilitate our understanding of the pathophysiology of multiple disorders and pathophysiologic, processes that cut across our current classification of diseases. Ultimately, the model provides a rational framework for the development of novel, myelin-centered treatments that may have widespread efficacy across multiple disease states and could potentially be used in delaying or even preventing some of the most devastating of human disorders. (C) 2003 Elsevier Inc. All rights reserved. C1 Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Lab Neuroimaging, Dept Neurol, Div Brain Mapping, Los Angeles, CA 90095 USA. Greater Los Angeles VA Healthcare Syst, Los Angeles, CA 90073 USA. RP Bartzokis, G (reprint author), Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90095 USA. 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Based on that literature, it was expected that reproductive and affiliative behaviors would be vastly decreased and aggression markedly increased in OT gene knockout (OTKO) mice. The initial publications reporting the behaviors of these mice did not include such phenotypes. Here, we compared single-unit activities recorded from the ventromedial hypothalamus in tissue slices of male and female OTKO mice and their wild-type littermate to test two hypotheses about OT functional genomics. First, we proposed that in OTKO mice, a very similar 9-amino-acid neuropeptide, arginine vasopressin (a likely gene duplication product), can 'cross over' and compensate for the lack of OT. This hypothesis was confirmed in both males and females. Further, we proposed that because of the lifelong absence of OT in OTKO, OT receptors would be more sensitive to OT in the knockout animals. We tested this idea in males and found that it was correct. Thus, an answer to the 'OTKO paradox' is put forth, with implications for OT-sensitive behaviors in a variety of species. Copyright (C) 2004 S. Karger AG, Basel. C1 Rockefeller Univ, Neurobiol & Behav Lab, Sch Med, New York, NY 10021 USA. Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, St Louis, MO 63110 USA. RP Kow, LM (reprint author), Rockefeller Univ, Neurobiol & Behav Lab, Sch Med, 1230 York Ave,Box 336, New York, NY 10021 USA. 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Large sets of images are mapped into a common coordinate system to study intra-population variability and inter-population differences, to provide voxel-wise mapping of functional sites, and help tissue and object segmentation via registration of anatomical labels. Common techniques often include the choice of a template image, which inherently introduces a bias. This paper describes a new method for unbiased construction of atlases in the large deformation diffeomorphic setting. A child neuroimaging autism study serves as a driving application. There is lack of normative data that explains average brain shape and variability at this early stage of development. We present work in progress toward constructing an unbiased MRI atlas of 2 years of children and the building of a probabilistic atlas of anatomical structures, here the caudate nucleus. Further, we demonstrate the segmentation of new subjects via atlas mapping. Validation of the methodology is performed by comparing the deformed probabilistic atlas with existing manual segmentations. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ N Carolina, Dept Radiat Oncol, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Comp Sci, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC 27599 USA. RP Joshi, S (reprint author), Univ N Carolina, Dept Radiat Oncol, Chapel Hill, NC 27599 USA. 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M., 2002, Computing and Visualization in Science, V5, DOI 10.1007/s00791-002-0084-6 Thompson P M, 1997, Med Image Anal, V1, P271, DOI 10.1016/S1361-8415(97)85002-5 Toga A.W., 1999, BRAIN WARPING WARFIELD SK, 2002, LECT NOTES COMPUTER, V2485, P298 Woods RP, 1998, J COMPUT ASSIST TOMO, V22, P155 Zou KH, 2003, ACAD RADIOL, V10, P1359, DOI 10.1016/S1076-6332(03)00538-5 NR 34 TC 249 Z9 249 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 1053-8119 J9 NEUROIMAGE JI Neuroimage PY 2004 VL 23 SU 1 BP S151 EP S160 DI 10.1016/j.neuroimage.2004.07.068 PG 10 WC Neurosciences; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 874UA UT WOS:000225374100014 PM 15501084 ER PT J AU Tani, P Lindberg, N Nieminen-von Wendt, T von Wendt, L Virkkala, J Appelberg, B Porkka-Heiskanen, T AF Tani, P Lindberg, N Nieminen-von Wendt, T von Wendt, L Virkkala, J Appelberg, B Porkka-Heiskanen, T TI Sleep in young adults with Asperger syndrome SO NEUROPSYCHOBIOLOGY LA English DT Article DE Asperger syndrome; sleep; polysomnography ID SOCIAL PHOBIA; INSOMNIA; ALEXITHYMIA; ARCHITECTURE; DISORDER; AUTISM AB Asperger syndrome (AS) is a neurodevelopmental disorder belonging to autism spectrum disorders. Both children and adults with AS have subjective impairment in the initiation and continuity of sleep, and studies using objective assessment are sparse. Twenty young AS adults with frequent complaints of low sleep quality were compared to 10 age-, gender- and education-matched controls without sleep complaints using polysomnography and spectral power analysis of slow-wave sleep. AS subjects displayed a similar polysomnographic profile as compared with controls. In spectral power analysis, a statistically nonsignificant trend towards decreased relative delta power and increased theta power in slow-wave sleep was found in the AS group. It seems that nonorganic insomnia, due to anxiety inherent in AS, is responsible for the low sleep quality in these subjects. Copyright (C) 2004 S. Karger AG, Basel. C1 Univ Helsinki, Dept Psychiat, SF-00180 Helsinki, Finland. Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Helsinki, Finland. Univ Helsinki, Inst Biomed, Helsinki, Finland. Tampere Univ Hosp, Clin Neurophysiol Sect, Tampere, Finland. RP Tani, P (reprint author), Univ Helsinki, Dept Physiol, Inst Biomed, Haartmaninkatu 8, FI-00290 Helsinki, Finland. 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However, most studies have examined whole blood levels of serotonin (5-HT), the vast majority of which is found in platelets. The aim of this study was to determine 5-HT levels in platelet-poor plasma (PPP) in a group of adult patients with autism. Methods: Levels of PPP 5-HT were compared between 10 adult drug-free autistic patients and 12 healthy controls. The Ritvo-Freeman Real-Life Rating Scale and the Overt Aggression Scale (OAS) were administered to the autistic group as a measure of symptom severity. Results: Significantly lower PPP 5-HT levels were observed in the autistic group as compared to the controls (p = 0.03). In addition, PPP 5-HT levels were inversely correlated with OAS scores among subjects with autism (r = -0.64, p < 0.05). Conclusion: PPP 5-HT ('free') levels appear to be low in autistic patients and may play a role in the pathophysiology and symptomatology of the disorder. Copyright (C) 2004 S. Karger AG, Basel. C1 Ness Ziona Mental Hlth Ctr, Res Unit, IL-74100 Ness Ziona, Israel. Tel Aviv Univ, Sackler Fac Med, IL-69978 Tel Aviv, Israel. Tel Aviv Sourasky Med Ctr, Lab Clin Biochem, Tel Aviv, Israel. Felsenstein Med Res Ctr, Lab Biol Psychiat, Petah Tiqwa, Israel. Geha Mental Hlth Ctr, Petah Tiqwa, Israel. Beer Yakov Mental Hlth Ctr, Beer Yaagov, Israel. RP Spivak, B (reprint author), Ness Ziona Mental Hlth Ctr, Res Unit, POB 1, IL-74100 Ness Ziona, Israel. 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Both conditions are also associated with impaired initiation and continuity of sleep. Twenty AS adults were compared with 10 healthy controls using the Toronto Alexithymia Scale and the Basic Nordic Sleep Questionnaire. AS subjects were significantly more alexithymic and reported lower sleep quality as compared with controls. AS and alexithymia are associated although the mediating factors are unknown. It is possible that alexithymic traits predispose to anxiety, which in turn lowers the sleep quality in AS adults. Alternatively, low sleep quality might be due to AS itself. Copyright (C) 2004 S. Karger AG, Basel. C1 Univ Helsinki, Dept Physiol, Inst Biomed, FI-00290 Helsinki, Finland. Univ Helsinki, Dept Psychiat, FI-00290 Helsinki, Finland. Univ Helsinki, Cent Hosp, Hosp Children & Adolescents, Helsinki, Finland. Univ Tampere, Tampere Sch Publ Hlth, Dept Social Psychiat, FIN-33101 Tampere, Finland. Tampere Univ Hosp, Dept Psychiat, Tampere, Finland. Paijat Hame Cent Hosp, Lahti, Finland. RP Tani, P (reprint author), Univ Helsinki, Dept Physiol, Inst Biomed, Haartmaninkatu 8, FI-00290 Helsinki, Finland. 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In the frontal lobe, patients had lower rGMR in medial/cingulate regions ( BA 32, 24, 25) but not in lateral regions ( BA 8 - 10) compared with healthy controls. Patients had higher rGMR in occipital ( BA 19) and parietal regions ( BA 39) compared with controls, but there were no group differences in temporal lobe regions. Among controls, better recall and use of the semantic-clustering strategy was associated with greater lateral and medial frontal rGMR, while decreased rGMR in medial-frontal regions was associated with greater perseverative/intrusion errors. Patients failed to show these patterns. Autism patients have dysfunction in some but not all of the key brain regions subserving verbal memory performance, and other regions may be recruited for task performance. Copyright (C) 2004 S. Karger AG, Basel. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. RP Hazlett, EA (reprint author), Mt Sinai Sch Med, Dept Psychiat, Box 1505,1 Gustave Levy Pl, New York, NY 10029 USA. 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SO NEUROPSYCHOLOGIA LA English DT Article DE autism; cognitive map; spatial orientation; visual-spatial; "what" pathway; "where" pathway; primary visual cortex ID PATH INTEGRATION; VISUAL MEMORY; INDIVIDUALS; IMPAIRMENT; NAVIGATION; KNOWLEDGE; DEFICITS; LESIONS; HUMANS; CORTEX AB This series of experiments was aimed at assessing spatial abilities in high functioning individuals with autism (HFA), using a human-size labyrinth. In the context of recent findings that the performance of individuals with HFA was superior to typically developing individuals in several non-social cognitive operations, it was expected that the HFA group would outperform a typically developing comparison group matched on full-scale IQ. Results showed that individuals with autism performed all spatial tasks at a level at least equivalent to the typically developing comparison group. No differences between groups were found in route and survey tasks. Superior performance for individuals with HFA was found in tasks involving maps, in the form of superior accuracy in graphic cued recall of a path, and shorter learning times in a map learning task. We propose that a superior ability to detect [Human Perception and Performance 27 (3) (2001) 719], match [Journal of Child Psychology and Psychiatry 34 (1993) 1351] and reproduce [Journal of Child Psychology and Psychiatry 40 (5) (1999) 743] simple visual elements yields superior performance in tasks relying on the detection and graphic reproduction of the visual elements composing a map. Enhanced discrimination, detection, and memory for visually simple patterns in autism may account for the superior performance of persons with autism on visuo-spatial tasks that heavily involve pattern recognition, either in the form of recognizing and memorizing landmarks or in detecting the similarity between map and landscape features. At a neuro-anatomical level, these findings suggest an intact dorso-lateral pathway, and enhanced performance in non social tasks relying on the infero-temporal pathway. (C) 2003 Elsevier Ltd. All rights reserved. C1 Hop Riviere Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. Univ Quebec, Dept Psychol, Montreal, PQ H3C 3P8, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. Univ Montreal, Inst Geriat, Ctr Rech, Montreal, PQ H3W 1W5, Canada. Hop Juif Readapt, Ctr Rech Interdisciplinaire Readaptat Montreal Me, Laval, PQ H7V 1R2, Canada. RP Mottron, L (reprint author), Hop Riviere Prairies, Clin Specialisee Troubles Envahissants Dev, 7070 Boul Perras, Montreal, PQ H1E 1A4, Canada. 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This review will examine artistic production in individuals with a variety of syndromes including achromatopsia, neglect, visual agnosia, aphasia, epilepsy, migraine, dementia and autism. From this review it appears that artists are not spared visual-motor deficits despite their special graphic abilities. Rather their talents allow them to express visual deficits with particular eloquence. By contrast, the effects of aphasia on art are variable. In addition to deficits, neuropsychological syndromes may be associated with positive phenomena. Such phenomena induced by epilepsy or migraines can serve to inspire artists. This review also makes clear that artists with neuropsychological deficits do not necessarily produce art of lesser quality. Rather, their art may change in content or in style, sometimes in surprising and aesthetically pleasing ways. The neuropsychology of visual art also touches on a few central questions about the nature of artistic expression itself. For example, what forms can artistic representations take? How are visual features used descriptively and expressively? What roles do knowing and seeing play in depiction? (C) 2004 Elsevier Ltd. All rights reserved. C1 Hosp Univ Penn, Dept Neurol, Philadelphia, PA 19104 USA. Hosp Univ Penn, Ctr Cognit Neurosci, Philadelphia, PA 19104 USA. RP Chatterjee, A (reprint author), Hosp Univ Penn, Dept Neurol, 3400 Spruce St,3 W Gates, Philadelphia, PA 19104 USA. 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Neuropsychological measures included a short form of the Wechsler Adult Intelligence Scale-Revised (D. Wechsler, 1981), the Hopkins Verbal Learning Test-Revised (R. H. B. Benedict, D. Schretlen, L. Groninger, & J. Brandt, 1998), the Brief Visuospatial Memory Test-Revised (R. H. B. Benedict, 1997), and the Edinburgh Handedness Inventory (S. M. Williams, 1986). Pedophilia showed significant negative correlations with IQ and immediate and delayed recall memory. Pedophilia was also related to non-right-handedness even after covarying age and IQ. These results suggest that pedophilia is linked to early neurodevelopmental perturbations. C1 Ctr Addict & Mental Hlth, Law & Mental Hlth Program, Toronto, ON M5T 1R8, Canada. Univ Toronto, Dept Psychiat, Toronto, ON, Canada. RP Cantor, JM (reprint author), Ctr Addict & Mental Hlth, Law & Mental Hlth Program, Clark Site,250 Coll St, Toronto, ON M5T 1R8, Canada. 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H., 2001, J INDIV PSYCHOL, V57, P51 TABACHNICK BARBARA G., 1989, USING MULTIVARIATE S, V2d TELLEGEN A, 1967, J CONSULT PSYCHOL, V31, P499, DOI 10.1037/h0024963 VIRKKUNEN M, 1976, ACTA PSYCHIAT SCAND, V53, P401, DOI 10.1111/j.1600-0447.1976.tb00087.x Vlachos FM, 1999, PERCEPT MOTOR SKILL, V88, P427, DOI 10.2466/PMS.88.2.427-428 Von Krafft-Ebing R., 1965, PSYCHOPATHIA SEXUALI Wechsler D, 1981, WECHSLER ADULT INTEL WILLIAMS SM, 1986, CORTEX, V22, P325 NR 54 TC 63 Z9 64 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0894-4105 J9 NEUROPSYCHOLOGY JI Neuropsychology PD JAN PY 2004 VL 18 IS 1 BP 3 EP 14 DI 10.1037/0894-4105.18.1.3 PG 12 WC Psychology, Clinical; Neurosciences; Psychology SC Psychology; Neurosciences & Neurology GA 766WJ UT WOS:000188398100001 PM 14744183 ER PT J AU O'Brien, J Spencer, J AF O'Brien, J Spencer, J TI Perceptual deficits in autism and Asperger syndrome: Form and motion processing SO PERCEPTION LA English DT Meeting Abstract C1 Brunel Univ, Dept Human Sci, Uxbridge UB8 3PH, Middx, England. EM justin.obrien@brunel.ac.uk NR 0 TC 1 Z9 1 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2004 VL 33 SU S BP 28 EP 28 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA 858NN UT WOS:000224198700087 ER PT J AU Phillips, WA Chapman, KLS Berry, PD AF Phillips, WA Chapman, KLS Berry, PD TI Size perception is less context-sensitive in males SO PERCEPTION LA English DT Article ID WEAK CENTRAL COHERENCE; RESIST VISUAL ILLUSIONS/; SEX-DIFFERENCES; COGNITIVE PHENOTYPE; FUNCTIONING AUTISM; SPATIAL ABILITIES; MENSTRUAL-CYCLE; CHILDREN; MODULATION; BOUNDARIES AB Context sensitivity of size perception has previously been used to study individual differences related to the distinction between local, analytic, or field-independent and global, holistic, or field-dependent perceptual styles. For example, it has been used in several recent studies of autistic spectrum disorders, which may involve an excessive bias toward local processing. Autism is much more common in males, and there is evidence that this may be in part because males in general tend to be less context-sensitive than females, and thus are more affected by conditions that further reduce context sensitivity. There is also evidence that a bias to local processing is more common in professions that require attention to detail. Context sensitivity of size perception was therefore studied as a function of sex and academic discipline in sixty-four university staff and students by a simple, sensitive, and specific psychophysical measure based on the Ebbinghaus illusion. The results show that in this task males are on average less context-sensitive than females, that the overlap is large, and that subjects with very high or very low context sensitivity tend to have the sex and profession predicted by the above hypotheses. C1 Univ Stirling, Dept Psychol, Ctr Cognit & Computat Neurosci, Stirling FK9 4LA, Scotland. RP Phillips, WA (reprint author), Univ Stirling, Dept Psychol, Ctr Cognit & Computat Neurosci, Stirling FK9 4LA, Scotland. EM Wap1@stir.ac.uk CR AGLIOTI S, 1995, CURR BIOL, V5, P679, DOI 10.1016/S0960-9822(95)00133-3 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BARONCOHEN S, 2002, TRENDS COGN SCI, V6, P216 Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206 Briskman J, 2001, J CHILD PSYCHOL PSYC, V42, P309, DOI 10.1111/1469-7610.00724 Bruno N, 2001, TRENDS COGN SCI, V5, P379, DOI 10.1016/S1364-6613(00)01725-3 Carey DP, 2001, TRENDS COGN SCI, V5, P109, DOI 10.1016/S1364-6613(00)01592-8 Franz VH, 2001, TRENDS COGN SCI, V5, P457, DOI 10.1016/S1364-6613(00)01772-1 HAMPSON E, 1990, BRAIN COGNITION, V14, P26, DOI 10.1016/0278-2626(90)90058-V Happe F, 2001, J CHILD PSYCHOL PSYC, V42, P299, DOI 10.1111/1469-7610.00723 HAPPE F, 1999, TRENDS COGN SCI, V3, P248 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x Hausmann M, 2000, BEHAV NEUROSCI, V114, P1245, DOI 10.1037/0735-7044.114.6.1245 Kay J, 1998, NEURAL NETWORKS, V11, P117, DOI 10.1016/S0893-6080(97)00110-X Kubovy M, 2001, TRENDS COGN SCI, V5, P93, DOI 10.1016/S1364-6613(00)01604-1 Milner D, 2003, TRENDS COGN SCI, V7, P10, DOI 10.1016/S1364-6613(02)00004-9 Milner D. 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A., 1954, PERSONALITY PERCEPTI NR 30 TC 27 Z9 27 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2004 VL 33 IS 1 BP 79 EP 86 DI 10.1068/p5110 PG 8 WC Psychology; Psychology, Experimental SC Psychology GA 806AS UT WOS:000220407400007 PM 15035330 ER PT J AU Jellema, T Lorteije, JAM van Rijn, S van t'Wout, M de Heer, F de Haan, EHF AF Jellema, T Lorteije, JAM van Rijn, S van t'Wout, M de Heer, F de Haan, EHF TI Failure to automate the semantic processing of social cues in autism SO PERCEPTION LA English DT Meeting Abstract C1 Univ Hull, Dept Psychol, Kingston Upon Hull HU6 7RX, N Humberside, England. Univ Utrecht, Helmholtz Inst, NL-3584 CS Utrecht, Netherlands. Univ Utrecht, Med Ctr, Dept Child & Adolescent Psychiat, NL-3584 CS Utrecht, Netherlands. EM T.Jellema@hull.ac.uk NR 0 TC 0 Z9 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2004 VL 33 SU S BP 101 EP 101 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA 858NN UT WOS:000224198700314 ER PT J AU Igliozzi, R Del Viva, MM Tancredi, R Brizzolara, D AF Igliozzi, R Del Viva, MM Tancredi, R Brizzolara, D TI Spatial and motion integration in children with autism SO PERCEPTION LA English DT Meeting Abstract C1 Univ Florence, CNR, Inst Neurosci, I-50100 Florence, Italy. CNR, Ist Neurofisiol, I-56100 Pisa, Italy. Univ Pisa, IRCCS Stella Maris, Div Neuropsychiat, I-56100 Pisa, Italy. EM roberta.igliozzi@inpe.unipi.it NR 0 TC 0 Z9 0 PU PION LTD PI LONDON PA 207 BRONDESBURY PARK, LONDON NW2 5JN, ENGLAND SN 0301-0066 J9 PERCEPTION JI Perception PY 2004 VL 33 SU S BP 130 EP 130 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA 858NN UT WOS:000224198700408 ER PT J AU Soderstrom, H Sjodin, AK Carlstedt, A Forsman, A AF Soderstrom, H Sjodin, AK Carlstedt, A Forsman, A TI Adult psychopathic personality with childhood-onset hyperactivity and conduct disorder: a central problem constellation in forensic psychiatry SO PSYCHIATRY RESEARCH LA English DT Article DE forensic psychiatry; violent crime; disruptive behavior disorders; comorbidity; risk factor ID ASPERGER-SYNDROME; 7-YEAR-OLD CHILDREN; TOTAL POPULATION; MENTAL DISORDER; BIRTH COHORT; COMORBIDITY; AUTISM; CRIME; EPIDEMIOLOGY; RELIABILITY AB To describe lifetime mental disorders among perpetrators of severe inter-personal crimes and to identify the problem domains most closely associated with aggression and a history of repeated violent criminality, we used structured interviews, clinical assessments, analyses of intellectual functioning, medical and social files, and collateral interviews in 100 consecutive subjects of pretrial forensic psychiatric investigations. Childhood-onset neuropsychiatric disorders [attention-deficit/hyperactivity disorder (AD/HD), learning disability, tics and autism spectrum disorders] affected 55% of the subjects and formed complex comorbidity patterns with adult personality disorders [including psychopathic traits according to the Psychopathy Checklist (PCL-R)], mood disorders and substance abuse. The closest psychiatric covariates to high Lifetime History of Aggression (LHA) scores and violent recidivism were the PCL-R scores and childhood conduct disorder (CD). Behavioral and affective PCL-R factors were closely associated with childhood AD/HD, CD, and autistic traits. The results support the notion that childhood-onset social and behavioral problems form the most relevant psychiatric symptom cluster in relation to pervasive adult violent behavior, while late-onset mental disorders are more often associated with single acts of violent or sexual aggression. (C) 2003 Elsevier Ireland Ltd. All rights reserved. C1 Univ Gothenburg, Dept Forens Psychiat, S-42204 Hisings Backa, Sweden. Univ Gothenburg, Inst Clin Neurosci, S-42204 Hisings Backa, Sweden. RP Soderstrom, H (reprint author), Univ Gothenburg, Dept Forens Psychiat, Box 4024, S-42204 Hisings Backa, Sweden. RI Anckarsater, Henrik/C-2244-2009 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Blom G, 1958, STAT ESTIMATES TRANS BROWN GL, 1982, AM J PSYCHIAT, V139, P741 Cooke DJ, 2001, PSYCHOL ASSESSMENT, V13, P171, DOI 10.1037//1040-3590.13.2.171 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x FAZEL S, 2002, LANCET, V360, P572 First M. 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PD JAN 1 PY 2004 VL 121 IS 3 BP 271 EP 280 DI 10.1016/S0165-1781(03)00270-1 PG 10 WC Psychiatry SC Psychiatry GA 759EY UT WOS:000187726400007 PM 14675746 ER PT J AU Webb, GF AF Webb, GF TI Autism: Neural basis and treatment possibilities SO PSYCHOLOGIST LA English DT Book Review CR *NOVARTIS FDN, 2003, AUTISM NEURAL BASIS NR 1 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 JAN PY 2004 VL 17 IS 1 BP 37 EP 37 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 759ZJ UT WOS:000187784500020 ER PT J AU Clark, E Olympia, DE Jensen, J Heathfield, LT Jenson, WR AF Clark, E Olympia, DE Jensen, J Heathfield, LT Jenson, WR TI Striving for autonomy in a contingency-governed world: Another challenge for individuals with developmental disabilities SO PSYCHOLOGY IN THE SCHOOLS LA English DT Article ID FOSTERING SELF-DETERMINATION; MENTAL-RETARDATION; MILD DISABILITIES; STUDENTS; BEHAVIOR; DISORDERS; RESOURCES; SCHOOL; PEOPLE; CHOICE AB The purpose of this article is to provide the reader with an orientation to the concepts and principles of autonomy and self-determination and the application of those concepts and principles to working with children and adolescents who have intellectual and developmental disabilities (ID/DD), including autism. Self-determination is essentially the ability of a person to be autonomous as to meaningful life choices and encompasses activities such as problem solving, decision making, goal setting, self-observation and evaluation, self-management and reinforcement, acquiring an internal locus of control, experiencing positive attributions of efficacy and outcome expectancy, developing a realistic and positive self-image, and self awareness. The lack of opportunities for self-determination, personal expression and consideration of personal preferences experienced by this population has been associated with increased psychiatric disturbance. Several principles supporting self-determination, including positive psychology and use of positive alternatives, are discussed by the authors. Further, practices that generate more opportunities for individuals to exercise personal control and autonomy across activities and environments in order to prevent psychological problems are discussed. Finally, the school psychologist's role in promoting the development of autonomy and self initiative among children and adolescents with ID/DD are outlined within the contexts of assessment practices, interventions and curriculums, positive behavior support technology, and continued educational reforms and systems change. (C) 2004 Wiley Periodicals, Inc. C1 Univ Utah, Salt Lake City, UT 84112 USA. RP Clark, E (reprint author), Univ Utah, 1705 E Campus Ctr Dr,Room 327, Salt Lake City, UT 84112 USA. CR Agran M, 1999, EDUC TRAIN MENT RET, V34, P293 ALGOZZINE B, 2000, REV EDUC RES, V71, P219 American Psychiatric Association, 2000, DIAGN STAT MAN MENT BAKER DJ, 2000, FOCUS AUTISM OTHER D, V15, P154, DOI 10.1177/108835760001500304 Browder DM, 2001, REM SPEC EDUC, V22, P233, DOI 10.1177/074193250102200407 BROWN F, 1993, EDUC TRAIN MENT RET, V28, P318 Brown F., 1996, PEOPLE DISABILITIES, P335 CARR EG, 1985, J APPL BEHAV ANAL, V18, P111, DOI 10.1901/jaba.1985.18-111 Clarke S, 1995, BEHAV DISORDERS, V20, P221 Durand V. M., 1990, SEVERE BEHAV PROBLEM Ezell D, 1999, EDUC TRAIN MENT RET, V34, P453 Field S., 1998, PRACTICAL GUIDE TEAC FLEISHER M, 1999, PSYCHIAT BEHAV DISOR, P317 Giangreco M. F., 1998, CHOOSING OUTCOMES AC HALLORAN W, 1993, RECENT ADV SPECIAL E Horner R. H., 2000, FOCUS AUTISM OTHER D, V15, P97, DOI 10.1177/108835760001500205 HORNER RH, 1996, PEOPLE DISABILITIES, P209 Koegel L. 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L., 1998, TEACHING SELF DETERM WEHMEYER ML, 1995, MENT RETARD, V33, P111 Wehmeyer ML, 1998, J ASSOC PERS SEVERE, V23, P5, DOI 10.2511/rpsd.23.1.5 Wehmeyer ML, 1996, AM J MENT RETARD, V100, P632 NR 48 TC 8 Z9 8 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0033-3085 J9 PSYCHOL SCHOOLS JI Psychol. Schools PD JAN PY 2004 VL 41 IS 1 BP 143 EP 153 DI 10.1002/pits.10146 PG 11 WC Psychology, Educational SC Psychology GA 757HJ UT WOS:000187556700014 ER PT J AU Fontenelle, LF Mendlowicz, MV de Menezes, GB Martins, RRD Versiani, M AF Fontenelle, LF Mendlowicz, MV de Menezes, GB Martins, RRD Versiani, M TI Asperger syndrome, obsessive-compulsive disorder, and major depression in a patient with 45,X/46,XY mosaicism SO PSYCHOPATHOLOGY LA English DT Article DE Asperger syndrome; pervasive developmental disorders; autism; obsessive-compulsive disorder; karyotype; mosaicism ID PERVASIVE DEVELOPMENTAL DISORDERS; REPETITIVE BEHAVIORS; AUTISTIC DISORDER; INFANTILE-AUTISM; CHILDREN; SUMATRIPTAN; CHROMOSOMES; ADOLESCENTS; AGGRESSION; ECT AB Background: Although previous reports have described the association of autism, mental retardation, and schizophrenia with a missing Y chromosome, we are not aware of any case showing an association between this particular chromosomal abnormality and Asperger syndrome. Method: We report the case of a male patient with a combination of Asperger syndrome, obsessive-compulsive disorder and 45,X/46,XY mosaicism. During the follow-up, this individual has also developed a severe episode of major depression, which was successfully treated with electroconvulsive therapy. Results: To the best of our knowledge, this is the first case in which a 45,X/46,XY mosaicism was described in association with Asperger syndrome, either alone or associated with other psychiatric disorders. Diagnostic and therapeutic aspects of this unique case are presented and discussed. Conclusions: Our findings suggest that a missing Y chromosome may play an etiological role in some cases of Asperger syndrome. Copyright (C) 2004 S. Karger AG, Basel. C1 Univ Fed Rio de Janeiro, Inst Psychiat, Anxiety & Depress Res Program, BR-21941 Rio De Janeiro, Brazil. Univ Fed Fluminense, Dept Psychiat & Mental Hlth, BR-24220000 Niteroi, RJ, Brazil. State Inst Diabet & Endocrinol Rio de Janeiro, Rio De Janeiro, Brazil. RP Fontenelle, LF (reprint author), Rua Lopes Trovao 88,Apt 1501,Bloco A, BR-24220071 Rio De Janeiro, Brazil. 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This article preliminarily identifies sleep problems that may exacerbate symptoms of autism; thus, possibly influencing effectiveness of daytime interventions. A database of parent report of sleep problems of children with autism (N = 55), ranging from 5 to 12 years of age (M = 8.2 years) was evaluated. Results suggested that fewer hours of sleep per night predicted overall autism scores and social skills deficits. Similarly, stereotypic behavior was predicted by fewer hours of sleep per night and screaming during the night. Increased sensitivity to environmental stimuli in the bedroom and screaming at night predicted communication problems. Finally, sensitivity to environmental stimuli in the bedroom also predicted fewer developmental sequence disturbances. The results indicate that sleep problems and the diagnostic characteristics of autism may be related. However, future research must be completed to determine the specific relationship. (C) 2004 Elsevier Ltd. All rights reserved. C1 Penn State Univ, Psychol Program, Middletown, PA 17057 USA. Ohio State Univ, Columbus Childrens Hosp, Columbus, OH 43210 USA. RP Schreck, KA (reprint author), Penn State Univ, Psychol Program, 777 W Harrisburg Pike, Middletown, PA 17057 USA. EM kas24@psu.edu CR American Psychiatric Association, 1994, DIAGN STAT MENT DIS American Sleep Disorders Association, 1991, INT CLASS SLEEP DIS Bonnet M. H., 1994, PRINCIPLES PRACTICE, P50 DURAND VM, 1996, J ASSOC PERS SEVERE, V21, P114 FENSKE EC, 1985, ANAL INTERVEN DEVEL, V5, P49, DOI 10.1016/S0270-4684(85)80005-7 Gilliam J. E., 1995, GILLIAM AUTISM RATIN GUILLEMINAULT C, 1982, EUR J PEDIATR, V139, P165, DOI 10.1007/BF01377349 HORNE JA, 1988, SLEEP, V11, P528 HOSHINO Y, 1984, FOLIA PSYCHIAT NEU J, V38, P45 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Lovaas O. 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A., 2003, J CHILD FAM STUD, V12, P349, DOI 10.1023/A:1023995912428 Schreck KA, 1997, THESIS OHIO STATE U Schreck KA, 2000, J AUTISM DEV DISORD, V30, P127, DOI 10.1023/A:1005407622050 Segawa Masaya, 1992, Brain Dysfunction, V5, P211 Smith T, 1997, AM J MENT RETARD, V102, P238, DOI 10.1352/0895-8017(1997)102<0238:IBTFPW>2.0.CO;2 *SPSS INC, 2000, STAT PACK SOC SCI RE *SPSS INC, 1995, STAT PACK SOC SCI RE Stores G, 1999, DEV MED CHILD NEUROL, V41, P568, DOI 10.1017/S001216229900119X THACKERAY EJ, 2000, THESIS RMIT U MELBOU Weiss MJ, 1999, BEHAV INTERVENT, V14, P3, DOI 10.1002/(SICI)1099-078X(199901/03)14:1<3::AID-BIN25>3.0.CO;2-F Wiggs L, 1999, J CHILD PSYCHOL PSYC, V40, P627, DOI 10.1017/S0021963099003881 Wiggs L, 1996, J INTELL DISABIL RES, V40, P518, DOI 10.1046/j.1365-2788.1996.799799.x NR 31 TC 86 Z9 87 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0891-4222 J9 RES DEV DISABIL JI Res. Dev. Disabil. PD JAN-FEB PY 2004 VL 25 IS 1 BP 57 EP 66 DI 10.1016/j.ridd.2003.04.007 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 768TH UT WOS:000188551100005 PM 14733976 ER PT J AU De Medinaceli, JC Rodriguez, OU AF De Medinaceli, JC Rodriguez, OU TI Asperger's syndrome in adolescents: A review of the concept and strategies for school integration SO REVISTA LATINOAMERICANA DE PSICOLOGIA LA Spanish DT Article DE Asperger syndrome; autism; school integration ID FUNCTIONING AUTISTIC-CHILDREN; FOLLOW-UP; MIND AB The present article provides a theoretical review of Asperger Syndrome, its history and links with autism, and discusses the main differences between these two diagnostic categories, based on the recent concept of autism spectrum. It includes the most important diagnostic criteria of Asperger syndrome, with more detailed descriptions of its characteristics in areas such as social interaction, language, cognition, and motor development. Finally, the importance on integration of people with Asperger to regular schools is discussed. Suggestions and strategies to be followed by schools teachers and peers in this process are presented. C1 Ctr Desarrollo Infantil, Bogota, Colombia. RP Rodriguez, OU (reprint author), Ctr Desarrollo Infantil, Transv 67 N 136-75, Bogota, Colombia. 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Latinoam. Psicol. PY 2004 VL 36 IS 3 BP 517 EP 530 PG 14 WC Psychology, Multidisciplinary SC Psychology GA 887EV UT WOS:000226289300011 ER PT J AU Lerman, DC Vorndran, CM Addison, L Kuhn, SC AF Lerman, DC Vorndran, CM Addison, L Kuhn, SC TI Preparing teachers in evidence-based practices for young children with autism SO SCHOOL PSYCHOLOGY REVIEW LA English DT Article ID PROFOUNDLY RETARDED INDIVIDUALS; INTERVENTION IMPLEMENTATION; BEHAVIORAL CONSULTATION; STIMULUS PREFERENCE; GENERAL-EDUCATION; FOLLOW-UP; STAFF; DISABILITIES; PARADIGM; PROGRAM AB Efforts to transfer research findings on autism into public schools would benefit from further evaluation of teacher preparation models. The purpose of this study was to evaluate a model program that was designed to prepare current teachers in evidence-based practices for children with autism. Drawn from the extensive literatures on caregiver teaching and behavioral interventions, this relatively comprehensive program was designed to be feasible within the constraints of typical school settings. Four certified special education teachers and a teacher-in-training participated in an intensive university-based summer program that incorporated both didactic and performance-based instruction. The teachers were taught a relatively large number of specific skills within three areas that have been the focus of extensive study for children with developmental disabilities (preference assessment, direct teaching, and incidental teaching). Results suggested that the teachers mastered all of these skills during role play and then implemented them successfully with 6 children who participated in the program. Teacher preparation also was associated with increases in correct task responses and communication among the children. C1 Louisiana State Univ, Baton Rouge, LA 70803 USA. 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H., 1989, STAFF MANAGEMENT HUM REID DH, 1990, HDB BEHAV MODIFICATI, P71 Sheridan SM, 2000, SCHOOL PSYCHOL REV, V29, P485 *US DEP ED, 2002, DIG ED STAT 2002 Watson TS, 1996, SCHOOL PSYCHOL QUART, V11, P267, DOI 10.1037/h0088933 NR 29 TC 30 Z9 30 PU NATL ASSOC SCHOOL PSYCHOLOGISTS PI BETHESDA PA 4340 EAST WEST HWY, STE 402, BETHESDA, MD 20814 USA SN 0279-6015 J9 SCHOOL PSYCHOL REV JI Sch. Psychol. Rev. PY 2004 VL 33 IS 4 BP 510 EP 526 PG 17 WC Psychology, Educational SC Psychology GA 886WD UT WOS:000226262700004 ER PT J AU Limoges, E Bolduc, C Chevrier, E Mottron, L Godbout, R AF Limoges, E Bolduc, C Chevrier, E Mottron, L Godbout, R TI Sleep in adults with high-functioning autism or Asperger syndrome SO SLEEP LA English DT Meeting Abstract CT 18th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 05-10, 2004 CL Philadelphia, PA SP Associated Profess Sleep Soc C1 Hop Riviere Prairies, Neurodev Disorders Program, Montreal, PQ, Canada. Hop Riviere Prairies, Ctr Rech Fernand Seguin, Montreal, PQ, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. NR 0 TC 0 Z9 0 PU AMER ACADEMY SLEEP MEDICINE PI WESTCHESTER PA ONE WESTBROOK CORPORATE CENTER STE 920, WESTCHESTER, IL 60154 USA SN 0161-8105 J9 SLEEP JI Sleep PY 2004 VL 27 SU S MA 768 BP 344 EP 344 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 844OX UT WOS:000223169400770 ER PT J AU Hughes, C Leekam, S AF Hughes, C Leekam, S TI What are the links between theory of mind and social relations? Review, reflections and new directions for studies of typical and atypical development SO SOCIAL DEVELOPMENT LA English DT Review DE theory of mind; social relationships; autism; language skills; disability ID THEORY-OF-MIND; INDIVIDUAL-DIFFERENCES; FALSE-BELIEF; MATERNAL SENSITIVITY; AUTISTIC-CHILDREN; BEHAVIOR PROBLEMS; VERBAL-ABILITY; PRETEND PLAY; SOCIOECONOMIC-STATUS; ATTACHMENT SECURITY AB Twenty years after research on children's 'theory of mind' began, this field continues to be a leading influence in the study of developmental psychology and psychopathology. In this review we examine the contribution of research on children's theories of mind to our understanding of children's developing social relationships. Evidence shows that for both typical and atypical populations this relationship is neither uniform nor unidirectional. Theory-of-mind skills are multifaceted and the nature of the developmental relationship between different aspects is not yet known, and there is evidence that theory-of-mind skills both transform and are transformed by interpersonal and family relationships and by language communities. To understand the multifaceted and complex nature of development in this area, we need clearer definitions of the skills under investigation, as well as research designs that capture the transactional nature of the relationship between theory of mind and social relations. Addressing these issues should help to clarify (i) the processes by which children's developing understanding of others is influenced by the social environment, and (ii) issues concerning the specificity of theory-of-mind impairments in atypical populations and the processes by which these impairments develop. C1 Univ Cambridge, Ctr Family Res, Cambridge CB2 3RF, England. Univ Durham, Durham DH1 3HP, England. 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Dev. PY 2004 VL 13 IS 4 BP 590 EP 619 DI 10.1111/j.1467-9507.2004.00285.x PG 30 WC Psychology, Developmental SC Psychology GA 861EB UT WOS:000224397800006 ER PT J AU Hrdlicka, M Komarek, V Faladova, L Zumrova, A Beranova, I Dudova, I Blatny, M Urbanek, T AF Hrdlicka, M Komarek, V Faladova, L Zumrova, A Beranova, I Dudova, I Blatny, M Urbanek, T TI EEG abnormalities are not associated with symptom severity in childhood autism SO STUDIA PSYCHOLOGICA LA English DT Article DE childhood autism; pervasive developmental disorders; EEG; psychopathology ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; INFANTILE-AUTISM; EPILEPSY; REGRESSION; CHILDREN AB We examined a group of 77 autistic children (61 boys, 16 girls) of an average age 9.1 +/- 5.3 years. The Childhood Autism Rating Scale (CARS), IQ test and 21 channel EEG (including night sleep EEG recording) were applied. It was possible to obtain evaluable EEG records in 63 patients. Missing EEG records were mostly due to noncooperation on the part of the autistic children. There were 29 normal EEGs (44.4%), 11 non-epileptiform abnormal EEGs (17.5%), and 24 abnormal EEGs with epileptiform discharges (38.1%). Using the median test, we compared the psychopathology in these three groups. No significant difference in the total CARS score was found among the groups. In the analysis of CARS items, there was only one significant difference among the groups in the 10th item - Fear or Nervousness (chi(2) = 7.963, df = 2, p = 0.019). C1 Charles Univ, Dept Child Psychiat, Sch Med 2, Prague 15006, Czech Republic. Charles Univ, Dept Child Neurol, Sch Med 2, Prague 15006, Czech Republic. Acad Sci, Inst Psychol, Brno, Czech Republic. RP Hrdlicka, M (reprint author), Charles Univ, Dept Child Psychiat, Sch Med 2, V Uvalu 84, Prague 15006, Czech Republic. RI Urbanek, Tomas/G-9427-2014; Blatny, Marek/H-4293-2014 OI Urbanek, Tomas/0000-0002-8807-4869; Blatny, Marek/0000-0001-9831-0637 CR Ballaban-Gil K, 2000, MENT RETARD DEV D R, V6, P300, DOI 10.1002/1098-2779(2000)6:4<300::AID-MRDD9>3.0.CO;2-R COFFEY CE, 1998, TXB PEDIAT NEUROPSYC Cohen D. 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PY 2004 VL 46 IS 3 BP 229 EP 234 PG 6 WC Psychology, Multidisciplinary SC Psychology GA 877PQ UT WOS:000225582900007 ER PT J AU Hill, EL AF Hill, EL TI Executive dysfunction in autism SO TRENDS IN COGNITIVE SCIENCES LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; CARD SORTING TEST; ASPERGER-SYNDROME; COGNITIVE DEFICITS; PRESCHOOL-CHILDREN; CHILDHOOD AUTISM; YOUNG-CHILDREN; BRAIN; MIND; PERFORMANCE AB 'Executive function' is an umbrella term for functions such as planning, working memory, impulse control, inhibition and mental flexibility, as well as for the initiation and monitoring of action. The primacy of executive dysfunction in autism is a topic of much debate, as are recent attempts to examine subtypes of executive function within autism and other neurodevelopmental disorders that are considered to implicate frontal lobe function. This article will review cognitive behavioural studies of planning, mental flexibility and inhibition in autism. It is concluded that more detailed research is needed to fractionate the executive system in autism by assessing a wide range of executive functions as well as their neuroanatomical correlates in the same individuals across the lifespan. C1 Univ London Goldsmiths Coll, Dept Psychol, London SE14 6NW, England. RP Hill, EL (reprint author), Univ London Goldsmiths Coll, Dept Psychol, Whitehead Bldg, London SE14 6NW, England. 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SCI. PD JAN PY 2004 VL 8 IS 1 BP 26 EP 32 DI 10.1016/j.tics.2003.11.003 PG 7 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 767GJ UT WOS:000188431600008 PM 14697400 ER PT S AU Hayes, GR Kientz, JA Truong, KN White, DR Abowd, GD Pering, T AF Hayes, GR Kientz, JA Truong, KN White, DR Abowd, GD Pering, T BE Davies, N Mynatt, E Siio, I TI Designing capture applications to support the education of children with autism SO UBICOMP 2004: UBIQUITOUS COMPUTING, PROCEEDINGS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 6th International Conference on Ubiquitous Computing CY SEP 07-10, 2004 CL Nottingham, ENGLAND SP Intel Corp, Nokia Corp, Fuji Xerox Palo Alto Lab, Microsoft Res, Samsung Adv Inst Technol, SMART Technol, Equator Interdisciplinary Res Collaborat, Engn Phys Sci Res Council, ACM SIGCHI, ACM SIGMOBILE, ACM SIGSOFT, ACM SIGWEB AB We explore the social and technical design issues involved in tracking the effectiveness of educational and therapeutic interventions for children with autism (CWA). Automated capture can be applied in a variety of settings to provide a means of keeping valuable records of interventions. We present the findings from qualitative studies and the designs of capture prototypes. These experiences lead to conclusions about specific considerations for building technologies to assist in the treatment of CWA, as well as other fragile demographics. Our work also reflects back on the automated capture problem itself, informing us as computer scientists how that class of applications must be reconsidered when the analysis of data in the access phase continually influences the capture needs and when social and practical constraints conflict with data collection needs. C1 Georgia Inst Technol, GVU Ctr, Atlanta, GA USA. Georgia Inst Technol, Coll Comp, Atlanta, GA USA. Intel Res, Santa Clara, CA USA. RP Hayes, GR (reprint author), Georgia Inst Technol, GVU Ctr, Atlanta, GA USA. EM gillian@cc.gatech.edu; julie@cc.gatech.edu; khai@cc.gatech.edu; drwhite@cc.gatech.edu; abowd@cc.gatech.edu; trevor.pering@intel.com CR Bellotti V, 1993, 3 EUR C COMP SUPP CO CHEN A, IEEE PERVASIVE COMPU, V1, P49 DEUEL R, 2002, IEEE PERVAS COMPUT, P7 *EUR COMM ART 29 W, 2004, OP 4 2004 PROC PERS GRUDIN J, COMMUNICATIONS ACM, V37, P82 *INCL TLC, 2003, EAR LESSIG L, 1998, TAIWAN NET 98 Mamykina L., 2004, ACM HUMAN FACTORS CO MAURICE C, 1996, BEHAV INTERVENTION Y *MILL SOFTW, 2004, LAB TUT PIERANGELO R, 1998, SPECIAL ED COMPLETE PLAISANT C, 1998, 1998 AM MED INF ASS, P76 Rimland B, 1999, AUTISM TREATMENT EVA SPRADLEY JP, 1980, PARTICIPANT OBERVATI Truong K.N., 2001, UBICOMP 2001, P209 WANT R, 2002, UBICOMP 2002 UBIQUIT 2000, COMPUTHERA 7 STEPS R NR 17 TC 9 Z9 9 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-22955-8 J9 LECT NOTES COMPUT SC PY 2004 VL 3205 BP 161 EP 178 PG 18 WC Computer Science, Hardware & Architecture; Computer Science, Theory & Methods SC Computer Science GA BAX42 UT WOS:000224085200010 ER PT S AU Gea-Megias, M Medina-Medina, N Rodriguez-Almendros, ML Rodriguez-Fortiz, MJ AF Gea-Megias, M Medina-Medina, N Rodriguez-Almendros, ML Rodriguez-Fortiz, MJ BE Stary, C Stephanidis, C TI Sc@ut: Platform for communication in ubiquitous and adaptive environments applied for children with autism SO USER-CENTERED INTERACTION PARADIGMS FOR UNIVERSAL ACCESS IN THE INFORMATION SOCEITY SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 8th ERCIM Workshop on User Interfaces for All CY JUN 28-29, 2004 CL Vienna, AUSTRIA SP European Res Consortium Informat & Math, Inst Comp Sci, Fdn Res & Technol, Austrian Assoc Res IT, Austrian Comp Soc, Johannes Kepler Univ Linz DE autism; PDAs; hypermedia; augmentative and alternative communication; adaptability AB Augmentative and Alternative Communication Systems (AAC) are an emergent technology for improving the,social integration of people with temporary or permanent communication difficulties. One problem which arises is the need to adapt these systems to the different users and situations by taking their capabilities, skills and progress into account. In this regard, we propose an adaptive architecture on a ubiquitous computation paradigm, which is being applied for children with autism. This paper proposes a two-tier architecture consisting of a communicator and, a context meta-model. It allows child communication to be represented and controlled using a PDA device by means of a wireless network. The main aim of the architecture is to facilitate communication, adapting to changes in user and scenario. C1 Univ Granada, ETSI, Dept Lenguajes & Sist Informat, E-18071 Granada, Spain. RP Gea-Megias, M (reprint author), Univ Granada, ETSI, Dept Lenguajes & Sist Informat, E-18071 Granada, Spain. EM mgea@ugr.es; nmedina@ugr.es; mlra@ugr.es; mjfortiz@ugr.es RI Medina Medina, Nuria/B-1743-2012 CR ALBACETE PL, 1982, ASSISTIVE TECHNOLOGY BAKER B, MINSPEAK SEMANTIC CO BLISS, 1965, SEMANTHOGRAPHY BLISS DAUTENHAHN K, 2002, DESIGN ISSUES INTERA Garcia-Cabrera L, 2002, J SOFTW MAINT EVOL-R, V14, P389, DOI 10.1002/smr.262 LYNAS W, 1998, COMMUNICATION OPTION MEDINAMEDINA N, 2002, LECT NOTES COMPUTER, V2347, P284 ORTEGA M, 2001, NEW PARADIGMS INTERA PADEREWSKIRODRI.P, 2004, IN PRESS J SYSTEMS A RODRIGUEZALMEND.ML, 2003, LECT NOTES COMPUTER, V2809, P50 RODRIGUEZFORTIZ MJ, 2004, IN PRESS ELECT NOTES Schlosser R. W., 1994, AUGMENTATIVE ALTERNA, V10, P207, DOI 10.1080/07434619412331276920 STEPHANIDIS C, 2001, UNIVERSAL AACESS INF VANDYKE JA, 1991, WORLD PREDICTION DIS NR 14 TC 2 Z9 2 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-23375-X J9 LECT NOTES COMPUT SC PY 2004 VL 3196 BP 50 EP 67 PG 18 WC Computer Science, Hardware & Architecture; Computer Science, Software Engineering; Computer Science, Theory & Methods SC Computer Science GA BBC01 UT WOS:000224665300005 ER PT J AU Massaro, DW Light, J AF Massaro, DW Light, J TI Improving the vocabulary of children with hearing loss SO VOLTA REVIEW LA English DT Article ID COMMUNICATION-SKILLS; SPEECH RECOGNITION; ACQUISITION; KNOWLEDGE; MEMORY; INSTRUCTION; FREQUENCY; AUTISM AB The goal of this study was to test the effectiveness of a Language Wizard/Player with Baldi, a computer-animated tutor, for teaching new vocabulary items to children with a hearing loss. Eight students with hearing loss, between the ages of 6 and 10, were tested and trained for about 20-30 minutes a day, 2 days a week for about 10 weeks on three categories of eight words each. The design of the experiment was based on a within-student multiple baseline design in which all three categories of words were continuously being tested while one of file categories was being trained. Knowledge of the words remained negligible without training and learning occurred fairly quickly for all words once training began, reaching asymptotic levels in each category. Knowledge of the trained words did not degrade after training once these words ended and training on other words took place. Finally, retention was nearly perfect, as indicated by a reassessment test 4 weeks after the experiment. C1 Univ Calif Santa Cruz, Perceptual Sci Lab, Santa Cruz, CA 95064 USA. McGill Univ, Montreal, PQ, Canada. 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PY 2004 VL 104 IS 4 BP 237 EP 255 PG 19 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 899SQ UT WOS:000227165700004 ER PT J AU Krasnoperova, MG AF Krasnoperova, MG TI Clinical peculiarities of childhood autism with endogenous manifesting psychosis and mental retardation SO ZHURNAL NEVROPATOLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE childhood autism; endogenous psychosis; mental retardation; catatonic symptoms AB Sixty-eight patients with childhood autism manifesting with psychoses of different psychopathological structure at the age up to 3 years have been observed. Four psychotic types - catatonic-regressive (19%), polymorphic-regressive (25%), catatonic with mental retardation during psychosis (32%), polymorphic with retardation of mental development during psychosis (24%) - are described. Correlations between a structure of deficit state and these psychoses were determined: 1) development of severe autistic state with pronounced mental development retardation and a lack of speech in the most cases of catatonic-regressive psychoses; 2) autistic state of moderate severity with mental development retardation of different severity and phrase speech formation in a les than half of the patients in polymorphic-regressive psychosis; 3) development of autistic state of moderate severity with mild mental development retardation and phrase speech formation in the majority of the cases in catatonic psychosis; (4) formation of moderately pronounced autistic state in the absence of mental development retardation or its mild degree and phrase speech acquirement after polymorphic psychosis. C1 Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. RP Krasnoperova, MG (reprint author), Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. 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S S Korsakova PY 2004 VL 104 IS 2 BP 5 EP 10 PG 6 WC Clinical Neurology; Pathology; Psychiatry SC Neurosciences & Neurology; Pathology; Psychiatry GA 815BM UT WOS:000221017800002 PM 15002313 ER PT J AU Zenkov, LR Konstantinov, PA Myasnikov, VN Sirazitdinova, EB Usacheva, EL AF Zenkov, LR Konstantinov, PA Myasnikov, VN Sirazitdinova, EB Usacheva, EL TI Nonconvulsion epileptic encepholopathies and their treatment SO ZHURNAL NEVROPATOLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article ID LANDAU-KLEFFNER-SYNDROME; CHILDREN; DISORDERS; APHASIA; AUTISM; REGRESSION; SEIZURES; SPIKES; CSWS C1 AY Kozhevnikov Nevrous Dis Clin, Moscow, Russia. IM Sechenov Med Acad, Moscow, Russia. Moscow City Psychiat Hosp 6, Moscow, Russia. RP Zenkov, LR (reprint author), AY Kozhevnikov Nevrous Dis Clin, Moscow, Russia. 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Psikhiatrii Im. S S Korsakova PY 2004 VL 104 IS 4 BP 30 EP 38 PG 9 WC Clinical Neurology; Pathology; Psychiatry SC Neurosciences & Neurology; Pathology; Psychiatry GA 826GX UT WOS:000221818400005 PM 15270297 ER PT J AU Krasnoperova, MG Simashkova, NV Bashina, VM AF Krasnoperova, MG Simashkova, NV Bashina, VM TI Use of cholinomimetics in the treatment of endogenous autism in children SO ZHURNAL NEVROPATOLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE children's autism; therapy; choline alfoscerate AB Twenty children with endogenous autism of mild and moderate severity (30-44,5 scores according to the CARS), aged 3-8 years, were treated with choline alfoscerate (CA), 400 mg/day, during 8 weeks in the presence of maintenanu therapy with neuroleptics (17 cases). Positive therapeutic effect was observed in 89% of the patients: significant improvement - in 61% and minimal efficacy - in 28%. Statistically significant positive changes in the patient's state were observed in the general improvement of behavior (p<0,001), development of social and communicative skills, as well as self-service, reduction of marked speech disturbances (p<0,001) and motor sphere (p<0,001), enhancement of learning activity and productivity (p<0,05). Good tolerability to the therapy, without patient's state worsening was registered. Some patients exhibited strengthening of affective lability in the first weeks of the treatment which attenuated to the 411 week as the CA dosages decreased to 400 mg every other day. CA may be recommended for combined therapy with neuroleptics as an effective and safe medicine for the treatment of cognitive and behavioral disorders in patients with children's autism. C1 Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. RP Krasnoperova, MG (reprint author), Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. 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S S Korsakova PY 2004 VL 104 IS 6 BP 35 EP 39 PG 5 WC Clinical Neurology; Pathology; Psychiatry SC Neurosciences & Neurology; Pathology; Psychiatry GA 836XS UT WOS:000222590100006 PM 15285632 ER PT J AU Levitt, JG O'Neill, J Blanton, RE Smalley, S Fadale, D McCracken, JT Guthrie, D Toga, AW Alger, JR AF Levitt, JG O'Neill, J Blanton, RE Smalley, S Fadale, D McCracken, JT Guthrie, D Toga, AW Alger, JR TI Proton magnetic resonance spectroscopic imaging of the brain in childhood autism SO BIOLOGICAL PSYCHIATRY LA English DT Review DE autism; child; magnetic resonance spectroscopy; brain; cingulate gyrus; caudate nucleus ID OBSESSIVE-COMPULSIVE DISORDER; ANTERIOR CINGULATE CORTEX; POSITRON-EMISSION-TOMOGRAPHY; GLUCOSE METABOLIC-RATE; CEREBRAL-BLOOD-FLOW; INFANTILE-AUTISM; IN-VIVO; VISUOSPATIAL ATTENTION; ASPERGERS-SYNDROME; ENERGY-METABOLISM AB Background: Autism is a developmental disorder of unknown neurologic basis. Based on prior work, we used proton magnetic resonance spectroscopic imaging (H-1-MRSI) to investigate brain structures, including cingulate and caudate, that we hypothesized would reveal metabolic abnormalities in subjects with autism. Methods: In 22 children with autism, 5 to 16 years old, and 20 age-matched healthy control subjects, H-1-MRSI assessed levels of N-acetyl compounds (NAA), choline compounds (Cho), and creatine plus phosphocreatine (Cr) at 272 msec echo-time and 1.5 T. Results: In subjects with autism compared with control subjects, Cho was 27.2% lower in left inferior anterior cingulate and 19.1% higher in the head of the right caudate nucleus; Cr was 21.1% higher in the head of the right caudate nucleus, but lower in the body of the left caudate nucleus (17.9%) and right occipital cortex (16.6%). Conclusions: Results are consistent with altered membrane metabolism, altered energetic metabolism, or both in the left anterior cingulate gyrus, both caudate nuclei, and right occipital cortex in subjects with autism compared with control subjects. C1 Univ Calif Los Angeles, Inst Neuropsychiat, Dept Psychiat & Biobehav Sci, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Lab Neuroimaging, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Dept Radiol Sci, Los Angeles, CA 90024 USA. RP Levitt, JG (reprint author), Univ Calif Los Angeles, Inst Neuropsychiat, Dept Psychiat & Biobehav Sci, 760 Westwood Plaza, Los Angeles, CA 90024 USA. 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Psychiatry PD DEC 15 PY 2003 VL 54 IS 12 BP 1355 EP 1366 DI 10.1016/S0006-3223(03)00688-7 PG 12 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 753UW UT WOS:000187249800008 PM 14675799 ER PT J AU Nelson, K AF Nelson, K TI Vaccine additives pose little risk to children SO LANCET LA English DT News Item ID THIMEROSAL; AUTISM CR Hviid A, 2003, JAMA-J AM MED ASSOC, V290, P1763, DOI 10.1001/jama.290.13.1763 Madsen KM, 2003, PEDIATRICS, V112, P604, DOI 10.1542/peds.112.3.604 2003, PEDIATRICS, V112, P1394 NR 3 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 DEC 13 PY 2003 VL 362 IS 9400 BP 1987 EP 1987 DI 10.1016/S0140-6736(03)15089-1 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 753BC UT WOS:000187210700018 ER PT J AU Offit, PA Coffin, SE AF Offit, PA Coffin, SE TI Communicating science to the public: MMR vaccine and autism SO VACCINE LA English DT Review DE MMR; autism; intestinal inflammation ID INFLAMMATORY-BOWEL-DISEASE; TETANUS-PERTUSSIS-VACCINE; MEASLES-VIRUS INFECTION; POLYMERASE-CHAIN-REACTION; RUBELLA VACCINATION; CROHNS-DISEASE; MUMPS-RUBELLA; NEUROLOGIC DISORDERS; CAUSAL ASSOCIATION; MULTIPLE-SCLEROSIS AB Media attention and consequent public concerns about vaccine safety followed publication of a small case-series of children who developed autism after receipt of the measles-mumps-rubella (MMR) vaccine. Many well-controlled studies performed subsequently found no evidence that MMR vaccine causes autism. However, despite these studies, some parents remain concerned that the MMR vaccine is not safe. We will discuss the origins of the hypothesis that the MMR vaccine causes autism, studies performed to test the hypothesis, how these studies have been communicated to the public, and some suggested strategies for how this communication can be improved. (C) 2003 Elsevier Ltd. All rights reserved. C1 Univ Penn, Childrens Hosp Philadelphia, Sch Med, Div Infect Dis, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Wistar Inst Anat & Biol, Philadelphia, PA 19104 USA. RP Offit, PA (reprint author), Univ Penn, Childrens Hosp Philadelphia, Sch Med, Div Infect Dis, Abramson Res Bldg,Room 1202C,34th St & Civic Ctr, Philadelphia, PA 19104 USA. 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NR 0 TC 3 Z9 3 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1090-0586 J9 APPL PSYCHOPHYS BIOF JI Appl. Psychophysiol. Biofeedback PD DEC PY 2003 VL 28 IS 4 BP 305 EP 306 PG 2 WC Psychology, Clinical SC Psychology GA 740NN UT WOS:000186408600006 ER PT J AU Jarusiewicz, B AF Jarusiewicz, B TI Efficacy of neurofeedback for children in the autistic spectrum: A pilot study SO APPLIED PSYCHOPHYSIOLOGY AND BIOFEEDBACK LA English DT Meeting Abstract DE autism; neurofeedback; Autism Treatment Evaluation Checklist; EEG biofeedback C1 Atlantic Res Inst Inc, Atlantic Highlands, NJ 07716 USA. NR 0 TC 3 Z9 3 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 1090-0586 J9 APPL PSYCHOPHYS BIOF JI Appl. Psychophysiol. Biofeedback PD DEC PY 2003 VL 28 IS 4 BP 311 EP 311 PG 1 WC Psychology, Clinical SC Psychology GA 740NN UT WOS:000186408600019 ER PT J AU Machado, MG Oliveira, HA Cipolotti, R Santos, CAGM de Oliveira, EF Donald, RM de Oliveira Krauss, MP AF Machado, MG Oliveira, HA Cipolotti, R Santos, CAGM de Oliveira, EF Donald, RM de Oliveira Krauss, MP TI Anatomical and functional abnormalities of central nervous system in autistic disorder: a MRI and SPECT study SO ARQUIVOS DE NEURO-PSIQUIATRIA LA Portuguese DT Article DE autism; MRI; SPECT ID INFANTILE-AUTISM; POSTERIOR-FOSSA; CHILDHOOD AUTISM; BRAIN; CEREBELLAR; TOMOGRAPHY; CHILDREN AB We present a study of anatomical and functional abnormalities of central nervous system (CNS) from patients with autistic disorder (AD); magnetic resonance imaging (MRI) and single photon emission computed tomography (SPECT) were used for the investigation. The population studied was composed of 24 patients, 15 (62.5%) males and 9 (17.5%) females, mean age 9 years. MRI was performed in all patients and SPECT was performed in 19 patients; 75% (n=18) of patients had anatomical abnormalities and all patients that realized SPECT had functional abnormalities. Anatomical abnormalities were preferentially noted in corpus callosum (25%), septum pellucidum (15.63%), cerebral ventricules (12.55%), cerebellum (9.38%), temporal lobes (6.25%), occipital lobes (6.25%) and hippocampus (6.25%). Functional abnormalities predominated in frontal lobes (53.13%), temporal lobes (28.13%), parietal lobes (15.63%) and basal ganglia (3.13%). However, anatomical and functional abnormalities of CNS are not priorities for diagnosis, which should have always clinical validation. C1 UFS, HU, Serv Neurol, Aracaju, SE, Brazil. RP Machado, MG (reprint author), UFS, HU, Serv Neurol, Aracaju, SE, Brazil. 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Neuro-Psiquiatr. PD DEC PY 2003 VL 61 IS 4 BP 957 EP 961 DI 10.1590/S0004-282X2003000600013 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 751JP UT WOS:000187063500013 PM 14762598 ER PT J AU Boucher, J Wolfberg, P AF Boucher, J Wolfberg, P TI Aims and design of the special issue SO AUTISM LA English DT Editorial Material ID AUTISM; CHILDREN; MIND C1 Univ Warwick, Warwick, England. Autism Inst Peer Relat & Play, San Francisco, CA USA. RP Boucher, J (reprint author), Univ Warwick, Warwick, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S., 1995, MIND BLINDNESS Baron-Cohen S, 2000, J ROY SOC MED, V93, P521 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Boucher J., 1999, CHILD LANG TEACH THE, V15, P1, DOI 10.1191/026565999676029298 Bretherton I, 1984, SYMBOLIC PLAY DEV SO Bruner J, 1986, ACTUAL MINDS POSSIBL Bruner J. L., 1985, PLAY ITS ROLE DEV EV Capps L., 1997, CHILDREN AUTISM DEV Garvey C., 1977, PLAY Hobson R. Peter, 1993, AUTISM DEV MIND HUGHES C, 2001, DEV AUTISM PERSPECTI LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 LEWIN PA, 1991, J LITHOTR STONE DIS, V3, P3 MUNDY P, 1995, DEV PSYCHOPATHOL, V7, P63 Perner Josef, 1991, UNDERSTANDING REPRES Piaget J, 1962, PLAY DREAMS IMITATIO RUBIN K, 1983, HDB CHILD PSYCHOL, P694 RUBIN KH, 1980, CHILDRENS PLAY, P69 Russell J., 1997, AUTISM EXECUTIVE DIS SMITH PK, 1986, CHILDRENS PLAY RES D, P37 Vygotsky Lev Semyonovitch, 1978, MIND SOC DEV HIGHER VYGOTSKY LS, 1966, SOV PSYCHOL, V12, P6 WELLMAN HM, 1991, CHILDS THEORY MIND Werner H., 1984, SYMBOL FORMATION Whiten A., 1991, NATURAL THEORIES MIN Wolfberg P. J., 1999, PLAY IMAGINATION CHI WOLFBERG PJ, 2003, PEER PLAY AUTIMS SPE NR 29 TC 6 Z9 6 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 339 EP 346 DI 10.1177/1362361303007004001 PG 8 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300001 PM 14678674 ER PT J AU Jordan, R AF Jordan, R TI Social play and autistic spectrum disorders - A perspective on theory, implications and educational approaches SO AUTISM LA English DT Article DE autism; autistic spectrum disorders; social play ID PRETEND PLAY; JOINT ATTENTION; YOUNG-CHILDREN; INTERVENTION; BEHAVIORS; PRESCHOOL; CHILDHOOD; DEFICITS; SKILLS AB The article considers the nature of the presumed social play deficit in autistic spectrum disorders (ASDs). The nature of play and its typical development is outlined and discussed in relation to play development in ASDs. It is suggested that social play is a confluence of two strands of development that are affected in autism: social and emotional development, and the cognitive development of play. It is shown that social play develops in a transactional way and in ASDs initial social difficulties prevent the development of social interaction, with its role in eliciting and enriching spontaneous play. At the same time, cognitive and affective difficulties prevent the play of children with autism developing to the extent of attracting other children and being of a complexity from which social play might develop. This cycle of impoverished play opportunities for children with ASDs may be broken through direct teaching and there are encouraging models of teaching social play with some success. C1 Univ Birmingham, Birmingham, W Midlands, England. RP Jordan, R (reprint author), Univ Birmingham, Birmingham, W Midlands, England. 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S., 2001, FOCUS AUTISM OTHER D, V16, P120, DOI DOI 10.1177/108835760101600208 THORP DM, 1995, J AUTISM DEV DISORD, V25, P265, DOI 10.1007/BF02179288 VANBECKELAERONN.IA, 1994, PLAY INTERVENTION Vygotsky Lev Semyonovitch, 1978, MIND SOC DEV HIGHER VYGOTSKY LS, 1966, SOV PSYCHOL, V12, P6 Watson LR, 1998, J AUTISM DEV DISORD, V28, P51, DOI 10.1023/A:1026063003289 WHITE C, 2002, GOOD AUTISM PRACTICE, V3, P63 Whiten A., 2000, AUTISM, V4, P185, DOI 10.1177/1362361300004002006 Whiten A., 1991, NATURAL THEORIES MIN WHYTE J, 1989, J SPEECH HEAR RES, V27, P364 Williams E, 2001, J AUTISM DEV DISORD, V31, P67, DOI 10.1023/A:1005665714197 Wing L, 2002, J CHILD PSYCHOL PSYC, V43, P307, DOI 10.1111/1469-7610.00023 Wolfberg P. J., 1999, PLAY IMAGINATION CHI Zercher C, 2001, AUTISM, V5, P374, DOI 10.1177/1362361301005004004 NR 72 TC 40 Z9 42 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 347 EP 360 DI 10.1177/1362361303007004002 PG 14 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300002 PM 14678675 ER PT J AU Williams, E AF Williams, E TI A comparative review of early forms of object-directed play and parent-infant play in typical infants and young children with autism SO AUTISM LA English DT Article DE autism; early object play; early; parent-infant play ID 1ST 2 YEARS; MOTHER-INFANT; JOINT ATTENTION; NONVERBAL-COMMUNICATION; SCHIZOPHRENIC CHILDREN; EXPLORATORY-BEHAVIOR; LANGUAGE-DEVELOPMENT; MASTERY MOTIVATION; RETARDED-CHILDREN; SYMBOLIC PLAY AB The article reviews the empirical evidence relating to the development of early solitary object and parent-infant play in typical infants and children diagnosed with autism. Whilst, collectively, the findings indicate that there may be both qualitative and quantitative differences in the early play of children with autism, relative to that of other children, it is also clear that significant gaps exist in our current knowledge. It is proposed that longitudinal studies, which make a detailed examination of the form and developmental trajectory of early play, are needed if we are to devise the most effective content, design and outcome measures for intervention programmes using play as a therapeutic medium. C1 Univ Surrey, Guildford GU2 5XH, Surrey, England. RP Williams, E (reprint author), Univ Surrey, Guildford GU2 5XH, Surrey, England. 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C., 1975, ASSESSMENT INFANCY VONDRA J, 1989, ACTION SOCIAL CONTEX WERTSCH JV, 1979, HUM DEV, V22, P1 Wetherby A., 1984, J SPEECH HEAR RES, V27, P367 WILLIAMS E, UNPUB COMP STUDY EXP Williams E, 2001, J AUTISM DEV DISORD, V31, P67, DOI 10.1023/A:1005665714197 WILLIAMS E, 2001, WORKSH DOING THINGS WING L, 1977, J CHILD PSYCHOL PSYC, V18, P167, DOI 10.1111/j.1469-7610.1977.tb00426.x WING L, 1969, J CHILD PSYCHOL PSYC, V10, P1, DOI 10.1111/j.1469-7610.1969.tb02066.x YARROW LJ, 1983, DEV PSYCHOL, V19, P159, DOI 10.1037/0012-1649.19.2.159 NR 97 TC 16 Z9 18 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 361 EP 377 DI 10.1177/1362361303007004003 PG 17 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300003 PM 14678676 ER PT J AU Jarrold, C AF Jarrold, C TI A review of research into pretend play in autism SO AUTISM LA English DT Review DE autism; autistic spectrum disorders; social play ID SYMBOLIC PLAY; NORMAL-CHILDREN; YOUNG-CHILDREN; LANGUAGE DISORDER; ELICITED PLAY; IMITATION; MIND; DEFICITS; SKILLS; COMPREHENSION AB Autism is currently diagnosed, in part at least, on the basis of problems in imagination. The article reviews the empirical evidence of difficulties in pretend play in autism, and focuses in particular on individuals' ability to engage in pretence in free play conditions, to produce pretence in more structured situations, and to make sense of pretend actions carried out by another person. These data suggest that individuals with autism have a marked difficulty in producing pretend play, but one that is reduced by providing substantial structure to the play situation or by testing comprehension of pretence. The implications of these findings for theories of pretend play in autism, in terms of an inability to conceive of non-literal situations, a difficulty in imposing a pretend usage on an object, or a failure to gain a benefit from engaging in pretend play, are discussed. C1 Univ Bristol, Bristol BS8 1TH, Avon, England. RP Jarrold, C (reprint author), Univ Bristol, Bristol BS8 1TH, Avon, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ATLAS JA, 1987, J CLIN PSYCHOL, V43, P17 BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 BARONCOHEN S, 1990, BRIT J DEV PSYCHOL, V8, P207 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BARONCOHEN S, 1991, BRIT J DEV PSYCHOL, V9, P301 BARTAK L, 1975, BRIT J PSYCHIAT, V126, P127, DOI 10.1192/bjp.126.2.127 BOUCHER J, 1990, BRIT J DEV PSYCHOL, V8, P205 Bruner J. S., 1976, PLAY ITS ROLE DEV EV Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 Charman T, 1997, J AUTISM DEV DISORD, V27, P325, DOI 10.1023/A:1025806616149 DEMYER MK, 1967, PSYCHOL REP, V21, P973 DOHERTY MB, 1984, J DEV BEHAV PEDIATR, V5, P26 ELKONIN D, 1966, SOV EDUC, V8, P35 FEIN GG, 1981, CHILD DEV, V52, P1095, DOI 10.1111/j.1467-8624.1981.tb03157.x HAMMER CU, 1981, J VOLCANOL GEOTH RES, V11, P3, DOI 10.1016/0377-0273(81)90071-8 Harris P., 1993, Understanding other minds: perspectives from autism Harris P., 1994, CHILDRENS EARLY UNDE Harris P. L., 1989, CHILDREN EMOTION HEIMANN M, 1992, BEHAV NEUROL, V5, P219, DOI 10.3233/BEN-1992-5404 HUTTENLOCHER J, 1978, MINNESOTA S CHILD PS, V11 JARROLD C, 1994, J AUTISM DEV DISORD, V24, P433, DOI 10.1007/BF02172127 Jarrold C, 1996, BRIT J DEV PSYCHOL, V14, P275 JARROLD C, 1994, J CHILD PSYCHOL PSYC, V35, P1473, DOI 10.1111/j.1469-7610.1994.tb01288.x JARROLD C, 1993, J AUTISM DEV DISORD, V23, P281, DOI 10.1007/BF01046221 KAVANAUGH RD, 1994, DEV PSYCHOL, V30, P847, DOI 10.1037/0012-1649.30.6.847 LESLIE AM, 1987, PSYCHOL REV, V94, P412, DOI 10.1037/0033-295X.94.4.412 Lewis V, 2000, INT J LANG COMM DIS, V35, P117 LEWIS V, 1995, J AUTISM DEV DISORD, V25, P105, DOI 10.1007/BF02178499 LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 Libby S, 1997, J AUTISM DEV DISORD, V27, P365, DOI 10.1023/A:1025801304279 Lillard A, 2001, DEV REV, V21, P495, DOI 10.1006/drev.2001.0532 LILLARD AS, 1993, CHILD DEV, V64, P348, DOI 10.1111/j.1467-8624.1993.tb02914.x MUNDY P, 1986, J CHILD PSYCHOL PSYC, V27, P657, DOI 10.1111/j.1469-7610.1986.tb00190.x Piaget J, 1962, PLAY DREAMS IMITATIO RIGUET CB, 1981, J AUTISM DEV DISORD, V11, P439 Scambler D, 2001, J AM ACAD CHILD PSY, V40, P1457, DOI 10.1097/00004583-200112000-00017 SIGMAN M, 1984, DEV PSYCHOL, V20, P293, DOI 10.1037/0012-1649.20.2.293 STONE WL, 1990, PEDIATRICS, V86, P267 Striano T, 2001, DEVELOPMENTAL SCI, V4, P442, DOI 10.1111/1467-7687.00186 UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 Vygotsky L. S., 1967, SOV PSYCHOL, V12, P62 WETHERBY AM, 1984, J SPEECH HEAR RES, V27, P364 WING L, 1977, J CHILD PSYCHOL PSYC, V18, P167, DOI 10.1111/j.1469-7610.1977.tb00426.x WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WOLFF SB, 1985, J AUTISM DEV DISORD, V15, P139 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 50 TC 47 Z9 47 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 379 EP 390 DI 10.1177/1362361303007004004 PG 12 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300004 PM 14678677 ER PT J AU Lewis, V AF Lewis, V TI Play and language in children with autism SO AUTISM LA English DT Article DE autism; language development; play ID SYMBOLIC PLAY; 2ND YEAR; COMMUNICATION AB It is well established that the play and language skills Of children with autism are impaired. The article considers the relationship between these developments in typically developing children and children with autism. First, the evidence for a relationship between these two areas in typically developing children is reviewed. Despite many methodological differences between studies, this evidence supports a relationship, with specific developments emerging first in play and subsequently in language. Second, evidence for a relationship between play and language in children with autism is reviewed. From published and some previously unpublished data it is concluded that if there is a relationship between play and language in children with autism it is weak, if it exists at all. Finally, the implications of these findings are discussed and it is suggested that any relationship between play and language may be mediated by how children and their parents interact when they are playing. C1 Open Univ, Milton Keynes MK7 6AA, Bucks, England. RP Lewis, V (reprint author), Open Univ, Milton Keynes MK7 6AA, Bucks, England. CR Carpenter M., 1998, MONOGRAPHS SOC RES C, V63 Charman T, 2000, COGNITIVE DEV, V15, P481, DOI 10.1016/S0885-2014(01)00037-5 CLIFT S, 1988, CHILD LANG TEACH THE, V14, P199 DOSWELL G, 1994, EUROPEAN J DISORDERS, V29, P291 Lewis V, 2000, INT J LANG COMM DIS, V35, P117 Lewis V., 2003, DEV DISABILITY LEWIS V, 1997, TEST PRETENT PLAY LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 MCCUNE L, 1995, DEV PSYCHOL, V31, P198, DOI 10.1037//0012-1649.31.2.198 MUNDY P, 1987, J AUTISM DEV DISORD, V17, P349, DOI 10.1007/BF01487065 OReilly AW, 1997, COGNITIVE DEV, V12, P185, DOI 10.1016/S0885-2014(97)90012-5 Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 Siller M, 2002, J AUTISM DEV DISORD, V32, P77, DOI 10.1023/A:1014884404276 Stone WL, 2001, AUTISM, V5, P341, DOI 10.1177/1362361301005004002 TAMISLEMONDA CS, 1994, DEV PSYCHOL, V30, P283, DOI 10.1037/0012-1649.30.2.283 UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 UNGERER JA, 1984, CHILD DEV, V55, P1448, DOI 10.2307/1130014 NR 17 TC 8 Z9 8 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 391 EP 399 DI 10.1177/1362361303007004005 PG 9 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300005 PM 14678678 ER PT J AU Stahmer, AC Ingersoll, B Carter, C AF Stahmer, AC Ingersoll, B Carter, C TI Behavioral approaches to promoting play SO AUTISM LA English DT Article DE applied behavior analysis; autism; behavioral teaching; naturalistic methods; play ID TEACHING AUTISTIC-CHILDREN; SELF-MANAGEMENT; GENERALIZED REDUCTION; DISRUPTIVE BEHAVIOR; SOCIODRAMATIC PLAY; APPROPRIATE PLAY; SOCIAL-BEHAVIOR; YOUNG-CHILDREN; SKILLS; DISABILITIES AB A variety of techniques grounded in behavioral psychology, and more specifically in applied behavior analysis, have been established to increase and improve play skills in children with autistic spectrum disorders. This article introduces a set of efficacious methods, which range from highly structured techniques to more naturalistic strategies. It focuses on object play as other authors in the issue discuss social play in greater depth. Behavioral techniques that are reviewed include: discrete trial training, use of stereotyped behaviors to increase play skills, pivotal response training, reciprocal imitation training, differential reinforcement of appropriate behavior, in vivo modeling and play scripts, and video modeling. A discussion of expanding behavior techniques to teach more complex play as well as training in varied environments is also presented. References are provided to allow the reader to obtain more in-depth information about each technique. C1 Univ Calif San Diego, San Diego, CA 92103 USA. RP Stahmer, AC (reprint author), Child & Adolescent Serv Res Ctr, 3020 Childrens Way MC 5033, San Diego, CA 92123 USA. RI Ingersoll, Brooke/A-9117-2012 CR Baker M. 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D., 1996, EARLY EDUC DEV, V7, P205, DOI 10.1027/s15566935eed0703_1 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 Smith M. J., 2001, TEACHING PLAY SKILLS Stahmer A. C., 2001, J POSIT BEHAV INTERV, V3, P75, DOI DOI 10.1177/109830070100300203 Stahmer A. C., 1999, CHILD LANG TEACH THE, V15, P29, DOI 10.1191/026565999672332808 STAHMER AC, 1995, J AUTISM DEV DISORD, V25, P123, DOI 10.1007/BF02178500 STAHMER AC, 1992, J APPL BEHAV ANAL, V25, P447, DOI 10.1901/jaba.1992.25-447 STAHMER AC, 1993, DISS ABSTR INT, V54, pB3331 STAHMER AC, 1994, M ASS BEH AN ATL GA SUGAI G, 1986, J AUTISM DEV DISORD, V16, P459, DOI 10.1007/BF01531711 Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 THORP DM, 1995, J AUTISM DEV DISORD, V25, P265, DOI 10.1007/BF02179288 TRYON AS, 1986, J ABNORM CHILD PSYCH, V14, P537, DOI 10.1007/BF01260522 WARREN SF, 1993, J SPEECH HEAR RES, V36, P83 Weiss M. J, 2001, REACHING OUT JOINING WOLERY M, 1985, J AUTISM DEV DISORD, V15, P149, DOI 10.1007/BF01531601 ZIHNI F, 2002, AZ METHOD USE VIDEO NR 57 TC 21 Z9 21 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 401 EP 413 DI 10.1177/1362361303007004006 PG 13 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300006 PM 14678679 ER PT J AU Van Berckelaer-Onnes, IA AF Van Berckelaer-Onnes, IA TI Promoting early play SO AUTISM LA English DT Article DE autism; intervention; perception; play; weak central coherence ID SYMBOLIC PLAY; AUTISTIC-CHILDREN AB Early forms of play involving the exploration of objects is repetitive and limited in scope in children with autism, consistent with a weak drive towards central coherence. The importance is stressed of early manipulative and relational play for the development of meaningful perceptual representations and the subsequent development of functional and symbolic play. It is argued that intervention designed to promote these early forms of play is therefore of critical importance. A toy-play intervention programme is described that was initially used in a research setting with 24 children with autism, using outcome measures and a 1 year follow-up assessment. The original intervention was successful. However, improvements in play were not maintained unless children continued to receive play support. A 'play stimulation' programme building on the toy-play programme is therefore now carried out with children in small groups after completion of the one-to-one toy-play programme. C1 Leiden Univ, Fac Social Sci, Dept Psychol & Special Educ, NL-2300 RB Leiden, Netherlands. RP Van Berckelaer-Onnes, IA (reprint author), Leiden Univ, Fac Social Sci, Dept Psychol & Special Educ, POB 9555, NL-2300 RB Leiden, Netherlands. CR DEMEYER MK, 1967, PSYCHOL REP, V21, P973 Frith U., 2003, AUTISM EXPLAINING EN GOULD J, 1986, J AUTISM DEV DISORD, V16, P199, DOI 10.1007/BF01531730 Howlin P, 1987, TREATMENT AUTISTIC C JARROLD C, 1993, J AUTISM DEV DISORD, V23, P281, DOI 10.1007/BF01046221 LEWIS V, 1988, BRIT J DEV PSYCHOL, V6, P325 Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 MCCUNENICOLICH L, 1980, MANUAL ANAL FREE PLA TILTON JR, 1964, PSYCHOL REP, V15, P967 UNGERER JA, 1981, J AM ACAD CHILD PSY, V20, P318, DOI 10.1016/S0002-7138(09)60992-4 VANBERCELAERONN.IA, 1994, PLAY INTERVENTIONS, P173 VANBERCKELAERON.IA, 1996, KINDER JEUGD PSYCHOT, V23, P77 VANBERCKELAERON.IA, 1988, KINDER JEUGD PSYCHOT, V15, P136 Verpoorten R. A. W., 1996, NEDERLANDS TIJDSCHRI, V22, P106 WING L, 1977, J CHILD PSYCHOL PSYC, V18, P167, DOI 10.1111/j.1469-7610.1977.tb00426.x WULFF SB, 1985, J AUTISM DEV DISORD, V15, P139, DOI 10.1007/BF01531600 NR 16 TC 10 Z9 11 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 415 EP 423 DI 10.1177/1362361303007004007 PG 9 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300007 PM 14678680 ER PT J AU Wieder, S Greenspan, SI AF Wieder, S Greenspan, SI TI Climbing the symbolic ladder in the DIR model through floor time/interactive play SO AUTISM LA English DT Article DE affect; autistic spectrum disorders; DIR; floor time; symbolic play AB The developmental, individual-difference, relationship-based model (DIR), a theoretical and applied framework for comprehensive intervention, examines the functional developmental capacities of children in the context of their unique biologically based processing profile and their family relationships and interactive patterns. As a functional approach, it uses the complex interactions between biology and experience to understand behavior and articulates the developmental capacities that provide the foundation for higher order symbolic thinking and relating. During spontaneous 'floor time' play sessions, adults follow the child's lead utilizing affectively toned interactions through gestures and words to move the child up the symbolic ladder by first establishing a foundation of shared attention, engagement, simple and complex gestures, and problem solving to usher the child into the world of ideas and abstract thinking. This process is illustrated by a case example of a young boy on the autism spectrum interacting with his father during 'floor time' over a 3 year period. C1 Interdisciplinary Council Dev & Learning Disorder, Bethesda, MD USA. George Washington Univ, Sch Med, Washington, DC 20052 USA. RP Wieder, S (reprint author), Interdisciplinary Council Dev & Learning Disorder, Bethesda, MD USA. CR BARON RA, 1992, MOTIV EMOTION, V16, P1, DOI 10.1007/BF00996485 GREENSPAN S, 1979, PSYCHOL ISSUES Greenspan S. I., 1992, INFANCY EARLY CHILDH Greenspan S. I., 1998, CHILD SPECIAL NEEDS Greenspan S. I., 1997, J DEV LEARNING DISOR, V1, P87 Greenspan S. I., 1989, DEV EGO IMPLICATIONS GREENSPAN SI, 2003, 1 IDEA SYMBOLS LANGU Greenspan S.I., 1997, DEV BASED PSYCHOTHER Greenstein S, 1997, IEEE MICRO, V17, P5, DOI 10.1109/40.592323 *ICDL, 2000, ICDL CLIN PRACT GUID *ICDL, 2002, P ICDL 6 INT C AUT D PIAGET J, 1962, CHILDHOOD PSYCHOPATH, P157 WIEDER S, 2001, ZERO 3, V21, P11 NR 13 TC 22 Z9 23 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 425 EP 435 DI 10.1177/1362361303007004008 PG 11 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300008 PM 14678681 ER PT J AU Yang, TR Wolfberg, PJ Wu, SC Hwu, PY AF Yang, TR Wolfberg, PJ Wu, SC Hwu, PY TI Supporting children on the autism spectrum in peer play at home and school - Piloting the integrated play groups model in Taiwan SO AUTISM LA English DT Article DE autism; Chinese culture; peers; play; social interaction ID SOCIAL-INTERACTION; BEHAVIOR; LANGUAGE AB The article focuses on integrated play groups (IPGs) as a model to support children with ASD in play with typically developing peers/siblings, and its recent adoption with children in a home and school setting in Taiwan. The first part provides a brief overview of the IPG model and its essential features. The second part reports on a pilot investigation that combined quantitative and qualitative methods to examine the effects of participation in IPGs on the symbolic and social play of two early elementary-aged children with autism. Preliminary findings suggest that each child made notable gains in reciprocal social interaction and symbolic/pretend play while participating in play groups. Implications are discussed in terms of play's role in enhancing socialization, imagination and peer cultural inclusion. C1 Natl Taipei Teachers Coll, Dept Special Educ, Taipei 106, Taiwan. Autism Inst Peer Relat & Play, San Francisco, CA USA. Jeu Guang Elementary Sch, Taipei, Taiwan. RP Yang, TR (reprint author), Natl Taipei Teachers Coll, Dept Special Educ, 134 Ho Ping E Rd,Sec 2, Taipei 106, Taiwan. 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W., 1984, SINGLE SUBJECT RES S Vygotsky Lev Semyonovitch, 1978, MIND SOC DEV HIGHER VYGOTSKY LS, 1966, SOV PSYCHOL, V12, P6 Westby C, 2000, PLAY DIAGNOSIS ASSES, P131 Wing L., 1987, HDB AUTISM PERVASIVE, P3 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wolfberg P., 1999, CHILD LANG TEACH THE, V15, P41, DOI 10.1191/026565999667036164 Wolfberg P. J., 1999, PLAY IMAGINATION CHI Wolfberg P. J., 2003, PEER PLAY AUTISM SPE WOLFBERG PJ, 1995, TEACHING CHILDREN AU Wolfberg PJ, 1999, J ASSOC PERS SEVERE, V24, P69, DOI 10.2511/rpsd.24.2.69 WOLFBERG PJ, 1994, DISS ABSTR INT WOLFBERG PJ, 1993, J AUTISM DEV DISORD, V23, P467, DOI 10.1007/BF01046051 WOLFBERG PJ, 1988, UNPUB INTEGRATED PLA WOLFBERG PJ, 1992, HO86D90016 OSERS DEP Zercher C, 2001, AUTISM, V5, P374, DOI 10.1177/1362361301005004004 NR 49 TC 14 Z9 18 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 437 EP 453 DI 10.1177/1362361303007004009 PG 17 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300009 PM 14678682 ER PT J AU Schuler, AL AF Schuler, AL TI Beyond echoplaylia - Promoting language in children with autism SO AUTISM LA English DT Article DE autism; echolalia; imaginative play; narrative; theory of mind; situation association ID PLAY; STORIES AB The article was written to support the use of play as a K medium to extend and enrich the communicative exchanges and, more specifically, the symbolic language of children on the autistic spectrum. The first argument in support of such use of play lies within the features of autistic communication, and particularly the extreme challenges encountered in imaginative play and narrative thought. The second argument on behalf of play lies within the selection of specific intervention strategies, which are discussed subsequently. Finally, the article presents a case illustration of how adult facilitated dramatic peer play led to a breakthrough in a range of symbolic behaviours in a 9-year-old girl with autism, who up to that point had not progressed beyond a semi-communicative use of echolalia, best described as 'situation association'. C1 San Francisco State Univ, San Francisco, CA 94132 USA. RP Schuler, AL (reprint author), San Francisco State Univ, 1600 Holloway Ave, San Francisco, CA 94132 USA. 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Jean-Paul Bovee explains the activities that were enjoyable for him and which were his play, although they were unusual and may not fit the typical definition of play. His mother, Dr Julie A. Donnelly, tells of her attempts to involve jean-Paul in typical play and how important play is as a bridge to social skills and involvement with peers. Jean-Paul concludes that his play is a part of the unique individual he has become. C1 Autism Support Serv, Columbia, MO 65202 USA. Univ Missouri, Kansas City, MO 64110 USA. RP Donnelly, J (reprint author), Autism Support Serv, 6901 Charlene, Columbia, MO 65202 USA. NR 0 TC 4 Z9 4 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2003 VL 7 IS 4 BP 471 EP 476 DI 10.1177/1362361303007004011 PG 6 WC Psychology, Developmental SC Psychology GA 749ZE UT WOS:000186959300011 PM 14678684 ER PT J AU Salinger, WL Ladrow, P Wheeler, C AF Salinger, WL Ladrow, P Wheeler, C TI Behavioral phenotype of the reeler mutant mouse: Effects of Reln gene dosage and social isolation SO BEHAVIORAL NEUROSCIENCE LA English DT Review ID QUANTITATIVE TRAIT LOCI; SPATIAL WORKING-MEMORY; THYROTROPIN-RELEASING-HORMONE; RECEPTIVE-FIELD PROPERTIES; F-1 HYBRIDS IMPLICATIONS; PREPULSE INHIBITION; ACOUSTIC STARTLE; KNOCKOUT MICE; HABITUATION DEFICITS; EXECUTIVE FUNCTION AB Reeler (rl/rl) and reeler/wild-type (+/rl) mice synthesize Reln at subnormal rates, as do patients with schizophrenia, bipolar disorder, and autism, thereby forming the basis for a Reln hypothesis for vulnerability to these psychopathologies and justifying attention to the behavioral phenotypes of Reln-deficient mice. Tests of gait, emotionality, social aggression, spatial working memory, novel-object detection, fear conditioning, and sensorimotor reflex modulation revealed the behavioral phenotype of rl/rl. but not +/rl, mice to be different from that of wild-type (+/+) mice. These results reveal no effect of Reln gene dosage and provide significant challenges to both the Reln and the neurodevelopmental hypotheses of the etiology of major psychopathologies. C1 Univ N Carolina, Dept Psychol, Greensboro, NC 27402 USA. RP Salinger, WL (reprint author), Univ N Carolina, Dept Psychol, POB 26170, Greensboro, NC 27402 USA. 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Neurosci. PD DEC PY 2003 VL 117 IS 6 BP 1257 EP 1275 DI 10.1037/0735-7044.117.6.1257 PG 19 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 755KP UT WOS:000187402300013 PM 14674845 ER PT J AU Grant, SGN AF Grant, SGN TI Synapse signalling complexes and networks: machines underlying cognition SO BIOESSAYS LA English DT Review ID LONG-TERM POTENTIATION; D-ASPARTATE RECEPTOR; POSTSYNAPTIC DENSITY-95; NMDA RECEPTOR; PROTEOMIC ANALYSIS; PROTEIN; HIPPOCAMPUS; PSD-95; SENSITIZATION; TRANSMISSION AB All thoughts and actions are encoded in patterns of neuronal electrical activity. Circuits of nerve cells connected by synapses are dedicated to processing information in these patterns. Information is not only transmitted across the synapse but also monitored by postsynaptic molecular machines. These machines are macromolecular complexes of similar to100 proteins organised into a network of protein interactions. 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We measured fractal dimension of human cerebellum ( CB) in magnetic resonance images of 24 healthy young subjects ( 12 men and 12 women). CB images were resampled to a series of image sets with different 3D resolutions. At each resolution, the skeleton of the CB white matter was obtained and the number of pixels belonging to the skeleton was determined. Fractal dimension of the CB skeleton was calculated using the box-counting method. The results indicated that the CB skeleton is a highly fractal structure, with a fractal dimension of 2.57 +/- 0.01. No significant difference in the CB fractal dimension was observed between men and women. C1 Cleveland Clin Fdn, Lemer Res Inst, Dept Biomed Engn, Cleveland, OH 44195 USA. Case Western Reserve Univ, Dept Phys, Cleveland, OH 44106 USA. Case Western Reserve Univ, Dept Biomed Engn, Cleveland, OH 44106 USA. RP Liu, JZ (reprint author), Cleveland Clin Fdn, Dept Biomed Engn ND20, 9500 Euclid Ave, Cleveland, OH 44195 USA. 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PD DEC PY 2003 VL 85 IS 6 BP 4041 EP 4046 DI 10.1016/S0006-3495(03)74817-6 PG 6 WC Biophysics SC Biophysics GA 747GX UT WOS:000186797800056 PM 14645092 ER PT J AU Foxton, JM Stewart, ME Barnard, L Rodgers, J Young, AH O'Brien, G Griffiths, TD AF Foxton, JM Stewart, ME Barnard, L Rodgers, J Young, AH O'Brien, G Griffiths, TD TI Absence of auditory 'global interference' in autism SO BRAIN LA English DT Article DE audition; autism; contour; pitch; weak central coherence ID CENTRAL COHERENCE; PITCH; INFORMATION; CHILDREN; CONTOUR; ABILITY; CORTEX; SAVANT AB There has been considerable recent interest in the cognitive style of individuals with Autism Spectrum Disorder (ASD). One theory, that of weak central coherence, concerns an inability to combine stimulus details into a coherent whole. Here we test this theory in the case of sound patterns, using a new definition of the details (local structure) and the coherent whole (global structure). Thirteen individuals with a diagnosis of autism or Asperger's syndrome and 15 control participants were administered auditory tests, where they were required to match local pitch direction changes between two auditory sequences. When the other local features of the sequence pairs were altered (the actual pitches and relative time points of pitch direction change), the control participants obtained lower scores compared with when these details were left unchanged. This can be attributed to interference from the global structure, defined as the combination of the local auditory details. In contrast, the participants with ASD did not obtain lower scores in the presence of such mismatches. This was attributed to the absence of interference from an auditory coherent whole. The results are consistent with the presence of abnormal interactions between local and global auditory perception in ASD. C1 Univ Newcastle Upon Tyne, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. 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The consistency in group means and intra-individual stability of developmental quotients (DQ) and non-verbal intelligence quotients (IQs) were compared for these two groups, which were matched by chronological age, initial non-verbal IQ/DQs, initial test given, and length of follow-up interval. The case group comprised 16 autistic children with average age at initial assessment of 3 years 8 months. The control group comprised 16 nonautistic developmental delayed children with average age at initial assessment of 3 years I I months. Mean DQ/non-verbal IQ at initial assessment was 73.9 +/- 23.9 for the case group and 80.3 +/- 23.2 for the control group. ANOVA yielded no significant effect of time or time X diagnosis interaction (F = 0.183, P = 0.675). The absolute difference in scores and group means were equivalent for both groups of children, with no difference in patterns of change. Correlations between DQ/non-verbal IQs at initial assessment and follow-up were significant and high for the two groups (autistic group: r = 0.87; control: r = 0.77). Intellectual functioning can be a valid measure in Taiwanese preschool children with autism, and has an equivalent meaning for children with autism and for non-autistic children with developmental delay. Though the follow-up period is too short for definite prognostic conclusions to be drawn, we think that non-verbal intelligence should be an essential assessment for preschool oriental autistic children so that sound expectation and treatment plan can be made. (C) 2003 Elsevier B.V. All rights reserved. C1 Kaohsiung Med Univ Hosp, Dept Pediat, Kaohsiung 807, Taiwan. Kaohsiung Municipal Hsiaokang Hosp, Kaohsiung 812, Taiwan. RP Jong, YJ (reprint author), Kaohsiung Med Univ Hosp, Dept Pediat, 482 Shan Ming Rd,Hsiao Kang Dist, Kaohsiung 807, Taiwan. 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Autistic disease (AD) is a severe neuropsychiatric disorder affecting 2-4 children per 10,000. We have recently shown reduction of Bcl-2 and increase in P53, two important markers of apoptosis, in parietal cortex of autistic subjects. 2. We hypothesized that brain levels of Bcl-2 and P53 would also be altered in superior frontal cortex and cerebellum of age-, sex, and postmortem-interval (PMI)-matched autistic subjects (N=5 autistic, N=4 controls). 3. Brain extracts were prepared from superior frontal cortex and cerebellum and subjected to Western blotting. 4. Results showed that levels of Bcl-2 decreased by 38% and 36% in autistic superior frontal and cerebellar cortices, respectively when compared to control tissues. By the same token, levels of P53 increased by 67.5% and 38% in the same brain areas in autistic subjects vs. controls respectively. Calculations of ratios of Bcl-2/P53 values also decreased by 75% and 43% in autistic frontal and cerebellar cortices vs. controls respectively. The autistic cerebellar values were significantly reduced (p<0.08) vs. control only. There were no significant differences in levels of β-actin between the two groups. Additionally, there were no correlations between Bcl-2, P53, and β-actin concentrations vs. age or PMI in either group. 5. These results confirm and extend previous data that levels of Bcl-2 and P53 are altered in three important brain tissues, i.e. frontal, parietal, and cerebellar cortices of autistic subjects, alluding to deranged apoptotic mechanisms in autism. C1 Univ Minnesota, Sch Med, Dept Psychiat, Div Neurosci Res, Minneapolis, MN 55455 USA. Univ Minnesota, Sch Med, Dept Neurosci, Div Neurosci Res, Minneapolis, MN 55455 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. 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Mol. Neurobiol. PD DEC PY 2003 VL 23 IS 6 BP 945 EP 952 DI 10.1023/B:CEMN.0000005322.27203.73 PG 8 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA 747AW UT WOS:000186783800007 PM 14964781 ER PT J AU Rondan, C Gepner, B Deruelle, C AF Rondan, C Gepner, B Deruelle, C TI Inner and outer face perception in children with autism SO CHILD NEUROPSYCHOLOGY LA English DT Article ID UPSIDE-DOWN FACES; GLOBAL PRECEDENCE; FACIAL EXPRESSION; RECOGNITION; REPRESENTATION; FEATURES; FAMILIAR; EMOTION; IDENTIFICATION; DISCRIMINATION AB Possible peculiarities in face perception in the autistic population were explored through two experiments. Fourteen autistic children (mean age=10 years 1 month) were individually matched to verbal mental age (VMA) and chronological age (CA) subjects. In a first experiment, subjects were to match faces on the basis of either their outer (hair, chin, ears) or their inner (eyes, nose, mouth) aspects. 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PD DEC PY 2003 VL 9 IS 4 BP 289 EP 297 DI 10.1076/chin.9.4.289.23516 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA 767LP UT WOS:000188453000005 PM 14972707 ER PT J AU Kamnasaran, D AF Kamnasaran, D TI Genetic analysis of psychiatric disorders associated with human chromosome 18 SO CLINICAL AND INVESTIGATIVE MEDICINE-MEDECINE CLINIQUE ET EXPERIMENTALE LA English DT Review ID BIPOLAR AFFECTIVE-DISORDER; SUSCEPTIBILITY LOCI; LINKAGE ANALYSIS; COMPLEX TRAITS; CHROMOSOME-18 MARKERS; GENOMEWIDE SCREEN; CAG/CTG REPEATS; GENOMIC SCREEN; SCHIZOPHRENIA; AUTISM AB Current models on the etiology of psychiatric disorders support the idea of a biologic cause as well as interactions of biologic systems with the environment. The elucidation of the genetic etiology is of paramount importance to understand the cause of psychiatric disorders. Human chromosome 18 was identified as one of the first chromosomes to be aberrant in psychiatric patients and has subsequently served as a model to identify the molecular cause. In this article I review a multitude of methodologies that can be used in determining the genetic basis of schizophrenia, affective disorder and autism associated with human chromosome 18. These strategies include the use of chromosome aberrations, linkage and association studies, mouse-human comparative genomics, mutation analysis on candidate genes, trinucleotide repeat expansion studies, search for genes demonstrating parental effects and bioinformatics. Current data from the use of these methods are cited from the literature. Linkage and association studies have suggested at least 2 candidate loci on the short and long arms of chromosome 18 for each of these psychiatric disorders. Some loci are supported by the mapping of chromosome aberrations from psychiatric patients. Mutation analyses of psychiatric patients with 4 candidate genes (NEDD4L, IMPA2, PACAP and GNAL) mapping within these loci have been unsuccessful, although an association was found with the IMPA2 gene in patients with schizophrenia. With these methods and findings, our understanding of the cause of psychiatric disorders associated with human chromosome 18 has improved and will advance, especially with emerging data from the human and rodent genome projects. (C) 2003 Canadian Medical Association. C1 Hosp Sick Children, Arthur & Sonia Labatts Brain Tumour Res Ctr, Toronto, ON M5G 1X8, Canada. RP Kamnasaran, D (reprint author), Hosp Sick Children, Arthur & Sonia Labatts Brain Tumour Res Ctr, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. 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Invest. Med.-Med. Clin. Exp. PD DEC PY 2003 VL 26 IS 6 BP 285 EP 302 PG 18 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 753QW UT WOS:000187242900004 PM 14690303 ER PT J AU Pescucci, C Meloni, I Bruttini, M Ariani, F Longo, I Mari, F Canitano, R Hayek, G Zappella, M Renieri, A AF Pescucci, C Meloni, I Bruttini, M Ariani, F Longo, I Mari, F Canitano, R Hayek, G Zappella, M Renieri, A TI Chromosome 2 deletion encompassing the MAP2 gene in a patient with autism and Rett-like features SO CLINICAL GENETICS LA English DT Article DE chromosome 2 deletion; MAP2 gene; preserved speech variant of Rett syndrome; Rett syndrome ID PROTEIN-2 MAP-2; EXPRESSION; BRAIN; ABNORMALITIES; DISINTEGRIN; NEOCORTEX; VARIANTS; MECP2 AB We present here a unique case of a 14-year-old female with autism and some features similar to Rett syndrome (RTT). Genetic analysis demonstrated a large deletion of chromosome 2q instead of a MECP2 mutation. Like a Rett patient, she is dyspraxic and shows frequent hand-washing stereotypic activities, hyperpnea, and bruxism. Like a preserved speech variant (PSV) of RTT, she is obese, able to speak in second and third persons, frequently echolalic, and has final normal head circumference and autistic behavior. In addition, she has dysmorphic features such as down-slanting palpebral fissures, low set ears without lobuli, bilateral flat feet, and bilateral syndactyly of the second and third toes, which do not belong to the Rett spectrum. She has a de novo chromosomal deletion in 2q34 of paternal origin. Gene content analysis of the deleted region showed the presence of 47 genes (14 putative and 33 known genes). This region contains some interesting genes such as ADAM23/MDC3, CREB1, KLF7, and MAP2. 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RI Mari, Francesca/E-7737-2012 OI Mari, Francesca/0000-0003-1992-1654 CR ARMSTRONG D, 1995, J NEUROPATH EXP NEUR, V54, P195, DOI 10.1097/00005072-199503000-00006 Armstrong DD, 2001, BRAIN DEV-JPN, V23, pS72, DOI 10.1016/S0387-7604(01)00332-1 BAUMAN ML, 1995, NEUROLOGY, V45, P1581 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Cal S, 2000, MOL BIOL CELL, V11, P1457 Colantuoni C, 2001, NEUROBIOL DIS, V8, P847, DOI 10.1006/nbdi.2001.0428 De Bona C, 2000, EUR J HUM GENET, V8, P325, DOI 10.1038/sj.ejhg.5200473 Guan ZH, 2002, CELL, V111, P483, DOI 10.1016/S0092-8674(02)01074-7 Johnston MV, 2003, EUR J PAEDIATR NEURO, V7, P105, DOI 10.1016/S1090-3798(03)00039-4 KALCHEVA N, 1995, P NATL ACAD SCI USA, V92, P10894, DOI 10.1073/pnas.92.24.10894 Kandel ER, 2001, SCIENCE, V294, P1030, DOI 10.1126/science.1067020 Kaufmann WE, 1997, EUR CHILD ADOLES PSY, V6, P75 KAUFMANN WE, 1995, NEUROPEDIATRICS, V26, P109, DOI 10.1055/s-2007-979738 Laub F, 2001, DEV BIOL, V233, P305, DOI 10.1006/dbio.2001.0243 Renieri A, 2003, J MOL MED-JMM, V81, P346, DOI 10.1007/s00109-003-0444-9 Sagane K, 1998, BIOCHEM J, V334, P93 SEABRIGH.M, 1971, LANCET, V2, P971 Shahbazian MD, 2002, AM J HUM GENET, V71, P1259, DOI 10.1086/345360 Shao YJ, 2002, AM J HUM GENET, V70, P1058, DOI 10.1086/339765 WENK GL, 1993, DEV BRAIN RES, V74, P67, DOI 10.1016/0165-3806(93)90084-N Zappella M, 2003, AM J MED GENET B, V119B, P102, DOI 10.1002/ajmg.b.10070 Zappella M, 2001, AM J MED GENET, V104, P14, DOI 10.1002/ajmg.10005 NR 22 TC 19 Z9 21 PU BLACKWELL MUNKSGAARD PI COPENHAGEN PA 35 NORRE SOGADE, PO BOX 2148, DK-1016 COPENHAGEN, DENMARK SN 0009-9163 J9 CLIN GENET JI Clin. Genet. PD DEC PY 2003 VL 64 IS 6 BP 497 EP 501 DI 10.1046/j.1399-0004.2003.00176.x PG 5 WC Genetics & Heredity SC Genetics & Heredity GA 745FV UT WOS:000186679400009 PM 14986829 ER PT J AU Pearce, BD AF Pearce, BD TI Modeling the role of infections in the etiology of mental illness SO CLINICAL NEUROSCIENCE RESEARCH LA English DT Review DE Boma disease virus (BDV); lymphocytic choriomeningitis virus (LCMV); interleukin-1; neurodevelopment; parvalburnin; hypothalamic-pituitary-adrenal axis ID BORNA-DISEASE-VIRUS; LYMPHOCYTIC CHORIOMENINGITIS VIRUS; CENTRAL-NERVOUS-SYSTEM; AUTISM SPECTRUM DISORDERS; INDIVIDUAL PATIENT DATA; HUMAN SERUM ANTIBODIES; OBSTETRIC COMPLICATIONS; VIRAL-INFECTION; PSYCHIATRIC-DISORDERS; ADULT SCHIZOPHRENIA AB There are numerous psychiatric disorders of unknown etiology that have been tentatively linked with microbial pathogens, particularly viruses. These include autism, major depression, bipolar disorder, schizophrenia, and chronic fatigue syndrome. These disorders likely have multiple contributing etiologies, and viruses or bacteria may be tapping into pathophysiological pathways that are shared by other environmental triggers. Animal models have been important for elucidating such pathways. Experiments in animals have demonstrated that infections can influence neurotransmission, cause neurobehavioral abnormalities, and produce developmental changes in the brain that become manifested latently, i.e. after sexual maturity. Animal models are helping to clarify the role of cytokines in sickness behavior, which could be relevant to major depression and chronic fatigue syndrome. Cytokines may also hold a central position in the neurodevelopmental origin for schizophrenia since there is emerging evidence that elevations in cytokines are associated with non-infectious obstetric complications (e.g. hypoxia) that have likewise been implicated as antecedents of schizophrenia. Nevertheless, infectious disease models in psychiatry have not come fully to fruition, and to realize their potential, they must continually incorporate new data from in vitro and human studies. (C) 2003 Published by Elsevier B.V. C1 Emory Univ, Sch Med, Dept Psychiat & Behav Sci, Atlanta, GA 30322 USA. RP Pearce, BD (reprint author), Emory Univ, Sch Med, Dept Psychiat & Behav Sci, 1639 Pierce Dr,WMB-4000, Atlanta, GA 30322 USA. 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Neurosci. Res. PD DEC PY 2003 VL 3 IS 4-5 BP 271 EP 282 DI 10.1016/S1566-2772(03)00098-7 PG 12 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 756JH UT WOS:000187461600008 ER PT J AU Naccari, C Ralat, JR Wong, S AF Naccari, C Ralat, JR Wong, S TI United States government unveils 10 year plan to fight autism SO CNS SPECTRUMS LA English DT News Item NR 0 TC 0 Z9 0 PU M B L COMMUNICATIONS, INC PI NEW YORK PA 333 HUDSON ST, 7TH FLOOR, NEW YORK, NY 10013 USA SN 1092-8529 J9 CNS SPECTRUMS JI CNS Spectr. PD DEC PY 2003 VL 8 IS 12 BP 880 EP 880 PG 1 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 895UW UT WOS:000226890300008 ER PT J AU Deisinger, JA AF Deisinger, JA TI Autism spectrum disorders: A transactional development perspective SO CONTEMPORARY PSYCHOLOGY-APA REVIEW OF BOOKS LA English DT Book Review C1 St Xavier Univ, Dept Psychol, Chicago, IL 60655 USA. RP Deisinger, JA (reprint author), St Xavier Univ, Dept Psychol, 3700 W 103rd St, Chicago, IL 60655 USA. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT BAKKEN JP, 2000, AUTISTIC SPECTRUM DI, P109 BURKHARDT S, 2001, AUTISTIC SPECTRUM DI, P211 Greenway C., 2000, ED PSYCHOL PRACTICE, V16, P469, DOI 10.1080/713666112 Herbert J. D., 2002, SCI REV MENTAL HLTH, V1, P23 HOOVER M, 2001, AUTISTIC SPECTRUM DI, P255 Kabot S, 2003, PROF PSYCHOL-RES PR, V34, P26, DOI 10.1037/0735-7028.34.1.26 LEASE CA, 2000, PSYCHOPATHOLOGY ADUL, P131 MYLES BS, 1999, ASPERGER SYNDROME DI Ramey CT, 1998, AM PSYCHOL, V53, P109, DOI 10.1037/0003-066X.53.2.109 Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 Walsh ME, 2002, COUNS PSYCHOL, V30, P682, DOI 10.1177/0011000002305002 Wetherby A. M., 2000, AUTISM SPECTRUM DISO Wicks-Nelson R., 2003, BEHAV DISORDERS CHIL NR 15 TC 0 Z9 0 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 0010-7549 J9 CONTEMP PSYCHOL JI Comtemp. Psychol. PD DEC PY 2003 VL 48 IS 6 BP 802 EP 804 PG 3 WC Psychology, Multidisciplinary SC Psychology GA 754ZY UT WOS:000187364400036 ER PT J AU Sherr, EH AF Sherr, EH TI The ARX story (epilepsy, mental retardation, autism, and cerebral malformations): one gene leads to many phenotypes SO CURRENT OPINION IN PEDIATRICS LA English DT Review DE ARX; cognitive impairment; epilepsy; cortical malformations; mental retardation ID ABSENT CORPUS-CALLOSUM; HOMEOBOX GENE; INFANTILE SPASMS; AMBIGUOUS GENITALIA; ABNORMAL GENITALIA; MUTATIONS; BRAIN; AGENESIS; HYPOTHERMIA; EXPRESSION AB Purpose of review Infantile spasms, mental retardation, autism, and dystonia represent disabling diseases for which little etiologic information is available. Mutations in the Aristaless related homeobox gene (ARX) have been found in patients with these conditions. This discovery provides important genetic information and may ultimately offer treatment options for these patients. Recent findings Recent work has demonstrated that mutations in ARX cause X-linked West syndrome, X-linked myoclonic epilepsy with spasticity and intellectual disability, Partington syndrome (mental retardation, ataxia, and dystonia), as well as nonsyndromic forms of mental retardation. Patients with these aforementioned diseases and ARX mutations were not reported to have brain imaging abnormalities. In contrast, mutations in ARX mutations have also been found in X-linked lissencephaly with abnormal genitalia, which typically includes severe brain malformations (lissencephaly, agenesis of the corpus callosum, and midbrain malformations), intractable seizures, and a severely shortened lifespan. ARX knockout mice manifest defects in overall neuroblast proliferation as well as selective abnormalities in gamma-aminobutyric acid-ergic interneuron migration. Consistent with these findings in mice, phenotype/genotype studies in humans suggest that truncating mutations cause X-linked lissencephaly with abnormal genitalia, and insertion/missense mutations result in epilepsy and mental retardation without cortical dysplasia. Summary Mutations in the homeobox gene, ARX, cause a diverse spectrum of disease that includes cognitive impairment, epilepsy, and in another group of patients severe cortical malformations. Although the precise prevalence of ARX mutations is unclear, ARX may rival Fragile X as a cause of mental retardation and epilepsy in males. C1 Univ Calif San Francisco, Dept Neurol, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. RP Sherr, EH (reprint author), Univ Calif San Francisco, Dept Neurol, 533 Parnassus Ave,Room U585c, San Francisco, CA 94143 USA. 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OPIN. PEDIATR. PD DEC PY 2003 VL 15 IS 6 BP 567 EP 571 DI 10.1097/00008480-200312000-00004 PG 5 WC Pediatrics SC Pediatrics GA 748XX UT WOS:000186887200004 PM 14631200 ER PT J AU Ziatas, K Durkin, K Pratt, C AF Ziatas, K Durkin, K Pratt, C TI Differences in assertive speech acts produced by children with autism, Asperger syndrome, specific language impairment, and normal development SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID MIND TASK-PERFORMANCE; MENTAL STATES; COMMUNICATIVE COMPETENCE; STORY CHARACTERS; SKILLS; ACQUISITION; INDIVIDUALS; DEFICITS; BELIEF; RELIABILITY AB The assertive speech acts of children with autism (n = 12) and Asperger syndrome (n = 12), individually matched to children with specific language impairment (SLI; n = 24) and children with normal development (n = 24) were studied in the context of gently structured conversation. These children also completed the false belief test of theory of mind. The children with autism used significantly lower proportions of assertions involving explanations and descriptions than the children with SLI or normal development and significantly lower proportions of assertions involving internal state and explanations than the children with Asperger syndrome. The children with autism used a higher proportion of assertions involving identifications than any other group. The assertions of the children with Asperger syndrome were generally not different than those of the children with SLI or normal development except for a higher proportion of assertions involving own internal state. Further analysis of the mental assertions revealed that the children with autism and Asperger syndrome predominantly referred to desire and made few references to thought and belief, whereas the children with SLI and those with normal development used a higher proportion of references to thought and belief. C1 Univ Western Australia, Dept Psychol, Crawley, WA 6907, Australia. La Trobe Univ, Bundoora, Vic, Australia. RP Ziatas, K (reprint author), Univ Western Australia, Dept Psychol, Mt Bay Rd, Crawley, WA 6907, Australia. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASTINGTON JW, 1990, NARRATIVE THOUGHT AND NARRATIVE LANGUAGE, P151 ASTINGTON JW, 1995, COGNITION EMOTION, V9, P151, DOI 10.1080/02699939508409006 Baron-Cohen S., 1993, UNDERSTANDING OTHER BARONCOHEN S, 1986, BRIT J DEV PSYCHOL, V4, P113 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 BARONCOHEN S, 1991, BRIT J DEV PSYCHOL, V9, P301 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BARTSCH K, 1995, CHILDRENS TALK MIND Bishop D. V. 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Arizona State Univ, Tempe, AZ 85287 USA. RP Perras, C (reprint author), Peel Dist Sch Board, Peel, ON, Canada. NR 0 TC 0 Z9 0 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 0013-1237 J9 EDUC TRAIN DEV DISAB JI Educ. Train. Dev. Disabil. PD DEC PY 2003 VL 38 IS 4 BP 355 EP 357 PG 3 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 808KZ UT WOS:000220569300001 ER PT J AU Yang, NK Schaller, JL Huang, TA Wang, MH Tsai, SF AF Yang, NK Schaller, JL Huang, TA Wang, MH Tsai, SF TI Enhancing appropriate social behaviors for children with autism in general education classrooms: An analysis of six cases SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article; Proceedings Paper CT 8th International Conference of the Council-for-Exceptional-Children-Division-on-Developmental-Disabilities (DDD) CY FEB 12-14, 2003 CL Kauai, HI SP Council Exceptional Children, Div Developmental Disabilities ID HIGH-FUNCTIONING CHILDREN; SKILLS; IMITATION; PRESCHOOLERS; DISORDERS; EMOTION; INTERVENTION; EXPRESSIONS; RECOGNITION; ADOLESCENTS AB This study compares generalized effects of a social-emotional skills training for girls and boys with autism in resource rooms on promoting positive social behaviors in general education classrooms in Taiwan. A single subject design was used to compare outcomes for 2 girls and 2 boys with autism in the experimental group with 2 boys with autism in the control group. Results of regression analyses revealed that all 4 participants in the experimental group significantly increased frequencies of positive social behaviors over time, while the two control participants did not demonstrate trends in the data. After adjusting for trends, the training had a medium effect size for 2 participants and a small effect size for 2 participants in the experimental group. This training was developed in response to educational services in Taiwan; suggestions are provided for development of interventions for children with autism that fit within general education classrooms. C1 Univ Texas, Dept Special Educ, Austin, TX 78712 USA. Min Tsu Elementary Sch, Kaohsiung, Taiwan. Poai Elementary Sch, Kaohsiung, Taiwan. RP Schaller, JL (reprint author), Univ Texas, Dept Special Educ, Austin, TX 78712 USA. CR Alberto P, 2002, APPL BEHAV ANAL TEAC Bauminger N, 2002, J AUTISM DEV DISORD, V32, P283, DOI 10.1023/A:1016378718278 BRAVERMAN M, 1989, J AUTISM DEV DISORD, V19, P301, DOI 10.1007/BF02211848 Brown L, 1990, MANUAL TEST NONVERBA Celani G, 1999, J AUTISM DEV DISORD, V29, P57, DOI 10.1023/A:1025970600181 CENTER BA, 1985, J SPEC EDUC, V19, P387 CHARMAN T, 2003, BIOL SCI, V358, P315 Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 CHEEK L, 1997, IMPROVING AGE APPROP Cohen J., 1988, STAT POWER ANAL BEHA, V2nd DAWSON G, 1990, J ABNORM CHILD PSYCH, V18, P335, DOI 10.1007/BF00916569 Dyck MJ, 2001, EUR CHILD ADOLES PSY, V10, P105 EDELSON MG, 1998, FOCUS AUTISM OTHER D, V13, P221 Field T, 2001, AUTISM, V5, P317, DOI 10.1177/1362361301005003008 Gena A, 1996, J APPL BEHAV ANAL, V29, P291, DOI 10.1901/jaba.1996.29-291 GOLDSTEIN H, 1992, J APPL BEHAV ANAL, V25, P289, DOI 10.1901/jaba.1992.25-289 Greenspan S. I., 2001, J DEV LEARNING DISOR, V5, P1 Hadwin J, 1996, DEV PSYCHOPATHOL, V8, P345 HANDLEMAN JS, 1983, CHILD FAMILY BEHAV T, V5, P73, DOI 10.1300/J019v05n01_05 HARING TG, 1989, J ASSOC PERS SEVERE, V14, P58 Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hobson RP, 1998, J AUTISM DEV DISORD, V28, P117, DOI 10.1023/A:1026088531558 HOBSON RP, 1986, J CHILD PSYCHOL PSYC, V27, P321, DOI 10.1111/j.1469-7610.1986.tb01836.x Hobson RP, 1999, J CHILD PSYCHOL PSYC, V40, P649, DOI 10.1111/1469-7610.00481 JAEDICKE S, 1994, DEV PSYCHOPATHOL, V6, P273, DOI 10.1017/S0954579400004582 Kanner L, 1943, NERV CHILD, V2, P217 Klin A, 1999, J AUTISM DEV DISORD, V29, P499, DOI 10.1023/A:1022299920240 Krantz PJ, 1998, J APPL BEHAV ANAL, V31, P191, DOI 10.1901/jaba.1998.31-191 MCGEE GG, 1991, J EARLY INTERVENTION, V15, P237 MCGEE GG, 1992, J APPL BEHAV ANAL, V25, P117, DOI 10.1901/jaba.1992.25-117 MESIBOV GB, 1984, J AUTISM DEV DISORD, V14, P395, DOI 10.1007/BF02409830 ODOM SL, 1986, J APPL BEHAV ANAL, V19, P59, DOI 10.1901/jaba.1986.19-59 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 POPLIN MS, 1988, J LEARN DISABIL, V21, P401 Roeyers H, 1996, J AUTISM DEV DISORD, V26, P303, DOI 10.1007/BF02172476 SNOW ME, 1987, J AM ACAD CHILD PSY, V26, P836, DOI 10.1097/00004583-198726060-00006 Stone WL, 1997, J ABNORM CHILD PSYCH, V25, P475, DOI 10.1023/A:1022685731726 Travis L, 2001, J AUTISM DEV DISORD, V31, P119, DOI 10.1023/A:1010705912731 Weiss MJ, 2001, BEHAV MODIF, V25, P785, DOI 10.1177/0145445501255007 WILLIAMS TI, 1989, J AUTISM DEV DISORD, V19, P143, DOI 10.1007/BF02212726 NR 40 TC 12 Z9 13 PU COUNCIL EXCEPTIONAL CHILDREN PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 0013-1237 J9 EDUC TRAIN DEV DISAB JI Educ. Train. Dev. Disabil. PD DEC PY 2003 VL 38 IS 4 BP 405 EP 416 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 808KZ UT WOS:000220569300007 ER PT J AU Perras, C Sharpe, V Perner, DE Zucker, SH AF Perras, C Sharpe, V Perner, DE Zucker, SH TI Research to practice in cognitive disabilities/mental retardation, autism, and related disabilities SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Editorial Material C1 Hood Coll, Frederick, MD 21701 USA. Bloomsburg Univ Penn, Bloomsburg, PA 17815 USA. Arizona State Univ, Tempe, AZ 85287 USA. NR 0 TC 0 Z9 0 PU COUNCIL EXCEPTIONAL CHILDREN, DIVISION EARLY CHILHOOD 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 DEC PY 2003 VL 38 IS 4 BP 355 EP 357 PG 3 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 753UP UT WOS:000187249200001 ER PT J AU Yang, NK Schaller, JL Huang, TA Wang, MH Tsai, SF AF Yang, NK Schaller, JL Huang, TA Wang, MH Tsai, SF TI Enhancing appropriate social behaviors for children with autism in general education classrooms: An analysis of six cases SO EDUCATION AND TRAINING IN MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES LA English DT Article; Proceedings Paper CT International Conference on Research to Practice in Cognitive Disabilities/Mental Retardation, Autism and Related Disabilities CY FEB 12-14, 2003 CL KAUAI, HAWAII SP Council Except Children Div Dev Disabilities ID HIGH-FUNCTIONING CHILDREN; PERVASIVE DEVELOPMENTAL DISORDER; FACIAL EXPRESSIONS; JOINT ATTENTION; SKILLS; IMITATION; PRESCHOOLERS; INTERVENTION; ADOLESCENTS; EMOTION AB This study compares generalized effects of a social-emotional skills training for girls and boys with autism in resource rooms on promoting positive social behaviors in general education classrooms in Taiwan. A single subject design was used to compare outcomes for 2 girls and 2 boys with autism in the experimental group with 2 boys with autism in the control group. Results of regression analyses revealed that all 4 participants in the experimental group significantly increased frequencies of positive social behaviors over time, while the two control participants did not demonstrate trends in the data. After adjusting for trends, the training had a medium effect size for 2 participants and a small effect size for 2 participants in the experimental group. This training was developed in response to educational services in Taiwan; suggestions are provided for development of interventions for children with autism that fit within general education classrooms. C1 Univ Texas, Dept Special Educ, Austin, TX 78712 USA. Min Tsu Elementary Sch, Kaohsiung, Taiwan. Poai Elementary Sch, Kaohsiung, Taiwan. RP Schaller, JL (reprint author), Univ Texas, Dept Special Educ, Austin, TX 78712 USA. CR Alberto P, 2002, APPL BEHAV ANAL TEAC Bauminger N, 2002, J AUTISM DEV DISORD, V32, P283, DOI 10.1023/A:1016378718278 BRAVERMAN M, 1989, J AUTISM DEV DISORD, V19, P301, DOI 10.1007/BF02211848 Brown L, 1990, MANUAL TEST NONVERBA Celani G, 1999, J AUTISM DEV DISORD, V29, P57, DOI 10.1023/A:1025970600181 CENTER BA, 1985, J SPEC EDUC, V19, P387 Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 Charman T, 2003, PHILOS T ROY SOC B, V358, P315, DOI 10.1098/rstb.2002.1199 CHEEK L, 1997, IMPROVING AGE APPROP Cohen J., 1988, STAT POWER ANAL BEHA, V2nd DAWSON G, 1990, J ABNORM CHILD PSYCH, V18, P335, DOI 10.1007/BF00916569 Dyck MJ, 2001, EUR CHILD ADOLES PSY, V10, P105 EDELSON MG, 1998, FOCUS AUTISM OTHER D, V13, P221 Field T, 2001, AUTISM, V5, P317, DOI 10.1177/1362361301005003008 Gena A, 1996, J APPL BEHAV ANAL, V29, P291, DOI 10.1901/jaba.1996.29-291 GOLDSTEIN H, 1992, J APPL BEHAV ANAL, V25, P289, DOI 10.1901/jaba.1992.25-289 Greenspan S. I., 2001, J DEV LEARNING DISOR, V5, P1 Hadwin J, 1996, DEV PSYCHOPATHOL, V8, P345 HANDLEMAN JS, 1983, CHILD FAMILY BEHAV T, V5, P73, DOI 10.1300/J019v05n01_05 HARING TG, 1989, J ASSOC PERS SEVERE, V14, P58 Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hobson RP, 1998, J AUTISM DEV DISORD, V28, P117, DOI 10.1023/A:1026088531558 HOBSON RP, 1986, J CHILD PSYCHOL PSYC, V27, P321, DOI 10.1111/j.1469-7610.1986.tb01836.x Hobson RP, 1999, J CHILD PSYCHOL PSYC, V40, P649, DOI 10.1111/1469-7610.00481 Howlin P., 1999, TEACHING CHILDREN AU JAEDICKE S, 1994, DEV PSYCHOPATHOL, V6, P273, DOI 10.1017/S0954579400004582 Kanner L, 1943, NERV CHILD, V2, P217 Kazdin A. E., 1982, SINGLE CASE RES DESI Klin A, 1999, J AUTISM DEV DISORD, V29, P499, DOI 10.1023/A:1022299920240 Krantz PJ, 1998, J APPL BEHAV ANAL, V31, P191, DOI 10.1901/jaba.1998.31-191 Kromrey JD, 1996, J EXP EDUC, V65, P73 Loveland KA, 2001, J AUTISM DEV DISORD, V31, P367, DOI 10.1023/A:1010608518060 MCGEE GG, 1991, J EARLY INTERVENTION, V15, P237 MCGEE GG, 1992, J APPL BEHAV ANAL, V25, P117, DOI 10.1901/jaba.1992.25-117 MESIBOV GB, 1984, J AUTISM DEV DISORD, V14, P395, DOI 10.1007/BF02409830 Njardvik U, 1999, J AUTISM DEV DISORD, V29, P287, DOI 10.1023/A:1022107318500 ODOM SL, 1986, J APPL BEHAV ANAL, V19, P59, DOI 10.1901/jaba.1986.19-59 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 POPLIN MS, 1988, J LEARN DISABIL, V21, P401 Roeyers H, 1996, J AUTISM DEV DISORD, V26, P303, DOI 10.1007/BF02172476 SNOW ME, 1987, J AM ACAD CHILD PSY, V26, P836, DOI 10.1097/00004583-198726060-00006 Stevenson H., 1992, LEARNING GAP WHY OUR Stone WL, 1997, J ABNORM CHILD PSYCH, V25, P475, DOI 10.1023/A:1022685731726 Travis L, 2001, J AUTISM DEV DISORD, V31, P119, DOI 10.1023/A:1010705912731 Weiss MJ, 2001, BEHAV MODIF, V25, P785, DOI 10.1177/0145445501255007 WHALEN C, 2001, THESIS U CALFORNIA S WILLIAMS TI, 1989, J AUTISM DEV DISORD, V19, P143, DOI 10.1007/BF02212726 YANG NK, 2003, SOCIAL EMOTIONAL SKI YIRMIYA N, 1989, J CHILD PSYCHOL PSYC, V30, P725, DOI 10.1111/j.1469-7610.1989.tb00785.x YIRMIYA N, 1994, DEV PSYCHOPATHOL, V6, P263, DOI 10.1017/S0954579400004570 YIRMIYA N, 1992, CHILD DEV, V63, P150, DOI 10.1111/j.1467-8624.1992.tb03603.x NR 51 TC 12 Z9 13 PU COUNCIL EXCEPTIONAL CHILDREN, DIVISION EARLY CHILHOOD 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 DEC PY 2003 VL 38 IS 4 BP 405 EP 416 PG 12 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 753UP UT WOS:000187249200007 ER PT J AU Heerey, EA Keltner, D Capps, LM AF Heerey, Erin A. Keltner, Dacher Capps, Lisa M. TI Making Sense of Self-Conscious Emotion: Linking Theory of Mind and Emotion in Children With Autism SO EMOTION LA English DT Article AB Self-conscious emotions such as embarrassment and shame are associated with 2 aspects of theory of mind (ToM): (a) the ability to understand that behavior has social consequences in the eyes of others and (b) an understanding of social norms violations. The present study aimed to link ToM with the recognition of self-conscious emotion. Children with and without autism identified facial expressions of self-conscious and non-self-conscious emotions from photographs. ToM was also measured. Children with autism performed more poorly than comparison children at identifying self-conscious emotions, though they did not differ in the recognition of non-self-conscious emotions. When ToM ability was statistically controlled, group differences in the recognition of self-conscious emotion disappeared. Discussion focused on the links between ToM and self-conscious emotion. C1 [Heerey, Erin A.; Keltner, Dacher; Capps, Lisa M.] Univ Calif Berkeley, Dept Psychol, Berkeley, CA 94720 USA. RP Heerey, EA (reprint author), Univ Calif Berkeley, Dept Psychol, 3210 Tolman Hall,Room 1650, Berkeley, CA 94720 USA. 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M., 1999, ANN M AM PSYCH SOC D Tager-Flusberg H, 1999, INT REV PSYCHIATR, V11, P325, DOI 10.1080/09540269974203 Tangney JP, 1996, J PERS SOC PSYCHOL, V70, P1256, DOI 10.1037/0022-3514.70.6.1256 Wallbott Harald G., 1995, P465 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd NR 31 TC 51 Z9 52 PU AMER PSYCHOLOGICAL ASSOC PI WASHINGTON PA 750 FIRST ST NE, WASHINGTON, DC 20002-4242 USA SN 1528-3542 J9 EMOTION JI Emotion PD DEC PY 2003 VL 3 IS 4 BP 394 EP 400 DI 10.1037/1528-3542.3.4.394 PG 7 WC Psychology, Experimental SC Psychology GA V21RS UT WOS:000208225300006 PM 14674831 ER PT J AU Waage-Baudet, H Lauder, JM Dehart, DB Kluckman, K Hiller, S Tint, GS Sulik, KK AF Waage-Baudet, H Lauder, JM Dehart, DB Kluckman, K Hiller, S Tint, GS Sulik, KK TI Abnormal serotonergic development in a mouse model for the Smith-Lemli-Opitz syndrome: implications for autism SO INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE LA English DT Article ID DEFECTIVE CHOLESTEROL-BIOSYNTHESIS; MONOAMINE-OXIDASE ACTIVITY; COMMISSURAL AXON GUIDANCE; DEVELOPING RAT-BRAIN; SONIC-HEDGEHOG; MEMBRANE CHOLESTEROL; INFANTILE-AUTISM; PRENATAL DEVELOPMENT; SPINAL-CORD; NEURONS AB The Smith-Lemli-Opitz syndrome (SLOS) is a malformation/mental retardation syndrome resulting from an inborn error in 3beta-hydroxysteroid Delta(7)-reductase (DHCR7), the terminal enzyme required for cholesterol biosynthesis. Using a targeting strategy designed to virtually eliminate Dhcr7 activity, we have created a SLOS mouse model that exhibits commissural deficiencies, hippocampal abnormalities, and hypermorphic development of serotonin (5-HT) neurons. The latter is of particular interest with respect to current evidence that serotonin plays a significant role in autism spectrum disorders and the recent clinical observation that 50% of SLOS patients present with autistic behavior. Immunohistochemical analyses have revealed a 306% increase in the area of 5-HT immunoreactivity (5-HT IR) in the hindbrains of mutant (Dhcr7(-/-)) mice as compared to age-matched wild type animals. Amount of 5-HT IR was measured as total area of IR per histological section. Additionally, a regional increase as high as 15-fold was observed for the most lateral sagittal hindbrain sections. In Dhcr7(-/-) mice, an expansion of 5-HT IR into the ventricular zone and floor plate region was observed. In addition, the rostral and caudal raphe groups exhibited a radial expansion in Dhcr7(-/-) mice, with 5-HT IR cells present in locations not seen in wild type mice. This increase in 5-HT IR appears to represent an increase in total number of 5-HT neurons and fibers. These observations may help explain the behavioral phenotype seen in SLOS, and provide clues for future therapeutic interventions that utilize pharmacological modulation of the serotonergic system. (C) 2003 ISDN. Published by Elsevier Ltd. All rights reserved. C1 Univ N Carolina, Sch Med, Dept Cell & Dev Biol, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Cell & Dev Pathol, Chapel Hill, NC 27599 USA. Univ N Carolina, Bowles Ctr Alcohol Studies, Chapel Hill, NC 27599 USA. VA Hosp E, Orange, NJ USA. RP Sulik, KK (reprint author), Univ N Carolina, Sch Med, Dept Cell & Dev Biol, 3019A Thurston Bowles Bldg,CB 7178, Chapel Hill, NC 27599 USA. 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J. Dev. Neurosci. PD DEC PY 2003 VL 21 IS 8 BP 451 EP 459 DI 10.1016/j.ijdevneu.2003.09.002 PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 761EJ UT WOS:000187887300005 PM 14659996 ER PT J AU Boucher, J AF Boucher, J TI Language development in autism SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY LA English DT Article; Proceedings Paper CT 8th International Congress of Paediatric Otorhinolaryngology CY SEP 11-14, 2002 CL OXFORD, ENGLAND DE communication; language profiles; psychological theories ID CHILDREN; DISORDERS; COMMUNICATION; DISCOURSE AB In this short review article, a summary of the behavioural impairments most commonly associated with the spectrum of autism-related disorders is presented, with a slightly amplified account of the defining communication impairment. The patterns of language ability and disability which typically occur in some forms of autism are then outlined, followed by a short section on possible cognitive, or psychological, explanations of these patterns. In particular, the hypothesis that defective socio-affective and socio-cognitive ('theory of mind') causes language impairments, and the hypothesis that temporal processing deficits cause these impairments, are outlined and briefly discussed. An extensive list of references is included, to support and amplify the summary data included in the review. (C) 2003 British Association for Paediatric Otorhinolaryngology. Published by Elsevier Ireland Ltd. All rights reserved. C1 Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. RP Boucher, J (reprint author), Univ Warwick, Dept Psychol, Coventry CV4 7AL, W Midlands, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BALTAXE CAM, 1992, J AUTISM DEV DISORD, V22, P1, DOI 10.1007/BF01046399 BOUCHER J, 2001, TIME MEMORY, P110 BROWN M, 1999, BR J OCCUPATIONAL TH, V62, P12 Carpenter M, 2002, J AUTISM DEV DISORD, V32, P91, DOI 10.1023/A:1014836521114 COHEN D, 1990, HDB AUTISM PERVASIVE, P195 DOBBINSON S, 2000, THESIS U SHEFFIELD DOBBINSON S, 1998, J COMMUN DISORD, V31, P1 ESKES GA, 1990, J AUTISM DEV DISORD, V20, P61, DOI 10.1007/BF02206857 FINE J, 1991, J CHILD PSYCHOL PSYC, V32, P771, DOI 10.1111/j.1469-7610.1991.tb01901.x FINE J, 1994, J AUTISM DEV DISORD, V24, P315, DOI 10.1007/BF02172230 GORDON AG, 1989, J AUTISM DEV DISORD, V19, P470, DOI 10.1007/BF02212945 Green D, 2002, J CHILD PSYCHOL PSYC, V43, P655, DOI 10.1111/1469-7610.00054 Happe F., 1994, AUTISM INTRO PSYCHOL Hobson R. 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R., 2000, ASPERGER SYNDROME, P25 Werner H., 1984, SYMBOL FORMATION World Health Organization, 1993, INT CLASS DIS NR 41 TC 18 Z9 18 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-5876 J9 INT J PEDIATR OTORHI JI Int. J. Pediatr. Otorhinolaryngol. PD DEC PY 2003 VL 67 SU 1 BP S159 EP S163 DI 10.1016/j.ijporl.2003.08.016 PG 5 WC Otorhinolaryngology; Pediatrics SC Otorhinolaryngology; Pediatrics GA 760BD UT WOS:000187789900023 PM 14662187 ER PT J AU Ruben, RJ AF Ruben, RJ TI Five children - vignettes of language disorders SO INTERNATIONAL JOURNAL OF PEDIATRIC OTORHINOLARYNGOLOGY LA English DT Article; Proceedings Paper CT 8th International Congress of Paediatric Otorhinolaryngology CY SEP 11-14, 2002 CL OXFORD, ENGLAND DE language delay; language abnormality; autism; pervasive developmental delay; social depravation; cochlear implant; otitis media with effusion; delayed diagnosis; language evaluation AB The pediatric otolaryngologist cares for children who have abnormal language as a primary or secondary deficiency. Five children, each with a different form of language disorder, are presented. These are children with specific language impairment (SLI) expressive, pervasive developmental delay (autism), expressive language delay associated with severe to profound hearing loss early in life, language delay secondary to a moderate to severe hearing toss diagnosed late and not cared for, and language delay secondary delay secondary to social deprivation and otitis media with effusion. (C) 2003 British Association for Paediatric Otorhinolaryngology. Published by Elsevier Ireland Ltd. All rights reserved. C1 Montefiore Med Ctr, Albert Einstein Coll Med, Dept Otolaryngol, Bronx, NY 10467 USA. RP Ruben, RJ (reprint author), Montefiore Med Ctr, Albert Einstein Coll Med, Dept Otolaryngol, 3400 Bainbridge Ave,3rd Floor, Bronx, NY 10467 USA. CR Coplan J., 1993, EARLY LANGUAGE MILES Coplan J, 1993, J Pediatr Health Care, V7, P212, DOI 10.1016/0891-5245(93)90006-4 RUBEN RJ, 1991, ARCH OTOLARYNGOL, V117, P1021 RUBEN RJ, 1982, LARYNGOSCOPE, V92, P38 NR 4 TC 1 Z9 1 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0165-5876 J9 INT J PEDIATR OTORHI JI Int. J. Pediatr. Otorhinolaryngol. PD DEC PY 2003 VL 67 SU 1 BP S125 EP S130 DI 10.1016/j.ijport.2003.08.010 PG 6 WC Otorhinolaryngology; Pediatrics SC Otorhinolaryngology; Pediatrics GA 760BD UT WOS:000187789900019 PM 14662183 ER PT J AU Bruneau, N Bonnet-Brilhault, F Gomot, M Adrien, JL Barthelemy, C AF Bruneau, N Bonnet-Brilhault, F Gomot, M Adrien, JL Barthelemy, C TI Cortical auditory processing and communication in children with autism: electrophysiological/behavioral relations SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Article DE autism; children; late auditory evoked potentials; N1c wave; T complex; temporal asymmetry; verbal and nonverbal communication ID TEMPORAL-LOBE DYSFUNCTION; CEREBRAL-BLOOD-FLOW; POTENTIALS N1 WAVE; EVOKED-POTENTIALS; BRAIN-STEM; CHILDHOOD AUTISM; SYSTEM ACTIVITY; DIPOLE MODEL; CORTEX; SPEECH AB The purpose of the present study was to investigate the relations between late auditory evoked potentials (AEPs) recorded at temporal sites (the N1c wave or Tb) and verbal and non-verbal abilities in children with autism. The study was performed in 26 mentally retarded children with autism (AUT) aged 4-8 years (mean age +/- S.E.M. = 71 +/- 2 months; mean verbal and non-verbal developmental quotient +/- S.E.M. = 36 +/- 4 and 48 +/- 3). The stimuli used were 750 Hz tone bursts of 200 ms duration delivered binaurally at different intensity levels (50, 60, 70, 80 dB SPL) with 3-5 s interstimulus intervals. Temporal AEPs were first compared to those of a group of 16 normal children (NOR) in the same age range (mean age +/- S.E.M. = 69 +/- 3 months). We then focused on the AUT group and considered relations between temporal AEPs and the severity of disorders of verbal and non-verbal communication assessed using a behavior rating scale. AEPs recorded on left and right temporal sites were of smaller amplitude in the AUT group than in the NOR group. Increasing intensity-related amplitude was observed on both sides in NOR and only on the right side in AUT. The lack of intensity effect on the left side resulted in a particular pattern of asymmetry at the highest level of intensity (80 dB SPL) with greater N1c amplitude on the right than on the left side (the reverse was found in the NOR group). Electro-clinical correlations indicated that the greater the amplitude of the right temporal N1c responses, the higher the verbal and non-verbal communication abilities. This suggests a developmental reorganization of left-right hemisphere functions in autism, with preferential activation of the right hemisphere for functions usually allocated to the left hemisphere, particularly those involving the secondary auditory areas situated on the lateral surface of the superior temporal gyrus where the N1c/Tb wave is generated. (C) 2003 Elsevier B.V. All rights reserved. C1 Univ Tours, Serv Explorat Fonctionnelles & Neurophysiol & Ped, F-37044 Tours, France. Univ Paris 05, Inst Psychol, F-75270 Paris 06, France. RP Bruneau, N (reprint author), Univ Tours, Serv Explorat Fonctionnelles & Neurophysiol & Ped, 2,Bd Tonnelle, F-37044 Tours, France. 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J. Psychophysiol. PD DEC PY 2003 VL 51 IS 1 BP 17 EP 25 DI 10.1016/S0167-8760(03)00149-1 PG 9 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 759LP UT WOS:000187739400003 PM 14629919 ER PT J AU Furnham, A Buck, C AF Furnham, A Buck, C TI A comparison of lay-beliefs about autism and obsessive-compulsive disorder SO INTERNATIONAL JOURNAL OF SOCIAL PSYCHIATRY LA English DT Article ID ATTRIBUTIONS; PERSPECTIVES AB The purpose of the two studies was to compare lay beliefs regarding the aetiology and treatment of autism (study 1) and obsessive-compulsive disorder (OCD) (study 2). It was hypothesised that beliefs about autism would be based primarily on a biomedical theory while beliefs regarding OCD primarily on psychological notions of cause and cure. Parents' interviews were conducted in study 1 and revealed that, as hypothesised, parents hold predominantly biomedical views about autism. Participants (n = 92) completed both questionnaires that involved rating a range of theories of aetiology and treatment approaches for each disorder. Statistical analysis confirmed that lay beliefs about autism were primarily biomedical and beliefs about OCD were primarily psychological. Multiple regression analyses indicated that a range of individual difference factors (religiousness, interest in mental illness, age and knowledge of autism) predicted beliefs about the importance of some of the five factors derived from factor analysis of belief statements. The relevance of investigating lay beliefs of aetiology and treatment of psychiatric disorders for clinical practice is also highlighted. C1 UCL, Dept Psychol, London WC1 0AP, England. RP Furnham, A (reprint author), UCL, Dept Psychol, 26 Bedford Way, London WC1 0AP, England. EM a.furnham@ucl.ac.uk CR Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Benveniste J, 1999, J Health Psychol, V4, P59, DOI 10.1177/135910539900400110 Bettleheim B., 1967, EMPTY FORTRESS CATTELL RB, 1966, MULTIVAR BEHAV RES, V1, P245, DOI 10.1207/s15327906mbr0102_10 Fombonne E, 1999, J AUTISM DEV DISORD, V29, P349, DOI 10.1023/A:1022123822135 FURNHAM A, 1990, J CLIN PSYCHOL, V46, P878, DOI 10.1002/1097-4679(199011)46:6<878::AID-JCLP2270460630>3.0.CO;2-T Furnham A, 1996, SOC SCI MED, V43, P29, DOI 10.1016/0277-9536(95)00330-4 Furnham A, 1997, J CLIN PSYCHOL, V53, P595 Furnham A, 1997, J GENET PSYCHOL, V158, P315 Furnham A., 1988, LAY THEORIES FURNHAM A, 1992, BRIT J PSYCHIAT, V161, P201, DOI 10.1192/bjp.161.2.201 Gray D E, 1995, Med Anthropol, V16, P99 Helps S, 1999, AUTISM, V3, P287, DOI 10.1177/1362361399003003006 JENIKE M, 1986, OBSESSIVE COMPULSIVE Kirk L., 1999, J RATION-EMOT COGN-B, V17, P137, DOI [10.1023/A:1023044729442, DOI 10.1023/A:1023044729442] Klein DF, 1981, ANXIETY NEW RES CHAN LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Meyer V., 1970, BEHAV THERAPY CLIN P OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 RACHMAN S, 1980, OBESSIONS COMPULSION RAUCH SL, 1993, PSYCHOSOMATICS, V34, P20 Furnham A, 1988, Int J Soc Psychiatry, V34, P212, DOI 10.1177/002076408803400307 RIPPERE V, 1977, BEHAV RES THER, V15, P465, DOI 10.1016/0005-7967(77)90002-X RIPPERE V, 1981, BEHAV RES THER, V19, P169, DOI 10.1016/0005-7967(81)90041-3 RUTTER M, 1993, NATURE NURTURE PSYCH, P269, DOI 10.1037/10131-013 Sanua V D, 1986, Int J Soc Psychiatry, V32, P16, DOI 10.1177/002076408603200203 STONE WL, 1987, J PEDIATR PSYCHOL, V12, P615, DOI 10.1093/jpepsy/12.4.615 WELCH M, 1989, PRE PERINATAL PSYCHO, V3, P319 NR 29 TC 24 Z9 24 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0020-7640 J9 INT J SOC PSYCHIATR JI Int. J. Soc. Psychiatr. PD DEC PY 2003 VL 49 IS 4 BP 287 EP 307 DI 10.1177/0020764003494006 PG 21 WC Psychiatry SC Psychiatry GA 764KQ UT WOS:000188206400006 PM 14727695 ER PT J AU Ahearn, WH Clark, KM Gardenier, NC Chung, BI Dube, W AF Ahearn, WH Clark, KM Gardenier, NC Chung, BI Dube, W TI Persistence of stereotypic behavior: Examining the effects of external reinforcers SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article; Proceedings Paper CT 28th Annual Meeting of the Association-for-Behavior-Analysis CY MAY, 2002 CL TORONTO, CANADA SP Assoc Behav Anal DE behavioral momentum; automatic reinforcement; resistance to change; stereotypy; autism ID SELF-INJURIOUS-BEHAVIOR; DEVELOPMENTAL-DISABILITIES; AUTOMATIC REINFORCEMENT; INTRINSIC MOTIVATION; MOMENTUM; INDIVIDUALS; RESISTANCE; REWARDS; PICA; LAW AB Basic research has shown that behavioral persistence is often positively related to rate of reinforcement. This relation, expressed in the metaphor of behavioral momentum, has potentially important implications for clinical application. The current study examined one prediction of the momentum metaphor for automatically reinforced behavior. Participants were 3 children who had been diagnosed with an autism spectrum disorder and who engaged in stereotypic behavior maintained by automatic reinforcement. Results suggested that stereotypic behavior was more resistant to disruption following periods of access to preferred stimuli delivered on a variable-time schedule than following periods without access to preferred stimuli. The implications of these findings for the treatment of automatically reinforced behavior are discussed. C1 New England Ctr Children, Southborough, MA 01772 USA. Yonsei Univ, Seoul 120749, South Korea. Univ Massachusetts, Sch Med, EK Shriver Ctr, Amherst, MA 01003 USA. RP Ahearn, WH (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. 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L., 1996, J BEHAV ANAL THERAPY, V1, P36 COWDERY GE, 1990, J APPL BEHAV ANAL, V23, P497, DOI 10.1901/jaba.1990.23-497 Deci EL, 1999, PSYCHOL BULL, V125, P627, DOI 10.1037/0033-2909.125.6.627 Dube WV, 2001, J EXP ANAL BEHAV, V75, P15, DOI 10.1901/jeab.2001.75-15 Dube WV, 2003, AM J MENT RETARD, V108, P134, DOI 10.1352/0895-8017(2003)108<0134:RREABM>2.0.CO;2 EMERSON E, 1992, RES DEV DISABIL, V13, P335, DOI 10.1016/0891-4222(92)90010-4 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Fisher WW, 1997, J APPL BEHAV ANAL, V30, P387, DOI 10.1901/jaba.1997.30-387 Grimes JA, 2001, J EXP ANAL BEHAV, V76, P179, DOI 10.1901/jeab.2001.76-179 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P215, DOI 10.1901/jaba.1994.27-215 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Mace FC, 2000, BEHAV BRAIN SCI, V23, P105, DOI 10.1017/S0140525X00372405 MACE FC, 1990, J EXP ANAL BEHAV, V54, P163, DOI 10.1901/jeab.1990.54-163 MCDOWELL JJ, 1982, AM PSYCHOL, V37, P771, DOI 10.1037/0003-066X.37.7.771 NEVIN JA, 1992, J EXP ANAL BEHAV, V57, P301, DOI 10.1901/jeab.1992.57-301 NEVIN JA, 1997, HDB LEARNING BEHAV T, P230 Nevin JA, 2000, BEHAV BRAIN SCI, V23, P73, DOI 10.1017/S0140525X00002405 NEVIN JA, 1990, J EXP ANAL BEHAV, V53, P359, DOI 10.1901/jeab.1990.53-359 Piazza CC, 2000, J APPL BEHAV ANAL, V33, P13, DOI 10.1901/jaba.2000.33-13 Piazza CC, 1998, J APPL BEHAV ANAL, V31, P165, DOI 10.1901/jaba.1998.31-165 Piazza CC, 2002, J APPL BEHAV ANAL, V35, P233, DOI 10.1901/jaba.2002.35-233 Plaud JJ, 1996, BEHAV MODIF, V20, P183, DOI 10.1177/01454455960202003 Reitman D, 1998, J BEHAV THER EXP PSY, V29, P101, DOI 10.1016/S0005-7916(98)00011-1 Romanczyk R. 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PD WIN PY 2003 VL 36 IS 4 BP 439 EP 448 DI 10.1901/jaba.2003.36-439 PG 10 WC Psychology, Clinical SC Psychology GA 763LY UT WOS:000188088500003 PM 14768664 ER PT J AU Carr, D AF Carr, D TI Effects of exemplar training in exclusion responding on auditory-visual discrimination tasks with children with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; exclusion-based learning; multiple-exemplar training; generalization ID SEVERE MENTAL-RETARDATION; BEHAVIOR ANALYSIS; CONDITIONAL-DISCRIMINATION; STIMULUS EQUIVALENCE; SPOKEN WORDS; LANGUAGE; INDIVIDUALS; COGNITION AB In Experiment I with 7 autistic children (3 to 6 years old), auditory-visual exclusion was tested with four unknown word-item pairs for each child. One child demonstrated exclusion and positive learning outcomes unequivocally with the four auditory-visual relations. Three children demonstrated exclusion, though inconsistently, and failed to demonstrate positive learning outcomes. The remaining 3 children failed to demonstrate exclusion; therefore, the learning outcome test was omitted. The 6 children who failed to demonstrate exclusion or positive learning outcomes participated in the second experiment. In Experiment 2, nonreinforced exclusion trials with four new unknown word-item pairs were included in trial blocks that also contained reinforced exclusion trials with the unknown exemplars from Experiment 1. Five children demonstrated exclusion with the new word-item pairs, and 4 of these demonstrated positive learning outcomes in further tests. One child demonstrated some limited but inconsistent improvement in exclusion and was not tested for learning outcomes. The data suggest that contemporaneous presentation of multiple examples of reinforced exclusion facilitated nonreinforced exclusion performances and that the resulting reduction in errors was critical in producing accurate learning outcomes with the new word-item discriminations. C1 Univ Wales Coll Med, Cardiff CF4 4XN, S Glam, Wales. RP Carr, D (reprint author), ARU, Welsh Ctr Learning Disabil, Meridian Court,North Rd, Cardiff CF14 3BG, S Glam, Wales. EM carrd1@cf.ac.uk RI turton, miranda/F-4682-2011 CR Adamson L. B., 1997, COMMUNICATION LANGUA, P75 Barnes D, 1996, J EXP ANAL BEHAV, V65, P264, DOI 10.1901/jeab.1996.65-264 BARNES D, 1996, PSYCHOL REC, V46, P236 BARNES D, 1991, PSYCHOL REC, V41, P19 BARNES D, 1994, PSYCHOL REC, V44, P91 Carey Susan, 1978, LINGUISTIC THEORY PS, P264 Carr D, 2000, J INTELLECT DEV DIS, V25, P181, DOI 10.1080/13668250020006295 de Rose J. C., 1992, UNDERSTANDING VERBAL, P69 deRose JC, 1996, J APPL BEHAV ANAL, V29, P451, DOI 10.1901/jaba.1996.29-451 DEVANY JM, 1986, J EXP ANAL BEHAV, V46, P243, DOI 10.1901/jeab.1986.46-243 DIXON LS, 1977, J EXP ANAL BEHAV, V27, P433, DOI 10.1901/jeab.1977.27-433 DOLLAGHAN CA, 1987, J SPEECH HEAR DISORD, V52, P218 GOLINKOFF RM, 1992, DEV PSYCHOL, V28, P99, DOI 10.1037/0012-1649.28.1.99 Hayes S. 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PD WIN PY 2003 VL 36 IS 4 BP 507 EP 524 DI 10.1901/jaba.2003.36-507 PG 18 WC Psychology, Clinical SC Psychology GA 763LY UT WOS:000188088500008 PM 14768669 ER PT J AU Seltzer, MM Krauss, MW Shattuck, PT Orsmond, G Swe, A Lord, C AF Seltzer, MM Krauss, MW Shattuck, PT Orsmond, G Swe, A Lord, C TI The symptoms of autism spectrum disorders in adolescence and adulthood SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; ADI-R; symptoms; life course development ID PSYCHIATRIC INTERVIEWING TECHNIQUES; ELICITING FACTUAL INFORMATION; RECEPTIVE LANGUAGE DISORDER; FOLLOW-UP; DIAGNOSTIC INTERVIEW; LIFE; CHILDREN; OUTCOMES; INDIVIDUALS AB This article describes the symptoms of autism spectrum disorders (ASD) manifested by 405 individuals between the ages of 10 and 53 years, all of whom had an ASD diagnosis. Data were collected using the Autism Diagnostic Interview -Revised (ADI-R) to assess the pattern of autism symptoms in adolescence and adulthood. Findings include that although virtually all sample members met the criteria for Autistic Disorder earlier in their childhood, just over half (54.8%) would have met autism criteria if current scores were used to complete the diagnostic algorithm; that adolescents were more likely to improve in the Reciprocal Social Interaction domain than the adults, whereas the adults were more likely to improve in the Restricted, Repetitive Behaviors and Interests domain, and there were no differences in severity of symptoms between cohorts in the Communication domain; and that individual symptoms showed unique trajectories, with greatest symptom abatement between lifetime and current ADI-R ratings for speaking in at least three-word phrases and the least symptom improvement for having friendships. Findings were interpreted in the context of life course development, reformulations of diagnostic criteria, and changing service contexts for individuals with autism spectrum disorders. 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W, 1992, QUESTIONS QUESTIONS, P65 Persson B, 2000, J AUTISM DEV DISORD, V30, P61, DOI 10.1023/A:1005464128544 Piven J, 1996, J AM ACAD CHILD PSY, V35, P523, DOI 10.1097/00004583-199604000-00019 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 RUMSEY JM, 1985, J AM ACAD CHILD PSY, V24, P465, DOI 10.1016/S0002-7138(09)60566-5 RUTTER M, 1981, BRIT J PSYCHIAT, V138, P456, DOI 10.1192/bjp.138.6.456 Schroeder SR, 1996, J AUTISM DEV DISORD, V26, P251, DOI 10.1007/BF02172022 Schultz SK, 1997, SCHIZOPHR RES, V23, P15, DOI 10.1016/S0920-9964(96)00087-4 SPERRY VW, 2001, FRAGILE SUCCESS 10 A Tantam D., 2000, ASPERGER SYNDROME, P367 Travis LL, 1998, MENT RETARD DEV D R, V4, P65, DOI 10.1002/(SICI)1098-2779(1998)4:2<65::AID-MRDD2>3.0.CO;2-W VOLKMAR FR, 1992, J AUTISM DEV DISORD, V22, P483, DOI 10.1007/BF01046323 Wing L, 1993, Eur Child Adolesc Psychiatry, V2, P61, DOI 10.1007/BF02098832 WOLF L, 1986, CAN J PSYCHIAT, V31, P550 World Health Organization, 1990, ICD 10 INT STAT CLAS NR 43 TC 148 Z9 149 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 2003 VL 33 IS 6 BP 565 EP 581 DI 10.1023/B:JADD.0000005995.02453.0b PG 17 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200002 PM 14714927 ER PT J AU Jennett, HK Harris, SL Mesibov, GB AF Jennett, HK Harris, SL Mesibov, GB TI Commitment to philosophy, teacher efficacy, and burnout among teachers of children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; applied behavior analysis; TEACCH; teacher efficacy; burnout; commitment AB Variables that may be related to burnout in teachers of students with autism, including commitment to an underlying philosophy of a treatment and professional self-efficacy, were explored. Teachers using one of two different treatment approaches to autism participated: those using Applied Behavior Analysis (n = 34), and those using TEACCH (Treatment and Education of Autistic and Related Communication-Related Handicapped Children) ( n = 30). Participants completed the Autism Treatment Philosophy Questionnaire, developed by the authors to differentiate between the philosophy of the approaches; Teacher Efficacy Scale, and Maslach Burnout Inventory. Results indicate a significant difference in philosophical commitment between the groups, but no differences in teaching efficacy or burnout. The relationship between a commitment to one's teaching approach and certain dimensions of teaching efficacy and burnout was found to be significant. Implications include the need for adequate training of teachers of students with autism. C1 State Univ New Jersey, Douglass Dev Disabil Ctr, Div Res & Training, New Brunswick, NJ 08901 USA. Univ N Carolina, Chapel Hill, NC USA. RP Jennett, HK (reprint author), State Univ New Jersey, Douglass Dev Disabil Ctr, Div Res & Training, 151 Ryders Lane, New Brunswick, NJ 08901 USA. EM heatherj@rci.rutgers.ed CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anderson S. 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A., 1999, UNDERSTANDING PREVEN, P166, DOI 10.1017/CBO9780511527784.010 Ghaith G, 1999, TEACH TEACH EDUC, V15, P487, DOI 10.1016/S0742-051X(99)00009-8 GIBSON S, 1984, J EDUC PSYCHOL, V76, P569, DOI 10.1037/0022-0663.76.4.569 Green G, 1996, BEHAV INTERVENTION Y, P29 GUSKEY TR, 1994, AM EDUC RES J, V31, P627, DOI 10.3102/00028312031003627 HARRIS SL, 1991, RES DEV DISABIL, V12, P17, DOI 10.1016/0891-4222(91)90020-S KAZDIN AE, 2001, BEHAV MODIFICATION A MASLACH C, 1981, J OCCUP BEHAV, V2, P99, DOI 10.1002/job.4030020205 Maslach C., 1996, MASLACH BURNOUT INVE, V3rd MESIBOV G, 1994, BEHAV ISSUES AUTISM MESIBOV GB, IN PRESS STRUCTURED WOOLFOLK AE, 1990, J EDUC PSYCHOL, V82, P81, DOI 10.1037//0022-0663.82.1.81 NR 24 TC 36 Z9 36 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD DEC PY 2003 VL 33 IS 6 BP 583 EP 593 DI 10.1023/B:JADD.0000005996.19417.57 PG 11 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200003 PM 14714928 ER PT J AU de Bildt, A Sytema, S Ketelaars, C Kraijer, D Volkmar, F Minderaa, R AF de Bildt, A Sytema, S Ketelaars, C Kraijer, D Volkmar, F Minderaa, R TI Measuring pervasive developmental disorders in children and adolescents with mental retardation: A comparison of two screening instruments used in a study of the total mentally retarded population from a designated area SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE PDD; MR; ABC; PDD-MRS; ADOS-G; ADI-R ID DIAGNOSTIC OBSERVATION SCHEDULE; ADAPTIVE-BEHAVIOR SCALES; AUTISTIC-CHILDREN; DEFICITS; EPIDEMIOLOGY; IMPAIRMENTS; INDIVIDUALS; RELIABILITY; INTERVIEW; AGREEMENT AB The performance of two screening instruments for Pervasive Developmental Disorders was studied in the total population of participants with mental retardation between 4 and 18 years (n = 1059) in Friesland, a northern province of the Netherlands. Parents completed the Autism Behavior Checklist (ABC), staff completed the Scale of Pervasive Developmental Disorder in Mentally Retarded Persons (PDD-MRS). The screening instruments were related to the Autism Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule - Generic for 184 participants. The agreement between ABC and PDD-MRS was fair (kappa =.24). The ABC had a better criterion-related validity compared with the Autism Diagnostic Interview - Revised, and the PDD-MRS compared to the Autism Diagnostic Observation Schedule - Generic. However, related to the clinical classification, both instruments performed equally well. Concluding, the ABC and PDD-MRS partially identify the same cases related to external criteria. In addition, each instrument has its own contribution. Both instruments are valuable in detecting children who are at high risk for PDD. C1 Univ Groningen, Dept Psychiat, Groningen, Netherlands. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP de Bildt, A (reprint author), Univ Groningen, Dept Psychiat Child & Adolescent Psychiat, Hanzepl 1, NL-9713 GZ Groningen, Netherlands. RI Sytema, Sjoerd/B-2058-2010 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bayley N., 1969, BAYLEY SCALES INFANT Bryson S. E., 1997, HDB AUTISM PERVASIVE, P41 Bryson SE, 1996, J AUTISM DEV DISORD, V26, P165, DOI 10.1007/BF02172005 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 CICCHETTI DV, 1981, AM J MENT DEF, V86, P127 Cicchetti DV, 2001, J CLIN EXP NEUROPSYC, V23, P695, DOI 10.1076/jcen.23.5.695.1249 Cicchetti DV, 1995, CHILD NEUROPSYCHOL, V1, P26, DOI 10.1080/09297049508401340 DEMYER MK, 1974, J AUTISM CHILD SCHIZ, V4, P42, DOI 10.1007/BF02104999 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Kanner L, 1943, NERV CHILD, V2, P217 Kraijer D. W., 1997, AUTISM AUTISTIC LIKE Krug D. A., 1980, AUTISM SCREENING INS LANDIS JR, 1977, BIOMETRICS, V33, P159, DOI 10.2307/2529310 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 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 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C., 1998, AUTISM DIAGNOSTIC OB MEULEN VF, 1983, BAYLEY ONTWIKKELINGS MURPHY JR, 1990, DEPRESSION PRIMARY C OSWALD DP, 1991, J AUTISM DEV DISORD, V21, P543, DOI 10.1007/BF02206876 RUTTER M, 1983, J CHILD PSYCHOL PSYC, V24, P513, DOI 10.1111/j.1469-7610.1983.tb00129.x Siegel B., 1996, WORLD AUTISTIC CHILD SNIJDERS JT, 1996, SNIJDERS OOMEN NIET Sparrow S, 1984, VINELAND ADAPTIVE BE *SPSS INC, 1999, SPSS WIND REL 10 0 5 Stata Corp, 2001, STAT STAT SOFTW REL STEFFENBURG S, 1986, BRIT J PSYCHIAT, V149, P81, DOI 10.1192/bjp.149.1.81 SZATMARI P, 1994, J AUTISM DEV DISORD, V24, P703, DOI 10.1007/BF02172281 Towbin KE, 1997, HDB AUTISM PERVASIVE, P123 Tsai LY, 1996, J AUTISM DEV DISORD, V26, P159, DOI 10.1007/BF02172004 Vander Steene G., 1986, WECHSLER INTELLIGENC VANDERSTEENE G, 1997, WECHSLER PERSCHOOL P VOLKMAR FR, 1987, J AM ACAD CHILD PSY, V26, P156, DOI 10.1097/00004583-198703000-00005 Wechsler D., 1989, WECHSLER PRESCHOOL P Wechsler D, 1974, WECHSLER INTELLIGENC WING L, 1981, J AUTISM DEV DISORD, V11, P31, DOI 10.1007/BF01531339 WING L, 1977, J CHILD PSYCHOL PSYC, V18, P167, DOI 10.1111/j.1469-7610.1977.tb00426.x WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 Wing L, 1997, HDB AUTISM PERVASIVE, P148 Wing L, 1993, Eur Child Adolesc Psychiatry, V2, P61, DOI 10.1007/BF02098832 World Health Organization, 1992, 10 REV INT CLASS DIS NR 43 TC 25 Z9 25 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 2003 VL 33 IS 6 BP 595 EP 605 DI 10.1023/B:JADD.0000005997.92287.a3 PG 11 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200004 PM 14714929 ER PT J AU Goldberg, WA Osann, K Filipek, PA Laulhere, T Jarvis, K Modahl, C Flodman, P Spence, MA AF Goldberg, WA Osann, K Filipek, PA Laulhere, T Jarvis, K Modahl, C Flodman, P Spence, MA TI Language and other regression: Assessment and timing SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; regression; assessment ID PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM DIAGNOSTIC INTERVIEW; SPEECH LOSS; CHILDREN; AGE; RECOGNITION; BEHAVIOR; ONSET AB Understanding of regression in autism has been hampered by variability in parental and clinical recognition and reporting of lost skills. This study introduced an instrument, the Regression Supplement Form, intended to supplement the Autism Diagnosis Interview-Revised and yield precise information about the types and timing of regression and events concurrent with loss and regain of skills. Data were collected from parents of 44 children (38 male, 6 female; mean age = 6 years) with Autistic Spectrum Disorder (37 Autistic Disorder, 7 Pervasive Developmental Disorder-Not Otherwise Specified). Parental responses on the Autism Diagnosis Interview-Revised indicated loss of skills during early development. The profile of regression that emerged included loss of skills between 18 and 21 months, on average, with language-only regression less common than loss of other, nonlanguage skills only or of full regression (loss of language and other skills). The onset of regression typically was gradual in nonlanguage areas and split between gradual and sudden loss for language skills. Some of the children were developing atypically before they lost other, nonlanguage skills, that is, their age at first words was delayed until age 2 years or older. Parents tended to attribute loss to medical factors such as immunizations. Many of the children regained some of the lost skills when they were 3.5-5 years of age, with therapeutic and instructional interventions given credit for the regain. C1 Univ Calif Irvine, Dept Psychol & Social Behav, Sch Social Ecol 3375 2, Irvine, CA 92697 USA. Univ Calif Irvine, Dept Med, Med Ctr, Irvine, CA 92717 USA. Univ Calif Irvine, Dept Pediat, Med Ctr, Irvine, CA 92717 USA. RP Goldberg, WA (reprint author), Univ Calif Irvine, Dept Psychol & Social Behav, Sch Social Ecol 3375 2, Irvine, CA 92697 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baranek GT, 2002, J AUTISM DEV DISORD, V32, P397, DOI 10.1023/A:1020541906063 Bayley N, 1993, BAYLEY SCALES INFANT Bristol MM, 1996, J AUTISM DEV DISORD, V26, P121, DOI 10.1007/BF02172002 Bristol-Power MM, 1999, J AUTISM DEV DISORD, V29, P435, DOI 10.1023/A:1021991718423 Sandler AD, 2001, PEDIATRICS, V107 COOPER J, 2001, INT M AUT RES SAN DI Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 Filipek P. A., 1999, J AUTISM DEV DISORD, V29, P437 Filipek PA, 2000, NEUROLOGY, V55, P468 HOLLINGSHEAD AB, 1975, 4 FACTOR MODEL SOCIA HOSHINO Y, 1987, JPN J PSYCHIAT NEUR, V41, P237 KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 Kurita H, 1996, PSYCHIAT CLIN NEUROS, V50, P181, DOI 10.1111/j.1440-1819.1996.tb02739.x LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 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 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x LORD C, 1993, INF MENTAL HLTH J, V14, P234, DOI 10.1002/1097-0355(199323)14:3<234::AID-IMHJ2280140308>3.0.CO;2-F Mullen E, 1995, MULLEN SCALES EARLY MUNDY P, 1995, DEV PSYCHOPATHOL, V7, P63 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 ROGERS SJ, 1990, J AM ACAD CHILD PSY, V29, P863, DOI 10.1097/00004583-199011000-00004 RUTTER M, 1987, LANGUAGE DEV DISORDE, P206 Shinnar S, 2001, PEDIATR NEUROL, V24, P183 SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 SHULMAN C, 1996, M INT SOC STUD BEH D Siegel B., 1996, WORLD AUTISTIC CHILD Thorndike RL, 1986, STANFORD BINET INTEL TOTH K, 2001, BIENN M SOC RES CHIL Tuchman R F, 1996, Rev Neurol, V24, P1446 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 VOLKMAR FR, 1985, AM J PSYCHIAT, V142, P1450 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 36 TC 91 Z9 94 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 2003 VL 33 IS 6 BP 607 EP 616 DI 10.1023/B:JADD.0000005998.47370.ef PG 10 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200005 PM 14714930 ER PT J AU Rogers, SJ Hepburn, S Wehner, E AF Rogers, SJ Hepburn, S Wehner, E TI Parent reports of sensory symptoms in toddlers with autism and those with other developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; developmental delays; sensory; parent report; fragile X syndrome ID ADI-R; CHILDREN; INDIVIDUALS AB The Short Sensory Profile was used to assess parental report of sensory reactivity across four groups of young children (n = 102). Groups were autism (n = 26), fragile X syndrome (n = 20), developmental disabilities of mixed etiology (n = 32), and typically developing children (n = 24). Groups were comparable on overall mental age (x = 22 months), and clinical groups were comparable on chronological age (x = 31 months). Significant differences were detected at alpha < .01 for tactile sensitivity [F(3,99) = 10.01], taste/smell sensitivity [F(3,99) = 11.63], underreactive/seeks stimulation [F(3,99) = 4.56], auditory filtering [F(3,99) = 19.67], and low energy/weak muscles [F(3,99) = 14.21]. Both children with fragile X syndrome and children with autism had significantly more sensory symptoms overall than the two comparison groups, and children with autism did not differ significantly from children with fragile X syndrome. Both groups were more impaired than developmentally delayed and typically developing children in tactile sensitivity and auditory filtering. Children with autism were more abnormal in responses to taste and smell than all other groups. Children with fragile X syndrome were more abnormal than all other groups in low energy/weak muscles. Sensory reactivity of children with developmental delays was comparable to mental age-matched typically developing toddlers. Correlational analyses indicated that neither overall developmental level nor IQ was related to abnormal sensory reactivity in children with autism or general developmental disorders. However, abnormal sensory reactivity had a significant relationship with overall adaptive behavior. C1 Univ Calif Davis, MIND Inst, Dept Psychiat, Sacramento, CA 95817 USA. Univ Colorado, Ctr Hlth, Dept Psychiat, Denver, CO 80202 USA. RP Rogers, SJ (reprint author), Univ Calif Davis, MIND Inst, Dept Psychiat, 2825 50th St, Sacramento, CA 95817 USA. CR Bishop DVM, 1997, Q J EXP PSYCHOL-A, V50, P899, DOI 10.1080/027249897391946 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 Dunn W., 1999, SENSORY PROFILE EXAM Dunn W, 2002, AM J OCCUP THER, V56, P97 Goldstein H, 2000, J AUTISM DEV DISORD, V30, P423, DOI 10.1023/A:1005599406819 Grandin T., 1986, EMERGENCE LABELED AU Hollingshead A. B., 1975, 4 FACTOR INDEX SOCIA Kientz MA, 1997, AM J OCCUP THER, V51, P530 Lord C., 1999, AUTISM DIAGNOSTIC OB LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x LORD C, 1993, INF MENTAL HLTH J, V14, P234, DOI 10.1002/1097-0355(199323)14:3<234::AID-IMHJ2280140308>3.0.CO;2-F McIntosh DN, 1999, SENSORY PROFILE EXAM MILLER LJ, 2001, UNDERSTANDING NATURE Miller LJ, 1999, AM J MED GENET, V83, P268, DOI 10.1002/(SICI)1096-8628(19990402)83:4<268::AID-AJMG7>3.3.CO;2-B Mullen E.M., 1995, MULLENS SCALES EARLY ORNITZ EM, 1977, J AUTISM CHILD SCHIZ, V7, P207, DOI 10.1007/BF01538999 Sparrow S, 1984, VINELAND ADAPTIVE BE THELEN E, 1966, STEROTYPED MOVEMENTS WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1969, J CHILD PSYCHOL PSYC, V10, P1, DOI 10.1111/j.1469-7610.1969.tb02066.x NR 22 TC 176 Z9 182 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 2003 VL 33 IS 6 BP 631 EP 642 DI 10.1023/B:JADD.0000006000.38991.a7 PG 12 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200007 PM 14714932 ER PT J AU Molloy, CA Dietrich, KN Bhattacharya, A AF Molloy, CA Dietrich, KN Bhattacharya, A TI Postural stability in children with autism spectrum disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article ID ASPERGER-SYNDROME; INFANTILE-AUTISM; BRAIN-STEM; MOTOR IMPAIRMENT; CORPUS-CALLOSUM; LEAD-EXPOSURE; CEREBELLAR; INDIVIDUALS; MR; ABNORMALITIES AB Maintaining upright posture is a complex process involving multiple afferent systems. The aim of this study was to measure the postural stability of children with Autism Spectrum Disorder (ASD) compared with children with typical neurodevelopment and to measure the relative contributions of the visual, somatosensory, and vestibular afferent systems in each group. Eight boys with ASD and eight age-, race-, and gender-matched controls participated in this study using force platform technology with customized software to measure postural sway under conditions designed to eliminate or modify visual and somatosensory input. Children with ASD had significantly larger sway areas under all test conditions in which afferent input was modified. These results are consistent with a deficit in the integration of visual, vestibular, and somatosensory input to maintain postural orientation. C1 Univ Cincinnati, Coll Med, Dept Pediat, Div Dev Disabil, Cincinnati, OH USA. Ctr Biostat & Epidemiol, Cincinnati, OH USA. Univ Cincinnati, Coll Med, Dept Environm Hlth, Div Epidemiol & Biostat, Cincinnati, OH 45267 USA. Univ Cincinnati, Coll Med, Dept Environm Hlth, Div Environm & Ind Hyg,Biomech Ergon Res Labs, Cincinnati, OH 45267 USA. RP Molloy, CA (reprint author), Cincinnati Childrens Hosp, Med Ctr, Ctr Biostat & Epidemiol, MLC 5041,3333 Burnet Ave, Cincinnati, OH 45229 USA. 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Autism Dev. Disord. PD DEC PY 2003 VL 33 IS 6 BP 643 EP 652 DI 10.1023/B:JADD.0000006001.00667.4c PG 10 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200008 PM 14714933 ER PT J AU Bosseler, A Massaro, DW AF Bosseler, A Massaro, DW TI Development and evaluation of a computer-animated tutor for vocabulary and language learning in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE vocabulary learning; animated tutor; multimedia; language learning; animated speech; tutoring children with autism; computer ID ACQUISITION; BEHAVIOR; COMMUNICATION AB Using our theoretical framework of multimodal processing, we developed and evaluated a computer-animated tutor, Baldi, to teach vocabulary and grammar for children with autism. Baldi was implemented in a Language Wizard/Player, which allows easy creation and presentation of a language lesson involving the association of pictures and spoken words. The lesson plan includes both the identification of pictures and the production of spoken words. In Experiment 1, eight children were given initial assessment tests, tutorials, and reassessment tests 30 days following mastery of the vocabulary items. All of the students learned a significant number of new words and grammar. A second within-subject design with six children followed a multiple baseline design and documented that the program was responsible for the learning and generalization of new words. The research indicates that children with autism are capable of learning new language within an automated program centered around a computer-animated agent, multimedia, and active participation and can transfer and use the language in a natural, untrained environment. C1 Univ Calif Santa Cruz, Dept Psychol, Santa Cruz, CA 95064 USA. RP Bosseler, A (reprint author), Univ Calif Santa Cruz, Dept Psychol, Santa Cruz, CA 95064 USA. 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W., 1998, PERCEIVING TALKING F MASSARO DW, 1999, P INT C PHON SCI SAN MASSARO DW, 2000, P INT SPEECH TECHN L Moore M, 2000, J AUTISM DEV DISORD, V30, P359, DOI 10.1023/A:1005535602064 PRIZANT BM, 1983, J SPEECH HEAR DISORD, V48, P296 RINCOVER A, 1975, J APPL BEHAV ANAL, V8, P235, DOI 10.1901/jaba.1975.8-235 SCHOPKER E, 1985, LEARNING COGNITION, P243 Schopler E, 1990, PSYCHOEDUCATIONAL PR Sparrow S, 1984, VINELAND ADAPTIVE BE STANOVICH KE, 1986, READ RES QUART, V21, P360, DOI 10.1598/RRQ.21.4.1 STOKES TF, 1974, J APPL BEHAV ANAL, V7, P599, DOI 10.1901/jaba.1974.7-599 TAGERFLUSBERG H, 1999, INT REV PSYCHIATR, V11, P355 Tager-Flusberg H, 2000, METHODS FOR STUDYING LANGUAGE PRODUCTION, P313 VANLANCKER D, 1991, DEV NEUROPSYCHOL, V7, P1 Vermeer A, 2001, APPL PSYCHOLINGUIST, V22, P217, DOI 10.1017/S0142716401002041 WECHSLER D, 1989, WECHSLER PROESCHOOL Wood J., 2001, LANGUAGE LEARNING TE, V5, P166 Yamamoto J, 1999, RES DEV DISABIL, V20, P355, DOI 10.1016/S0891-4222(99)00017-7 NR 42 TC 75 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 DEC PY 2003 VL 33 IS 6 BP 653 EP 672 DI 10.1023/B:JADD.0000006002.82367.4f PG 20 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200009 PM 14714934 ER PT J AU Ingersoll, B Schreibman, L Tran, QH AF Ingersoll, B Schreibman, L Tran, QH TI Effect of sensory feedback on immediate object imitation in children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; imitation; sensory feedback; social motivation; joint attention; affect ID JOINT ATTENTION; MOTOR IMITATION; YOUNG-CHILDREN; DOWN-SYNDROME; PRETEND PLAY; DISORDERS; INFANCY AB This study examined the effect of sensory feedback (e. g., flashing lights and sound) on the imitation performance of children with autism and typical children group-matched for mental age. Participants were administered an immediate object-imitation task with six novel toys constructed for this study: three with a sensory effect that could be activated by imitating the modeled action and three without a sensory effect. Although overall imitation performance did not differ significantly between the two groups, the imitation performance of the participants with autism was significantly higher with sensory toys than with nonsensory toys. Typical participants' imitation performance did not differ between the two sets of toys. Both groups played significantly more with the sensory toys during free play, indicating that sensory toys were more reinforcing for both groups. Additional results demonstrated that typical children used significantly more social behaviors during imitation than children with autism, but they did not differ in object-oriented behaviors, replicating previous findings. It is argued that children with autism may be less motivated to imitate by social interaction, but may be motivated to imitate to receive a nonsocial reward ( sensory feedback). C1 Oregon Hlth Sci Univ, Child Dev & Rehabil Ctr, Portland, OR 97239 USA. Univ Calif San Diego, La Jolla, CA 92093 USA. RP Ingersoll, B (reprint author), Oregon Hlth Sci Univ, Child Dev & Rehabil Ctr, 3181 SW Sam Jackson Pk Rd, Portland, OR 97239 USA. RI Ingersoll, Brooke/A-9117-2012 CR ABRAVANEL E, 1976, CHILD DEV, V47, P1032, DOI 10.1111/j.1467-8624.1976.tb02284.x BARONCOHEN S, 1988, J AUTISM DEV DISORD, V18, P379, DOI 10.1007/BF02212194 Bayley N, 1993, BAYLEY SCALES INFANT Brown J. D., 1998, INTERSUBJECTIVE COMM, P260 Charman T, 1997, DEV PSYCHOL, V33, P781, DOI 10.1037//0012-1649.33.5.781 CHARMAN T, 1994, DEV PSYCHOPATHOL, V6, P403, DOI 10.1017/S0954579400006015 CURCIO F, 1978, J AUTISM CHILD SCHIZ, V8, P281, DOI 10.1007/BF01539631 DAWSON G, 1990, J ABNORM CHILD PSYCH, V18, P335, DOI 10.1007/BF00916569 DEMYER MK, 1972, J AUTISM CHILD SCHIZ, V2, P264, DOI 10.1007/BF01537618 Eckerman CO, 1996, DEV PSYCHOL, V32, P141, DOI 10.1037/0012-1649.32.1.141 ECKERMAN CO, 1990, DEV PSYCHOL, V26, P370, DOI 10.1037/0012-1649.26.3.370 Gilliam J. E., 1995, GILLIAM AUTISM RATIN HAMMES JGW, 1981, J AUTISM DEV DISORD, V11, P331, DOI 10.1007/BF01531515 Hobson RP, 1999, J CHILD PSYCHOL PSYC, V40, P649, DOI 10.1111/1469-7610.00481 JONES V, 1985, J AUTISM DEV DISORD, V15, P37, DOI 10.1007/BF01837897 KASARI C, 1990, J AUTISM DEV DISORD, V20, P87, DOI 10.1007/BF02206859 Kugiumutzakis G., 1999, IMITATION INFANCY, P36 Libby S, 1997, J AUTISM DEV DISORD, V27, P365, DOI 10.1023/A:1025801304279 MAURICE C, 1996, BEHAV INTERVENTION Y MELTZOFF AN, 1988, CHILD DEV, V59, P217, DOI 10.2307/1130404 MORGAN SB, 1989, J CHILD PSYCHOL PSYC, V30, P857, DOI 10.1111/j.1469-7610.1989.tb00287.x MUNDY P, 1995, DEV PSYCHOPATHOL, V7, P63 Nadel J., 1999, IMITATION INFANCY, P209 OHTA M, 1987, J AUTISM DEV DISORD, V17, P45, DOI 10.1007/BF01487259 Pierce K, 1997, J AUTISM DEV DISORD, V27, P265, DOI 10.1023/A:1025898314332 PIERCE K, 1995, J APPL BEHAV ANAL, V28, P285, DOI 10.1901/jaba.1995.28-285 Roeyers H, 1998, DEV PSYCHOPATHOL, V10, P441, DOI 10.1017/S0954579498001680 Rogers S. J., 1991, DEV PSYCHOPATHOL, V3, P137, DOI DOI 10.1017/S0954579400000043 Rogers S. J., 2000, AUTISM SPECTRUM DISO, P79 Rogers SJ, 1996, CHILD DEV, V67, P2060, DOI 10.2307/1131609 Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 SIGMAN M, 1984, DEV PSYCHOL, V20, P293, DOI 10.1037/0012-1649.20.2.293 Smith IM, 1998, COGNITIVE NEUROPSYCH, V15, P747, DOI 10.1080/026432998381087 SMITH IM, 1994, PSYCHOL BULL, V116, P259, DOI 10.1037/0033-2909.116.2.259 Stone WL, 1997, J ABNORM CHILD PSYCH, V25, P475, DOI 10.1023/A:1022685731726 Trevarthen C., 1999, IMITATION INFANCY, P127 UZGIRIS I, 1990, SOCIAL INFLUENCES SO, P215 UZGIRIS IC, 1981, INT J BEHAV DEV, V4, P1 NR 38 TC 36 Z9 36 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 2003 VL 33 IS 6 BP 673 EP 683 DI 10.1023/B:JADD.0000006003.26667.f8 PG 11 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200010 PM 14714935 ER PT J AU Barry, TD Klinger, LG Lee, JM Palardy, N Gilmore, T Bodin, SD AF Barry, TD Klinger, LG Lee, JM Palardy, N Gilmore, T Bodin, SD TI Examining the effectiveness of an outpatient clinic-based social skills group for high-functioning children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger's syndrome; social skills; therapy; greeting ID EXECUTIVE FUNCTION; BEHAVIOR; MIND; PRESCHOOLERS; INTERVENTIONS; LONELINESS; PROFILES; PEERS; SELF AB Although social skills group interventions for children with autism are common in outpatient clinic settings, little research has been conducted to determine the efficacy of such treatments. This study examined the effectiveness of an outpatient clinic-based social skills group intervention with four high-functioning elementary-aged children with autism. The group was designed to teach specific social skills, including greeting, conversation, and play skills in a brief therapy format (eight sessions total). At the end of each skills-training session, children with autism were observed in play sessions with typical peers. Typical peers received peer education about ways to interact with children with autism. Results indicate that a social skills group implemented in an outpatient clinic setting was effective in improving greeting and play skills, with less clear improvements noted in conversation skills. In addition, children with autism reported increased feelings of social support from classmates at school following participation in the group. However, parent report data of greeting, conversation, and play skills outside of the clinic setting indicated significant improvements in only greeting skills. Thus, although the clinic-based intervention led to improvements in social skills, fewer changes were noted in the generalization to nonclinic settings. C1 Univ Alabama, Dept Psychol, Tuscaloosa, AL 35487 USA. Texas A&M Univ, Dept Psychol, College Stn, TX 77843 USA. RP Klinger, LG (reprint author), Univ Alabama, Dept Psychol, Box 870348, Tuscaloosa, AL 35487 USA. RI Bodin, Steven/E-2771-2011 CR AHRTER S, 1985, SOCIAL SUPPORT SCALE American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASHER SR, 1985, J CONSULT CLIN PSYCH, V53, P500, DOI 10.1037/0022-006X.53.4.500 Baker MJ, 1998, J ASSOC PERS SEVERE, V23, P300, DOI 10.2511/rpsd.23.4.300 Barnhill G. P., 2001, FOCUS AUTISM OTHER D, V16, P46, DOI 10.1177/108835760101600112 Baron-Cohen S., 1993, AUTISM FACTS BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Chin HY, 2000, J AUTISM DEV DISORD, V30, P569, DOI 10.1023/A:1005639427185 COHEN J, 1960, EDUC PSYCHOL MEAS, V20, P37, DOI 10.1177/001316446002000104 COTTER MW, 1997, THESIS U ALABAMA TUS Courchesne E., 1994, ATYPICAL COGNITIVE D, P101 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 Fleiss JL, 1981, STAT METHODS RATES P FRITH U, 2000, CHILDHOOD COGNITIVE, P324 GAYLORDROSS RJ, 1984, J APPL BEHAV ANAL, V17, P229, DOI 10.1901/jaba.1984.17-229 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P279 GOLDSTEIN H, 1992, J APPL BEHAV ANAL, V25, P289, DOI 10.1901/jaba.1992.25-289 Gonzalez-Lopez A., 1997, FOCUS AUTISM OTHER D, V12, P2 GRAY C, 1993, TAMING RECESS JUNGLE Gresham F. M., 1990, SOCIAL SKILLS RATING Happe F, 1996, BRAIN, V119, P1377, DOI 10.1093/brain/119.4.1377 HARING TG, 1987, J ASSOC PERS SEVERE, V12, P280 Harrell L. G., 1998, ED TREATMENT CHILDRE, V21, P107 HARTER S, 1981, PICTORIAL SCALE PERC HUGHES C, 1994, NEUROPSYCHOLOGIA, V32, P477, DOI 10.1016/0028-3932(94)90092-2 Hughes JN, 1997, DEV PSYCHOPATHOL, V9, P75 Hwang B, 2000, J AUTISM DEV DISORD, V30, P331, DOI 10.1023/A:1005579317085 KAMPS DM, 1992, J APPL BEHAV ANAL, V25, P281, DOI 10.1901/jaba.1992.25-281 Kaufman A. S., 1990, KAUFMAN BRIEF INTELL Klinger LG, 2000, J CLIN CHILD PSYCHOL, V29, P479, DOI 10.1207/S15374424JCCP2904_3 Koegel LK, 2001, BEHAV MODIF, V25, P745, DOI 10.1177/0145445501255005 KOEGEL RL, 1993, J APPL BEHAV ANAL, V26, P369, DOI 10.1901/jaba.1993.26-369 Laushey KM, 2000, J AUTISM DEV DISORD, V30, P183, DOI 10.1023/A:1005558101038 MARRIAGE KJ, 1995, AUST NZ J PSYCHIAT, V29, P58, DOI 10.3109/00048679509075892 MATSON JL, 1991, J CLIN CHILD PSYCHOL, V20, P428, DOI 10.1207/s15374424jccp2004_11 MCEVOY RE, 1993, J CHILD PSYCHOL PSYC, V34, P563, DOI 10.1111/j.1469-7610.1993.tb01036.x MCGEE GG, 1992, J APPL BEHAV ANAL, V25, P117, DOI 10.1901/jaba.1992.25-117 MESIBOV GB, 1986, SOCIAL BEHAV AUTISM, P265 Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 MIRIN SM, 1991, HOSP COMMUNITY PSYCH, V42, P1007 ODOM SL, 1986, J APPL BEHAV ANAL, V19, P59, DOI 10.1901/jaba.1986.19-59 OKE NJ, 1990, J AUTISM DEV DISORD, V20, P479, DOI 10.1007/BF02216054 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 OZONOFF S, 1994, DEV PSYCHOPATHOL, V6, P415, DOI 10.1017/S0954579400006027 Ozonoff S, 1999, J AUTISM DEV DISORD, V29, P171, DOI 10.1023/A:1023052913110 Rogers SJ, 2000, J AUTISM DEV DISORD, V30, P399, DOI 10.1023/A:1005543321840 SAINATO DM, 1992, J APPL BEHAV ANAL, V25, P127, DOI 10.1901/jaba.1992.25-127 Schroeder C. S., 2002, ASSESSMENT TREATMENT SHAFER MS, 1984, J APPL BEHAV ANAL, V17, P461, DOI 10.1901/jaba.1984.17-461 THORP DM, 1995, J AUTISM DEV DISORD, V25, P265, DOI 10.1007/BF02179288 NR 51 TC 74 Z9 74 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 2003 VL 33 IS 6 BP 685 EP 701 DI 10.1023/B:JADD.0000006004.86556.e0 PG 17 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200011 PM 14714936 ER PT J AU Duarte, CS Bordin, IAS de Oliveira, A Bird, H AF Duarte, CS Bordin, IAS de Oliveira, A Bird, H TI The CBCL and the identification of children with autism and related conditions in Brazil: Pilot findings SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; pervasive developmental disorders; CBCL ID DIAGNOSIS; COMMUNITY; DISORDERS AB The Child Behavior Checklist (CBCL)/4-18 is one of the few standardized means available for assessing child mental health in Brazil. In this context, the identification of a specific pathology such as autism by the CBCL/4-18 is relevant. To examine the validity of the CBCL/4-18 for the identification of autism, the CBCL/4-18 was applied to 101 children: 36 with autism and related conditions, 31 with other psychiatric disorders, and 34 schoolchildren. Children ranged in age from 4 to 11 years. A CBCL factor called Autistic/Bizarre and the narrow-band Thought Problems scale differentiated autistic conditions from other psychiatric disorders and schoolchildren. Conclusion: The CBCL/4-16 can identify autistic children in clinical and school settings in Brazil. C1 Columbia Univ, New York State Psychiat Inst, Dept Child & Adolescent Psychiat, New York, NY 10032 USA. Univ Fed Sao Paulo, UNIFESP EPM, Escola Paulista Med, Dept Psychiat, Sao Paulo, Brazil. RP Duarte, CS (reprint author), Columbia Univ, New York State Psychiat Inst, Dept Child & Adolescent Psychiat, 1051 Riverside Dr,Unit 43, New York, NY 10032 USA. CR Achenbach TM, 2001, RATINGS RELATIONS DS Achenbach TM, 1991, MANUAL CHILD BEHAV C Bolte S, 1999, PSYCHOPATHOLOGY, V32, P93, DOI 10.1159/000029072 Bordin I. A. S., 1995, Revista ABP-APAL (Associacao Brasileira de Psiquiatria-Asociacion Psiquiatrica de la America Latina), V17, P55 Clark A, 1999, J CHILD PSYCHOL PSYC, V40, P287, DOI 10.1017/S0021963098003400 Sandler AD, 2001, PEDIATRICS, V107 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x GOULD MS, 1993, J ABNORM CHILD PSYCH, V21, P287, DOI 10.1007/BF00917536 Heubeck BG, 2000, J ABNORM CHILD PSYCH, V28, P439, DOI 10.1023/A:1005131605891 Hosmer Jr DW, 1989, APPL LOGISTIC REGRES Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Leaf PJ, 1996, J AM ACAD CHILD PSY, V35, P889, DOI 10.1097/00004583-199607000-00014 Powell JE, 2000, DEV MED CHILD NEUROL, V42, P624, DOI 10.1017/S001216220000116X RESCORLA L, 1988, J AUTISM DEV DISORD, V18, P475, DOI 10.1007/BF02211868 NR 14 TC 40 Z9 41 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 2003 VL 33 IS 6 BP 703 EP 707 DI 10.1023/B:JADD.0000006005.31818.1c PG 5 WC Psychology, Developmental SC Psychology GA 749AJ UT WOS:000186896200012 PM 14714937 ER PT J AU Malone, RP Delaney, MA Gifford, C AF Malone, RP Delaney, MA Gifford, C TI Ziprasidone treatment in adolescents with autism: A pilot study SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT 43rd Annual Meeting of the New-Clinical-Drug-Evaluation-Unit CY MAY 27-30, 2003 CL BOCA RATON, FLORIDA SP New Clin Drug Evaluat Unit, NIMH C1 Drexel Univ, Coll Med, EPPI, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 PU MARY ANN LIEBERT INC PUBL PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD WIN PY 2003 VL 13 IS 4 BP 414 EP 415 PG 2 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 772QB UT WOS:000188851800009 ER PT J AU Yaryura-Tobias, JA Rabinowitz, DC Neziroglu, F AF Yaryura-Tobias, JA Rabinowitz, DC Neziroglu, F TI Possible basal ganglia pathology in children with complex symptoms SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID OBSESSIVE-COMPULSIVE DISORDER; SELF-STIMULATORY BEHAVIOR; LA-TOURETTE SYNDROME; PERCEPTUAL REINFORCEMENT; REPETITIVE BEHAVIORS; PARKINSONS-DISEASE; PERSPECTIVE; SPECTRUM; AUTISM AB Background: Clinical observation of children presenting with a myriad of motor, behavioral, emotional, and sensorial symptoms who do not respond to treatment led to the hypothesis that these children may constitute a unique population, perhaps even a new clinical entity. The literature on child and adolescent psychopathology does not specifically address the phenomenological, diagnostic, and etiological factors that make these children unique. For this reason, a preliminary study was conducted to identify additional symptoms and features that make these children different. Method: Data were collected in 2001 on 7 children with complex symptomatology using the Behavior Assessment System for Children, the Anxiety Disorders Interview Schedule for DSM-IV, and a neurological illnesses and symptoms questionnaire designed by the authors. Results: On average, these children met full DSM-IV criteria for 1 to 5 diagnoses. The most prevalent diagnoses were attention-deficit/hyperactivity disorder, obsessive-compulsive disorder, oppositional defiant disorder, and pervasive developmental disorder. These children also exhibited a high incidence of sensory hyperarousal, aggressiveness, hypersexuality, and neuroethological behaviors. Almost all of the children also had indications of a history of bacterial or viral infection. Conclusion: The specific symptoms identified and the biological factors found in many of the children seem to suggest basal ganglia involvement. C1 Bio Behav Inst, Great Neck, NY 11021 USA. NYU, Dept Psychiat, New York, NY 10016 USA. Hofstra Univ, Dept Psychol, Hempstead, NY 11550 USA. RP Yaryura-Tobias, JA (reprint author), Bio Behav Inst, 935 No Blvd,Suite 102, Great Neck, NY 11021 USA. CR ALBANO AM, 1996, ANXIETY DISORDERS IN ALEXANDER GE, 1986, ANNU REV NEUROSCI, V9, P357, DOI 10.1146/annurev.ne.09.030186.002041 ALLEN AJ, 1995, J AM ACAD CHILD PSY, V34, P307, DOI 10.1097/00004583-199503000-00015 Allen G, 2003, AM J PSYCHIAT, V160, P262, DOI 10.1176/appi.ajp.160.2.262 Baxter LR, 2000, OBSESSIVE COMPULSIVE, P573 Coghill GE, 1936, PEDAGOG SEMIN J GEN, V48, P3 Creak M, 1935, J MENT SCI, V81, P834 DODMAN NH, 1997, OBSESSIVE COMPULSIVE, P99 DRAKE ME, 1992, CLIN ELECTROENCEPHAL, V23, P19 Geller DA, 1996, J AM ACAD CHILD PSY, V35, P1637, DOI 10.1097/00004583-199612000-00016 Gilles de la Tourette G, 1885, ARCH NEUROL-CHICAGO, V9, P19 HENDRICKS I, 1927, AM J PSYCHIAT, V7, P989 Hoche A, 1912, Z GESAMTE NEUROL PSY, V12, P540 Jeffery KJ, 1997, AM J PSYCHIAT, V154, P156 KNOBLOCK H, 1974, GESELL AMATRUDAS DEV Leahy SR, 1921, J AMER MED ASSOC, V76, P373 Leckman J., 1999, TOURETTES SYNDROME T, P155 LEWIS MH, 1987, J APPL BEHAV ANAL, V20, P253, DOI 10.1901/jaba.1987.20-253 LOURIE RS, 1949, AM J PSYCHIAT, V105, P653 LOVAAS I, 1987, J APPL BEHAV ANAL, V20, P45, DOI 10.1901/jaba.1987.20-45 Mathew S J, 2001, CNS Spectr, V6, P555 MAYERGROSS W, 1921, Z GES NEUROL PSYCH, V73, P283, DOI 10.1007/BF02895297 MCDOUGLE CJ, 1994, J CLIN PSYCHIAT, V55, P24 Mesulam M. 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Psychiatry PD DEC PY 2003 VL 64 IS 12 BP 1495 EP 1501 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 758DK UT WOS:000187617300014 PM 14728112 ER PT J AU Bishop, J AF Bishop, J TI The Internet for educating individuals with social impairments SO JOURNAL OF COMPUTER ASSISTED LEARNING LA English DT Article DE autism; collaboration; emotion recognition; social phobia; special education; wireless agents ID PHOBIA; AUTISM; AGENTS AB Social impairments materialise in a number of forms, from developmental disabilities such as autistic spectrum disorder, to psychiatric conditions such as social phobia. The individuals diagnosed with these problems find it difficult to deal with social situations through either the inability to perform in these situations or the fear of not being able to do so. The study investigated the social and practical implications of using Mobile Internet technology to deliver information relating to a social situation in real-time to participants with Autistic Spectrum Disorders (n = 10) and General Social Phobia (n = 3) diagnosed using DSM-IV. The participants used the agent on their mobile phone to convert phrases they found offensive or confusing into more concise and understandable definitions. Analysing their attitudes revealed that the technology enables socially impaired individuals to learn the meaning of emotions and understand more about how they communicate with their peers. However, the study concludes that governmental organisations, education providers and society as a whole need to adopt a cohesive approach to communication to ensure socially impaired individuals are fully included in society C1 Univ Glamorgan, Sch Comp, Pontypridd CF37 1DL, M Glam, Wales. RP Bishop, J (reprint author), Univ Glamorgan, Sch Comp, Llantwit Rd, Pontypridd CF37 1DL, M Glam, Wales. RI Bishop, Jonathan/E-8882-2015 OI Bishop, Jonathan/0000-0002-9919-7602 CR *APA, 1996, DIAGN STAT MAN MENT, P7 Attwood T., 2000, ASPERGERS SYNDROME G BERGER HJC, 1993, J AUTISM DEV DISORD, V23, P341, DOI 10.1007/BF01046224 Blades M, 2000, NUTR FOOD SCI, V30, P137, DOI 10.1108/00346650010319741 BOGELS S, 2001, BEHAV RES THER, V40, P1367 BURCHARDT T, 2000, DYNAMICS BEING DISAB Chou CY, 2003, COMPUT EDUC, V40, P255, DOI 10.1016/S0360-1315(02)00130-6 Clark DM, 2002, BIOL PSYCHIAT, V51, P92, DOI 10.1016/S0006-3223(01)01296-3 Di Martino A, 2001, PEDIATR NEUROL, V25, P199, DOI 10.1016/S0887-8994(01)00276-4 Fairbrother N, 2002, BEHAV RES THER, V40, P1291, DOI 10.1016/S0005-7967(01)00139-5 Fasel B, 2003, PATTERN RECOGN, V36, P259, DOI 10.1016/S0031-3203(02)00052-3 Fishbein M., 1980, UNDERSTANDING ATTITU FRENCH S, 1991, NEW BEACON, V75, P886 FRENCH S, 1991, NEW BEACON, V75, P153 FRITH U, 1991, AUTISM ASPERGER SYND, P3 Harvey A., 2000, INCLUSION AUTISM IS HORLEY K, 2001, J ANXIETY DIORD, V410, P1 Kelly EB, 2001, GENET ENG NEWS, V21, P1 Klin A, 2002, ARCH GEN PSYCHIAT, V59, P809, DOI 10.1001/archpsyc.59.9.809 Lange DB, 1999, COMMUN ACM, V42, P88, DOI 10.1145/295685.298136 Lupton D, 2000, SOC SCI MED, V50, P1851, DOI 10.1016/S0277-9536(99)00422-0 MOORE D, 2000, INNOV EDUC TRAIN INT, V37, P3 Oliver M., 1983, SOCIAL WORK DISABLED Parsons S, 2002, J INTELL DISABIL RES, V46, P430, DOI 10.1046/j.1365-2788.2002.00425.x PETRUSHIN V, 2000, 2000 FALL S SOC INT ROULSTONE A, 1993, DISABLING BARRIERS E, P241 Schneier FR, 2001, J CLIN PSYCHIAT, V62, P43 VANAMERINGEN M, 2002, J ANXIETY DIORD, V433, P1 van Dam-Baggen R, 2000, J ANXIETY DISORD, V14, P437, DOI 10.1016/S0887-6185(00)00038-4 WELELR M, 2002, DELIVERING LEARNING NR 30 TC 9 Z9 9 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0266-4909 J9 J COMPUT ASSIST LEAR JI J. Comput. Assist. Learn. PD DEC PY 2003 VL 19 IS 4 BP 546 EP 556 DI 10.1046/j.0266-4909.2003.00057.x PG 11 WC Education & Educational Research SC Education & Educational Research GA 752UC UT WOS:000187184700014 ER PT J AU Levy, SE Mandell, DS Merhar, S Ittenbach, RF Pinto-Martin, JA AF Levy, SE Mandell, DS Merhar, S Ittenbach, RF Pinto-Martin, JA TI Use of complementary and alternative medicine among children recently diagnosed with autistic spectrum disorder SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE complementary and alternative medicine; autistic spectrum disorder ID BEHAVIORAL TREATMENT; YOUNG-CHILDREN; ASTHMA; FAMILIES; THERAPY AB This study examined the prevalence and correlates of use of different types of complementary and alternative medicine (CAM) among a sample of children With suspected or recently diagnosed autism. The authors' review of 284 charts of children seen at the Regional Autism Center of The Children's Hospital of Philadelphia, Pennsylvania, found that more than 30% of children were using some CAM, and that 9% were using potentially harmful CAM. Having an additional diagnosis was protective against CAM use and being Latino was associated with CAM use. Having seen a prior provider regarding the child's health condition was predictive of potentially harmful CAM use. Further research is required on cultural differences in treatment decisions about CAM, as well as the reasons for the association between the use of prior providers and CAM. The high prevalence of CAM use among a recently diagnosed sample indicates that clinicians should discuss CAM early in the assessment process. C1 Childrens Hosp Philadelphia, Reg Autism Ctr, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Psychiat, Philadelphia, PA 19104 USA. Univ Penn, Sch Med, Dept Pediat, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Div Biostat, Philadelphia, PA USA. Univ Penn, Sch Nursing, Philadelphia, PA USA. RP Levy, SE (reprint author), Childrens Hosp Philadelphia, Reg Autism Ctr, Childrens Seashore House,3405 Civic Ctr Blvd, Philadelphia, PA 19104 USA. RI Mandelld, David/A-1044-2007; Mandell, David/H-2730-2012 OI Mandell, David/0000-0001-8240-820X CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bussing R, 2002, PSYCHIATR SERV, V53, P1096, DOI 10.1176/appi.ps.53.9.1096 Campbell M, 1996, J AM ACAD CHILD PSY, V35, P134, DOI 10.1097/00004583-199602000-00005 Sandler AD, 2001, PEDIATRICS, V107, P1221 Davis MP, 2003, ARCH PEDIAT ADOL MED, V157, P393, DOI 10.1001/archpedi.157.4.393 Flores G, 2002, JAMA-J AM MED ASSOC, V288, P82, DOI 10.1001/jama.288.1.82 Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 GRAY DE, 1993, SOC SCI MED, V36, P1037, DOI 10.1016/0277-9536(93)90121-J Gray D E, 1995, Med Anthropol, V16, P99 Horvath K, 2002, CURR OPIN PEDIATR, V14, P583, DOI 10.1097/01.MOP.0000030221.71203.46 Howlin P, 1997, EUR CHILD ADOLES PSY, V6, P55 Hurvitz EA, 2003, DEV MED CHILD NEUROL, V45, P364, DOI 10.1017/S0012162203000707 Hyman SL, 2000, CONT PEDIAT, V17, P101 Kanner L, 1943, NERV CHILD, V2, P217 KLEINMAN A., 1980, PATIENTS HEALERS CON Levy SE, 2002, INFANT YOUNG CHILD, V14, P33 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 Lovaas O. I., 1997, PREVENTION TREATMENT, P61 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 Nickel RE, 1996, INFANT YOUNG CHILD, V8, P29 Pachter LM, 2002, J ASTHMA, V39, P119, DOI 10.1081/JAS-120002193 PACHTER LM, 1993, J DEV BEHAV PEDIATR, V14, P163 PACHTER LM, 1995, ARCH PEDIAT ADOL MED, V149, P982 Reznik M, 2002, ARCH PEDIAT ADOL MED, V156, P1042 Richdale AL, 1999, DEV MED CHILD NEUROL, V41, P60, DOI 10.1017/S0012162299000122 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 Sandler AD, 2001, PEDIATRICS, V107, P598 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Volkmar Fred, 1999, Journal of the American Academy of Child and Adolescent Psychiatry, V38, p32S 1995, CAM RES METH C APR 7 NR 31 TC 69 Z9 69 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD DEC PY 2003 VL 24 IS 6 BP 418 EP 423 DI 10.1097/00004703-200312000-00003 PG 6 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 755TV UT WOS:000187428300003 PM 14671475 ER PT J AU Williams, G Oliver, JM Allard, AM Sears, L AF Williams, G Oliver, JM Allard, AM Sears, L TI Autism and associated medical and familial factors: A case control study SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE pervasive developmental disorder; developmental disability; medical conditions; primary healthcare; etiology; family history; behavior disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; HEAD CIRCUMFERENCE; CHILDREN; PARENTS; BIRTH; SIBLINGS; HISTORY; SEASON; INDIVIDUALS AB To systematically review medical and familial conditions in autistic subjects (AU) as compared to other developmentally disabled controls (DD). Data was gathered prospectively for 102 AUs and 106 DDs who were comparable for age, sex, and nonverbal intelligence. Chi-square and t test analyses were used to evaluate the data collected for AUs and DDs. Demographic data for AUs and DDs was similar for age, sex, and nonverbal IQ scores. The only statistically significant demographic differences were higher educational levels in mothers of AUs and increased number of firstborn AUs. Family history data revealed a greater number of reported maternal learning disabilities for DDs and increased paternal mental retardation for AUs but no differences in familial medical or psychiatric disorders. No prenatal or perinatal risk factors were identified in the AU group although increased alcohol use during pregnancy and decreased gestational age was found in the DD group. Review of developmental and behavioral issues revealed delayed toileting, tantrums, strong food preferences, and preoccupations to be significantly increased in AUs as compared to DDs. No significant differences were noted between the two groups in health problems or doctor visits. However, AUs had significantly larger mean head size than DDs. This study confirmed several previously established findings in autism including 4 to 1 male prevalence, increased head size, strong food preferences, and lack of prenatal/perinatal findings specifically associated with autism. However, the data suggested no increased prevalence of health problems among AUs or their family members compared to DDs. Several biologic interventions and etiologic theories of autism have been based on the assumption of medical differences in this population, an assumption called into question by current data. C1 Univ Louisville, Sch Med, Dept Pediat, Child Evaluat Ctr, Louisville, KY 40204 USA. RP Williams, G (reprint author), Univ Louisville, Sch Med, Dept Pediat, Child Evaluat Ctr, 571 S Floyd,Suite 100, Louisville, KY 40204 USA. 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Dev. Phys. Disabil. PD DEC PY 2003 VL 15 IS 4 BP 335 EP 349 DI 10.1023/A:1026310216069 PG 15 WC Rehabilitation SC Rehabilitation GA 735XF UT WOS:000186139300003 ER PT J AU Murphy, D AF Murphy, D TI Admission and cognitive details of male patients diagnosed with Asperger's Syndrome detained in a Special Hospital: comparison with a schizophrenia and personality disorder sample SO JOURNAL OF FORENSIC PSYCHIATRY & PSYCHOLOGY LA English DT Article DE Asperger's Syndrome; admission details; neuropsychological functioning ID AUTISM; VIOLENCE; COMMUNICATION; PREVALENCE; INTERVIEW AB This study examined whether male patients with Asperger's Syndrome detained in a high-security psychiatric hospital could be distinguished from patients with schizophrenia or with personality disorder on the basis of selected admission and neuropsychological details. Exploratory comparisons found that those patients with Asperger's Syndrome were less likely to have a history of alcohol or illicit substance abuse and had lower index offence violence ratings than the other patient groups. Age at admission was less discriminating and Mental Health Act 1983 section information did not suggest any bias. However, within the Asperger's Syndrome group approximately half had received either a mental Illness classification or a psychopathic disorder classification respectively. Within the neuropsychological measures patients with Asperger's Syndrome displayed in performance both similarities to and differences from the other patient groups. Tentative conclusions and implications for assessment and treatment are highlighted, along with the methodological limitations. C1 Broadmoor Hosp, Dept Psychol, Crowthorne RG45 7EG, Berks, England. RP Murphy, D (reprint author), Broadmoor Hosp, Dept Psychol, Crowthorne RG45 7EG, Berks, England. 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Forensic Psychiatry Psychol. PD DEC PY 2003 VL 14 IS 3 BP 506 EP 524 DI 10.1080/1478994031000152736 PG 19 WC Criminology & Penology; Psychiatry SC Criminology & Penology; Psychiatry GA 772NA UT WOS:000188847100003 ER PT J AU Suzuki, Y Critchley, HD Rowe, A Howlin, P Murphy, DGM AF Suzuki, Y Critchley, HD Rowe, A Howlin, P Murphy, DGM TI Impaired olfactory identification in Asperger's syndrome SO JOURNAL OF NEUROPSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article ID FACIAL EXPRESSIONS; AUTISM; DISCRIMINATION; NEUROANATOMY; DISORDER; BRAIN; MIND AB The authors measured odor detection threshold and odor identification in 12 males with Asperger's syndrome and 12 matched control subjects. Relative to control subjects, Asperger's syndrome subjects were not impaired at odor detection but were significantly impaired at olfactory identification. C1 Univ London St Georges Hosp, Sch Med, Dept Psychol, London SW17 0RE, England. Univ London Kings Coll, Inst Psychiat, Dept Psychol Med, London WC2R 2LS, England. Univ London Kings Coll, Guys Kings & St Thomas Sch Med, Dept Hlth Care Elderly, Clin Age Res Unit, London WC2R 2LS, England. RP Suzuki, Y (reprint author), Nagoya Univ, Grad Sch Med, Program Hlth & Community Med, Dept Geriatr Med Growth & Aging,Showa Ku, 65 Tsurumai Cho, Nagoya, Aichi 4668550, Japan. RI Howlin, Patricia/A-7622-2011; critchley, hugo/G-9267-2011 CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 ADOLPHS R, 1994, NATURE, V372, P669, DOI 10.1038/372669a0 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 Barnett R, 1999, PSYCHOL MED, V29, P1227, DOI 10.1017/S0033291799008818 CAIN WS, 1983, AM J OTOLARYNG, V4, P252, DOI 10.1016/S0196-0709(83)80068-4 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 DOTY RL, 1984, PHYSIOL BEHAV, V32, P489, DOI 10.1016/0031-9384(84)90269-5 ESLINGER PJ, 1985, NEUROLOGY, V35, P1731 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x Saitoh O, 1998, PSYCHIAT CLIN NEUROS, V52, pS219 TANABE T, 1975, J NEUROPHYSIOL, V38, P1284 ZATORRE RJ, 1991, BRAIN, V114, P71 NR 15 TC 34 Z9 35 PU AMER PSYCHIATRIC PRESS, INC PI WASHINGTON PA 1400 K ST, N W, STE 1101, WASHINGTON, DC 20005 USA SN 0895-0172 J9 J NEUROPSYCH CLIN N JI J. Neuropsychiatr. Clin. Neurosci. PD WIN PY 2003 VL 15 IS 1 BP 105 EP 107 DI 10.1176/appi.neuropsych.15.1.105 PG 3 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 641RH UT WOS:000180759300016 PM 12556580 ER PT J AU Sturmey, P AF Sturmey, P TI Video technology and persons with autism and other developmental disabilities: An emerging technology for PBS SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article RP Sturmey, P (reprint author), CUNY Queens Coll, Dept Psychol, 86-15,Kissena Blvd, Flushing, NY 11365 USA. CR BARONCOHEN S, 1989, HDB AUTISM PERVASIVE, P880 McClannahan L. E., 1997, ENVIRON BEHAV, P271 SPRADLIN JE, 1999, AUTISM BEHAV ANAL PE, P49 Swettenham J, 1996, J CHILD PSYCHOL PSYC, V37, P157, DOI 10.1111/j.1469-7610.1996.tb01387.x NR 4 TC 15 Z9 15 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD WIN PY 2003 VL 5 IS 1 BP 3 EP 4 DI 10.1177/10983007030050010401 PG 2 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LY UT WOS:000180573500002 ER PT J AU D'Ateno, P Mangiapanello, K Taylor, BA AF D'Ateno, P Mangiapanello, K Taylor, BA TI Using video modeling to teach complex play sequences to a preschooler with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID CHILDREN AB The identification of efficient teaching procedures to address deficits in imaginative play skills, which are commonly seen in children with autism, is a challenge for professionals who are designing treatment programs. In the present study, video modeling was used to teach play skills to a preschool child with autism. Videotaped play sequences included both verbal and motor responses. A multiple-baseline procedure across three response categories (having a tea party, shopping, and baking) was implemented to demonstrate experimental control. No experimenter-implemented reinforcement or correction procedures were used during the intervention. Results indicated that the video modeling intervention led to to the rapid acqusition of both verbal and motor responses for all play sequences. This procedure was shown to be an efficient technique for teaching relatively long sequences of responses in relatively few teaching sessions in the absence of chaining procedures. In addition, the complex sequences of verbal and motor responses were acquired without the use of error-correction procedures or explicit experimenter-implemented reinforcement contingencies. C1 CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA. CUNY, Grad Ctr, New York, NY USA. RP D'Ateno, P (reprint author), CUNY Queens Coll, Dept Psychol, 65-30 Kissena Blvd, Flushing, NY 11367 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 Charlop-Christy M. H., 1999, AUTISM BEHAV ANAL PE, P167 Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd STAHMER AC, 1995, J AUTISM DEV DISORD, V25, P123, DOI 10.1007/BF02178500 STOKES TF, 1977, J APPL BEHAV ANAL, V10, P349, DOI 10.1901/jaba.1977.10-349 Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 NR 7 TC 84 Z9 84 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD WIN PY 2003 VL 5 IS 1 BP 5 EP 11 DI 10.1177/10983007030050010801 PG 7 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LY UT WOS:000180573500003 ER PT J AU Charlop-Christy, MH Daneshvar, S AF Charlop-Christy, MH Daneshvar, S TI Using video modeling to teach perspective taking to children with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID MIND; SKILLS; BELIEF AB Perspective taking refers to the ability to determine mental states of others in order to explain or predict behavior. in typically developing children, this skill appears around age 4 years (Baron-Cohen, Leslie, & Frith, 1985), but it is delayed or absent in children with autism. In the present study, video modeling was used to teach perspective taking to three children with autism. A multiple-baseline design across children and within child across tasks was used to assess learning. Generalization across untrained similar stimuli was also assessed. Video modeling was a fast and effective tool for teaching perspective-taking tasks to children with autism, resulting in both stimulus and response generalization. These results concurred with previous research that perspective taking can be taught. Unlike other studies, however, wider ranges of generalization were found. C1 Claremont Mckenna Coll, Dept Psychol, Claremont, CA 91711 USA. Claremont Grad Univ, Claremont, CA USA. RP Charlop-Christy, MH (reprint author), Claremont Mckenna Coll, Dept Psychol, P-6,850 Columbia, Claremont, CA 91711 USA. CR ALCANTARA PR, 1994, EXCEPT CHILDREN, V61, P40 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th 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 CHANDLER M, 1989, CHILD DEV, V60, P1263, DOI 10.1111/j.1467-8624.1989.tb04001.x CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 Charlop-Christy MH, 2000, J AUTISM DEV DISORD, V30, P537, DOI 10.1023/A:1005635326276 CHARLOPCHRISTY MH, 1997, TREAT CHILD AUTISM G Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd FANTZ RL, 1964, SCIENCE, V146, P668, DOI 10.1126/science.146.3644.668 Frith U., 1989, AUTISM EXPLAINING EN GOPNIK A, 1991, CHILD DEV, V62, P98, DOI 10.1111/j.1467-8624.1991.tb01517.x HAPPE FGE, 1994, J CHILD PSYCHOL PSYC, V35, P1461, DOI 10.1111/j.1469-7610.1994.tb01287.x Happe F, 1996, NEUROREPORT, V8, P197, DOI 10.1097/00001756-199612200-00040 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 IHRIG K, 1988, J AUTISM DEV DISORD, V18, P67, DOI 10.1007/BF02211819 Matson J. L., 1994, AUTISM CHILDREN ADUL, P241 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x SCHOPLER E, 1983, AUTISM ADOLESCENTS A Schreibman L., 1988, AUTISM Siegler R. S., 1986, CHILDRENS THINKING STOKES TF, 1977, J APPL BEHAV ANAL, V10, P349, DOI 10.1901/jaba.1977.10-349 Swettenham J, 1996, J CHILD PSYCHOL PSYC, V37, P157, DOI 10.1111/j.1469-7610.1996.tb01387.x Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 NR 25 TC 81 Z9 82 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD WIN PY 2003 VL 5 IS 1 BP 12 EP 21 DI 10.1177/10983007030050010101 PG 10 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LY UT WOS:000180573500004 ER PT J AU Kinney, EM Vedora, J Stromer, R AF Kinney, EM Vedora, J Stromer, R TI Computer-presented video models to teach generative spelling to a child with an autism spectrum disorder SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID STIMULUS-CONTROL; TECHNOLOGY AB We examined the use of computer video models and video rewards to teach generative spelling to a child with an autism spectrum disorder. In Phase I, Ana viewed video models of her teacher writing target words. After Ana wrote the words correctly, she watched videos of play routines unique to each training word. Ana rapidly learned to spell three five-word sets based on pictures and dictation. In Phase 2, Ana learned to spell four novel words (e.g., lore and tock) that were based on the elements of five words learned in Phase I (e.g., tore and lock) and arranged into a teaching matrix of three beginning consonants and three word endings. In Phases 3 and 4, Ana learned to spell subsets of four three-by-three matrices, then immediately proved capable of spelling the remaining words in each matrix. Ana also succeeded on generalization and maintenance tests at home and school throughout the study. Generative spelling thus may be derived from a teaching package that (a) involves video models and rewards and (b) arranges opportunities for learning to recombine initial consonants and word endings. Ana's proficiency in spelling helped her acquire literacy skills commensurate with her general school placement. C1 Univ Massachusetts, Sch Med, Shriver Ctr, Waltham, MA USA. Northeastern Univ, Boston, MA 02115 USA. BEACON Serv, Milford, MA USA. RP Kinney, EM (reprint author), 82 West St, Milford, MA 01757 USA. CR CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 deRose JC, 1996, J APPL BEHAV ANAL, V29, P451, DOI 10.1901/jaba.1996.29-451 GOLDSTEIN H, 1989, J APPL BEHAV ANAL, V22, P245, DOI 10.1901/jaba.1989.22-245 McClannahan L. E., 1997, ENVIRON BEHAV, P271 Mueller MM, 2000, J APPL BEHAV ANAL, V33, P515, DOI 10.1901/jaba.2000.33-515 Remington B., 1990, MENT HANDICAP RES, V3, P33 RINCOVER A, 1975, J APPL BEHAV ANAL, V8, P235, DOI 10.1901/jaba.1975.8-235 Schreibman L., 2000, J POSIT BEHAV INTERV, V2, P3, DOI 10.1177/109830070000200102 Sherer M, 2001, BEHAV MODIF, V25, P140, DOI 10.1177/0145445501251008 Sparrow S, 1984, VINELAND ADAPTIVE BE STOKES TF, 1977, J APPL BEHAV ANAL, V10, P349, DOI 10.1901/jaba.1977.10-349 Stromer R, 1996, J APPL BEHAV ANAL, V29, P25, DOI 10.1901/jaba.1996.29-25 Stromer R., 1992, J BEHAVIORAL ED, V2, P139, DOI 10.1007/BF00947117 STROMER R, 2002, UNPUB ACTIVITY SCHED Taylor BA, 1999, J DEV PHYS DISABIL, V11, P253, DOI 10.1023/A:1021800716392 VEDORA J, 2002, UNPUB COMPUTER BASED Yamamoto J, 1999, RES DEV DISABIL, V20, P355, DOI 10.1016/S0891-4222(99)00017-7 NR 17 TC 50 Z9 51 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD WIN PY 2003 VL 5 IS 1 BP 22 EP 29 DI 10.1177/10983007030050010301 PG 8 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LY UT WOS:000180573500005 ER PT J AU Wert, BY Neisworth, JT AF Wert, BY Neisworth, JT TI Effects of video self-modeling on spontaneous requesting in children with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article AB Video self-modeling (VSM) is a promising intervention to teach new skills and improve the use of existing skills in young children with autism. VSM includes observation and imitation of one's self on videotape that records specific desirable child behaviors. The purpose of this study was to test the effectiveness of VSM for training young children with autism to make spontaneous requests in school settings. Four young children with autism participated. Experimental control was demonstrated using a multiple-baseline design across participants. Introduction of VSM led to a large increase in requesting behavior in all four children. VSM was effective in causing an increase in spontaneous requesting in young children with autism. C1 Penn State Univ, University Pk, PA 16802 USA. RP Wert, BY (reprint author), Bloomsburg Univ Penn, Dept Except Programs, 101-C Navy Hall, Bloomsburg, PA 17815 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bandura A., 1977, SOCIAL LEARNING THEO Buggey T., 1999, J POSIT BEHAV INTERV, V1, P205, DOI 10.1177/109830079900100403 CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 Dowrick PW, 1999, APPL PREV PSYCHOL, V8, P23, DOI 10.1016/S0962-1849(99)80009-2 FREEMAN S, 1996, TEACH ME LANGUAGE LA HOSFORD RE, 1981, COUNS PSYCHOL, V9, P45, DOI 10.1177/001100008000900113 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 MCGEE GG, 1999, FUNCTIONAL ANAL PROB, P171 MEHARG SS, 1990, ADV BEHAV RES THER, V12, P85, DOI 10.1016/0146-6402(90)90008-E WETHERBY AM, 1998, SEMINARS SPEECH LANG, V19 ZIHNI F, 1995, AZ METHOD USE VIDEO NR 12 TC 58 Z9 59 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD WIN PY 2003 VL 5 IS 1 BP 30 EP 34 DI 10.1177/10983007030050010501 PG 5 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LY UT WOS:000180573500006 ER PT J AU McGrath, AM Bosch, S Sullivan, CL Fuqua, RW AF McGrath, AM Bosch, S Sullivan, CL Fuqua, RW TI Training reciprocal social interactions between preschoolers and a child with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID NONHANDICAPPED PEERS; INTERVENTION; BEHAVIOR; SKILLS AB Previous research has suggested that children diagnosed with autism have severe social deficits that require active intervention. As such, the current study investigated the effectiveness of peer and individual social skills training for a preschooler diagnosed with autism. The goal of the training was to increase the rate of reciprocal social interactions. Results indicated that the frequency of appropriate initiations and responses did increase and that these changes were socially valid (a) as measured by expert ratings of change and (b) in comparison to typical peer-to-peer social behavior. Results are discussed in terms of their applicability to classrooms serving children diagnosed with autism. C1 Univ Kansas, Med Ctr, Dept Pediat, Kansas City, KS 66160 USA. Western Michigan Univ, Kalamazoo, MI 49008 USA. Eastern Maine Med Ctr, Bangor, ME USA. RP McGrath, AM (reprint author), Univ Kansas, Med Ctr, Dept Pediat, 3901 Rainbow Blvd, Kansas City, KS 66160 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Kamps D., 1997, J BEHAV ED, V7, P335, DOI 10.1023/A:1022879607019 Koegel LK, 2001, BEHAV MODIF, V25, P745, DOI 10.1177/0145445501255005 KOHLER FW, 1992, BEHAV MODIF, V16, P525, DOI 10.1177/01454455920164005 KRANTZ PJ, 1993, J APPL BEHAV ANAL, V26, P121, DOI 10.1901/jaba.1993.26-121 Lee S, 1996, J ASSOC PERS SEVERE, V21, P88 LORD C, 1986, J AUTISM DEV DISORD, V16, P249, DOI 10.1007/BF01531658 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MCGEE GG, 1992, J APPL BEHAV ANAL, V25, P117, DOI 10.1901/jaba.1992.25-117 Pierce K, 1997, J APPL BEHAV ANAL, V30, P157, DOI 10.1901/jaba.1997.30-157 Roeyers H, 1996, J AUTISM DEV DISORD, V26, P303, DOI 10.1007/BF02172476 ROFF M, 1961, J ABNORM SOC PSYCH, V63, P333, DOI 10.1037/h0041004 STRAIN PS, 1981, EXCEPTIONAL ED Q, V1, P83 STRAIN PS, 1986, EXCEPT CHILDREN, V52, P543 STRAIN PS, 1984, REM SPEC EDUC, V5, P21 TREMBLAY A, 1981, BEHAV MODIF, V5, P237, DOI 10.1177/014544558152006 Weiss MJ, 2001, BEHAV MODIF, V25, P785, DOI 10.1177/0145445501255007 NR 17 TC 11 Z9 11 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD WIN PY 2003 VL 5 IS 1 BP 47 EP 54 DI 10.1177/10983007030050010701 PG 8 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LY UT WOS:000180573500008 ER PT J AU Boettcher, M Koegel, RL McNerney, EK Koegel, LK AF Boettcher, M Koegel, RL McNerney, EK Koegel, LK TI A family-centered prevention approach to PBS in a time of crisis SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Editorial Material ID BEHAVIORAL SUPPORT AB This article describes a family-wide prevention approach to positive behavior support (PBS) interventions during a period of potential crisis for a family with a child with autism. Specifically, the mother in this family was to have major invasive surgery that would require extensive time for recovery. Past functional assessment data and anecdotal evidence indicated that lack of predictability, structure, supervision, and systematic behavior supports all contributed to problem behaviors in this family. As a result, a multicomponent intervention plan was implemented to prevent such problems. The procedures included the following elements: (a) priming intervention, (b) stakeholder meeting, (c) coordination of services and schedules, (d) family-wide PBS plan, and (e) ongoing support. The outcome of this intervention was that the child with autism and her siblings showed decreases in their disruptive behaviors (as opposed to the expected increases), and the family experienced other family-wide collateral positive effects from this proactive intervention approach. C1 Univ Calif Santa Barbara, Gevirtz Grad Sch Educ, Autism Res Ctr, Santa Barbara, CA 93106 USA. Univ Calif Santa Barbara, Gevirtz Grad Sch Educ, Counseling Clin Sch Psychol Program, Santa Barbara, CA 93106 USA. RP Boettcher, M (reprint author), Univ Calif Santa Barbara, Gevirtz Grad Sch Educ, Autism Res Ctr, Santa Barbara, CA 93106 USA. CR Carr EG, 2002, J POSIT BEHAV INTERV, V4, P4, DOI 10.1177/109830070200400102 DUNLAP G, 2001, ADDRESSING SOCIAL AC, P43 HORNER RH, 1990, J ASSOC PERS SEVERE, V15, P125 Horner R. H., 2000, FOCUS AUTISM OTHER D, V15, P97, DOI 10.1177/108835760001500205 Horner RH, 1997, J SPEC EDUC, V31, P84 Koegel L. K., 1996, POSITIVE BEHAV SUPPO Lucyshyn J. M., 2002, FAMILIES POSITIVE BE Wilde L. D., 1992, INCREASING SUCCESS S NR 8 TC 7 Z9 7 PU PRO-ED INC PI AUSTIN PA 8700 SHOAL CREEK BLVD, AUSTIN, TX 78757-6897 USA SN 1098-3007 J9 J POSIT BEHAV INTERV JI J. Posit. Behav. Interv. PD WIN PY 2003 VL 5 IS 1 BP 55 EP 59 DI 10.1177/10983007030050010901 PG 5 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 638LY UT WOS:000180573500009 ER PT J AU McClellan, JM Werry, JS AF McClellan, JM Werry, JS TI Evidence-based treatments in child and adolescent psychiatry: An inventory SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Review DE evidence-based medicine; pharmacology; psychotherapy; children; adolescents ID OBSESSIVE-COMPULSIVE DISORDER; DEFICIT HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; RANDOMIZED CLINICAL-TRIAL; COGNITIVE-BEHAVIORAL-THERAPY; PLACEBO-CONTROLLED TRIAL; 2-YEAR FOLLOW-UP; HOSPITALIZED AGGRESSIVE-CHILDREN; EMPIRICALLY SUPPORTED TREATMENTS; POSTTRAUMATIC STRESS SYMPTOMS AB Objective: To provide a list of evidence-based psychopharmacology and psychotherapy treatments for child psychiatry. Method: Published reviews and Medline searches were examined to generate a list of treatments supported by randomized controlled trials. Results: For psychopharmacology, the best evidence to date supports the use of stimulant medications for attention-deficit/hyperactivity disorder and selective serotonin reuptake inhibitors (SSRIs) for obsessive-compulsive disorder. There is also reasonable evidence addressing SSRIs for anxiety disorders and moderate to severe major depressive disorder, and risperidone for autism. The psychosocial interventions best supported by well-designed studies are cognitive-behavioral and behavioral interventions, especially for mood, anxiety, and behavioral disorders. Family-based and systems of care interventions also have been found effective. Conclusions: Although the number of evidence-based treatments for child psychiatry is growing, much of clinical practice remains based on the adult literature and traditional models of care. Challenges toward adopting evidence-based practices are discussed. C1 Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. Univ Auckland, Auckland 1, New Zealand. RP McClellan, JM (reprint author), Childrens Hosp, 4800 Sand Point Way,NE, Seattle, WA 98125 USA. 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PD DEC PY 2003 VL 42 IS 12 BP 1388 EP 1400 DI 10.1097/01.chi.0000092322.84052.88 PG 13 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 746CP UT WOS:000186729200005 PM 14627873 ER PT J AU Arnold, LE Vitiello, B McDougle, C Scahill, L Shah, B Gonzalez, NM Chuang, S Davies, M Hollway, J Aman, MG Cronin, P Koenig, K Kohn, AE McMahon, DJ Tierney, E AF Arnold, LE Vitiello, B McDougle, C Scahill, L Shah, B Gonzalez, NM Chuang, S Davies, M Hollway, J Aman, MG Cronin, P Koenig, K Kohn, AE McMahon, DJ Tierney, E TI Parent-defined target symptoms respond to risperidone in RUPP autism study: Customer approach to clinical trials SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article DE autism; pervasive developmental disorder; treatment; assessment; instruments ID MINIMAL BRAIN-DYSFUNCTION; DEXTROAMPHETAMINE; LEVOAMPHETAMINE; NETWORK AB Objective: A consumer-oriented efficacy assessment in clinical trials should measure changes in chief complaint and consumer request (symptoms of most concern to patient/caregiver), which may be diluted in change scores of multisymptom scales. Method: In the Research Units on Pediatric Psychopharmacology (RUPP) Autism Network 8-week double-blind trial of risperidone versus placebo, the chief concerns of parents were collected at 0, 4, and 8 weeks (endpoint), in addition to standardized primary measures. Blinded clinical judges rated change from baseline to 4 and 8 weeks on a 9-point scale (1 = normalized, 5 = unchanged, 9 = disastrous); 94 participants had usable data. Results: The most common symptoms identified by parents were tantrums, aggression, and hyperactivity. Interrater reliability was excellent. Mean ratings at endpoint were 2.8 +/- 1.2 on risperidone and 4.5 +/- 1.3 on placebo (p < .001). Ratings were collinear with Clinical Global Impression-improvement and Aberrant Behavior Checklist Irritability subscale (primary dimensional measure). Effect size d was 1.4, compared to 1.2 on the Aberrant Behavior Checklist Irritability subscale. 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PD DEC PY 2003 VL 42 IS 12 BP 1443 EP 1450 DI 10.1097/01.chi.0000091946.28938.54 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 746CP UT WOS:000186729200011 PM 14627879 ER PT J AU Skegg, DCG AF Skegg, DCG TI Autism and measles-mumps-rubella (MMR) vaccination: A challenge for pharmacoepidemiology SO PHARMACOTHERAPY LA English DT Editorial Material ID PRACTICE RESEARCH DATABASE; EPIDEMIOLOGIC EVIDENCE; DISORDER; ASSOCIATION; CALIFORNIA; PREVALENCE; SPECTRUM; CHILDREN; CAUSAL CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, P66 BAILEY A, 1995, PSYCHOL MED, V25, P63 BAUM C, 1994, PHARMACOEPIDEM DR S, P125 Bignall J, 1998, LANCET, V351, P966 Black C, 2002, BRIT MED J, V325, P419, DOI 10.1136/bmj.325.7361.419 Chen RT, 1998, LANCET, V351, P611, DOI 10.1016/S0140-6736(05)78423-3 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 Furlano RI, 2001, J PEDIATR-US, V138, P366, DOI 10.1067/mpd.2001.111323 Gangarosa EJ, 1998, LANCET, V351, P356, DOI 10.1016/S0140-6736(97)04334-1 Rodriguez LAG, 1998, BRIT J CLIN PHARMACO, V45, P419 Jick H, 2003, PHARMACOTHERAPY, V23, P1524, DOI 10.1592/phco.23.15.1524.31955 Kanner L, 1943, NERV CHILD, V2, P217 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Lee JW, 1998, LANCET, V351, P905, DOI 10.1016/S0140-6736(98)26012-0 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Medical Research Council, 2001, MRC REV AUT RES EP C SKEGG DCG, 1986, MONITORING DRUG SAFE, P291 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 VENNING GR, 1983, BRIT MED J, V286, P458 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 1999, LANCET, V354, P949, DOI 10.1016/S0140-6736(05)75696-8 *WHO, 1992, ICD 10 CLASS MENT BE, P252 WIHOLM BE, 1994, PHARMACOEPIDEM DR S, P139 Wilson K, 2003, ARCH PEDIAT ADOL MED, V157, P628, DOI 10.1001/archpedi.157.7.628 Wing L, 1997, LANCET, V350, P1761, DOI 10.1016/S0140-6736(97)09218-0 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 2000, LANCET, V355, P1379 NR 29 TC 0 Z9 0 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER, 806, 750 WASHINGTON ST, BOSTON, MA 02111 USA SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD DEC PY 2003 VL 23 IS 12 BP 1521 EP 1523 DI 10.1592/phco.23.15.1521.31956 PG 3 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 749VQ UT WOS:000186950500001 PM 14695030 ER PT J AU Jick, H Kaye, JA AF Jick, H Kaye, JA TI Epidemiology and possible causes of autism SO PHARMACOTHERAPY LA English DT Article DE MMR vaccine; epidemiology; autism ID PRACTICE RESEARCH DATABASE; RUBELLA VACCINE; MEASLES; MUMPS; PREVALENCE; CALIFORNIA; DISORDER AB Objectives. To review the recent literature on possible causes of the increase in frequency of diagnosed autism reported from three countries, and to compare the medical diagnoses and drug therapy from a new series of autistic boys and their mothers with that of comparable nonautistic boys and their mothers. Design. Case-control evaluation. Participants. Members of over 250 general practices in the United Kingdom. Measurements and Main Results. Frequency of exposure to drugs and presence of preexisting clinical illnesses in autistic children and their mothers were compared with nonautistic children and their mothers over time. According to published studies, the incidence of boys diagnosed with autism rose dramatically in the 1990s. Numerous published studies have concluded that the measles-mumps-rubella vaccine is not responsible for the large rise in diagnosed autism. in our study, boys diagnosed with autism had medical and drug histories, such as vaccines, before diagnosis, that were closely similar to those of nonautistic boys, except that developmental and sensory disorders were far more common in autistic boys. No material differences during pregnancy were found between the mothers of autistic boys and those of nonautistic boys in relation to illness or drug therapy. In the early 1990s, boys with diagnosed developmental disorders were infrequently diagnosed with autism. In the later 1990s, such boys more often were diagnosed with autism. Conclusion. A major cause of the recent large increase in the number of boys diagnosed with autism probably is due to changing diagnostic practices. C1 Boston Univ, Sch Med, Boston Collaborat Drug Surveillance Program, Lexington, MA 02421 USA. RP Jick, H (reprint author), Boston Univ, Sch Med, Boston Collaborat Drug Surveillance Program, 11 Muzzey St, Lexington, MA 02421 USA. CR BAILEY A, 1995, PSYCHOL MED, V25, P63 Black C, 2002, BRIT MED J, V325, P419, DOI 10.1136/bmj.325.7361.419 Croen LA, 2002, J AUTISM DEV DISORD, V32, P207, DOI 10.1023/A:1015453830880 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 FITZPATRICK M, MMR TRUTH JICK H, 2003, EPIDEMIOLOGY, V14, P431 Jick SS, 2003, PHARMACOTHERAPY, V23, P686, DOI 10.1592/phco.23.5.686.32205 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Lamb JA, 2000, HUM MOL GENET, V9, P861, DOI 10.1093/hmg/9.6.861 Last JM, 2001, DICT EPIDEMIOLOGY Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 PHILLIPS M, 2003, UK DAILY MAIL 0311, P10 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 *UK MRC, 2001, MRC REV AUT RES EP C Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 1999, LANCET, V354, P949, DOI 10.1016/S0140-6736(05)75696-8 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 NR 17 TC 37 Z9 37 PU PHARMACOTHERAPY PUBLICATIONS INC PI BOSTON PA NEW ENGLAND MEDICAL CENTER, 806, 750 WASHINGTON ST, BOSTON, MA 02111 USA SN 0277-0008 J9 PHARMACOTHERAPY JI Pharmacotherapy PD DEC PY 2003 VL 23 IS 12 BP 1524 EP 1530 DI 10.1592/phco.23.15.1524.31955 PG 7 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 749VQ UT WOS:000186950500002 PM 14695031 ER PT J AU Sarimski, K AF Sarimski, K TI Crisis and behavioral disorders in mental retardation and autism SO PRAXIS DER KINDERPSYCHOLOGIE UND KINDERPSYCHIATRIE LA German DT Book Review CR THEUNISSEN G, 2003, KRISEN VERHALTENSAUF NR 1 TC 0 Z9 0 PU VANDENHOECK & RUPRECHT PI GOTTINGEN PA THEATERSTRASSE 13,, D-37073 GOTTINGEN, GERMANY SN 0032-7034 J9 PRAX KINDERPSYCHOL K JI Prax. Kinderpsychol. Kinderpsychiatr. PD DEC PY 2003 VL 52 IS 10 BP 823 EP 824 PG 2 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 755PR UT WOS:000187418400010 ER PT J AU Okada, T Sato, W Murai, T Kubota, Y Toichi, M AF Okada, T Sato, W Murai, T Kubota, Y Toichi, M TI Eye gaze triggers visuospatial attentional shift in individuals with autism SO PSYCHOLOGIA LA English DT Article DE autism; gaze; visuospatial attention; joint attention ID CHILDREN; RECOGNITION; PERCEPTION; MONKEYS; MIND AB We examined whether eye gaze triggers reflexive attentional shift in autism. First, autistic individuals who were lacking both joint attention behaviors and theory-of-mind abilities were examined. Targets were randomly presented to either the left or right side of a gazing face. Autistic subjects localized the targets faster when targets were congruent with than against gaze directions. The occurrence of this gaze-triggered attentional shift was further examined using different stimulus onset asynchronies (SOAs) in autistic individuals and non-autistic controls. Autistic subjects similar to non-autistic controls responded faster when the targets were congruent with than against gaze directions for short SOA conditions. These results suggest that autistic individuals, even those lacking joint attention behaviors, respond reflexively to another person's gaze directions. C1 Kyoto Univ, Fac Med, Dept Neuropsychiat, Sakyo Ku, Kyoto 6068507, Japan. Case Western Reserve Univ, Univ Hosp Cleveland, Cleveland, OH 44106 USA. Shiga Univ Med Sci, Shiga, Japan. RP Okada, T (reprint author), Kyoto Univ, Fac Med, Dept Neuropsychiat, Sakyo Ku, 54 Shogoin Kawaharacho, Kyoto 6068507, Japan. EM tksokada@kuhp.kyoto-u.ac.jp CR American Psychiatric Association, 2000, DSM 4 TR DIAGN STAT, VFourth BARONCOHEN S, 1995, MINDBINDNESS ESSAY A Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 BARONCOHEN S, 1989, BRIT J DEV PSYCHOL, V7, P113 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 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Butterworth G., 1991, NATURAL THEORIES MIN CAMPBELL R, 1990, NEUROPSYCHOLOGIA, V28, P1123, DOI 10.1016/0028-3932(90)90050-X Chawarska K, 2003, CHILD DEV, V74, P1108, DOI 10.1111/1467-8624.00595 Driver J, 1999, VIS COGN, V6, P509 Emery NJ, 2000, NEUROSCI BIOBEHAV R, V24, P581, DOI 10.1016/S0149-7634(00)00025-7 Friesen CK, 1998, PSYCHON B REV, V5, P490, DOI 10.3758/BF03208827 HEYWOOD CA, 1992, PHILOS T ROY SOC B, V335, P31, DOI 10.1098/rstb.1992.0004 Hoffman EA, 2000, NAT NEUROSCI, V3, P80, DOI 10.1038/71152 Langton SRH, 1999, VIS COGN, V6, P541 Leekam SR, 1998, J CHILD PSYCHOL PSYC, V39, P951, DOI 10.1017/S0021963098003035 MUNDY P, 1986, J CHILD PSYCHOL PSYC, V27, P657, DOI 10.1111/j.1469-7610.1986.tb00190.x PERRETT DI, 1985, PROC R SOC SER B-BIO, V223, P293, DOI 10.1098/rspb.1985.0003 Povinelli DJ, 1996, J COMP PSYCHOL, V110, P336 Schuller AM, 2001, NEUROREPORT, V12, P2381, DOI 10.1097/00001756-200108080-00019 SIGMAN M, 1986, J CHILD PSYCHOL PSYC, V27, P647, DOI 10.1111/j.1469-7610.1986.tb00189.x NR 22 TC 15 Z9 17 PU PSYCHOLOGIA SOC PI KYOTO PA DEPT EDUC PSYCHOL FAC EDUC KYOTO UNIV, KYOTO, 606, JAPAN SN 0033-2852 J9 PSYCHOLOGIA JI Psychologia PD JAN PY 2003 VL 46 IS 4 BP 246 EP 254 DI 10.2117/psysoc.2003.246 PG 9 WC Psychology, Multidisciplinary SC Psychology GA 776FY UT WOS:000189107000004 ER PT J AU Marquette, JM AF Marquette, JM TI Siblings of children with autism: A guide for families (2nd edition) SO RESEARCH AND PRACTICE FOR PERSONS WITH SEVERE DISABILITIES LA English DT Book Review C1 Univ Louisville, Louisville, KY 40292 USA. RP Marquette, JM (reprint author), Univ Louisville, Louisville, KY 40292 USA. CR FERGUSON PM, 1988, J ASSOC PERS SEVERE, V13, P177 Gray David E., 1992, Australia and New Zealand Journal of Developmental Disabilities, V18, P83 Harris S. L., 2003, SIBLINGS CHILDREN AU MARQUETTE JM, 2002, ANN C ASS U CTR DIS Sharpley CF, 1997, J INTELLECT DEV DIS, V22, P19, DOI 10.1080/13668259700033261 NR 5 TC 0 Z9 0 PU TASH PI BALTIMORE PA 29 W SUSQUEHANNA AVE, STE 210, BALTIMORE, MD 21204-5201 USA SN 0274-9483 J9 RES PRACT PERS SEV D JI Res. Pract. Pers. Sev. Disabil. PD WIN PY 2003 VL 28 IS 4 BP 232 EP 234 DI 10.2511/rpsd.28.4.232 PG 3 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 832BS UT WOS:000222242800007 ER PT J AU Alpas, B Akcakin, M AF Alpas, B Akcakin, M TI The adaptation, reliability and validity study of the Vineland Adaptive Behavior Scales - Survey Form - (Vineland) for Turkish babies SO TURK PSIKOLOJI DERGISI LA Turkish DT Article DE Vineland Adaptive Behavior Scales (Survey Form); adaptation; reliability; validity; infancy and early childhood stage; adaptive behavior ID CHILDREN; AUTISM; CONVERGENT; EDITION; SAMPLE; SKILLS; MOTOR AB The aim of this study was to investigate the adaptation, reliability and validity of the Vineland Adaptive Behavior Scales - Survey Form - (Vineland) for Turkish babies, whose original was developed by Sparrow et all in 1984. The Vineland was administered on total 561 (283 girls, 278 boys) normal children and total 23 (5 girls, 18 boys) autistic children. This children between four different age ranges (0 - 11 months, 12 - 23 months, 24 - 35 months and 36 - 47 months) from three different SES group (low, middle and high) were selected for this study. Results indicated that as children grew older, their total scores on the scale also increased. There were no significant differences in sex. In the 24 - 35 and 36 - 47 months age ranges, high SES children's scores were higher than the others (low and middle SES). When the age was divorced in the month ranges, there were no significant differences from birth to 24 months age ranges. Reliability studies of scale included Interrater Reliability (97 - .99), Test Retest (91 and .98) and Internal Consistency Analysis (95 - .97). Validity studies assessed with three different methods: Construct Validity (factor analysis), and two different Criterion Validity studies. This results revealed that the Vineland could be used as a qualitative and a quantitative assessment instrument in infancy and early childhood stages of Turkish children. C1 Ankara Univ, Cocuk Ruh Sagligi Hastaliklari Anabilim Dali, TR-06590 Cebeci Ankara, Turkey. RP Alpas, B (reprint author), Ankara Univ, Cocuk Ruh Sagligi Hastaliklari Anabilim Dali, TR-06590 Cebeci Ankara, Turkey. CR AKCAKIN M, 1993, TURK PSIKOL DERG, V29, P3 Akcakin M., 2002, COCUK GENCLIK RUH SA, V9, P3 AKCAKIN M, 1993, TURK PSIKIYATR DERG, V4, P39 American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Anastasi A., 1968, PSYCHOL TESTING, V3rd ATKINSON L, 1992, J SCHOOL PSYCHOL, V30, P165, DOI 10.1016/0022-4405(92)90028-4 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BRITTON WH, 1986, AM J MENT RETARD, V91, P105 DELEMOS MM, 1989, PSYCHOL TEST B, V2, P3 DELGADO LD, 1990, AVANCES PSICOLOGIA C, V8, P99 Doll E. 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PD DEC PY 2003 VL 18 IS 52 BP 57 EP 71 PG 15 WC Psychology, Multidisciplinary SC Psychology GA 754WY UT WOS:000187357000004 ER PT J AU Singer, E AF Singer, E TI US draws up plans to tackle autism SO NATURE LA English DT News Item CR 2003, NATURE, V425, P438 NR 1 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI LONDON PA MACMILLAN BUILDING, 4 CRINAN ST, LONDON N1 9XW, ENGLAND SN 0028-0836 J9 NATURE JI Nature PD NOV 27 PY 2003 VL 426 IS 6965 BP 373 EP 373 DI 10.1038/426373b PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 747JE UT WOS:000186800800007 PM 14647347 ER PT J AU Gage, NM Siegel, B Callen, M Roberts, TPL AF Gage, NM Siegel, B Callen, M Roberts, TPL TI Cortical sound processing in children with autism disorder: an MEG investigation SO NEUROREPORT LA English DT Article DE auditory cortex; auditory perception; autism disorder; development; hemispheric asymmetry; language; Magnetoencephalography; M100; neurodevelopmental disorder ID NEUROMAGNETIC M100; EVOKED-POTENTIALS; AUDITORY-CORTEX; PERCEPTION; MATURATION; LATENCY; FIELDS; SPEECH AB Previous work investigating frequency encoding mechanisms in human auditory cortex has provided evidence that latency of the auditory evoked M100 is strongly proportional to frequency, with low frequency (100-200 Hz) tones associated with similar to 30 ms longer latencies than mid-range frequency (1-2 kHz) tones. Motivated by pervasive speech and auditory perception deficits observed in autism spectrum disorder, we evaluated M100 frequency dependence in children with autism disorder and typically developing controls. Results indicate that for control children, the dynamic range of frequency modulation was similar to previous reports for healthy adults. Children with autism had a much reduced range of modulation in right hemisphere sites. Findings indicate that frequency encoding mechanisms may follow a differential maturational path in autism spectrum disorder. C1 Univ Calif Irvine, Dept Radiol, Biomagnet Imaging Lab, Irvine, CA 92697 USA. Univ Calif San Francisco, Pervas Dev Disorders Clin, San Francisco, CA 94143 USA. RP Gage, NM (reprint author), Univ Calif Irvine, Dept Radiol, Biomagnet Imaging Lab, Mail Code 5100,3151 Social Sci Plaza A, Irvine, CA 92697 USA. EM ngage@uci.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN AM PS, V4th California-Department-of-Developmental-Services, 2002, AUT SPECTR DIS BEST EGGERMONT JJ, 1988, ELECTROEN CLIN NEURO, V70, P293, DOI 10.1016/0013-4694(88)90048-X Gage N, 1998, BRAIN RES, V814, P236, DOI 10.1016/S0006-8993(98)01058-0 Gage NM, 2002, COGNITIVE BRAIN RES, V14, P303, DOI 10.1016/S0926-6410(02)00128-3 GAGE NM, IN PRESS DEV BRAIN R GREENBERG S, 1997, INT S HEAR BELT WOOD JACOBSON GP, 1992, EAR HEART, V13, P3887 Jancke L, 2002, NEUROIMAGE, V15, P733, DOI 10.1006/nimg.2001.1027 LORD C, 1997, J AUTISM DEV DISORD, V27, P510 Ornitz E. M., 1989, AUTISM NATURE DIAGNO, P174 PAETAU R, 1995, J CLIN NEUROPHYSIOL, V12, P177, DOI 10.1097/00004691-199503000-00008 Pell MD, 1999, BRAIN LANG, V69, P161, DOI 10.1006/brln.1999.2065 Poldrack RA, 2001, J COGNITIVE NEUROSCI, V13, P687, DOI 10.1162/089892901750363235 Ponton C, 2002, CLIN NEUROPHYSIOL, V113, P407, DOI 10.1016/S1388-2457(01)00733-7 Rapin I., 1992, HDB NEUROPSYCHOLOGY, P111 Roberts TPL, 1998, NEUROREPORT, V9, P3265, DOI 10.1097/00001756-199810050-00024 Roberts TPL, 2000, J CLIN NEUROPHYSIOL, V17, P114, DOI 10.1097/00004691-200003000-00002 Rojas DC, 1998, NEUROREPORT, V9, P1543 VERKINDT C, 1995, EVOKED POTENTIAL, V96, P143, DOI 10.1016/0168-5597(94)00242-7 WOODS DL, 1993, HEARING RES, V66, P46, DOI 10.1016/0378-5955(93)90258-3 Zatorre RJ, 2002, TRENDS COGN SCI, V6, P37, DOI 10.1016/S1364-6613(00)01816-7 Zatorre RJ, 2001, CEREB CORTEX, V11, P946, DOI 10.1093/cercor/11.10.946 NR 23 TC 46 Z9 49 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD NOV 14 PY 2003 VL 14 IS 16 BP 2047 EP 2051 DI 10.1097/01.wnr.0000090030.460874a PG 5 WC Neurosciences SC Neurosciences & Neurology GA 803CH UT WOS:000220208700008 PM 14600495 ER PT J AU Stokstad, E AF Stokstad, E TI Vaccine-autism link dealt blow (vol 301, pg 1454, 2003) SO SCIENCE LA English DT Correction CR Madsen KM, 2003, PEDIATRICS, V112, P604, DOI 10.1542/peds.112.3.604 Stokstad E, 2003, SCIENCE, V301, P1454 NR 2 TC 0 Z9 0 PU AMER ASSOC ADVANCEMENT SCIENCE PI WASHINGTON PA 1200 NEW YORK AVE, NW, WASHINGTON, DC 20005 USA SN 0036-8075 J9 SCIENCE JI Science PD NOV 14 PY 2003 VL 302 IS 5648 BP 1152 EP 1152 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 742XW UT WOS:000186544300027 ER PT J AU Hubl, D Bolte, S Feineis-Matthews, S Lanfermann, H Federspiel, A Strik, W Poustka, F Dierks, T AF Hubl, D Bolte, S Feineis-Matthews, S Lanfermann, H Federspiel, A Strik, W Poustka, F Dierks, T TI Functional imbalance of visual pathways indicates alternative face processing strategies in autism SO NEUROLOGY LA English DT Article ID FRONTAL EYE FIELDS; OBJECT RECOGNITION; FACIAL EXPRESSIONS; NEURAL SYSTEMS; HUMAN BRAIN; ACTIVATION; AREA; CHILDREN; CORTEX; DISCRIMINATION AB Objective: To investigate whether autistic subjects show a different pattern of neural activity than healthy individuals during processing of faces and complex patterns. Methods: Blood oxygen level-dependent (BOLD) signal changes accompanying visual processing of faces and complex patterns were analyzed in an autistic group (n=7; 25.3 [6.9] years) and a control group (n=7; 27.7 [7.8] years). Results: Compared with unaffected subjects, autistic subjects demonstrated lower BOLD signals in the fusiform gyrus, most prominently during face processing, and higher signals in the more object-related medial occipital gyrus. Further signal increases in autistic subjects vs controls were found in regions highly important for visual search: the superior parietal lobule and the medial frontal gyrus, where the frontal eye fields are located. Conclusions: The cortical activation pattern during face processing indicates deficits in the face-specific regions, with higher activations in regions involved in visual search. These findings reflect different strategies for visual processing, supporting models that propose a predisposition to local rather than global modes of information processing in autism. C1 Univ Hosp Clin Psychiat, Dept Psychiat Neurophysiol, CH-3000 Bern, Switzerland. Univ Frankfurt, Dept Radiol, Inst Neuroradiol, D-6000 Frankfurt, Germany. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. RP Hubl, D (reprint author), Univ Hosp Clin Psychiat, Dept Psychiat Neurophysiol, Bolligenstr 111, CH-3000 Bern, Switzerland. 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Med. J. PD NOV 8 PY 2003 VL 327 IS 7423 BP 1069 EP 1069 DI 10.1136/bmj.327.7423.1069-c PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 742QW UT WOS:000186530400013 ER PT J AU Vicente, MP Antoranz, AV Moreo, LG AF Vicente, MP Antoranz, AV Moreo, LG TI Review on the study of the theory of the mind in pervasive development disorders and schizophrenia SO ACTAS ESPANOLAS DE PSIQUIATRIA LA Spanish DT Review DE theory of mind; schizophrenia; pervasive developemental disorders metarepresentation ID AUTISM; PEOPLE; SYMPTOMATOLOGY; CONSCIOUSNESS; IMPAIRMENTS; INTENTIONS; COGNITION; CHILDREN; OTHERS AB The theory of mind (ToM) is a new concept which could be defined as the ability to make inferences on the intentions of others. This capacity has been used to explain childhood autism symptoms and recently an attempt has been made to refer it to schizophrenia The authors aim to review the theory of mind concept, the different questions that could appear in neurocognitive sciences and the utilities that this hypothetical model has been given in the clinical practice. The authors also consider the contributions and restrictions that its use has in the field of pervasive developmental disorders and schizophrenia. C1 Univ Madrid, Hosp La Princesa, Madrid 28006, Spain. RP Vicente, MP (reprint author), Univ Madrid, Hosp La Princesa, Diego Leon 62, Madrid 28006, Spain. 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Psiquiatri. PD NOV-DEC PY 2003 VL 31 IS 6 BP 339 EP 346 PG 8 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 755NC UT WOS:000187413700005 ER PT J AU Bonora, E Lamb, JA Abbott, A Redhead, N Ragoussis, I Bailey, AJ Monaco, AP AF Bonora, E Lamb, JA Abbott, A Redhead, N Ragoussis, I Bailey, AJ Monaco, AP TI Linkage to the AUTS1 locus and analysis of candidate genes for autism on chromosome 7q. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. Univ Oxford, Warneford Hosp, Dept Psychiat, Oxford, England. RI Bailey, Anthony/J-2860-2014 OI Bailey, Anthony/0000-0003-4257-972X NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 108 BP 183 EP 183 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700110 ER PT J AU Gharani, N Benayed, R Brzustowicz, LM Millonig, JH AF Gharani, N Benayed, R Brzustowicz, LM Millonig, JH TI Association of the homeodomain transcription factor ENGRAILED 2 with autism spectrum disorder. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Rutgers State Univ, Dept Genet, Piscataway, NJ USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Psychiat, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Dept Cell Biol & Neurosci, Piscataway, NJ 08854 USA. Univ Med & Dent New Jersey, Robert Wood Johnson Med Sch, Ctr Adv Biotechnol, Piscataway, NJ 08854 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 107 BP 183 EP 183 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700107 ER PT J AU Vieland, VJ Sheffield, V Wassink, T Beck, J Goedken, R Childress, D Piveri, J AF Vieland, VJ Sheffield, V Wassink, T Beck, J Goedken, R Childress, D Piveri, J TI A new genome screen for autism based on the posterior probability of linkage (PPL) and incorporating language-based phenotypes finds evidence of linkage to several genomic locations, each supported by independent sources of information. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Iowa, Iowa City, IA 52242 USA. Univ N Carolina, Chapel Hill, NC USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 174 BP 196 EP 196 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700175 ER PT J AU Thatcher, KN Braunschweig, D Samaco, RC LaSalle, JM AF Thatcher, KN Braunschweig, D Samaco, RC LaSalle, JM TI Homologous pairing of 15q11-13 imprinted domains in brain is developmentally regulated but deficient in Rett and autism samples. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Calif Davis, Sch Med, Davis, CA 95616 USA. RI LaSalle, Janine/A-4643-2008 OI LaSalle, Janine/0000-0002-3480-2031 NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 279 BP 217 EP 217 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700278 ER PT J AU Arnold, GL Hyman, SL Delucia, L Mooney, RA AF Arnold, GL Hyman, SL Delucia, L Mooney, RA TI Gluten and dairy restricted diets alter plasma amino acids and neurotransmitter precursors in autism SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Rochester, Sch Med & Dent, Dept Pediat & Pathol, Rochester, NY USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 513 BP 258 EP 258 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700516 ER PT J AU Luc-Chese, S Takahashi, N Miles, J AF Luc-Chese, S Takahashi, N Miles, J TI Is autism caused by numerous genetic and cytogenetic syndromes? SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Missouri, Dept Child Hlth, Med Gen Div, Columbia, MO 65201 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 589 BP 270 EP 270 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700590 ER PT J AU Foran, T Bocian, M Flodman, P Miles, JH Spence, MA AF Foran, T Bocian, M Flodman, P Miles, JH Spence, MA TI Minor physical anomalies in autism SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Calif Irvine, Dept Pediat, Div Human Genet, Irvine, CA USA. Univ Missouri, Childrens Hosp, Columbia, MO USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 690 BP 287 EP 287 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700689 ER PT J AU Miles, J Bocian, M Farmer, J Takahashi, N Spence, M Braddock, S Martin, R Hong, J AF Miles, J Bocian, M Farmer, J Takahashi, N Spence, M Braddock, S Martin, R Hong, J TI Autism and dysmorphology: A valid observational measure SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ MO Hosp, Dept Child Hlth, Div Med Gen, Columbia, MO USA. Univ MO, Dept Hlth Psych, Columbia, MO USA. Univ Calif Irvine, Div Hum Gen & Birth Defects, Orange, CA 92668 USA. Washington Univ, Sch Med, St Louis, MO USA. NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 693 BP 288 EP 288 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700696 ER PT J AU Edelmann, L Shanske, AL Gosset, P Kardon, NB Levy, B AF Edelmann, L Shanske, AL Gosset, P Kardon, NB Levy, B TI A 13 Mb deletion on 2q21 in a patient with a t(1;2)(31;q21), autism and multiple congenital anomalies. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Mt Sinai Sch Med, Dept Human Genet, New York, NY USA. Albert Einstein Coll Med, Childrens Hosp Montefiore, Bronx, NY 10467 USA. Hop Necker Enfants Malad, Dept Genet, Paris, France. Hop Necker Enfants Malad, Unite INSERM U393, Paris, France. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 758 BP 299 EP 299 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700759 ER PT J AU Christian, SL Weiss, LA Fritz, HL Lord, C Akshoomoff, N Courchesne, E Wu, X Leventhal, BL Cook, EH AF Christian, SL Weiss, LA Fritz, HL Lord, C Akshoomoff, N Courchesne, E Wu, X Leventhal, BL Cook, EH TI Maternal duplication of 15q11-q13 identified in one autism patient during linkage disequilibrium mapping. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. Univ Michigan, Dept Psychol, Ann Arbor, MI 48109 USA. Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Childrens Hosp, Res Ctr, San Diego, CA USA. Univ Chicago, Dept Pediat, Chicago, IL 60637 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 783 BP 304 EP 304 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700784 ER PT J AU Samaco, RC Nagarajan, RP Braunschweig, D Lasalle, JM AF Samaco, RC Nagarajan, RP Braunschweig, D Lasalle, JM TI Multiple pathways regulate MeCP2 in normal brain development and exhibit defects in non-MECP2 mutant Rett and autism samples. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Calif Davis, Sch Med, Davis, CA 95616 USA. RI LaSalle, Janine/A-4643-2008 OI LaSalle, Janine/0000-0002-3480-2031 NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 903 BP 324 EP 324 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700906 ER PT J AU Martin, CL Ilkin, Y Powell, C Rao, K Whichello, A Cook, E AF Martin, CL Ilkin, Y Powell, C Rao, K Whichello, A Cook, E TI Breakpoint mapping of a de novo 15p;16p translocation reveals a candidate gene for autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Duke Univ, Sch Nursing, Durham, NC USA. Univ N Carolina, Div Genet & Metab, Chapel Hill, NC USA. Univ Chicago, Dept Human Genet, Chicago, IL 60637 USA. NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 910 BP 325 EP 325 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700910 ER PT J AU Jaworski, J Ashley-Koch, AE Menold, M Abramson, RK DeLong, GR Wright, HH Cuccaro, ML Gilbert, JR Pericak-Vancl, MA AF Jaworski, J Ashley-Koch, AE Menold, M Abramson, RK DeLong, GR Wright, HH Cuccaro, ML Gilbert, JR Pericak-Vancl, MA TI Investigation of parent of origin effects for Autism susceptibility loci on chromosomes 2, 7 and 15. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Duke Univ, Med Ctr, Durham, NC USA. Univ S Carolina, Columbia, SC 29208 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 965 BP 334 EP 334 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599700964 ER PT J AU Reddy, K AF Reddy, K TI Autism: Incidence of cytogenetic abnormality and fragile-X syndrome. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Genzyme Genet, Diagnost Team, Orange, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1178 BP 372 EP 372 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701178 ER PT J AU Wolpert, CM Grubber, J Donnelly, SL DeLong, GR Ravan, SA Abramson, RA Wright, HH Gilbert, JR Cuccaro, ML Pericak-Vance, MA AF Wolpert, CM Grubber, J Donnelly, SL DeLong, GR Ravan, SA Abramson, RA Wright, HH Gilbert, JR Cuccaro, ML Pericak-Vance, MA TI Evidence supporting the MFTM in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Duke Univ, Med Ctr, Durham, NC 27706 USA. Univ S Carolina, Columbia, SC 29208 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1179 BP 372 EP 372 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701181 ER PT J AU Szatmari, P Merette, C Emond, C Zwaigenbaum, L Maziade, M Roy, MA Palmour, R AF Szatmari, P Merette, C Emond, C Zwaigenbaum, L Maziade, M Roy, MA Palmour, R TI Disentangling the autism phenotype; a sib-pair analysis. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 McMaster Univ, Dept Psychiat, Hamilton, ON L8S 4L8, Canada. Univ Laval, Dept Psychiat, Quebec City, PQ, Canada. McMaster Univ, Dept Pediat, Hamilton, ON L8S 4L8, Canada. McGill Univ, Dept Psychiat, Montreal, PQ H3A 2T5, Canada. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1292 BP 391 EP 391 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701292 ER PT J AU Scardovi, AL Ottolenghi, C Soli, F Stanghellini, I Caffo, E Forabosco, A AF Scardovi, AL Ottolenghi, C Soli, F Stanghellini, I Caffo, E Forabosco, A TI Automated transcript mapping detects brain-specific gene transcripts in a region on 16p13 associated with autism SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Modena, I-41100 Modena, Italy. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1559 BP 436 EP 436 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701559 ER PT J AU Carlo, S Arciniegas, NJ Valencia, D Acevedo, JR Ramos, I Reis, AA Massanet, JM Ramirez, N Cornier, AS AF Carlo, S Arciniegas, NJ Valencia, D Acevedo, JR Ramos, I Reis, AA Massanet, JM Ramirez, N Cornier, AS TI Presence of lactic Acidemia and elevated lactate-pyruvate ratio in patients with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Ponce Sch Med, Dept Biochem, Ponce, PR USA. Genet Diagnost Grp, Mayaguez, PR USA. Univ Puerto Rico, Arecibo, PR USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1612 BP 445 EP 445 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701611 ER PT J AU Stodgell, CJ Wanek, N O'Bara, M Hyman, SL Bryson, S Rodier, PM AF Stodgell, CJ Wanek, N O'Bara, M Hyman, SL Bryson, S Rodier, PM TI Association of HOXD1 and GBX2 allelic variants with autism spectrum disorders. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Rochester, Rochester, NY 14627 USA. Rochester Inst Technol, Rochester, NY 14623 USA. Dalhousie Univ, IWK Hlth Ctr, Halifax, NS B3H 3J5, Canada. RI Stodgell, Christopher/A-1161-2007 NR 0 TC 1 Z9 1 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1760 BP 470 EP 470 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701762 ER PT J AU Ashley-Koch, AE Martin, ER Jaworski, J Menold, MM Haynes, CA Cuccaro, ML Gilbert, JR Pericak-Vance, MA AF Ashley-Koch, AE Martin, ER Jaworski, J Menold, MM Haynes, CA Cuccaro, ML Gilbert, JR Pericak-Vance, MA TI Examination of multilocus association of the GABAA receptor subunit genes in multiplex autism families. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Duke Univ, Med Ctr, Durham, NC USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1885 BP 491 EP 491 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701885 ER PT J AU Pericak-Vance, MA Rabionet, R Skaar, D Abramson, RK Wright, HH DeLong, GR Cuccaro, ML Gilbert, JR AF Pericak-Vance, MA Rabionet, R Skaar, D Abramson, RK Wright, HH DeLong, GR Cuccaro, ML Gilbert, JR TI Evidence for linkage to chromosome 19 in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Duke Univ, Med Ctr, Durham, NC USA. Univ S Carolina, Columbia, SC 29208 USA. RI rabionet, raquel/A-7407-2009 OI rabionet, raquel/0000-0001-5006-8140 NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1912 BP 495 EP 495 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701913 ER PT J AU Sutcliffe, JS Olson, LM McCauley, JL Dowd, M Winkloski, B Rosen-Sheidley, B Crockett, G Folstein, SE Haines, JL AF Sutcliffe, JS Olson, LM McCauley, JL Dowd, M Winkloski, B Rosen-Sheidley, B Crockett, G Folstein, SE Haines, JL TI A genome-wide screen for autism susceptibility loci identifies significant linkage on 19p SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Vanderbilt Univ, Dept Mol Physiol & Biophys, Program Human Genet, Nashville, TN USA. Tufts Univ, New England Med Ctr, Dept Psychiat, Boston, MA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1937 BP 500 EP 500 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701938 ER PT J AU Spence, SJ Kim, SH Geschwind, DH Alarcon, M AF Spence, SJ Kim, SH Geschwind, DH Alarcon, M TI Chromosome 7q linkage in autism: No evidence for strengthened signal by including parental information or stratification based on language delay SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Calif Los Angeles, AGRE, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 1951 BP 502 EP 502 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599701951 ER PT J AU Wassink, TH Piven, J Vieland, VJ Jenkins, L Goedken, P Spence, MA Smith, M Sheffield, VC AF Wassink, TH Piven, J Vieland, VJ Jenkins, L Goedken, P Spence, MA Smith, M Sheffield, VC TI Evidence supporting CENTG2 as an autism susceptibility gene. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Iowa, Carver Coll Med, Dept Psychiat, Iowa City, IA USA. Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. Univ Iowa, Coll Publ Hlth, Dept Biostat, Iowa City, IA USA. Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. Univ Calif Irvine, Dept Pediat, Iowa City, IA USA. Univ Iowa, Carver Coll Med, Dept Pediat, Iowa City, IA USA. Univ Iowa, Carver Coll Med, Howard Hughes Med Inst, Iowa City, IA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2011 BP 512 EP 512 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702010 ER PT J AU Smith, M Flodman, P Woodroffe, A Bocian, ME Hariouni, M Spence, MA AF Smith, M Flodman, P Woodroffe, A Bocian, ME Hariouni, M Spence, MA TI Chromosome microdeletions as etiological factors in autism: Report of 4 cases and identification of autism candidate genes. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Calif Irvine, Dept Pediat, Irvine, CA 92717 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2017 BP 513 EP 513 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702016 ER PT J AU Woodroffe, A Ramanathan, S Flodman, P Bocian, M Mays, L Modahl, C Hanouni, M Spence, MA Smith, M AF Woodroffe, A Ramanathan, S Flodman, P Bocian, M Mays, L Modahl, C Hanouni, M Spence, MA Smith, M TI Molecular genetic analysis of a chromosome 4q31.3-34 deletion associated with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Calif Irvine, Irvine, CA 92717 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2013 BP 513 EP 513 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702014 ER PT J AU Talebizadeh, Z Bittel, DC Kibiryeva, N Butler, MG AF Talebizadeh, Z Bittel, DC Kibiryeva, N Butler, MG TI X chromosome inactivation and candidate gene studies in females with autism SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Childrens Mercy Hosp & Clin, Kansas City, MO USA. Univ Missouri, Sch Med, Kansas City, MO 64108 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2020 BP 514 EP 514 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702023 ER PT J AU Vicente, AM Silva, S Coutinho, AM Bento, C Marques, C Atade, A Miguel, T Borges, L Oliveira, G AF Vicente, AM Silva, S Coutinho, AM Bento, C Marques, C Atade, A Miguel, T Borges, L Oliveira, G TI Evidence for the involvement of the BDNF gene in autism and relation to family history of depression SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Gulbenkian Inst Sci, P-2781 Oeiras, Portugal. Hosp Pediat Coimbra, Coimbra, Portugal. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2022 BP 514 EP 514 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702024 ER PT J AU Shah, AB Faustino, J Zordan, R Angeli, S Gitschier, J AF Shah, AB Faustino, J Zordan, R Angeli, S Gitschier, J TI Identification of ethyl mercury-related genetic determinants that may increase susceptibility towards autism using a yeast deletion based assay SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Calif San Francisco, Howard Hughes Med Inst, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA. Univ Calif San Francisco, Dept Pediat, San Francisco, CA 94143 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2026 BP 515 EP 515 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702029 ER PT J AU Skaar, DA Christ, L Cucarro, ML Gilbert, JR Schwartz, S Pericak-Vance, MA AF Skaar, DA Christ, L Cucarro, ML Gilbert, JR Schwartz, S Pericak-Vance, MA TI Identification of chromosome 7 breakpoints in an autistic family indicates candidate genes for autism susceptibility SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Duke Univ, Ctr Human Genet, Med Ctr, Durham, NC USA. Case Western Reserve Univ, Dept Genet, Cleveland, OH 44106 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2051 BP 519 EP 519 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702051 ER PT J AU Moreira, ES Orabona, GM Avelar, LO Vadasz, E Biason, LM Takahashi, VNO Abe, K Vianna-Morgante, AM Passos-Bueno, MR AF Moreira, ES Orabona, GM Avelar, LO Vadasz, E Biason, LM Takahashi, VNO Abe, K Vianna-Morgante, AM Passos-Bueno, MR TI Molecular and cytogenetic analyses in Brazilian patients affected by autism spectrum disorders SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Sao Paulo, Inst Biociencias, Ctr Estudos Genoma Humano, Dept Biol, Sao Paulo, Brazil. Univ Sao Paulo, Fac Med, Hosp Clin, SEPIA,Inst Psiquiatria, Sao Paulo, Brazil. RI Moreira, Eloisa/K-9155-2014 NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2055 BP 520 EP 520 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702056 ER PT J AU Sahoo, T Jiang, Y Shinawi, M Michaelis, RC Buyse, I Kashork, CD Schroer, RJ Roa, BB Stockton, DW Spielman, RS Stevenson, RE Shaffer, LG Beaudet, AL AF Sahoo, T Jiang, Y Shinawi, M Michaelis, RC Buyse, I Kashork, CD Schroer, RJ Roa, BB Stockton, DW Spielman, RS Stevenson, RE Shaffer, LG Beaudet, AL TI A mixed epigenetic-genetic model for autism with the ubiquitin ligase UBE3A as a candidate principal gene. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Baylor Coll Med, Houston, TX 77030 USA. Greenwood Genet Ctr, Greenwood, SC USA. Univ Penn, Philadelphia, PA 19104 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2072 BP 522 EP 522 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702073 ER PT J AU Feng, J Shibayama, A Glanzmann, C Yan, J Cook, E Craddock, N Jones, I Goldman, D Heston, L Sommer, S AF Feng, J Shibayama, A Glanzmann, C Yan, J Cook, E Craddock, N Jones, I Goldman, D Heston, L Sommer, S TI MECP2 variants in psychiatric diseases: Possible association with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 City Hosp Natl Med Ctr, Dept Mol Genet, Duarte, CA USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Birmingham, Div Neurosci, Queen Elizabeth Psychiat Hosp, Birmingham, W Midlands, England. NIAAA, NIH, Bethesda, MD USA. Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. RI Jones, Ian/B-4925-2009 NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2078 BP 523 EP 523 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702079 ER PT J AU Coutinho, AM Oliveira, G Fesel, C Marques, C Ataide, A Miguel, T Borges, L Vicente, AM AF Coutinho, AM Oliveira, G Fesel, C Marques, C Ataide, A Miguel, T Borges, L Vicente, AM TI Association of the serotonin receptor 5-HT5A with autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Gulbenkian Inst Sci, Oeiras, Portugal. Hosp Pediat Coimbra, Coimbra, Portugal. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2096 BP 526 EP 526 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702097 ER PT J AU McCauley, JL Olson, LM Delahanty, R Amin, T Organ, EL Nurmi, EL Jacobs, MM Folstein, SE Haines, JL Sutcliffe, JS AF McCauley, JL Olson, LM Delahanty, R Amin, T Organ, EL Nurmi, EL Jacobs, MM Folstein, SE Haines, JL Sutcliffe, JS TI High-density linkage disequilibrium mapping at the 15q12 GABA receptor subunit cluster identifies association in autism. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Vanderbilt Univ, Program Human Genet, Dept Physiol & Mol Biophys, Nashville, TN USA. Tufts Univ, New England Med Ctr, Dept Psychiat, Medford, MA 02155 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2138 BP 533 EP 533 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702139 ER PT J AU Stone, JL Tsai, S Merriman, B Cantor-Chiu, RM Geschwind, DH Nelson, SF AF Stone, JL Tsai, S Merriman, B Cantor-Chiu, RM Geschwind, DH Nelson, SF CA AGRE Consortium TI High density SNP based association study of 21 candidate genes in autism spectrum disorder. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA USA. Univ Calif Los Angeles, Dept Neurol, Program Neurogenet, Sch Med, Los Angeles, CA 90024 USA. Univ Calif Los Angeles, Inst Neuropsychiat, Ctr Neurobehav Genet, Sch Med, Los Angeles, CA 90024 USA. Autism Genet Resource Exchange, Los Angeles, CA USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2145 BP 535 EP 535 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702146 ER PT J AU Michaelis, RC Steiner, CE Lobo-Menendez, F Skinner, C Wright, CM Schroer, RJ AF Michaelis, RC Steiner, CE Lobo-Menendez, F Skinner, C Wright, CM Schroer, RJ TI Tuberous sclerosis 2 (TSC2) gene variants in patients with autism and seizures. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Greenwood Genet Ctr, JC Self Res Inst, Greenwood, SC 29646 USA. Univ Sao Paulo, Campinas, Brazil. Presbyterian Coll, Clinton, SC USA. RI Steiner, Carlos/B-9319-2014 OI Steiner, Carlos/0000-0001-5148-3063 NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2166 BP 538 EP 538 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702168 ER PT J AU Rabionet, R Jaworski, J Cuccaro, ML Benton, JL Walters, S Wright, HH Abramson, RK DeLong, GR Gilbert, JR Pericak-Vance, MA AF Rabionet, R Jaworski, J Cuccaro, ML Benton, JL Walters, S Wright, HH Abramson, RK DeLong, GR Gilbert, JR Pericak-Vance, MA TI Analysis of Methyl Binding Domain (MBD) genes in autism risk. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Duke Univ, Med Ctr, Durham, NC 27706 USA. Univ S Carolina, Columbia, SC 29208 USA. RI rabionet, raquel/A-7407-2009 OI rabionet, raquel/0000-0001-5006-8140 NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2174 BP 539 EP 539 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702175 ER PT J AU Goedken, R Piven, J Sheffield, V Wassink, T Beck, J Vieland, V AF Goedken, R Piven, J Sheffield, V Wassink, T Beck, J Vieland, V TI How multiple data sets are combined affects autism genome screen results: 'Pooled' compared to sequentially updated linkage analyses. SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Meeting Abstract CT Annual Meeting of the American-Society-of-Human-Genetics CY NOV 04-08, 2003 CL LOS ANGELES, CALIFORNIA SP Amer Soc Human Genet C1 Univ Iowa, Iowa City, IA 52242 USA. Univ N Carolina, Chapel Hill, NC 27515 USA. NR 0 TC 0 Z9 0 PU UNIV CHICAGO PRESS PI CHICAGO PA 1427 E 60TH ST, CHICAGO, IL 60637-2954 USA SN 0002-9297 J9 AM J HUM GENET JI Am. J. Hum. Genet. PD NOV PY 2003 VL 73 IS 5 MA 2572 BP 607 EP 607 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 726LC UT WOS:000185599702575 ER PT J AU Bigler, ED Tate, DF Neeley, ES Wolfson, LJ Miller, MJ Rice, SA Cleavinger, H Anderson, C Coon, H Ozonoff, S Johnson, M Dinh, E Lu, J Mc Mahon, W Lainhart, JE AF Bigler, ED Tate, DF Neeley, ES Wolfson, LJ Miller, MJ Rice, SA Cleavinger, H Anderson, C Coon, H Ozonoff, S Johnson, M Dinh, E Lu, J Mc Mahon, W Lainhart, JE TI Temporal lobe, autism, and macrocephaly SO AMERICAN JOURNAL OF NEURORADIOLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; TRAUMATIC BRAIN INJURY; HIGH-RESOLUTION MRI; HEAD CIRCUMFERENCE; INCIDENTAL FINDINGS; MENTAL-RETARDATION; TUBEROUS SCLEROSIS; ASPERGER-SYNDROME; CHILDREN; INDIVIDUALS AB BACKGROUND AND PURPOSE: Because of increased prevalence of macrocephaly in autism, head size must be controlled for in studies that examine volumetric findings of the temporal lobe in autistic subjects. We prospectively examined temporal lobe structures in individuals with autism who were normocephalic or macrocephalic (head circumference > 97th percentile) and in control subjects who were normocephalic or macrocephalic or who had a reading disorder (unselected for head size). The rationale for the reading disorder group was to have control subjects with potential temporal lobe anomalies, but who were not autistic. METHODS: In individuals aged 7-31 years, autism was diagnosed on the basis of standardized interview and diagnostic criteria. Control subjects ranged in age from 7 to 22 years. All subjects were male. MR morphometrics of the major temporal lobe structures were based on ANALYZE segmentation routines, in which total brain volume and total intracranial volume (TICV) were calculated. Both group comparisons and developmental analyses were performed. RESULTS: No distinct temporal lobe abnormalities of volume were observed once head size (TICV) was controlled for. In autistic and control subjects, robust growth patterns were observed in white and gray matter that differed little between the groups. Although subtle differences were observed in some structures (ie, less white matter volume in the region of the temporal stem and overall temporal lobe), none was statistically significant. CONCLUSION. No major volumetric anomalies of the temporal lobe were found in cases of autism when IQ, TICV, and age were controlled. Temporal lobe abnormalities that may be associated with autism are likely to be more related to functional organization within the temporal lobe than to any gross volumetric difference. C1 Brigham Young Univ, Dept Psychol & Neurosci, Provo, UT 84602 USA. Brigham Young Univ, Dept Stat, Provo, UT 84602 USA. Univ Utah, Dept Psychiat, Salt Lake City, UT 84112 USA. Univ Calif Davis, Dept Psychiat, MIND Inst, Davis, CA 95616 USA. RP Bigler, ED (reprint author), Brigham Young Univ, Dept Psychol & Neurosci, 1001 SWKT, Provo, UT 84602 USA. 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PD NOV-DEC PY 2003 VL 24 IS 10 BP 2066 EP 2076 PG 11 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 746KD UT WOS:000186744800027 PM 14625235 ER PT J AU Boddaert, N Belin, P Chabane, N Poline, JB Barthelemy, C Mouren-Simeoni, MC Brunelle, F Samson, Y Zilbovicius, M AF Boddaert, N Belin, P Chabane, N Poline, JB Barthelemy, C Mouren-Simeoni, MC Brunelle, F Samson, Y Zilbovicius, M TI Perception of complex sounds: Abnormal pattern of cortical activation in autism SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID CEREBRAL-BLOOD-FLOW; FUNCTIONAL NEUROANATOMY; AUDITORY-PERCEPTION; CHILDHOOD AUTISM; DISCRIMINATION; DYSFUNCTION; INDIVIDUALS; CHILDREN; LANGUAGE; AREA AB Objective: Bilateral temporal hypoperfusion at rest was recently described in autism. In normal adults, these regions are activated by listening to speech-like sounds. To investigate auditory cortical processing in autism, the authors performed a positron emission tomography activation study. Method: Regional cerebral blood flow was measured in five autistic adults and eight comparison subjects during rest and while listening to speech-like sounds. Results: Similar to the comparison subjects, autistic patients showed a bilateral activation of the superior temporal gyrus. However, an abnormal pattern of hemispheric activation was observed in the autistic group. The volume of activation was larger on the right side in the autistic patients, whereas the reverse pattern was found in the comparison group. The direct comparison between the two groups showed that the right middle frontal gyrus exhibited significantly greater activation in the autistic group. Conversely, the left temporal areas exhibited less activation in autistic patients. Conclusions: These findings suggest that abnormal auditory cortical processing is implicated in the language impairments and the inadequate response to sounds typically seen in autism. C1 CEA, Serv Hosp Frederic Joliot, INSERM, Dept Rech Med,ERM0205, F-91406 Orsay, France. Assistance Publ Hop Paris, Serv Radiol Pediat, Paris, France. Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada. Assistance Publ Hop Paris, Hop Robert Debre, Serv Pedopsychiat, Paris, France. Inst Natl Sante & Rech Med, Tours, France. Assistance Publ Hop, Grp Hosp Pitie Salpetriere, Serv Urgences Cerebro Vasc, Paris, France. RP Zilbovicius, M (reprint author), CEA, Serv Hosp Frederic Joliot, INSERM, Dept Rech Med,ERM0205, 4 Pl Gen Leclerc, F-91406 Orsay, France. 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J. Psychiat. PD NOV PY 2003 VL 160 IS 11 BP 2057 EP 2060 DI 10.1176/appi.ajp.160.11.2057 PG 4 WC Psychiatry SC Psychiatry GA 740PB UT WOS:000186409800027 PM 14594758 ER PT J AU Fidler, DJ AF Fidler, DJ TI Parental vocalizations and perceived immaturity in Down syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID PRADER-WILLI-SYNDROME; MENTAL-RETARDATION; MOTHERS SPEECH; YOUNG-CHILDREN; LIFE-SPAN; STRESS; FAMILIES; INFANTS; AUTISM; IMPRESSIONS AB Previous findings suggest that children with Down syndrome may be perceived as more youthful than other children with mental retardation. In this study whether perceptions of youthfulness can be linked to parenting behavior, in particular increased prosodic adjustments characteristic of infant-directed speech, is investigated. The prosodic characteristics of parental language targeted to children with Down syndrome and children with other etiologies of mental retardation were compared. Results show that parents of children with Down syndrome raised their voice pitch significantly more (i.e., spoke in a higher register) and spoke with a significantly wider mean pitch variance than parents of children in the comparison group. Implications are discussed for parent-child interactions in children with different genetic mental retardation syndromes. C1 Colorado State Univ, Ft Collins, CO 80526 USA. RP Fidler, DJ (reprint author), Colorado State Univ, 110 Gifford Bldg, Ft Collins, CO 80526 USA. 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PD NOV PY 2003 VL 33 IS 6 BP 717 EP 717 PG 1 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 732TN UT WOS:000185961800087 ER PT J AU Wynn, JW Smith, T AF Wynn, JW Smith, T TI Generalization between receptive and expressive language in young children with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article ID BEHAVIORAL TREATMENT; COMPREHENSION; ACQUISITION; PRESCHOOLERS; IMITATION; WORD AB Generalization between expressive and receptive language was studied in six boys with autism (chronological age 47-76 months, language age 13-42 months). Each participant received training on three or four word pairs (e.g. hot/cold). Half the pairs were taught expressively and then receptively; the other half were taught in the reverse order. Data were obtained on generalization from the trained to untrained modality, generalization errors, and between- and within-subject differences. Across participants, the 'expressive first' condition led to cross-modal generalization more often than the 'receptive first' condition. However, one child displayed the opposite pattern, and three other children's patterns varied across training stimuli. Error analyses indicated that, when children failed to demonstrate receptive-to-expressive generalization, they did generalize in another manner: responding based on physical resemblance between cues used in the study and those used in previous training. The results suggest ways to individualize instruction and better understand cross-modal generalization. Copyright (C) 2003 John Wiley Sons, Ltd. C1 Childrens Hosp, Autism Ctr, Intens Behav Intervent Clin, Westerville, OH 43082 USA. Univ Calif Los Angeles, Los Angeles, CA USA. Univ Rochester, Med Ctr, Rochester, NY 14642 USA. RP Wynn, JW (reprint author), Childrens Hosp, Autism Ctr, Intens Behav Intervent Clin, 433 N Cleveland Ave, Westerville, OH 43082 USA. 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PD NOV PY 2003 VL 18 IS 4 BP 245 EP 266 DI 10.1002/bin.142 PG 22 WC Psychology, Clinical SC Psychology GA 748FZ UT WOS:000186853000002 ER PT J AU LeBlanc, LA Miguel, CF Cummings, AR Goldsmith, TR Carr, JE AF LeBlanc, LA Miguel, CF Cummings, AR Goldsmith, TR Carr, JE TI The effects of three stimulus-equivalence testing conditions on emergent US geography relations of children diagnosed with autism SO BEHAVIORAL INTERVENTIONS LA English DT Article ID DISCRIMINATION; SAMPLE AB Two children with autism were trained in US geography using a match to sample procedure. Different testing procedures commonly used in stimulus equivalence research were compared, including some conditions with reinforcement for responding to enhance motivation. Both children were able to master the trained geography relations and emergent stimulus relations were also noted. All three testing procedures produced similar effects, suggesting that incorporation of procedures to enhance motivation to respond does not invalidate testing in a stimulus equivalence preparation. Copyright (C) 2003 John Wiley Sons, Ltd. C1 Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. RP LeBlanc, LA (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. 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Intervent. PD NOV PY 2003 VL 18 IS 4 BP 279 EP 289 DI 10.1002/bin.144 PG 11 WC Psychology, Clinical SC Psychology GA 748FZ UT WOS:000186853000004 ER PT J AU Good, CD Lawrence, K Thomas, NS Price, CJ Ashburner, J Friston, KJ Frackowiak, RSJ Oreland, L Skuse, DH AF Good, CD Lawrence, K Thomas, NS Price, CJ Ashburner, J Friston, KJ Frackowiak, RSJ Oreland, L Skuse, DH TI Dosage-sensitive X-linked locus influences the development of amygdala and orbitofrontal cortex, and fear recognition in humans SO BRAIN LA English DT Article DE amygdala; Turner syndrome; X-chromosome; fear; emotion ID TURNER-SYNDROME; MONOAMINE-OXIDASE; COGNITIVE DEFICITS; SEX-DIFFERENCES; SHORT STATURE; EYE GAZE; AUTISM; BRAIN; CHROMOSOME; CHILDREN AB The amygdala, which plays a critical role in emotional learning and social cognition, is structurally and functionally sexually dimorphic in humans. We used magnetic neuroimaging and molecular genetic analyses with healthy subjects and patients possessing X-chromosome anomalies to find dosage-sensitive genes that might influence amygdala development. If such X-linked genes lacked a homologue on the Y-chromosome they would be expressed in one copy in normal 46,XY males and two copies in normal 46,XX females. We showed by means of magnetic neuroimaging that 46,XY males possess significantly increased amygdala volumes relative to normal 46,XX females. However, females with Turner syndrome (45,X) have even larger amygdalae than 46,XY males. This finding implies that haploinsufficiency for one or more X-linked genes influences amygdala development irrespective of a direct or indirect (endocrinological) mechanism involving the Y-chromosome. 45,X females also have increased grey matter volume in the orbitofrontal cortex bilaterally, close to a region implicated in emotional learning. They are as poor as patients with bilateral amygdalectomies in the recognition of fear from facial expressions. We attempted to localize the gene(s) responsible for these deficits in X-monosomy by means of a deletion mapping strategy. We studied female patients possessing structural X-anomalies of the short arm. A genetic locus (no greater than 4.96 Mb in size) at Xp11.3 appears to play a key role in amygdala and orbitofrontal structural and (by implication) functional development. Females with partial X-chromosome deletions, in whom this critical locus is deleted, have normal intelligence. Their fear recognition is as poor as that of 45,X females and their amygdalae are correspondingly enlarged. This 4.96 Mb region contains, among others, the genes for monoamine oxidase A (MAOA) and B (MAOB), which are involved in the oxidative deamination of several neurotransmitters, including dopamine and serotonin. 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Although the randomized controlled trial (RCT) is a major methodological breakthrough extending the limits of objectivity in clinical medical science, clinical trials of surgery have seldom included placebo surgery as a control, for ethical reasons. Especially in clinical studies intended eventually to establish a new intervention for developmental conditions, it has been recognized that there is huge examiner bias. In addition, the many miraculous cases that have been reported in nonsurgical open trials for developmental conditions and have eventually been evaluated as nonspecific positive outcomes in RCTs suggest that empirically promising interventions must be subjected to scientific scrutiny as soon as possible in the field of developmental conditions. Application to pediatric neurosurgery. Therefore, in childhood neurosurgery, clinical studies to establish a new therapeutic measure for developmental conditions should be designed as rigorously as possible using optimized scientific methods. The worldwide ethical guideline, the Declaration of Helsinki issued by the World Medical Association, can provide principles for the establishment of a new intervention in the treatment of a patient when proven therapeutic methods do not exist or methods used thus far have been ineffective. Physicians' discretion to use unproven or new therapeutic measures for such patients is approved in the presence of efforts of an ethical and scientific approach. Even if the measure is a very promising intervention, the research aspects must completely be demonstrated for informed consent and review by the ethical committee and the trial must be regarded as a clinical research. Especially when an RCT is not possible for ethical reasons, appropriate epidemiological data or animal experiments should suggest that the new measure is effective before a clinical trial. In a clinical setting, where neither epidemiological studies nor animal experimentation can be introduced, if necessary the researcher should collaborate with experts to obtain multidisciplinary justification for clinical testing. C1 Nagahama Shinryojyo, Inst EGT, Shimokoshiki, Kagoshima 8961411, Japan. RP Ijichi, S (reprint author), Nagahama Shinryojyo, Inst EGT, 8-3 Nagahama, Shimokoshiki, Kagoshima 8961411, Japan. 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PD NOV PY 2003 VL 19 IS 10-11 BP 711 EP 715 DI 10.1007/s00381-003-0846-6 PG 5 WC Clinical Neurology; Pediatrics; Surgery SC Neurosciences & Neurology; Pediatrics; Surgery GA 746JR UT WOS:000186743700001 PM 14566420 ER PT J AU Steffenburg, S Steffenburg, U Gillberg, C AF Steffenburg, S Steffenburg, U Gillberg, C TI Autism spectrum disorders in children with active epilepsy and learning disability: comorbidity, pre- and perinatal background, and seizure characteristics SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID MENTALLY-RETARDED CHILDREN; PERVASIVE DEVELOPMENTAL DISORDERS; PSYCHIATRIC-DISORDERS; DIAGNOSTIC INTERVIEW; PATHOGENETIC ASPECTS; CHILDHOOD EPILEPSY; ASPERGER-SYNDROME; RETARDATION; PREVALENCE; INDIVIDUALS AB The aim of this study was to examine the comorbidity pattern, seizure characteristics, and aetiology in a representative group of children with a combination of autism spectrum disorder (ASD), active epilepsy, and learning disability.* Ninety children (47 males, 43 females; mean age 11 years 2 months, range 8 to 16 years at the time of psychiatric examination) with active epilepsy and learning disability, identified in a population-based study in Goteborg, Sweden, were subdivided into those with and those without ASD and compared with respect to aetiology, additional neuroimpairments, and seizure characteristics. In addition, the cohorts were examined for trends of prevalence over a period of time. Results indicated that established aetiology was much more often present in the prenatal period than in the peri- or postnatal periods in the ASD group. Cerebral palsy and visual impairment were under-represented in the ASD group. Partial seizures tended to be more common and generalized seizures less common in the ASD group compared with the non-ASD group. Seizure onset was later in the ASD group. Many of the significant differences were accounted for by a large group of psychiatrically unclassifiable participants in the non-ASD group. There was no trend towards an increase of affected children over the 12-year period. 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To test for a sensory function, we applied a topical anesthetic to the participant's skin. SIB was reduced by 20 to 60% after application of the dermal anesthetic. These results support an automatic reinforcement hypothesis. Implications for treatment are discussed. C1 Lehigh Univ, Coll Educ, Bethlehem, PA 18015 USA. Univ N Texas, Denton, TX 76203 USA. Ctr Child Study, Denton, TX 76203 USA. RP Kern, L (reprint author), Lehigh Univ, Coll Educ, 111 Res Dr, Bethlehem, PA 18015 USA. 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PD NOV PY 2003 VL 45 IS 11 BP 769 EP 771 DI 10.1017/S0012162003001427 PG 3 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 738GU UT WOS:000186279000008 PM 14580133 ER PT J AU German, TP Nichols, S AF German, TP Nichols, S TI Children's counterfactual inferences about long and short causal chains SO DEVELOPMENTAL SCIENCE LA English DT Article ID FALSE BELIEF TASKS; MIND; REPRESENTATION; DIFFICULTY; DECEPTION; REALITY; AUTISM AB Recent findings on counterfactual reasoning in children have led to the claim that children's developing capacities in the domain of `theory of mind' might reflect the emergence of the ability to engage in counterfactual thinking over the preschool period (e.g Riggs, Peterson, Robinson & Mitchell, 1998). In the study reported here, groups of 3- and 4-year old children were presented with stories describing causal chains of several events, and asked counterfactual thinking tasks involving changes to different points in the chain. The ability to draw successful counterfactual inferences depended strongly on the inferential length of the problem, and the age of the children; while 3-year-olds performed above chance on short inference counterfactuals, they performed below chance on problems involving longer inference chains. Four-year-old children were above chance on all problems. Moreover, it was found that while success on longer chain inference problems was significantly correlated with the ability to pass tests of standard false belief, there was no such relationship for short inference problems, which were significantly easier than false belief problems. These results are discussed in terms of the developmental relationships between causal knowledge, counterfactual thinking and calculating the contents of mental states. C1 Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA. Coll Charleston, Dept Philosophy, Charleston, SC 29401 USA. 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PD NOV PY 2003 VL 6 IS 5 BP 514 EP 523 DI 10.1111/1467-7687.00309 PG 10 WC Psychology, Developmental; Psychology, Experimental SC Psychology GA 747CQ UT WOS:000186788000010 ER PT J AU Graul, AI AF Graul, AI TI Annual update 2003: Drugs for psychiatric disorders and substance abuse SO DRUGS OF THE FUTURE LA English DT Editorial Material AB This month's Annual Update 2003, dedicated to Drugs for Psychiatric Disorders and Substance Abuse, is comprised of a compendium of 137 drugs for the treatment of anxiety disorders, depression, bipolar disorder, schizophrenia, autism, attention deficit hyperactivity disorder, sleep disorders, alcohol abuse and alcoholism, drug abuse and addiction, and smoking cessation. The table of drugs includes products which have been launched for the first time since 2002 and others that were previously marketed for another indication. Products featured in the monograph updates section include agomelatine, aripiprazole, blonanserin, duloxetine hyrochloride, escitalopram oxalate, eszopiclone, gepirone hydrochloride, indiplon, INN-00835, lamotrigine, nalmefene, naltrexone hydrochloride, ocinaplon, olanzapine, pregabalin, quetiapine fumarate, TAK-375 and venlafaxine hydrochloride. NR 0 TC 3 Z9 3 PU PROUS SCIENCE, SA PI BARCELONA PA PO BOX 540, PROVENZA 388, 08025 BARCELONA, SPAIN SN 0377-8282 J9 DRUG FUTURE JI Drug Future PD NOV PY 2003 VL 28 IS 11 BP 1103 EP 1121 PG 19 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 777AA UT WOS:000189150700007 ER PT J AU Jacobson, RM AF Jacobson, RM TI Vaccine safety SO IMMUNOLOGY AND ALLERGY CLINICS OF NORTH AMERICA LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; ADDRESSING PARENTS CONCERNS; MEASLES VACCINATION; ROTAVIRUS VACCINE; RUBELLA VACCINATION; ADVERSE EVENTS; CROHNS-DISEASE; AUTISM; MUMPS; IMMUNIZATION AB Although tremendously successful in reducing the threat of many deadly childhood diseases, vaccination remains at the forefront of public debate due to safety concerns. This debate has interrupted vaccine delivery and has resulted in preventable disease and outbreaks. This article addresses issues that concern most or all vaccines as a class and specific vaccines routinely used in children and adults. A discussion of the processes in place for evaluating vaccine safety is included. C1 Mayo Clin, Vaccine Res Grp, Rochester, MN 55905 USA. Mayo Clin, Dept Pediat & Adolescent Med, Rochester, MN 55905 USA. RP Jacobson, RM (reprint author), Mayo Clin, Vaccine Res Grp, 200 1st St SW, Rochester, MN 55905 USA. 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Allerg. Clin. North Am. PD NOV PY 2003 VL 23 IS 4 BP 589 EP + DI 10.1016/S0889-8561(03)00090-0 PG 16 WC Allergy; Immunology SC Allergy; Immunology GA 757UZ UT WOS:000187581000003 PM 14753382 ER PT J AU Kurup, RK Kurup, PA AF Kurup, RK Kurup, PA TI A hypothalamic digoxin-mediated model for autism SO INTERNATIONAL JOURNAL OF NEUROSCIENCE LA English DT Article DE autism; digoxin; dolichol; ubiquinone ID RAT-BRAIN; GLYCOSAMINOGLYCANS; SCHIZOPHRENICS; GLUTATHIONE; TRYPTOPHAN; METABOLISM; GLUTAMATE; ILLNESSES; LIVER; SERUM AB The isoprenoid pathway and its metabolites-digoxin, dolichol, and ubiquinone were assessed in autism. The isoprenoid pathway and digoxin status was also studied for comparison in individuals of differing hemispheric dominance to determine the role of cerebral dominance in the genesis of autism. There was an upregulation of the isoprenoid pathway as evidenced by elevated HUG CoA reductase activity in autism. Digoxin, an endogenous Na+-K+ ATPase inhibitor secreted by the hypothalamus, was found to be elevated and RBC membrane Na+-K+ ATPase activity was found to be reduced in autism. Membrane Na+-K+ ATPase inhibition can result in increased intracellular Ca2+ and reduced magnesium levels. Hypothalamic digoxin can modulate conscious and subliminal perception and its dysfunction may lead to autism. Digoxin can also preferentially upregulate tryptophan transport over tyrosine resulting in increased levels of depolarizing tryptophan catabolites-serotonin, quinolinic acid (NMDA agonist), strychnine (blocks glycinergic inhibitory transmission), and nicotine (promotes dopamine release) and decreased levels of hyperpolarizing tyrosine catabolites-dopamine, noradrenaline, and morphine-contributing to membrane Na+-K+ ATPase inhibition. Increased nicotine levels can produce increased dopaminergic transmission in the presence of low dopamine levels. NMDA excitotoxicity could result from hypomagnesemia induced by membrane Na+-K+ ATPase inhibition and quinolinic acid, an NMDA agonist acting on the NMDA receptor Hypomizgnesemia and increased dolichol Level can affect glycoconjugate metabolism and membranogenesis leading on to disordered synaptic connectivity in the limbic allocortex and defective presentation of viral antigens and neuronal antigens contributing to autoimmunity and viral persistance important in the pathogenesis. Membrane Na+-K+ ATPase inhibition can produce immune activation, a component of autoimmunity. Mitochondrial dysfunction consequent to altered calcium/magnesium ratios and reduced ubiquinone levels can result in increased free radical generation and reduced free radical scavenging and defective opoptosis leading to abnormal synaptogenesis. Autism can thus be considered a syndrome of hypothalamic digoxin hypersecretion consequent to an upregulated isoprenoid pathway. 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J. Neurosci. PD NOV PY 2003 VL 113 IS 11 BP 1537 EP 1559 DI 10.1080/00207450390231482 PG 23 WC Neurosciences SC Neurosciences & Neurology GA 744AD UT WOS:000186605000006 PM 14585753 ER PT J AU Grigorenko, EL Klin, A Volkmar, F AF Grigorenko, EL Klin, A Volkmar, F TI Annotation: Hyperlexia: disability or superability? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; comprehension; dyslexia; pervasive developmental disorder; reading; specific language impairment ID PERVASIVE DEVELOPMENTAL DISORDER; WORD-RECOGNITION SKILLS; READING-COMPREHENSION; AUTISTIC-SAVANT; POOR COMPREHENDERS; PHONEMIC AWARENESS; LANGUAGE DISORDER; INFANTILE-AUTISM; YOUNG CHILDREN; READERS AB Background: Hyperlexia is the phenomenon of spontaneous and precocious mastery of single-word reading that has been of interest to clinicians and researchers since the beginning of the last century. Methods: An extensive search of publications on the subject of hyperlexia was undertaken and all available publications were reviewed. Results: The literature can be subdivided into discussions of the following issues: (1) whether hyperlexia is a phenomenon that is characteristic only of specific clinical populations (e.g., children with developmental delays) or whether it can also be observed in the general population; (2) whether hyperlexia is a distinct syndrome comorbid with a number of different disorders or whether it is a part of the spectrum of some other clinical condition(s); (3) whether hyperlexia should be defined through single-word reading superiority with regard to reading comprehension, vocabulary, general intelligence, any combination of the three, or all three characteristics; (4) whether there is a specific neuropsychological profile associated with hyperlexia; (5) whether hyperlexia is characterized by a particular developmental profile; and (6) whether hyperlexia should be viewed as a disability (deficit) or superability (talent). Conclusions: We interpret the literature as supporting the view that hyperlexia is a superability demonstrated by a very specific group of individuals with developmental disorders (defined through unexpected single-word reading in the context of other-wise suppressed intellectual functioning) rather than as a disability exhibited by a portion of the general population (defined through a discrepancy between levels of single-word reading and comprehension). We simultaneously argue, however, that multifaceted and multi-methodological approaches to studying the phenomenon of hyperlexia, defined within the research framework of understanding single-word reading, are warranted and encouraged. C1 Yale Univ, Ctr Child Study, New Haven, CT 06510 USA. Yale Univ, Dept Psychol, New Haven, CT 06520 USA. Moscow MV Lomonosov State Univ, Dept Psychol, Moscow, Russia. RP Grigorenko, EL (reprint author), Yale Univ, Ctr Child Study, 230 S Frontage Rd, New Haven, CT 06510 USA. CR Aaron P. 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PD NOV PY 2003 VL 44 IS 8 BP 1079 EP 1091 DI 10.1111/1469-7610.00193 PG 13 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 741CX UT WOS:000186442100002 PM 14626452 ER PT J AU Rutter, M Caspi, A Moffitt, TE AF Rutter, M Caspi, A Moffitt, TE TI Using sex differences in psychopathology to study causal mechanisms: unifying issues and research strategies SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Review DE sex (gender) differences; psychopathology; epidemiology; measurement; significance testing; research strategies; molecular genetics; quantitative genetics; cognitive styles; psychosocial influences ID DSM-III-R; PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM DIAGNOSTIC INTERVIEW; NATIONAL-COMORBIDITY-SURVEY; ATTENTION DEFICIT DISORDER; MILD LANGUAGE DELAY; GENDER DIFFERENCES; ANOREXIA-NERVOSA; PSYCHIATRIC-DISORDERS; CONDUCT DISORDER AB Background: Although there is an extensive literature, both speculative and empirical, on postulated differences between males and females in their rates of particular types of disorder, very little is known about the mechanisms that underlie these sex differences. The study of mechanisms is important because it may provide clues on aetiological processes. The review seeks to outline what is known, what are the methodological hazards that must be dealt with, and the research strategies that may be employed. Methods: We note the need for representative general samples, and for adequate measurement and significance testing if valid conclusions are to be drawn. We put forward three levels of causes that have to be considered: a genetically determined distal basic starting point; the varied consequences of being male or female; and the proximal risk or protective factors that are more directly implicated in the causal mechanisms that predispose to psychopathology. In delineating these, we argue that three key sets of evidential criteria have to be met: a) that the risk factors differ between males and females; b) that they provide for risk or protection within each sex; and c) that when introduced into a causal model, they eliminate or reduce the sex differences in the disorders being studied. Results: A male excess mainly applies to early onset disorders that involve some kind of neurodevelopmental impairment. A female excess mainly applies to adolescent-onset emotional disorders. No variables have yet met all the necessary criteria but some good leads are available. The possible research strategies that may be employed are reviewed. Conclusions: The systematic investigation of sex differences constitutes an invaluable tool for the study of the causal processes concerned with psychopathology. C1 Kings Coll London, Inst Psychiat, SGDP Ctr, London, England. 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Child Psychol. Psychiatry Allied Discip. PD NOV PY 2003 VL 44 IS 8 BP 1092 EP 1115 DI 10.1111/1469-7610.00194 PG 24 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 741CX UT WOS:000186442100003 PM 14626453 ER PT J AU Ashwood, P Murch, SH Anthony, A Pellicer, AA Torrente, F Thomson, MA Walker-Smith, JA Wakefield, AJ AF Ashwood, P Murch, SH Anthony, A Pellicer, AA Torrente, F Thomson, MA Walker-Smith, JA Wakefield, AJ TI Intestinal lymphocyte populations in children with regressive autism: Evidence for extensive mucosal immunopathology SO JOURNAL OF CLINICAL IMMUNOLOGY LA English DT Article DE inflammation; mucosa; T lymphocyte; B lymphocyte; human ID DEVELOPMENTAL DISORDERS; NODULAR HYPERPLASIA; MEASLES; ASSOCIATION; MUMPS AB Inflammatory intestinal pathology has been reported in children with regressive autism (affected children). Detailed analysis of intestinal biopsies in these children indicates a novel lymphocytic enterocolitis with autoimmune features; however, links with cognitive function remain unclear. To characterize further, the nature and extent of this disease we examined the mucosal infiltrate using flow cytometry. Duodenal, ileal, and colonic biopsies were obtained from 52 affected children, 25 histologically normal, and 54 histologically inflamed, developmentally normal controls. Epithelial and lamina propria lymphocyte populations were isolated and examined by multicolor flow cytometry. Adjacent biopsies were assessed by semiquantitative histopathology. At all sites, CD3(+) and CD3(+) CD8(+) IEL as well as CD3(+) LPL were significantly increased in affected children compared with developmentally normal noninflamed control groups (p < 0.01) reaching levels similar to inflamed controls. In addition, two populations - CD3(+)CD4(+) IEL and LP CD19(+) B cells - were significantly increased in affected children compared with both noninflamed and inflamed control groups including IBD, at all sites examined (p < 0.01). Histologically there was a prominent mucosal eosinophil infiltrate in affected children that was significantly lower in those on a gluten- and casein-free diet, although lymphocyte populations were not influenced by diet. The data provide further evidence of a pan-enteric mucosal immunopathology in children with regressive autism that is apparently distinct from other inflammatory bowel diseases. C1 UCL Royal Free & Univ Coll Med Sch, Iflammatory Bowel Dis Study Grp, London, England. UCL Royal Free & Univ Coll Med Sch, Ctr Paediat Gastroenterol, London, England. UCL Royal Free & Univ Coll Med Sch, Dept Histopathol, London, England. Gaslini Inst, Genoa, Italy. RP Ashwood, P (reprint author), Univ Calif Davis, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA. EM p.ashwood@rfc.ucl.ac.uk CR ABOUZAKOUK M, 1996, J IMMUNOL METHODS, V194, P211 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASHWOOD P, 2002, J PEDIAT GASTROENTER, V34, pO18 BARONCOHEN S, 1996, BRIT J PSYCHIAT, V168, P158, DOI DOI 10.1192/BJP.168.2.158 Baron-Cohen S, 2000, J ROY SOC MED, V93, P521 BERTRAND J, 2001, PEDIATRICS, V108, P1156 Bolte ER, 1998, MED HYPOTHESES, V51, P133, DOI 10.1016/S0306-9877(98)90107-4 Comi AM, 1999, J CHILD NEUROL, V14, P388, DOI 10.1177/088307389901400608 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 DEufemia P, 1996, ACTA PAEDIATR, V85, P1076, DOI 10.1111/j.1651-2227.1996.tb14220.x Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 Furlano RI, 2001, J PEDIATR-US, V138, P366, DOI 10.1067/mpd.2001.111323 Gupta S, 1998, J NEUROIMMUNOL, V85, P106, DOI 10.1016/S0165-5728(98)00021-6 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 KAYE JA, 2001, BMJ, V322 Knivsberg AM, 1995, SCAND J EDUC RES, V39, P223, DOI 10.1080/0031383950390304 Knivsberg AM, 2002, NUTR NEUROSCI, V5, P251, DOI 10.1080/10281450290028945 LUDVIKSSON BR, 1992, J PEDIATR-US, V121, P23, DOI 10.1016/S0022-3476(05)82535-1 Murch SM, 1999, GUT, V44, pA127 Sandler RH, 2000, J CHILD NEUROL, V15, P429, DOI 10.1177/088307380001500701 Shah N, 1999, NEW ENGL J MED, V340, P891 Singh VK, 1998, CLIN IMMUNOL IMMUNOP, V89, P105, DOI 10.1006/clin.1998.4588 Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Torrente F, 2002, MOL PSYCHIATR, V7, P375, DOI 10.1038/sj/mp/4001077 UHLMANN V, 2002, MOL PATHOL, V55 vanGent T, 1997, J CHILD PSYCHOL PSYC, V38, P337 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 Wakefield AJ, 2002, ALIMENT PHARM THER, V16, P663, DOI 10.1046/j.1365-2036.2002.01206.x Wakefield AJ, 2000, AM J GASTROENTEROL, V95, P2285 Waring RH, 1997, DEV BRAIN DYSFUNCT, V10, P40 Warren RP, 1996, MOL CHEM NEUROPATHOL, V28, P77, DOI 10.1007/BF02815207 Whiteley P, 1999, AUTISM, V3, P45, DOI 10.1177/1362361399003001005 NR 33 TC 84 Z9 84 PU SPRINGER/PLENUM PUBLISHERS PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0271-9142 EI 1573-2592 J9 J CLIN IMMUNOL JI J. Clin. Immunol. PD NOV PY 2003 VL 23 IS 6 BP 504 EP 517 DI 10.1023/B:JOCI.0000010427.05143.bb PG 14 WC Immunology SC Immunology GA 758PL UT WOS:000187659300008 PM 15031638 ER PT J AU Burford, B Kerr, AM Macleod, HA AF Burford, B Kerr, AM Macleod, HA TI Nurse recognition of early deviation in development in home videos of infants with Rett disorder SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE developmental deviation; infancy; nurse recognition; Rett disorder ID AUTISM; SYMPTOMS; MOVIES; AGE AB Background In the genetic Rett disorder (RD), infants make some progress then suffer a dramatic developmental regression, usually before 2 years of age. Home videos, taken before the problems are recognized, offer an objective source for detecting early signs. Methods Thirty-six health visitors and midwives were invited to view brief examples from home videos of a cohort of 14 infants with RD and 11 control infants with normal development in the first year of life, and to indicate, by pressing a button, points in the recordings which aroused their suspicion of developmental deviation. They were then invited to comment on their selection. The participants were blind as to whether any individual example showed an infant with normal development or one with some form of developmental disturbance. Results From the first month of life and throughout the first year, infants with RD received more button presses than controls (46%, 361 out of 778 viewings) in comparison with the control group (12%, 67 of 558). The consistent nature of the health professionals' comments made possible their categorization under four headings: appearance, posture, movement and contact. In the first month of life, the hand postures of infants with RD received particular comment from midwives (23 out of 37 comments overall on posture). Conclusions The present study strongly suggests the presence of early signs of developmental deviation in infants with RD, although, in most cases, formal developmental screening procedures have failed to detect these before the ages of 12 or 18 months. C1 Univ Edinburgh, Dept Educ Studies, Edinburgh, Midlothian, Scotland. Univ Glasgow, Dept Psychol Med, Glasgow, Lanark, Scotland. Univ Edinburgh, Dept Community & Higher Educ, Edinburgh, Midlothian, Scotland. RP Burford, B (reprint author), Univ Glasgow, Acad Ctr, Gartnavel Royal Hosp, Dept Psychol Med, 1055 Great Western Rd, Glasgow G12 9XH, Lanark, Scotland. CR ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 Amir RE, 1999, NAT GENET, V23, P185 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 Buck R., 1981, DEV SOCIAL PSYCHOL, P127 BURFORD B, 2000, USING VIDEO RES PEOP Burford B., 1993, THESIS U EDINBURGH E CarmagnatDubois F, 1997, ENCEPHALE, V23, P273 Guy J, 2001, NAT GENET, V27, P322, DOI 10.1038/85899 HAGBERG B, 1983, ANN NEUROL, V14, P471, DOI 10.1002/ana.410140412 Kerr A., 2001, RETT DISORDER DEV BR, P1 KERR AM, 1987, BRAIN DEV-JPN, V9, P487 KERR AM, 2001, BRAIN DEV, V23, P44 KERR AM, 1995, NEUROPEDIATRICS, V26, P67, DOI 10.1055/s-2007-979725 KERR AM, 1995, NEUROPEDIATRICS, V26, P72, DOI 10.1055/s-2007-979726 Leonard H, 1999, AM J MED GENET, V83, P88, DOI 10.1002/(SICI)1096-8628(19990312)83:2<88::AID-AJMG3>3.0.CO;2-7 Leonard H, 1998, DEV MED CHILD NEUROL, V40, P115 MACLEOD HA, 1993, PSYCHOL TEACHING REV, V2, P115 PERCY AK, 1992, BRAIN DEV S, V14, P57 Rett A, 1966, Wien Med Wochenschr, V116, P723 SHABAZIAN MD, 2001, CURRENT OPINIONS NEU, V14, P171 Trevarthen C., 2001, RETT DISORDER DEV BR, P303 TREVATHAN E, 1988, ANN NEUROL, V23, P425 NR 22 TC 23 Z9 23 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD NOV PY 2003 VL 47 BP 588 EP 596 DI 10.1046/j.1365-2788.2003.00476.x PN 8 PG 9 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 736KA UT WOS:000186168900003 PM 14641806 ER PT J AU Baghdadli, A Pascal, C Grisi, S Aussilloux, C AF Baghdadli, A Pascal, C Grisi, S Aussilloux, C TI Risk factors for self-injurious behaviours among 222 young children with autistic disorders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE autistic disorders; children; risk factors; self-injurious behaviours ID INTELLECTUAL DISABILITY; SCALE; EPIDEMIOLOGY; ADULTS AB The aim of this study was to identify risk factors for self-injurious behaviours (SIBs) in children with autistic disorders. The occurrence of SIB was examined in comparison with the following variables: chronological age, sex, adaptive skills, speech level, associated medical condition, degree of autism and parental social class. The subjects were 222 children aged under 7 years and all of them fulfilled the ICD-10 criteria for infantile autism. Retrospective data were collected on demographic characteristics and medical condition. Children were assessed in terms of speech, degree of autism and adaptive skills in communication, socialization and daily living skills domains. Results indicated that 50% of the children experienced SIB and 14.6% had severe SIBs. Lower chronological age, associated perinatal condition, a higher degree of autism and a higher daily living skills delay were risk factors of SIBs but parental class, sex and epilepsy were not. C1 CHU Montpellier, Clin Peyre Plantade, Child & Adolescent Psychiat Dept, F-34295 Montpellier 5, France. RP Baghdadli, A (reprint author), CHU Montpellier, Clin Peyre Plantade, Child & Adolescent Psychiat Dept, 291 Ave Doyen Giraud, F-34295 Montpellier 5, France. 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Rev. Immunol. PD NOV PY 2003 VL 3 IS 11 BP 913 EP 918 DI 10.1038/nri1228 PG 6 WC Immunology SC Immunology GA 743EC UT WOS:000186558600017 PM 14608376 ER PT J AU Tuchman, R AF Tuchman, R TI Autism SO NEUROLOGIC CLINICS LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; AUDITORY-EVOKED-POTENTIALS; POSTERIOR-FOSSA STRUCTURES; SPECTRUM DISORDERS; BRAIN-STEM; INFANTILE-AUTISM; YOUNG-CHILDREN; IMMUNOLOGICAL TREATMENTS; MINICOLUMNAR PATHOLOGY AB Autism is a complex neurodevelopmental disorder that is behaviorally defined. The behavioral manifestations that define autism include qualitative deficits in social interaction and communication and restricted repetitive and stereotyped patterns of behavior, activities, and interests [1]. Autism defines children at a behavioral level and is associated with multiple etiologies. The phenotypic presentation of autism is influenced by factors that are not part of the defining features of this disorder. One aspect of autism that is not part of the diagnostic criteria but is an important prognostic indicator is cognitive ability. The wide range of social skills, communication abilities, and patterns of behavior that occur in autism are best captured by the term "autism spectrum disorders" (ASDs) [2,3]. Autism is a prototype disorder of sociocognitive development that provides an important opportunity to observe and delineate the regions of the brain that are responsible for behaviors that define social cognition and communication. Recent reports indicate that there is an explosion of children given the diagnosis of an ASD. Prevalence figures range from 4 to 10 per 10,000 up to 2 to 5 per 1000 [4]. Reports disagree, however, on whether or not prevalence truly has increased. One explanation for the increased diagnosis is that there is a greater awareness of the ASDs, especially in mildly affected children and in those with severe mental retardation [5]. 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PD NOV PY 2003 VL 21 IS 4 BP 915 EP + DI 10.1016/S0733-8619(03)00011-2 PG 19 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 733VU UT WOS:000186022000011 PM 14743656 ER PT J AU Sergeant, JA Geurts, H Huijbregts, S Scheres, A Oosterlaan, J AF Sergeant, JA Geurts, H Huijbregts, S Scheres, A Oosterlaan, J TI The top and the bottom of ADHD: a neuropsychological perspective SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Article; Proceedings Paper CT Symposium on Do Different Branches of Mesocorticolimbic System Underlie Different ADHD Variants CY APR 14-20, 2002 CL ELECTR NETWORK DE attention deficit/hyperactivity disorder; executive function; working memory; inhibition; delay aversion; selective attention; higher function autism; reward ID DEFICIT-HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; ANTERIOR CINGULATE CORTEX; AGGRESSIVE CONDUCT DISORDER; WORKING-MEMORY; RESPONSE-INHIBITION; EXECUTIVE FUNCTION; PREFRONTAL CORTEX; DEVELOPMENTAL PSYCHOPATHOLOGY; TREATED PHENYLKETONURIA AB Five models of attention deficit/hyperactivity disorder (ADHD) are reviewed. 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Biobehav. Rev. PD NOV PY 2003 VL 27 IS 7 BP 583 EP 592 DI 10.1016/j.neubiorev.2003.08.004 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 747NN UT WOS:000186810900002 PM 14624803 ER PT J AU Klug, MG Burd, L Kerbeshian, J Benz, B Martsolf, JT AF Klug, MG Burd, L Kerbeshian, J Benz, B Martsolf, JT TI A comparison of the effects of parental risk markers on pre- and perinatal variables in multiple patient cohorts with fetal alcohol syndrome, autism, Tourette syndrome, and sudden infant death syndrome: an enviromic analysis SO NEUROTOXICOLOGY AND TERATOLOGY LA English DT Article DE autism; birth certificate; fetal alcohol syndrome; parents; risk markers; sudden infant death syndrome; Tourette syndrome ID NORTH-DAKOTA; PREVALENCE; CHILDREN AB The prevalence and magnitude of effect of individual risk markers for specific developmental disorders vary widely across diagnostic category. The four study cohorts for this project were patients from four diagnostic registries in North Dakota for fetal alcohol syndrome (FAS), autism, sudden infant death syndrome (SIDS), and Tourette syndrome. These four cohorts were used to estimate prevalence and magnitude of effect of parental risk markers in patients with developmental disabilities. Cases with North Dakota birth certificates were matched with controls. Using birth certificate data, we then examined five parental risk markers for each cohort and estimated direct and indirect effects for each risk marker by cohort. The authors found two significant paternal risk markers (age in SIDS and education in FAS). Significant maternal markers were age in SIDS, education in FAS, autism, and SIDS. Marital status was a significant risk marker in FAS. Effect sizes were estimated using paired t tests, odds ratios, and population attributable risk (PAR) for both direct and indirect effects for each marker. We estimated both direct and indirect effects to allow for direct comparisons of the differential effect estimates of each of these markers. The direct effect of parental markers differs across diagnostic cohorts of patients. Use of cohorts from similar denominator populations obtained from prevalence studies is a useful methodological tool for estimating the prevalence and magnitude of effect of risk markers. (C) 2003 Elsevier Inc. All rights reserved. C1 Univ N Dakota, Sch Med & Hlth Sci, N Dakota Fetal Alcohol Syndrome Ctr, Grand Forks, ND 58202 USA. RP Burd, L (reprint author), Univ N Dakota, Sch Med & Hlth Sci, N Dakota Fetal Alcohol Syndrome Ctr, Box 9037,501 N Columbia Rd, Grand Forks, ND 58202 USA. 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Teratol. PD NOV-DEC PY 2003 VL 25 IS 6 BP 707 EP 717 DI 10.1016/j.ntt.2003.07.018 PG 11 WC Neurosciences; Toxicology SC Neurosciences & Neurology; Toxicology GA 748RX UT WOS:000186875800010 PM 14624970 ER PT J AU Osborne, JW Summitt, J AF Osborne, JW Summitt, J TI Autism caused by dental amalgam? SO OPERATIVE DENTISTRY LA English DT Editorial Material C1 Univ Colorado, Ctr Hlth Sci, Dept Restorat Dent, Boulder, CO 80309 USA. Univ Texas, Hlth Sci Ctr, Dept Restorat Dent, San Antonio, TX USA. RP Osborne, JW (reprint author), Univ Colorado, Ctr Hlth Sci, Dept Restorat Dent, Boulder, CO 80309 USA. CR Bernard S, 2001, MED HYPOTHESES, V56, P462, DOI 10.1054/mehy.2000.1281 Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 Nelson KB, 2003, PEDIATRICS, V111, P674, DOI 10.1542/peds.111.3.674 1988, DORLANDS ILLUSTRATED, P169 NR 4 TC 1 Z9 1 PU OPERATIVE DENTISTRY INC PI INDIANAPOLIS PA INDIANA UNIV SCHOOL DENTISTRY, ROOM S411, 1121 WEST MICHIGAN ST, INDIANAPOLIS, IN 46202-5186 USA SN 0361-7734 J9 OPER DENT JI Oper. Dent. PD NOV-DEC PY 2003 VL 28 IS 6 BP 665 EP 666 PG 2 WC Dentistry, Oral Surgery & Medicine SC Dentistry, Oral Surgery & Medicine GA 740KM UT WOS:000186401600001 PM 14653277 ER PT J AU Verstraeten, T Davis, RL DeStefano, F Lieu, TA Rhodes, PH Black, SB Shinefield, H Chen, RT AF Verstraeten, T Davis, RL DeStefano, F Lieu, TA Rhodes, PH Black, SB Shinefield, H Chen, RT CA Vaccine Safety Datalink Team TI Safety of thimerosal-containing vaccines: A two-phased study of computerized health maintenance organization databases SO PEDIATRICS LA English DT Article DE cohort study; computerized medical record systems; language development disorders; speech disorders; thimerosal; vaccines ID SEYCHELLES CHILD-DEVELOPMENT; LOW-BIRTH-WEIGHT; METHYLMERCURY EXPOSURE; INTRAVENOUS-INJECTION; MERCURY; OUTCOMES; INFANTS; NEUROTOXICITY; VACCINATION; DATALINK AB Objective. To assess the possible toxicity of thimerosal-containing vaccines (TCVs) among infants. Methods. A 2-phased retrospective cohort study was conducted using computerized health maintenance organization (HMO) databases. Phase I screened for associations between neurodevelopmental disorders and thimerosal exposure among 124170 infants who were born during 1992 to 1999 at 2 HMOs (A and B). In phase II, the most common disorders associated with exposure in phase I were reevaluated among 16717 children who were born during 1991 to 1997 in another HMO (C). Relative risks for neurodevelopmental disorders were calculated per increase of 12.5 mug of estimated cumulative mercury exposure from TCVs in the first, third, and seventh months of life. Results. In phase I at HMO A, cumulative exposure at 3 months resulted in a significant positive association with tics (relative risk [RR]: 1.89; 95% confidence interval [CI]: 1.05-3.38). At HMO B, increased risks of language delay were found for cumulative exposure at 3 months (RR: 1.13; 95% CI: 1.01-1.27) and 7 months (RR: 1.07; 95% CI: 1.01-1.13). In phase II at HMO C, no significant associations were found. In no analyses were significant increased risks found for autism or attention-deficit disorder. Conclusions. No consistent significant associations were found between TCVs and neurodevelopmental outcomes. Conflicting results were found at different HMOs for certain outcomes. For resolving the conflicting findings, studies with uniform neurodevelopmental assessments of children with a range of cumulative thimerosal exposures are needed. C1 Ctr Dis Control & Prevent, Epidem Intelligence Serv Program, Epidemiol Program Off, Atlanta, GA 30333 USA. Ctr Dis Control & Prevent, Vaccine Safety & Dev Act, Epidemiol & Surveillance Div, Natl Immunizat Program, Atlanta, GA USA. Univ Washington, Seattle, WA 98195 USA. Grp Hlth Cooperat Puget Sound, Seattle, WA 98121 USA. Childrens Hosp, Div Gen Pediat, Boston, MA 02115 USA. Harvard Pilgrim Hlth Care, Dept Ambulatory Care & Prevent, Ctr Child Hlth Care Studies, Boston, MA USA. 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Increased prevalence of familial autoimmune disease is a common finding among probands with various autoimmune disorders. Autistic disorder ( autism) is a highly genetic disorder with known immune and immunogenetic abnormalities. Previous research has found an increased frequency of autoimmune disorders in families with autistic probands. We further investigated this association by determining the frequency of autoimmune disorders in families that have probands with pervasive developmental disorders (PDDs), including autism, compared with 2 control groups. Methods. Three well-defined study groups, including 1) families that have a child with a PDD, 2) families that have a child with an autoimmune disorder, and 3) families with a healthy control child, constituted the sample. A questionnaire inquiring about which first- and second-degree family members had received a diagnosis of having specific autoimmune disorders was completed by 101 families in each group. Results. The frequency of autoimmune disorders was significantly higher in families of the PDD probands compared with families of both the autoimmune and healthy control probands. Autoimmunity was highest among the parents of PDD probands compared with parents of the healthy control subjects. Hypothyroidism/ Hashimoto's thyroiditis and rheumatic fever were significantly more common in families with PDD probands than in the healthy control families. Conclusions. Autoimmunity was increased significantly in families with PDD compared with those of healthy and autoimmune control subjects. These preliminary findings warrant additional investigation into immune and autoimmune mechanisms in autism. C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. Indiana Univ, Sch Med, Dept Pediat, Indianapolis, IN 46202 USA. James Whitcomb Riley Hosp Children, Indianapolis, IN 46202 USA. St Vincent Hosp, Indianapolis, IN USA. RP McDougle, CJ (reprint author), Indiana Univ, Sch Med, Dept Psychiat, Psychiat Bldg A305,1111 W 10th St, Indianapolis, IN 46202 USA. 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Since BDV-infected rats exhibited an inhibition of postnatal weight gain, the present study sought to evaluate a contribution of nutritional status to virus-induced neurodevelopmental injury. We compared neuroanatomical, neurochemical, and behavioral alterations following neonatal BDV infection and rearing in the oversized litters in Fischer344 rats on postnatal day (PND) 26. Despite a comparable weight gain inhibition, different patterns of brain pathology, alterations in brain monoamine systems, and behavioral deficits were observed in the BDV-infected rats compared to the malnourished rats. While no appreciable cell injury was noted in the brains of the malnourished rats, a significant loss of Purkinje cells (PC) and early signs of degeneration of the hippocampal dentate gyrus were found in the BDV-infected rats. Both neonatal BDV infection and postnatal malnourishment increased tissue concentrations of serotonin [5-hydroxytryptamine (5-HT)] in the hippocampus. In contrast, increased turnover of 5-HT in the cortex and hippocampus and elevated turnover of dopamine (DA) in the striatum were found in the malnourished rats only, suggesting that different pathogenic mechanisms might underlie monoamine disturbances in virus-infected and malnourished rats. The observed dissimilar neuroanatomical and neurochemical abnormalities might explain the different responses to novelty in the BDV-infected and malnourished rats. Compared to the control rats, the BDV-infected rats exhibited novelty-induced hyperactivity, while no differences in locomotion were noted between the control and malnourished rats. Taken together, the present data indicate that virus-associated inhibition of postnatal weight gain is unlikely to account for the major BDV-associated neurodevelopmental alterations that seem to be due to specific effects of neonatal BDV infection. (C) 2003 Elsevier Inc. All rights reserved. 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PD NOV PY 2003 VL 80 IS 2-3 BP 359 EP 366 DI 10.1016/j.physbeh.2003.08.011 PG 8 WC Psychology, Biological; Behavioral Sciences SC Psychology; Behavioral Sciences GA 750DT UT WOS:000186976600024 PM 14637236 ER PT J AU [Anonymous] AF [Anonymous] TI Stars shine for 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 NOV PY 2003 VL 16 IS 11 BP 572 EP 572 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 744AY UT WOS:000186606800002 ER PT J AU McDonald, ME Hemmes, NS AF McDonald, ME Hemmes, NS TI Increases in social initiation toward an adolescent with autism: reciprocity effects SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE social initiation; social reciprocity; autism ID PRESCHOOL-CHILDREN; SPONTANEOUS SPEECH; YOUNG-CHILDREN; TIME-DELAY; BEHAVIOR; PRAISE; REINFORCEMENT; INTERVENTION; LANGUAGE; SKILLS AB Level of spontaneous social initiating by three adult caregivers toward a youth with autism was studied during a program to increase the youth's level of social initiating. The adult participants were three staff members of a program for individuals with autism; they were assigned to the classroom of the youth participant, but none was directly involved in his educational program. Under a multiple-baseline across subject design, in combination with a multi-element design, the youth's social initiations toward each adult were systematically reinforced. Two sessions were conducted daily: one in which prompts, token reinforcers, and verbal praise for the youth's social behavior were presented (baseline and training sessions), and one in which prompts were absent and only verbal praise was presented (probe sessions). Frequency of spontaneous initiating toward the youth increased for each adult during treatment when the youth's frequency of initiating toward a given adult increased. It was higher during training vs. probe sessions, where level of social initiating by the youth was also higher. (C) 2003 Published by Elsevier Ltd. C1 CUNY, Grad Ctr, Plainview, NY 11804 USA. CUNY, Queens Coll, Plainview, NY 11804 USA. Genesis Sch, Plainview, NY 11804 USA. RP McDonald, ME (reprint author), CUNY, Grad Ctr, 270 Washington Ave,Suite 6, Plainview, NY 11804 USA. 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PD NOV PY 2003 VL 26 IS 11 BP 618 EP 624 DI 10.1016/j.tins.2003.09.004 PG 7 WC Neurosciences SC Neurosciences & Neurology GA 741HN UT WOS:000186452800010 PM 14585602 ER PT J AU Zoghbi, HY AF Zoghbi, HY TI Postnatal neurodevelopmental disorders: Meeting at the synapse? SO SCIENCE LA English DT Article ID LINKED MENTAL-RETARDATION; CPG-BINDING PROTEIN-2; RETT-SYNDROME BRAIN; AUTISTIC DISORDER; MECP2 MUTATIONS; DNA METHYLATION; PROXIMAL 15Q; ANGELMAN-SYNDROME; INFANTILE-AUTISM; SYNDROME GENE AB We often think of neurodevelopmental disorders as beginning before birth, and many certainly do. A handful, however, strike many months after birth, following a period of apparently normal growth and development. Autism and Rett syndrome are two such disorders, and here I consider some of their similarities at the phenotypic and pathogenic levels. I propose that both disorders result from disruption of postnatal or experience-dependent synaptic plasticity. C1 Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. Baylor Coll Med, Dept Neurol, Houston, TX 77030 USA. Baylor Coll Med, Dept Mol & Human Genet, Div Neurosci, Houston, TX 77030 USA. Baylor Coll Med, Howard Hughes Med Inst, Houston, TX 77030 USA. RP Zoghbi, HY (reprint author), Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. 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OBSESSIVE-COMPULSIVE DISORDER; BASAL GANGLIA; BANK VOLES; CLETHRIONOMYS-GLAREOLUS; JUMPING STEREOTYPY; SPECTRUM DISORDERS; LABORATORY MICE; BEHAVIOR; PERSEVERATION; INHIBITION AB Spontaneously occurring abnormal behaviors in animals have recently received considerable attention, both in veterinary medicine and as a potential model for abnormal behavior in several human mental disorders. Stereotypies are abnormal repetitive, unvarying, and functionless behaviors that are often performed by captive and domesticated animals housed in barren environments. They closely resemble the stereotypies of autistic and mentally retarded patients, stereotypies of unmedicated chronic schizophrenic patients, certain classes of simple tic in Tourette's syndrome, and several drug-induced behaviors. However, evidence for a common mechanism has been lacking. Stereotypies in human mental disorders are indicative of profound brain dysfunction involving the basal ganglia, and are associated with pervasive voluntary-motor impairments and psychological distress. Here we show that stereotypy in captive Orange-Wing Amazon Parrots (Amazona amazonica) is correlated with poor performance on the same psychiatric task (the 'gambling task') as stereotypy in autistic and schizophrenic patients. The task measures recurrent perseveration-the tendency to inappropriately repeat responses. Thus, the more stereotypy a parrot performed, the more likely it was to inappropriately repeat itself from trial-to-trial on the task; and the more rapidly it made repeated, but not switched, responses. These results parallel the executive motor impairments seen in human patients, and therefore suggest that, like in human patients, stereotypy in caged parrots reflects a general disinhibition of the behavioral control mechanisms of the dorsal basal ganglia. If this result holds true in other laboratory species, stereotypic animals are likely to be of questionable utility in behavior, neuroscience, and neuropharmacological experiments. In humans, stereotypies and obsessive-compulsive behaviors are considered to be mutually exclusive categories of behavior, with different neural substrates, and different treatment strategies. These results, therefore, suggest that the pharmacological treatment of stereotypies in veterinary medicine based on the assumption that they are equivalent to human Obsessive-Compulsive Disorder may be inappropriate. As stereotypies in captive animals develop in response to the captive environment, these results also emphasize the role that the environment may play in eliciting or exacerbating stereotypy in human patients. Finally, by parallel to human patients, there is a potential psychological distress in animals showing these behaviors. (C) 2003 Elsevier Science B.V. All rights reserved. C1 Univ Calif Davis, Dept Anim Sci, Davis, CA 95616 USA. RP Garner, JP (reprint author), Univ Calif Davis, Dept Anim Sci, 1 Shields Ave, Davis, CA 95616 USA. 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PD OCT 17 PY 2003 VL 145 IS 1-2 BP 125 EP 134 DI 10.1016/S0166-4328(03)00115-3 PG 10 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 734TD UT WOS:000186073300013 PM 14529811 ER PT J AU Hammer, S Dorrani, N Hartiala, J Stein, S Schanen, NC AF Hammer, S Dorrani, N Hartiala, J Stein, S Schanen, NC TI Rett syndrome in a 47,XXX patient with a de novo MECP2 mutation SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE MECP2; Rett syndrome; trisomy; X-chromosome ID X-CHROMOSOME INACTIVATION; LINKED MENTAL-RETARDATION; SYNDROME FAMILY; SYNDROME GENE; PHENOTYPE; MALES; BOYS AB Rett syndrome is caused by mutation in MECP2, a gene located on Xq28 and subject to X-inactivation. MECP2 encodes methyl CpG-binding protein 2, a widely expressed transcriptional repressor of methylated DNA. Mutations in MECP2 are primarily de novo events in the male germ line and thus lead to an excess of affected females. Here we report the identification of a unique 47,XXX girl with relatively mild atypical Rett syndrome leading initially to a diagnosis of infantile autism with regression. Mutation analysis of the MECP2 gene identified a de novo MECP2 mutation, L100V. Examination of a panel of X-linked microsatellite markers indicated that her supernumerary X chromosome is maternally derived. X-inactivation patterns were determined by analysis of methylation of the androgen receptor locus, and indicated preferential inactivation of her paternal allele. The parental origin of her MECP2 mutation could not be determined because she was uninformative for intronic polymorphisms flanking her mutation. This is the first reported case of sex chromosome trisomy and MECP2 mutation in a female, and it illustrates the importance of allele dosage on the severity of Rett syndrome phenotype. (C) 2003 Wiley-Liss, Inc. C1 Alfred I Dupont Hosp Children, Nemours Res Inst, Wilmington, DE 19899 USA. Univ Calif Los Angeles, Sch Med, Dept Human Genet, Los Angeles, CA USA. Eastern Maine Med Ctr, Dept Pediat, Bangor, ME USA. Eastern Maine Med Ctr, Neurol Res Lab, Bangor, ME USA. Univ Maine, Dept Vet & Anim Sci, Orono, ME USA. Univ Maine, Dept Biochem, Orono, ME USA. Univ Maine, Dept Microbiol, Orono, ME USA. Univ Maine, Dept Mol Biol, Orono, ME USA. Univ Maine, Dept Biol Sci, Orono, ME USA. RP Schanen, NC (reprint author), Alfred I Dupont Hosp Children, Nemours Res Inst, 1600 rockland Rd,POB 269, Wilmington, DE 19899 USA. 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J. Med. Genet. A PD OCT 15 PY 2003 VL 122A IS 3 BP 223 EP 226 DI 10.1002/ajmg.a.20320 PG 4 WC Genetics & Heredity SC Genetics & Heredity GA 724NC UT WOS:000185492800005 PM 12966522 ER PT J AU Brambilla, P Hardan, A di Nemi, SU Perez, J Soares, JC Barale, F AF Brambilla, P Hardan, A di Nemi, SU Perez, J Soares, JC Barale, F TI Brain anatomy and development in autism: review of structural MRI studies SO BRAIN RESEARCH BULLETIN LA English DT Review DE neuroimaging; cerebellum; vermis; amygdala; hippocampus; corpus callosum ID POSTERIOR-FOSSA STRUCTURES; INFANTILE-AUTISM; CORPUS-CALLOSUM; HEAD CIRCUMFERENCE; CEREBELLAR VERMIS; PSYCHIATRIC-DISORDERS; STEM INVOLVEMENT; 4TH VENTRICLE; FRONTAL-LOBE; CHILDREN AB Autism is a neurodevelopmental disorder that severely disrupts social and cognitive functions. MRI is the method of choice for in vivo and non-invasively investigating human brain morphology in children and adolescents. The authors reviewed structural MRI studies that investigated structural brain anatomy and development in autistic patients. All original MRI research papers involving autistic patients, published from 1966 to May 2003, were reviewed in order to elucidate brain anatomy and development of autism and rated for completeness using a 12-item check-list. Increased total brain, parieto-temporal lobe, and cerebellar hemisphere volumes were the most replicated abnormalities in autism. Interestingly, recent findings suggested that the size of amygdala, hippocampus, and corpus callosum may also be abnormal. It is conceivable that abnormalities in neural network involving fronto-temporo-parietal cortex, limbic system, and cerebellum may underlie the pathophysiology of autism, and that such changes could result from abnormal brain development during early life. Nonetheless, available MRI studies were often conflicting and could have been limited by methodological issues. Future MRI investigations should include well-characterized groups of autistic and matched healthy individuals, while taking into consideration confounding factors such as IQ, and socioeconomic status. (C) 2003 Elsevier Inc. All rights reserved. C1 Giovanni di Dio Hosp Fatebenefratelli, IRCCS S, Biol Psychiat Unit, I-25125 Brescia, Italy. Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15260 USA. Univ Pavia, Matteo Hosp, Sch Med, IRCCS S,Dept Psychiat, I-27100 Pavia, Italy. Cascina Rossago Rehabil Ctr Autism, Pavia, Italy. Univ Texas, Hlth Sci Ctr, Dept Psychiat, San Antonio, TX 78284 USA. S Texas VA Hlth Care Syst, San Antonio, TX USA. RP Brambilla, P (reprint author), Giovanni di Dio Hosp Fatebenefratelli, IRCCS S, Biol Psychiat Unit, Via Pilastroni 4, I-25125 Brescia, Italy. 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Bull. PD OCT 15 PY 2003 VL 61 IS 6 BP 557 EP 569 DI 10.1016/j.brainresbull.2003.06.001 PG 13 WC Neurosciences SC Neurosciences & Neurology GA 776TN UT WOS:000189133800001 PM 14519452 ER PT J AU Volkmar, FR Pauls, D AF Volkmar, FR Pauls, D TI Autism SO LANCET LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; PLACEBO-CONTROLLED TRIAL; LATENT-CLASS ANALYSIS; LINKAGE-DISEQUILIBRIUM; SPECTRUM DISORDERS; ASPERGER-SYNDROME; RUBELLA VACCINE; FAMILY HISTORY; GENOMIC SCREEN; PERSONALITY-CHARACTERISTICS AB Autism is a disorder characterised by severe difficulties in social interaction and communication, and with unusual behaviours. Once thought of as rare, autism is now recognised as being common. The role of CNS factors in pathogenesis is suggested by high rates of seizure disorder; research has highlighted the role of several specific brain regions in syndrome pathogenesis. 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In this follow-up analysis we have increased the sample size threefold, while holding the study design constant, so that we now report 345 multiplex families, each with at least two siblings affected with autism or ASD phenotype. Along with 235 new multiplex families, 73 new microsatellite markers were also added in 10 regions, thereby increasing the marker density at these strategic locations from 10 cM to similar to2 cM and bringing the total number of markers to 408 over the entire genome. Multipoint maximum LOD scores (MLS) obtained from affected-sib-pair analysis of all 345 families yielded suggestive evidence for linkage on chromosomes 17, 5, 11, 4, and 8 (listed in order by MLS) (P < .01). The most significant findings were an MLS of 2.83 (P = .00029) on chromosome 17q, near the serotonin transporter (5-hydroxytryptamine transporter [5-HTT]), and an MLS of 2.54 (P = .00059) on 5p. The present follow-up genome scan, which used a consistent research design across studies and examined the largest ASD sample collection reported to date, gave either equivalent or marginally increased evidence for linkage at several chromosomal regions implicated in our previous scan but eliminated evidence for linkage at other regions. C1 Columbia Univ, Columbia Genome Ctr, New York, NY 10032 USA. Columbia Univ, Dept Genet & Dev, New York, NY 10032 USA. Columbia Univ, Dept Psychiat, New York, NY 10032 USA. Columbia Univ, Dept Epidemiol, New York, NY 10032 USA. New York State Psychiat Inst & Hosp, New York, NY 10032 USA. Univ Calif Los Angeles, Ctr Neurobehav Genet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Neuropsychiat Res Inst, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Program Neurogenet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, David Geffen Sch Med, Los Angeles, CA 90095 USA. RP Gilliam, TC (reprint author), Columbia Univ, Columbia Genome Ctr, 1150 St Nicholas Ave,Room 508, New York, NY 10032 USA. RI Juo, Suh-Hang/A-1765-2010; Juo, Suh-Hang/C-9545-2009; Palmer, Abraham/L-2158-2014 OI Palmer, Abraham/0000-0003-3634-0747 CR ADAMS P, 1994, GENET EPIDEMIOL, V11, P87, DOI 10.1002/gepi.1370110109 Aita VM, 1999, AM J HUM GENET, V64, P210, DOI 10.1086/302185 Alarcon M, 2002, AM J HUM GENET, V70, P60, DOI 10.1086/338241 American Psychiatric Association, 2000, DIAGN STAT MAN MENT [Anonymous], 1992, INT STAT CLASS DIS R Auranen M, 2002, AM J HUM GENET, V71, P777, DOI 10.1086/342720 BADNER JA, 2002, MOL PSYCHIATR, V7, P56 BAILEY A, 1995, PSYCHOL MED, V25, P63 Barrett S, 1999, AM J MED GENET, V88, P609 Broman KW, 1998, AM J HUM GENET, V63, P1563, DOI 10.1086/302112 Broman KW, 1998, AM J HUM GENET, V63, P861, DOI 10.1086/302011 Buxbaum JD, 2001, AM J HUM GENET, V68, P1514, DOI 10.1086/320588 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Charman T, 2002, EUR CHILD ADOLES PSY, V11, P249, DOI 10.1007/s00787-002-0297-8 Cook Edwin H. 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J. Hum. Genet. PD OCT PY 2003 VL 73 IS 4 BP 886 EP 897 DI 10.1086/378778 PG 12 WC Genetics & Heredity SC Genetics & Heredity GA 727TL UT WOS:000185676100015 PM 13680528 ER PT J AU Muller, RA Kleinhans, N Kemmotsu, N Pierce, K Courchesne, E AF Muller, RA Kleinhans, N Kemmotsu, N Pierce, K Courchesne, E TI Abnormal variability and distribution of functional maps in autism: An fMRI study of visuomotor learning SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 1st International Meeting for Autism Research CY NOV 09-10, 2001 CL SAN DIEGO, CALIFORNIA ID POSITRON-EMISSION-TOMOGRAPHY; CEREBRAL BLOOD-FLOW; MAGNETIC-RESONANCE; INFANTILE-AUTISM; SPATIAL ATTENTION; ASPERGER-SYNDROME; CEREBELLAR CONTRIBUTION; CHILDHOOD AUTISM; POSTERIOR-FOSSA; BRAIN-STEM AB Objective: Autism is a neurally based psychiatric disorder, but there is no consensus regarding the underlying neurofunctional abnormalities. Previous functional magnetic resonance imaging (fMRI) studies of simple movement suggested individually variable and scattered functional brain organization in autism. The authors examined whether such abnormalities generalize to multimodal processing (visually driven motor sequence learning). Method: Eight male autistic patients and eight comparison subjects matched with the patients on age, gender, and handedness were examined by using fMRI while they performed finger press movements prompted by visually presented repeating six-digit sequences. Hemodynamic responses to the six-digit sequences were statistically compared to responses to single-digit stimuli in one experiment and to regular six-digit sequences in another experiment. Results: Both groups showed activations in bilateral premotor, superior parietal, and occipital cortices in both experiments. Task-by-group interactions showed that superior parietal activations were less pronounced in the autism group, whereas prefrontal cortex and more posterior parietal loci showed greater activation in the autism group than in the comparison group. The distances between Individual subjects' activation peaks and the group-wise peak were greater in the autism group than in the comparison group. Conclusions: The results support earlier findings of abnormal variability and scatter of functional maps in autism. They are consistent with evidence from other studies suggesting early-onset disturbances in the development of cerebello-thalamo-cortical pathways in autism. C1 San Diego State Univ, Dept Psychol, San Diego, CA 92120 USA. Childrens Hosp, Res Ctr, Lab Neurosci Autism, La Jolla, CA USA. Univ Calif San Diego, Dept Cognit Sci, La Jolla, CA 92093 USA. San Diego State Univ, Joint Doctoral Program Clin Psychol, San Diego, CA 92182 USA. 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J. Psychiat. PD OCT PY 2003 VL 160 IS 10 BP 1847 EP 1862 DI 10.1176/appi.ajp.160.10.1847 PG 16 WC Psychiatry SC Psychiatry GA 731JJ UT WOS:000185880300023 PM 14514501 ER PT J AU Gillberg, C AF Gillberg, C TI Deficits in attention, motor control, and perception: a brief review SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Review ID DEVELOPMENTAL COORDINATION DISORDER; MINOR NEUROLOGICAL DYSFUNCTION; SWEDISH 7-YEAR-OLD CHILDREN; HYPERACTIVITY DISORDER; 6-YEAR-OLD CHILDREN; ASPERGER-SYNDROME; ADHD; AGE; ALCOHOL; DRUG AB The concept of DAMP (deficits in attention, motor control, and perception) has been in clinical use in Scandinavia for about 20 years. DAMP is diagnosed on the basis of concomitant attention deficit/hyperactivity disorder and developmental coordination disorder in children who do not have severe learning disability or cerebral palsy. In clinically severe form it affects about 1.5% of the general population of school age children; another few per cent are affected by more moderate variants. Boys are overrepresented; girls are currently probably underdiagnosed. There are many comorbid problems/overlapping conditions, including conduct disorder, depression/anxiety, and academic failure. There is a strong link with autism spectrum disorders in severe DAMP. Familial factors and pre- and perinatal risk factors account for much of the variance. Psychosocial risk factors appear to increase the risk of marked psychiatric abnormality in DAMP. Outcome in early adult age was psychosocially poor in one study in almost 60% of unmedicated cases. There are effective interventions available for many of the problems encountered in DAMP. C1 Gothenburg Univ, Dept Child & Adolescent Psychiat, S-41119 Gothenburg, Sweden. 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F., 1971, EXCEPTIONAL INFANT S, P343 Whitaker AH, 1997, ARCH GEN PSYCHIAT, V54, P847 NR 40 TC 107 Z9 110 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD OCT PY 2003 VL 88 IS 10 BP 904 EP 910 DI 10.1136/adc.88.10.904 PG 7 WC Pediatrics SC Pediatrics GA 723KW UT WOS:000185432400017 PM 14500312 ER PT J AU Langdon, R AF Langdon, R TI Theory of mind and psychopathology: Autism versus schizophrenia SO AUSTRALIAN AND NEW ZEALAND JOURNAL OF PSYCHIATRY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU BLACKWELL PUBLISHING ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 0004-8674 J9 AUST NZ J PSYCHIAT JI Aust. N. Z. J. Psych. PD OCT PY 2003 VL 37 SU 1 BP A47 EP A47 PG 1 WC Psychiatry SC Psychiatry GA 744MF UT WOS:000186635700171 ER PT J AU Ferrante, P Saresella, M Guerini, FR Marzorati, M Musetti, MC Cazzullo, AG AF Ferrante, P Saresella, M Guerini, FR Marzorati, M Musetti, MC Cazzullo, AG TI Significant association of HLA A2-DR11 with CD4 naive decrease in autistic children SO BIOMEDICINE & PHARMACOTHERAPY LA English DT Article DE CD4 naive; HLA; autistic syndrome AB Nine autistic children and 37 ethnically homogenous controls were enrolled in the study to assess their human leukocyte antigen (HLA) pattern, and eight healthy children were studied to define their peripheral blood cell subsets. We observed a significant decrease in CD4+ naive and an increase in CD4+ memory T cells in autistic children. These differences were significantly more pronounced in the autistic children bearing the HLA A2 and DR11 alleles. These data support the hypothesis that autism could be due to an immune imbalance occurring in genetically predisposed children. (C) 2003 Editions scientifiques et medicales Elsevier SAS. All rights reserved. C1 IRCCS, Don C Gnocchi Fdn, Lab Biol, I-20148 Milan, Italy. LITA, Dept Sci & Biomed Technol, Chair Virol, I-20090 Segrate, Italy. Univ Milan, Sch Med, Chair Childhood Neurol & Psychiat, I-20122 Milan, Italy. RP Ferrante, P (reprint author), IRCCS, Don C Gnocchi Fdn, Lab Biol, Via Capecelatro 66, I-20148 Milan, Italy. RI Saresella, Marina/G-7810-2012; Guerini, Franca/G-8055-2012 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th DELGIUDICEASCH G, 1997, INT J NEUROPSYCHIAT, V2, P61 Denney DR, 1996, J AUTISM DEV DISORD, V26, P87, DOI 10.1007/BF02276236 Filipek PA, 2000, NEUROLOGY, V55, P468 WARREN RP, 1990, IMMUNOL INVEST, V19, P245, DOI 10.3109/08820139009041839 Warren RP, 1996, J NEUROIMMUNOL, V67, P97 NR 6 TC 19 Z9 20 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0753-3322 J9 BIOMED PHARMACOTHER JI Biomed. Pharmacother. PD OCT PY 2003 VL 57 IS 8 BP 372 EP 374 DI 10.1016/S0753-3322(03)00099-4 PG 3 WC Medicine, Research & Experimental; Pharmacology & Pharmacy SC Research & Experimental Medicine; Pharmacology & Pharmacy GA 742RB UT WOS:000186530900008 PM 14568232 ER PT J AU Chang, SJ Crothers, C Lai, SH Lamm, S AF Chang, SJ Crothers, C Lai, SH Lamm, S TI Pediatric neurobehavioral diseases in Nevada counties with respect to perchlorate in drinking water: An ecological inquiry SO BIRTH DEFECTS RESEARCH PART A-CLINICAL AND MOLECULAR TERATOLOGY LA English DT Article DE perchlorate; ADHD; autism; drinking water; evironmental health ID NEONATAL THYROXINE; THYROID-HORMONE; BIRTH-DEFECTS; HEALTH; CONTAMINATION; CHILDREN; LEVEL; AGE AB BACKGROUND: Contamination of drinking water with Perchlorate, a known thyrotropic agent, has been demonstrated in areas in the western United States. The health consequences of that exposure have been studied, particularly in the State of Nevada. Previous studies in Nevada, comparing the area with Perchlorate in the drinking water and the areas without perchlorate in the drinking water, have found no difference in neonatal thyroxine (T-4) or thyrotropin (TSH) levels, or in the prevalences of thyroid diseases and thyroid cancer. This same study design has now been applied to the major neurobehavioral diseases of childhood (i.e., attention deficit-hyperactivity disorder (ADHD) and autism) and to school performance in order to determine whether those conditions are more frequent in the area with perchlorate-contaminated water. METHODS: Medical services data on ADHD and autism were obtained from the Nevada Medicaid system for the period of January 1, 1996, to December 31, 2000, with county of residence used as the basis for residential information. Analyses of fourth-grade school performance results for two recent time periods came from the state government. Perchlorate concentrations in drinking water had been determined by local water authorities. ADHD and autism rates for the area with Perchlorate in the drinking water (Clark County) were calculated and compared with the rates for the other areas in the state, as were fourth-grade school performances. RESULTS: Analysis of the data from the Nevada Medicaid program shows that the rates for ADHD and for autism in the area where Perchlorate was in the drinking water did not exceed the rates in those areas where there was no Perchlorate contamination in the drinking water. Fourth-grade standardized test results for students in Clark County were not different from those of the remainder of the state. CONCLUSIONS: This ecological study of children in the exposure area did not find evidence of an increased risk of either ADHD or of autism caused by Perchlorate contamination in the drinking water. Furthermore, no difference in overall fourth-grade school performance was observed. No evidence was found that children from the area with Perchlorate in the drinking water (up to 24 mug/liter) had either an increase in pediatric neurobehavioral disease (ADHD and autism) or a decrease in fourth-grade academic performance. The limitations of this ecological study relate to diagnostic criteria and ascertainment of geographic and demographic differences and to data on individual residence and water consumption during pregnancy. (C) 2003 Wiley-Liss, Inc. C1 CEOH, Washington, DC 20007 USA. Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Baltimore, MD USA. Neveda Dept Educ, Carson City, NV USA. RP Lamm, S (reprint author), CEOH, 2428 Wisconsin Ave NW, Washington, DC 20007 USA. 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Part A-Clin. Mol. Teratol. PD OCT PY 2003 VL 67 IS 10 BP 886 EP 892 DI 10.1002/bdra.10089 PG 7 WC Developmental Biology; Toxicology SC Developmental Biology; Toxicology GA 736AR UT WOS:000186148500009 PM 14745943 ER PT J AU Welch, MG Keune, JD Welch-Horan, TB Anwar, N Anwar, M Ruggiero, DA AF Welch, MG Keune, JD Welch-Horan, TB Anwar, N Anwar, M Ruggiero, DA TI Secretin activates visceral brain regions in the rat including areas abnormal in autism SO CELLULAR AND MOLECULAR NEUROBIOLOGY LA English DT Review DE secretin; autism; stress; c-fos; ependyma; visceral brain; stress adaptation networks ID VASOACTIVE INTESTINAL PEPTIDE; NUCLEUS-TRACTUS-SOLITARII; ROSTRAL VENTROLATERAL MEDULLA; CHRONIC-INTERMITTENT HYPOXIA; MEDIAL PREFRONTAL CORTEX; PLACEBO-CONTROLLED TRIAL; VAGAL NERVE-STIMULATION; NITRIC-OXIDE; C-FOS; BEHAVIORAL-IMPLICATIONS AB 1. The aim of this study was to determine whether central networks are involved in the presumptive behavioral and autonomic regulatory actions of secretin, a gut hormone that has been reported to have ameliorative effects in autistic children. 2. Central neural responses monitored by regional c-fos gene expression were examined in response to intracerebroventricular secretin injection in awake, freely-moving Sprague-Dawley rats. Tissue sections were incubated in an antibody to the c-fos gene product, Fos, and processed immunohistochemically. 3. Qualitative differences in Fos immunoreactivity in stress adaptation and visceral representation areas of the brain were observed between secretin- and vehicle-infused age-matched pairs (n = 4 pairs). Secretin-activated regions include the area postrema, dorsal motor nucleus, medial region of the nucleus of the solitary tract and its relay station in the lateral tegmentum, locus ceruleus, ventral periaqueductal gray, periventricular thalamic nucleus, paraventricular hypothalamus magnocellularis, medial and central amygdala, lateral septal complex as well as ependymal and subependymal nuclei lining the third ventricle. Specific areas of the cerebral cortex were heavily labeled in secretin- treated rats, as compared to controls: the medial bank of the anterior prefrontal cortex, orbitofrontal cortex, the piriform cortex, and the anterior olfactory nucleus. Secretin attenuated Fos immunoreactivity in the dorsal periaqueductal gray, intralaminar thalamus, medial parvicellular compartment of the hypothalamus, supraoptic nucleus of the hypothalamus, lateral amygdala, motor cortex, and the somatosensory and association areas of the parietal cortex. 4. Secretin alters the activity of structures involved in behavioral conditioning of stress adaptation and visceral reflex reactions. This study predicts a possible cellular mechanism, activation of third ventricular ependymal and subependymal cells, as well as central regulatory actions of secretin. The physiological effects of secretin on behavioral, endocrine, autonomic and sensory neuronal activation patterns, together, contribute to central c-fos activation. Secretin alters the activity of structures involved in behavioral conditioning of stress adaptation and visceral reflex reactions. This study predicts a possible cellular mechanism, activation of third ventricular ependymal and subependymal cells, and central regulatory actions of secretin. The physiological effects of secretin on behavioral, endocrine, autonomic and sensory neuronal activation patterns, together, contribute to central c-fos activation. These findings mandate further investigation of secretin as a brain/gut stress regulatory hormone. C1 Columbia Univ Coll Phys & Surg, Dept Psychiat, NYSPI, New York, NY 10032 USA. Columbia Univ Coll Phys & Surg, Dept Anat & Cell Biol, NYSPI, New York, NY 10032 USA. Columbia Univ Coll Phys & Surg, Div Neurosci, Lab Childhood Regulatory Disorders, NYSPI, New York, NY 10032 USA. Columbia Univ Coll Phys & Surg, Div Neurosci, Lab Behav Neuroanat, NYSPI, New York, NY 10032 USA. RP Welch, MG (reprint author), Columbia Univ Coll Phys & Surg, Dept Psychiat, NYSPI, 1051 Riverside Dr, New York, NY 10032 USA. 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Mol. Neurobiol. PD OCT PY 2003 VL 23 IS 4-5 BP 817 EP 837 DI 10.1023/A:1025013322194 PG 21 WC Cell Biology; Neurosciences SC Cell Biology; Neurosciences & Neurology GA 708UX UT WOS:000184589000030 PM 14514034 ER PT J AU Belmonte, MK Yurgelun-Todd, DA AF Belmonte, MK Yurgelun-Todd, DA TI Functional anatomy of impaired selective attention and compensatory processing in autism SO COGNITIVE BRAIN RESEARCH LA English DT Article DE autism; visual attention; arousal; fMRI; parietal; intraparietal sulcus ID POSITRON-EMISSION-TOMOGRAPHY; DEVELOPMENTAL CEREBELLAR ABNORMALITY; VISUAL-SPATIAL ATTENTION; EVENT-RELATED POTENTIALS; MAGNETIC-RESONANCE; SHIFTING ATTENTION; BRAIN ACTIVITY; ODDBALL TASKS; VISUOSPATIAL ATTENTION; STIMULUS LOCATION AB In autism, physiological indices of selective attention have been shown to be abnormal even in situations where behaviour is intact. This divergence between behaviour and physiology suggests the action of some compensatory process of attention, one which may hold clues to the aetiology of autism's characteristic cognitive phenotype. Six subjects with autism spectrum disorders and six normal control subjects were studied with functional magnetic resonance imaging while performing a bilateral visual spatial attention task. In normal subjects. the task evoked activation in a network of cortical regions including the superior parietal lobe (P<0.001), left middle temporal gyrus (P=0.002), left inferior (P<0.001) and middle (P<0.02) frontal gyri, and medial frontal gyrus (P<0.02). Autistic subjects, in contrast, showed activation in the bilateral ventral occipital cortex (P<0.03) and striate cortex (P<0.05). Within the task condition, a region-of-interest comparison of attend-left versus attend-right conditions indicated that modulation of activation in the autistic brain as a function of the lateral focus of spatial attention was abnormally decreased in the left ventral occipital cortex (P<0.03), abnormally increased in the left intraparietal sulcus (P<0.01), and abnormally variable in the superior parietal lobe (P<0.03). These results are discussed in terms of a model of autism in which a pervasive defect of neural and synaptic development produces over-connected neural systems prone to noise and crosstalk, resulting in hyper-arousal and reduced selectivity. These low-level attentional traits may be the developmental basis for higher-order cognitive styles such as weak central coherence. (C) 2003 Elsevier B.V. All rights reserved. C1 McLean Hosp, Cognit Neuroimaging Lab, Belmont, MA 02478 USA. Harvard Univ, Sch Med, Boston, MA 02115 USA. 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Brain Res. PD OCT PY 2003 VL 17 IS 3 BP 651 EP 664 DI 10.1016/S0926-6410(03)00189-7 PG 14 WC Computer Science, Artificial Intelligence; Neurosciences; Neuroimaging SC Computer Science; Neurosciences & Neurology GA 739QY UT WOS:000186359000011 ER PT J AU Foster, B King, BH AF Foster, B King, BH TI Asperger syndrome: to be or not to be? SO CURRENT OPINION IN PEDIATRICS LA English DT Review DE asperger; autism; pervasive developmental disorder; high-functioning autism ID PERVASIVE DEVELOPMENTAL DISORDER; AUTISTIC SPECTRUM DISORDERS; HIGH-FUNCTIONING AUTISM; PRESCHOOL-CHILDREN; MOTOR IMPAIRMENT; PREVALENCE; ADOLESCENTS; DIAGNOSIS; BEHAVIOR; DEFICIT AB Purpose of review Asperger syndrome is a pervasive developmental disorder characterized by impairments in social interactions, such as nonverbal behaviors, failure to develop peer relationships, and lack of social reciprocity with restricted, repetitive and stereotyped patterns of interest or behavior. The diagnosis of Asperger syndrome is increasingly common, and it is timely to review its phenomenology and treatment. Recent findings As there is a growing public awareness and acceptance of Asperger syndrome, clinical research has produced mixed results that do not clearly discriminate Asperger syndrome from high-functioning autism. However, research does indicate that children with pervasive developmental disorder achieve better outcomes when diagnosis is made early and appropriate community supports can be marshaled. Summary The history and phenomenology of Asperger syndrome is briefly reviewed, and recent literature relating to assessment and treatment is highlighted. C1 Dartmouth Coll Sch Med, Lebanon, NH USA. Childrens Hosp Dartmouth, Lebanon, NH USA. RP King, BH (reprint author), 1 Med Ctr Dr, Lebanon, NH 03756 USA. CR American Psychiatric Association, 2002, DIAGN STAT MAN MENT Barnhill G. P., 2001, FOCUS AUTISM OTHER D, V16, P46, DOI 10.1177/108835760101600112 Barnhill G. 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PD OCT PY 2003 VL 15 IS 5 BP 491 EP 494 DI 10.1097/00008480-200310000-00008 PG 4 WC Pediatrics SC Pediatrics GA 728DA UT WOS:000185698900008 PM 14508298 ER PT J AU Coplan, J AF Coplan, J TI Atypicality, intelligence, and age: a conceptual model of autistic spectrum disorder SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; FOLLOW-UP; LONGITUDINAL EXAMINATION; DIAGNOSTIC INTERVIEW; INFANTILE-AUTISM; CLUSTER-ANALYSIS; CHILDREN; PROGNOSIS; CLASSIFICATION; INDIVIDUALS RP Coplan, J (reprint author), Childrens Seashore House,Room 210A,3405 Civ Ctr B, Philadelphia, PA 19104 USA. 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PD OCT PY 2003 VL 111 IS 13 BP A693 EP A693 DI 10.1289/ehp.111-a693a PG 1 WC Environmental Sciences; Public, Environmental & Occupational Health; Toxicology SC Environmental Sciences & Ecology; Public, Environmental & Occupational Health; Toxicology GA 732JU UT WOS:000185940800007 ER PT J AU Soderstrom, H AF Soderstrom, H TI Psychopathy as a disorder of empathy SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Editorial Material DE personality; theory of mind; autism; social brain; forensic ID ASPERGER-SYNDROME; AUTISM; MIND; ADULTS C1 Dept Forens Psychiat, S-42204 Hisings Backa, Sweden. RP Soderstrom, H (reprint author), Dept Forens Psychiat, Box 4024, S-42204 Hisings Backa, Sweden. 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PD OCT PY 2003 VL 12 IS 5 BP 249 EP 252 DI 10.1007/s00787-003-0338-y PG 4 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 724HH UT WOS:000185481800006 PM 14667112 ER PT J AU Martin, LA Goldowitz, D Mittleman, G AF Martin, LA Goldowitz, D Mittleman, G TI The cerebellum and spatial ability: dissection of motor and cognitive components with a mouse model system SO EUROPEAN JOURNAL OF NEUROSCIENCE LA English DT Article DE chimera; lurcher; navigation; persistence; search; water maze ID LURCHER MUTANT MICE; INFERIOR OLIVARY NEURONS; CHANNEL DELTA-2 SUBUNIT; MORRIS WATER MAZE; INFANTILE-AUTISM; PURKINJE-CELL; CHIMERIC MICE; BRAIN; RATS; NEURODEGENERATION AB The cerebellum has recently been linked to spatial navigation, as indicated by the inferior performance of cerebellar mutant or cerebellar lesioned animals in the water maze. The inability to dissociate motor from cognitive deficits in the impaired water maze performance has been a confounding variable in previous studies, however. In this study, we sought to define clearly the role of the cerebellar system in spatial navigation outside of motor control by creating a mouse model of Purkinje cell loss with intact motor ability, and testing these mice in the water maze. To this end, we made aggregation chimeras between Lc/+ mice, which lose all Purkinje cells postnatally, and +/+ control mice. Lc/+ mice are ataxic and show impaired rotor-rod performance. By contrast, we show that Lc/+ <----> +/+ chimeras above a threshold of Purkinje cell loss show no outward signs of motor impairment and demonstrated normal rotor-rod ability. In the water maze, we found that Lc/+ mice showed impaired performance in the place, cue and platform removal tasks, whereas Lc/+<---->+/+ chimeras performed similarly to controls in all tasks. 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PD OCT PY 2003 VL 2 IS 5 BP 253 EP 254 DI 10.1046/j.1601-183X.2003.00040.x PG 2 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 743QQ UT WOS:000186585400001 PM 14606690 ER PT J AU Rubenstein, JLR Merzenich, MM AF Rubenstein, JLR Merzenich, MM TI Model of autism: increased ratio of excitation/inhibition in key neural systems SO GENES BRAIN AND BEHAVIOR LA English DT Review DE autism; genetics; model; neural excitation; neural inhibition; neural systems ID GLUTAMIC-ACID DECARBOXYLASE; SEROTONIN TRANSPORTER GENE; PRIMARY AUDITORY-CORTEX; MONKEY CEREBRAL-CORTEX; FRAGILE-X-SYNDROME; MENTAL-RETARDATION; CORTICAL REPRESENTATION; DEVELOPMENTAL DISORDERS; GABAERGIC INHIBITION; PREFRONTAL CORTEX AB Autism is a severe neurobehavioral syndrome, arising largely as an inherited disorder, which can arise from several diseases. Despite recent advances in identifying some genes that can cause autism, its underlying neurological mechanisms are uncertain. 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PD OCT PY 2003 VL 2 IS 5 BP 255 EP 267 DI 10.1046/j.1601-183X.2003.00037.x PG 13 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 743QQ UT WOS:000186585400002 PM 14606691 ER PT J AU Tropepe, V Sive, HL AF Tropepe, V Sive, HL TI Can zebrafish be used as a model to study the neurodevelopmental causes of autism? SO GENES BRAIN AND BEHAVIOR LA English DT Review DE autism; brain; development; genetic behavior; zebrafish ID CENTRAL-NERVOUS-SYSTEM; EMBRYONIC STEM-CELLS; RETINOIC ACID; DANIO-RERIO; TRANSGENIC ZEBRAFISH; BRACHYDANIO-RERIO; GENE-EXPRESSION; NEURAL PLATE; IN-VIVO; LARVAL ZEBRAFISH AB The zebrafish has proven to be an excellent model for analyzing issues of vertebrate development. In this review we ask whether the zebrafish is a viable model for analyzing the neurodevelopmental causes of autism. In developing an answer to this question three topics are considered. First, the general attributes of zebrafish as a model are discussed, including low cost maintenance, rapid life cycle and the multitude of techniques available. These techniques include large-scale genetic screens, targeted loss and gain of function methods, and embryological assays. Second, we consider the conservation of zebrafish and mammalian brain development, structure and function. Third, we discuss the impressive use of zebrafish as a model for human disease, and suggest several strategies by which zebrafish could be used to dissect the genetic basis for autism. We conclude that the zebrafish system could be used to make important contributions to understanding autistic disorders. C1 Whitehead Inst Biomed Res, MIT, Cambridge, MA 02142 USA. RP Sive, HL (reprint author), Whitehead Inst Biomed Res, MIT, 9 Cambridge Ctr, Cambridge, MA 02142 USA. 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A comparative analysis of amygdala neuroanatomy in normal vs. autistic brains would be aided by the availability of molecular markers to unambiguously recognize these different amygdala substructures. Here We report on the development of methods to identify genes enriched in the central, lateral and medial nuclei of the rodent amygdala. Our results suggest that laser-capture microdissection of specific amygdala subnuclei, when combined with linear amplification of cRNA probes for oligonucleotide microarray hybridization, can efficiently identify genes whose expression is confined to these substructures. Importantly, many of these genes were missed in previous gene expression-profiling experiments using whole amygdala tissue. 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These findings, along with recent functional neuroimaging data, have led Baron-Cohen et al. (2000) to propose that dysfunction of the amygdala may be responsible, in part, for the impairment of social behavior that is a hallmark feature of autism. Recent data from studies in our laboratory on the effects of amygdala lesions in the adult and infant macaque monkey do not support a fundamental role for the amygdala in social behavior. If the amygdala is not essential for the component processes of social behavior, as seems to be case in both non-human primates and selected patients with bilateral amygdala damage, then it is unlikely to be the primary substrate for the impaired social behavior of autism. However, damage to the amygdala does have an effect on a monkey's response to normally fear-inducing stimuli, such as snakes, and removes a natural reluctance to engage novel conspecifics in social interactions. 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PD OCT PY 2003 VL 2 IS 5 BP 295 EP 302 DI 10.1034/j.1601-183X.2003.00043.x PG 8 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 743QQ UT WOS:000186585400005 PM 14606694 ER PT J AU Yonan, AL Palmer, AA Smith, KC Feldman, I Lee, HK Yonan, JM Fischer, SG Pavlidis, P Gilliam, TC AF Yonan, AL Palmer, AA Smith, KC Feldman, I Lee, HK Yonan, JM Fischer, SG Pavlidis, P Gilliam, TC TI Bioinformatic analysis of autism positional candidate genes using biological databases and computational gene network prediction SO GENES BRAIN AND BEHAVIOR LA English DT Review DE 17q; AGRE sample; autism; association studies; bioinformatics; candidate genes ID CYSTIC-FIBROSIS GENE; SPECTRUM DISORDERS; GENOMEWIDE SCREEN; TRANSMISSION DISEQUILIBRIUM; NO ASSOCIATION; SACCHAROMYCES-CEREVISIAE; SUSCEPTIBILITY LOCUS; RNA INTERFERENCE; INFANTILE-AUTISM; COMPLEX TRAITS AB Common genetic disorders are believed to arise from the combined effects of multiple inherited genetic variants acting in concert with environmental factors, such that any given DNA sequence variant may have only a marginal effect on disease outcome. As a consequence, the correlation between disease status and any given DNA marker allele in a genomewide linkage study tends to be relatively weak and the implicated regions typically encompass hundreds of positional candidate genes. Therefore, new strategies are needed to parse relatively large sets of 'positional' candidate genes in search of actual disease-related gene variants. Here we use biological databases to identify 383 positional candidate genes predicted by genomewide genetic linkage analysis of a large set of families, each with two or more members diagnosed with autism, or autism spectrum disorder (ASD). Next, we seek to identify a subset of biologically meaningful, high priority candidates. The strategy is to select autism candidate genes based on prior genetic evidence from the allelic association literature to query the known transcripts within the 1-LOD (logarithm of the odds) support interval for each region. We use recently developed bioinformatic programs that automatically search the biological literature to predict pathways of interacting genes (PATHWAYASSIST and GENEWAYS). To identify gene regulatory networks, we search for coexpression between candidate genes and positional candidates. The studies are intended both to inform studies of autism, and to illustrate and explore the increasing potential of bioinformatic approaches as a compliment to linkage analysis. C1 Columbia Univ, Columbia Genome Ctr, New York, NY 10032 USA. Columbia Univ, Dept Genet & Dev, New York, NY USA. Columbia Univ, Dept Psychiat, New York, NY USA. New York State Psychiat Inst & Hosp, New York, NY USA. Columbia Univ, Div Mol Genet, Dept Pediat, New York, NY USA. Columbia Univ, Dept Med, New York, NY USA. Columbia Univ, Dept Biomed Informat, New York, NY USA. RP Gilliam, TC (reprint author), Columbia Univ, Columbia Genome Ctr, 1150 St Nicholas Ave,Room 508, New York, NY 10032 USA. 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PD OCT PY 2003 VL 2 IS 5 BP 303 EP 320 DI 10.1046/j.1601-183X.2003.00041.x PG 18 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 743QQ UT WOS:000186585400006 PM 14606695 ER PT J AU Prizant, BM Wetherby, AM Rubin, E Laurent, AC AF Prizant, BM Wetherby, AM Rubin, E Laurent, AC TI The SCERTS model - A transactional, family-centered approach to enhancing communication and socioemotional abilities of children with autism spectrum disorder SO INFANTS AND YOUNG CHILDREN LA English DT Article DE autistic spectrum disorder; autism; developmental; early intervention; education; communication; emotional regulation; family support; social ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; INTERVENTION; LANGUAGE; ECHOLALIA; PROFILES; ISSUES AB A range of educational/treatment approaches is currently available for young children with autism spectrum disorders (ASD). A recent comprehensive review by an expert panel on ASD (National Research Council, 2001) concluded that a number of approaches have demonstrated positive outcomes, but nonetheless, not all children benefit equally from any one approach. Efforts to increase communicative and socioemotional abilities are widely regarded as among the most critical priorities, and growth in these areas is closely related to prognosis and long-term positive outcomes. However, some widely disseminated approaches are, not based on the most contemporary developmental research on social and communication development in children with and without disabilities, nor do they draw from current understanding of the learning style of children with ASD. This article describes the SCERTS Model, which prioritizes Social Communication, Emotional Regulation, and Transactional Support as the primary developmental dimensions that must be addressed in a comprehensive program designed to support the development of young children with ASD and their families. The SCERTS Model has been derived from a theoretical as well as empirically based foundation and addresses core challenges of children with ASD as they relate to social communication, emotional regulation, and transactional support. The SCERTS Model also is consistent with empirically supported interventions and it reflects current and emerging "recommended practices" (National Research Council, 2001). C1 Brown Univ, Childhood Commun Serv, Providence, RI 02912 USA. Brown Univ, Ctr Study Human Dev, Providence, RI 02912 USA. Florida State Univ, Dept Commun Disorders, Ctr Autism & Related Disorders, Tallahassee, FL 32306 USA. Commun Crossroads, Monterey, CA USA. 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PD OCT-DEC PY 2003 VL 16 IS 4 BP 296 EP 316 PG 21 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 725MH UT WOS:000185546600004 ER PT J AU McCann, J Peppe, S AF McCann, J Peppe, S TI Prosody in autism spectrum disorders: a critical review SO INTERNATIONAL JOURNAL OF LANGUAGE & COMMUNICATION DISORDERS LA English DT Review DE prosody; intonation; autism; Asperger's syndrome ID HIGH-FUNCTIONING AUTISM; IMMEDIATE ECHOLALIA; LINGUISTIC PROSODY; CONTRASTIVE STRESS; ASPERGER-SYNDROME; CHILDS APPRAISAL; LANGUAGE; VOICE; IMPAIRMENTS; EXPRESSIONS AB Background: Many individuals with autism spectrum disorders present with unusual or odd-sounding prosody. Despite this widely noted observation, prosodic ability in autism spectrum disorders is often perceived as an under-researched area. Aims: This review seeks to establish whether there is a prosodic disorder in autism, what generalizations can be made about its various manifestations and whether these manifestations vary according to the diagnosis. A literature review was carried out to establish what areas of prosody in autism spectrum disorders have been researched to date, what the findings have been and to determine what areas are yet to be researched. Main contribution: It is shown that prosody in autism spectrum disorders is an under-researched area and that where research has been undertaken, findings often conflict. The findings of these conflicting studies are compared and recommendations are made for areas of future research. Conclusions: Research in this area has covered mostly prosodic expression, although some more recent studies cover comprehension, processing and the relationship of receptive prosodic ability to theory of mind. Findings conflict and methodology varies greatly. 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PD OCT-DEC PY 2003 VL 38 IS 4 BP 325 EP 350 DI 10.1080/1368282031000154204 PG 26 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 733QF UT WOS:000186011600001 PM 14578051 ER PT J AU Hviid, A Stellfeld, M Wohlfahrt, J Melbye, M AF Hviid, A Stellfeld, M Wohlfahrt, J Melbye, M TI Association between thimerosal-containing vaccine and autism SO JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION LA English DT Article ID POPULATION; REGISTER; MERCURY AB Context Mercuric compounds are nephrotoxic and neurotoxic at high doses. Thimerosal, a preservative used widely in vaccine formulations, contains ethylmercury. Thus it has been suggested that childhood vaccination with thimerosal-containing vaccine could be causally related to neurodevelopmental disorders such as autism. Objective To determine whether vaccination with a thimerosal-containing vaccine is associated with development of autism. Design, Setting, and Participants Population-based cohort study of all children born in Denmark from January 1, 1990, until December 31, 1996 (N =467450) comparing children vaccinated with a thimerosal-containing vaccine with children vaccinated with a thimerosal-free formulation of the same vaccine. Main Outcome Measures Rate ratio (RR) for autism and other autistic-spectrum disorders, including trend with dose of ethylmercury. Results During 2986654 person-years, we identified 440 autism cases and 787 cases of other autistic-spectrum disorders. The risk of autism and other autistic-spectrum disorders did not differ significantly between children vaccinated with thimerosal-containing vaccine and children vaccinated with thimerosal-free vaccine (RR, 0.85 [95% confidence interval (0), 0.60-1.20] for autism; RR, 1.12 [95% Cl, 0.88-1.43] for other autistic-spectrum disorders). Furthermore, we found no evidence of a dose-response association (increase in RR per 25 mug of ethylmercury, 0.98 [95% Cl, 0.90-1.06] for autism and 1.03 [95% Cl, 0.98-1.09] for other autistic-spectrum disorders). Conclusion The results do not support a causal relationship between childhood vaccination with thimerosal-containing vaccines and development of autistic-spectrum disorders. C1 Statens Serum Inst, Dept Epidemiol Res, Danish Epidemiol Sci Ctr, DK-2300 Copenhagen S, Denmark. Statens Serum Inst, Dept Med, DK-2300 Copenhagen, Denmark. RP Hviid, A (reprint author), Statens Serum Inst, Dept Epidemiol Res, Danish Epidemiol Sci Ctr, Artillerivej 5, DK-2300 Copenhagen S, Denmark. 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PD OCT 1 PY 2003 VL 290 IS 13 BP 1763 EP 1766 DI 10.1001/jama.290.13.1763 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 726NQ UT WOS:000185606100026 PM 14519711 ER PT J AU Begeer, S Rieffe, C Terwogt, MM Stockmann, L AF Begeer, S Rieffe, C Terwogt, MM Stockmann, L TI Theory of Mind-based action in children from the autism spectrum SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; PDDNOS; high-functioning; Theory of Mind; action ID PERVASIVE DEVELOPMENTAL DISORDER; FALSE-BELIEF TASKS; DECEPTION; EMOTIONS; ADULTS; ABILITIES; KNOWLEDGE; BEHAVIOR AB In this study we investigated whether task interest facilitated the application of Theory of Mind capacities in high-functioning children from the autism spectrum. Children were invited to carry out two simple tasks. Sabotage of both tasks by a third party resulted in the experimenter appearing to have a false belief. Whereas pervasive developmental disorder not otherwise specified (PDDNOS) children tended to correct the experimenter's false belief in the rewarded task condition, children with autism were not influenced by task condition. These results highlight the role played by social and communicative factors in the application of Theory of Mind knowledge in the former clinical group. C1 Vrije Univ Amsterdam, Dept Dev Psychol, NL-1081 BT Amsterdam, Netherlands. Paedolog Inst, Duivendrecht, Netherlands. Univ London, Sch Psychol & Human Dev, Inst Educ, London, England. RP Begeer, S (reprint author), Vrije Univ Amsterdam, Dept Dev Psychol, Van de Boechorststr 1, NL-1081 BT Amsterdam, Netherlands. RI Begeer, Sander/I-3383-2012 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron-Cohen S, 1993, UNDERSTANDING OTHER BARONCOHEN S, 1992, J CHILD PSYCHOL PSYC, V33, P1141, DOI 10.1111/j.1469-7610.1992.tb00934.x BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BOWLER DM, 1992, J CHILD PSYCHOL PSYC, V33, P877, DOI 10.1111/j.1469-7610.1992.tb01962.x Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 Capps L., 1998, AUTISM, V2, P325, DOI DOI 10.1177/1362361398024002 CARRUTHERS P, 1996, THEORIES THEORIES MI COTTON JW, 1993, STAT TXB MONOGRAPHS, P147 DUNLAP G, 1984, J EXP CHILD PSYCHOL, V37, P41, DOI 10.1016/0022-0965(84)90057-2 EISENMAJER R, 1991, BRIT J DEV PSYCHOL, V9, P351 FOMBONNE E, 1994, EUR CHILD ADOLES PSY, V3, P176 Frith U., 1994, SOCIAL DEV, V3, P108, DOI DOI 10.1111/J.1467-9507.1994.TB00031.X Frith U, 1989, EXPLAINING ENIGMA Happe F, 1996, BRAIN, V119, P1377, DOI 10.1093/brain/119.4.1377 HAPPE FGE, 1994, J AUTISM DEV DISORD, V24, P129, DOI 10.1007/BF02172093 Heavey L, 2000, J AUTISM DEV DISORD, V30, P225, DOI 10.1023/A:1005544518785 Hughes C, 2000, J CHILD PSYCHOL PSYC, V41, P483, DOI 10.1017/S0021963099005533 Jolliffe T, 1999, J AUTISM DEV DISORD, V29, P395, DOI 10.1023/A:1023082928366 KOEGEL RL, 1985, J CHILD PSYCHOL PSYC, V26, P185, DOI 10.1111/j.1469-7610.1985.tb02259.x Newton P, 2000, BRIT J DEV PSYCHOL, V18, P297, DOI 10.1348/026151000165706 ODELL M, 1981, 1981 ANN CONV AM SPE ODELL MC, 1983, AM PSYCH ASS ANN CON PERNER J, 1985, J EXP CHILD PSYCHOL, V39, P437, DOI 10.1016/0022-0965(85)90051-7 PERNER J, 1989, CHILD DEV, V60, P689, DOI 10.1111/j.1467-8624.1989.tb02749.x PESKIN J, 1992, DEV PSYCHOL, V28, P84, DOI 10.1037//0012-1649.28.1.84 Piaget J., 1929, CHILDS CONCEPTION WO Premack D., 1978, BEHAV BRAIN SCI, V1, P512, DOI 10.1016/j.tics.2008.02.010 Rieffe C, 2000, INFANT CHILD DEV, V9, P147, DOI 10.1002/1522-7219(200009)9:3<147::AID-ICD226>3.3.CO;2-S RIEFFE C, 1996, JB ONTWIKKELINGSPSYC, V2, P216 Rieffe C, 2000, J CHILD PSYCHOL PSYC, V41, P601, DOI 10.1017/S0021963099005843 Rieffe C, 2000, J AUTISM DEV DISORD, V30, P195, DOI 10.1023/A:1005540417877 Roeyers H, 2001, J CHILD PSYCHOL PSYC, V42, P271, DOI 10.1111/1469-7610.00718 Searle John R., 1983, INTENTIONALITY Serra M, 1999, EUR CHILD ADOLES PSY, V8, P301 Sicotte C, 1999, J AUTISM DEV DISORD, V29, P225, DOI 10.1023/A:1023032122489 SIEGAL M, 1991, COGNITION, V38, P1, DOI 10.1016/0010-0277(91)90020-5 SODIAN B, 1992, J CHILD PSYCHOL PSYC, V33, P591, DOI 10.1111/j.1469-7610.1992.tb00893.x SODIAN B, 1991, CHILD DEV, V62, P468, DOI 10.1111/j.1467-8624.1991.tb01545.x TERWOGT MM, 1998, INT J BEHAV DEV, V23, P113 TERWOGTKOUWENHO.KM, 1993, NEDERLANDS TIJDSCHRI, V48, P136 Travis L, 2001, J AUTISM DEV DISORD, V31, P119, DOI 10.1023/A:1010705912731 VANDERGAAG RJ, 1996, KIND ADOLESCENT, V17, P57 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd Wing Lorna, 1988, DIAGNOSIS ASSESSMENT, P91 NR 46 TC 22 Z9 24 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 2003 VL 33 IS 5 BP 479 EP 487 DI 10.1023/A:1025875311062 PG 9 WC Psychology, Developmental SC Psychology GA 725HT UT WOS:000185538700002 PM 14594328 ER PT J AU Bauminger, N Shulman, C Agam, G AF Bauminger, N Shulman, C Agam, G TI Peer interaction and loneliness in high-functioning children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE peer interaction; high-functioning autism; loneliness ID NONHANDICAPPED PEERS; SOCIAL INTERACTIONS; TEACHING THEORY; BEHAVIOR; PLAY; INITIATIONS; ADOLESCENTS; COMPETENCE; EMOTIONS; SKILLS AB Social interaction with peers and the understanding and feelings of loneliness were examined in 18 high-functioning children with autism and 17 typically developing children matched for IQ, chronological age, gender, and maternal education. Observations were conducted on children's spontaneous social initiations and responses to their peers in natural settings such as recess and snack time, and children reported on their understanding and feelings of loneliness and social interaction. Overall, children with autism revealed a good understanding of both social interaction and loneliness, and they demonstrated a high level of social initiation. However, they spent only half the time in social interactions with peers compared with their matched counterparts, and they interacted more often with a typically developing child than with another special education child. Despite the intergroup differences in frequency of interaction, a similar distribution of interactions emerged for both groups, who presented mostly positive social behaviors, fewer low-level behaviors, and very infrequent negative behaviors. Children with autism reported higher degrees of loneliness than their typical age-mates, as well as a lower association between social interaction and loneliness, suggesting their poorer understanding of the relations between loneliness and social interaction. Research and practice implications of these findings are discussed. C1 Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. Hebrew Univ Jerusalem, Jerusalem, Israel. RP Bauminger, N (reprint author), Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asher S. R., 1990, PEER REJECTION CHILD, P253 ASHER SR, 1984, CHILD DEV, V55, P1456, DOI 10.2307/1130015 ASHER SR, 1985, J CONSULT CLIN PSYCH, V53, P500, DOI 10.1037/0022-006X.53.4.500 Bacon AL, 1998, J AUTISM DEV DISORD, V28, P129, DOI 10.1023/A:1026040615628 Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Bauminger N, 2002, J AUTISM DEV DISORD, V32, P283, DOI 10.1023/A:1016378718278 BORMANNKISCHKEL C, 1995, J CHILD PSYCHOL PSYC, V36, P1243, DOI 10.1111/j.1469-7610.1995.tb01368.x BRADY MP, 1987, J AUTISM DEV DISORD, V17, P375, DOI 10.1007/BF01487067 Burgess K. B., 1999, LONELINESS CHILDHOOD, P109, DOI 10.1017/CBO9780511551888.006 CAPPS L, 1995, DEV PSYCHOPATHOL, V7, P137 CAPPS L, 1992, J CHILD PSYCHOL PSYC, V33, P1169, DOI 10.1111/j.1469-7610.1992.tb00936.x CASSIDY J, 1992, CHILD DEV, V63, P350, DOI 10.1111/j.1467-8624.1992.tb01632.x Chamberlain B., 2001, DEV AUTISM PERSPECTI DEWEY D, 1988, CAN J PSYCHOL, V42, P242, DOI 10.1037/h0084183 GAYLORDROSS RJ, 1984, J APPL BEHAV ANAL, V17, P229, DOI 10.1901/jaba.1984.17-229 Gonzalez-Lopez A., 1997, FOCUS AUTISM OTHER D, V12, P2 Gray C.A., 1998, ASPERGER SYNDROME HI, P167 Hadwin J, 1997, J AUTISM DEV DISORD, V27, P519, DOI 10.1023/A:1025826009731 Hadwin J, 1996, DEV PSYCHOPATHOL, V8, P345 Hauck M, 1995, J AUTISM DEV DISORD, V25, P579, DOI 10.1007/BF02178189 Hermelin B, 1985, COMMUNICATION PROBLE, P283 HOBSON RP, 1993, PHILOS PSYCHOL, V6, P227, DOI 10.1080/09515089308573090 JAEDICKE S, 1994, DEV PSYCHOPATHOL, V6, P273, DOI 10.1017/S0954579400004582 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1995, DEV PSYCHOPATHOL, V7, P611 LORD C, 1986, J AUTISM DEV DISORD, V16, P249, DOI 10.1007/BF01531658 Loveland KA, 1997, DEV PSYCHOPATHOL, V9, P579 MARGALIT M, 1994, LEARN DISABILITY Q, V17, P297, DOI 10.2307/1511126 ODEM SL, 1984, AM J ORTHOPSYCHIAT, V54, P544 OKE NJ, 1990, J AUTISM DEV DISORD, V20, P479, DOI 10.1007/BF02216054 OZONOFF S, 1995, J AUTISM DEV DISORD, V25, P415, DOI 10.1007/BF02179376 Parker JG, 1995, DEV PSYCHOPATHOL, V2, P96 RENSHAW PD, 1993, CHILD DEV, V64, P1271, DOI 10.1111/j.1467-8624.1993.tb04200.x Roeyers H, 1996, J AUTISM DEV DISORD, V26, P303, DOI 10.1007/BF02172476 Shores R. E, 1987, BEHAVIORAL DISORDERS, V12, P233 Sigman M, 1999, MONOGR SOC RES CHILD, V64, P1, DOI 10.1111/1540-5834.00002 STONE WL, 1990, J AUTISM DEV DISORD, V20, P437, DOI 10.1007/BF02216051 Strain Phillip S., 1998, Seminars in Speech and Language, V19, P391, DOI 10.1055/s-2008-1064056 Volkmar F., 1997, HDB AUTISM PERVASIVE, P173 VOLKMAR FR, 1989, J AM ACAD CHILD PSY, V28, P82, DOI 10.1097/00004583-198901000-00015 Wechsler D, 1974, WISC R MANUAL WECHSL Weiss R. S, 1973, LONELINESS EXPERIENC WOLFBERG PJ, 1993, J AUTISM DEV DISORD, V23, P467, DOI 10.1007/BF01046051 Zercher C, 2001, AUTISM, V5, P374, DOI 10.1177/1362361301005004004 NR 46 TC 98 Z9 98 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 2003 VL 33 IS 5 BP 489 EP 507 DI 10.1023/A:1025827427901 PG 19 WC Psychology, Developmental SC Psychology GA 725HT UT WOS:000185538700003 PM 14594329 ER PT J AU Baron-Cohen, S Wheelwright, S AF Baron-Cohen, S Wheelwright, S TI The friendship questionnaire: An investigation of adults with Asperger syndrome or high-functioning autism, and normal sex differences SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE empathy; high-functioning autism; Asperger syndrome; social relationships; friendship; Theory of Mind ID CHILDREN; BRAIN AB Friendship is an important part of normal social functioning, yet there are precious few instruments for measuring individual differences in this domain. In this article, we report a new self-report questionnaire, the Friendship Questionnaire (FQ), for use with adults of normal intelligence. A high score on the FQ is achieved by the respondent reporting that they enjoy close, empathic, supportive, caring friendships that are important to them; that they like and are interested in people; and that they enjoy interacting with others for its own sake. The FQ has a maximum score of 135 and a minimum of zero. In Study 1, we carried out a study of n = 76 (27 males and 49 females) adults from a general population, to test for previously reported sex differences in friendships. This confirmed that women scored significantly higher than men. In Study 2, we employed the FQ with n = 68 adults (51 males, 17 females) with Asperger Syndrome or high-functioning autism to test the theory that autism is an extreme form of the male brain. The adults with Asperger Syndrome or high-functioning autism scored significantly lower on the FQ than both the male and female controls from Study 1. The FQ thus reveals both a sex difference in the style of friendship in the general population, and provides support for the extreme male brain theory of autism. C1 Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, Cambridge CB2 2AH, England. Univ Cambridge, Dept Psychiat, Cambridge CB2 2AH, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Autism Res Ctr, Dept Expt Psychol, 18B Trumpington Rd, Cambridge CB2 2AH, England. CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Baron-Cohen S., 2001, J DEV LEARNING DISOR, V5, P47 Baron-Cohen S., 1999, NEURODEVELOPMENTAL D Baron-Cohen S, 1997, ADV INFANCY RES, V11, P193 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BARONCOHEN S, 2002, HDB COGNITIVE DEV BaronCohen S, 1997, J COGNITIVE NEUROSCI, V9, P548, DOI 10.1162/jocn.1997.9.4.548 Baron-Cohen S, 1999, J AUTISM DEV DISORD, V29, P407, DOI 10.1023/A:1023035012436 BARONCOHEN S, IN PRESS J AUTISM DE Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 BARONCOHEN S, 2000, COGNITIVE NEUROSCIEN Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x BaronCohen S, 1997, J CHILD PSYCHOL PSYC, V38, P813, DOI 10.1111/j.1469-7610.1997.tb01599.x Bauminger N, 2000, CHILD DEV, V71, P447, DOI 10.1111/1467-8624.00156 Caplan P. J., 1997, GENDER DIFFERENCES H Davis M. H., 1994, EMPATHY SOCIAL PSYCH Fivush R., 1994, GENDER DEV Geary David, 1998, MALE FEMALE EVOLUTIO HINES M, 1994, CHILD DEV, V65, P1042 Bailey A, 1998, HUM MOL GENET, V7, P571 Kimura D., 1999, SEX COGNITION LAWSON J, IN PRESS J AUSTISM D Maccoby E. E., 1999, 2 SEXES GROWING APAR WESCHLER D, 1939, MEASUREMENT ADULT IN WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1994, INT CLASS DIS NR 27 TC 59 Z9 59 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 2003 VL 33 IS 5 BP 509 EP 517 DI 10.1023/A:1025879411971 PG 9 WC Psychology, Developmental SC Psychology GA 725HT UT WOS:000185538700004 PM 14594330 ER PT J AU Aman, MG Lam, KSL Collier-Crespin, A AF Aman, MG Lam, KSL Collier-Crespin, A TI Prevalence and patterns of use of psychoactive medicines among individuals with autism in the Autism Society of Ohio SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE AED; psychotropic drugs; antileptic drugs; Autism ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDREN; DISABILITIES; DRUGS; PYRIDOXINE; VARIABLES; RATES AB To date, there have been few surveys of psychotropic and antiepileptic drug (AED) prevalence in individuals with autism-spectrum conditions. We surveyed 747 families in the Autism Society of Ohio regarding the use of psychotropic drugs, AEDs, and over-the-counter (OTC) preparations for autism. In all, 417 families (55.8%) replied. A total of 45.6% were taking some form of psychotropic agent (including St. John's wort and melatonin), whereas 11.5% were taking AEDs, and 10.3% took OTC autism preparations. The most common psychotropic agents included antidepressants (21.6%), antipsychotics (14.9%), antihypertensives (12.5%), and stimulants (11.3%). Some 51.6% were prescribed psychotropic drugs or AEDs, and 55.4% took psychotropic drugs, AEDs, or autism supplements. Demographic variables frequently found to be associated with medication use included greater age, more severe autism, more severe intellectual handicap, and housing outside the family home. Whereas there is empirical support for the use of some of these psychotropic agents in autism, others are being prescribed with minimal research support. OTC autism preparations were used in substantial numbers of individuals, despite limited research support and the possibility of toxic effects. C1 Ohio State Univ, Nisonger Ctr Mental Retardat & Dev Disabil, Columbus, OH 43210 USA. RP Aman, MG (reprint author), Ohio State Univ, Nisonger Ctr UAP, 1581 Dodd Dr, Columbus, OH 43210 USA. CR Aman MG, 1996, J DEV PHYS DISABIL, V8, P347, DOI 10.1007/BF02578400 Aman MG, 1999, MENT RETARD DEV D R, V5, P253, DOI 10.1002/(SICI)1098-2779(1999)5:4<253::AID-MRDD2>3.0.CO;2-R AMAN MG, 1995, J AM ACAD CHILD PSY, V34, P1672, DOI 10.1097/00004583-199512000-00018 Aman MG, 1999, MENT RETARD DEV D R, V5, P279, DOI 10.1002/(SICI)1098-2779(1999)5:4<279::AID-MRDD5>3.0.CO;2-6 AMAN MG, 1995, AM J MENT RETARD, V99, P500 Aman MG, 2000, J AUTISM DEV DISORD, V30, P451, DOI 10.1023/A:1005559725475 BATES WJ, 1986, AM J MENT RETARD, V90, P363 Baumeister A., 1998, PSYCHOTROPIC MED DEV, P133 Findling RL, 1997, J AUTISM DEV DISORD, V27, P467, DOI 10.1023/A:1025861522935 FRASER WI, 1998, PSYCHOTROPIC MED DEV, P271 HAGERMAN R, 1998, PSYCHOTROPIC MED DEV, P259 HEBERLEIN TA, 1978, AM SOCIOL REV, V43, P447, DOI 10.2307/2094771 KERLINGER FN, 2000, FDN BEHAV RES, P599 Martin A, 1999, J AM ACAD CHILD PSY, V38, P923, DOI 10.1097/00004583-199907000-00024 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 RIMLAND B, 1988, J CHILD NEUROL, V3, pS68 RINCK C, 1998, PSYCHOTROPIC MED DEV, P31 RUSH AJ, 2000, AM J MENTAL RETARDAT, V105 SCHAUMBURG H, 1983, NEW ENGL J MED, V309, P445, DOI 10.1056/NEJM198308253090801 Schlesselman J., 1982, CASE CONTROL STUDIES Singh NN, 1997, J CHILD ADOL PSYCHOP, V7, P255, DOI 10.1089/cap.1997.7.255 SINGH NN, 1998, PSYCHOTROPIC MED DEV, P311 WALTER SD, 1987, AM J EPIDEMIOL, V125, P319 NR 23 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 OCT PY 2003 VL 33 IS 5 BP 527 EP 534 DI 10.1023/A:1025883612879 PG 8 WC Psychology, Developmental SC Psychology GA 725HT UT WOS:000185538700006 PM 14594332 ER PT J AU Watanabe, M Sturmey, P AF Watanabe, M Sturmey, P TI The effect of choice-making opportunities during activity schedules on task engagement of adults with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE choice; activity; schedule; engagement ID PERFORMANCE; CHILDREN AB Increasing choice and participation by adults with autism spectrum disorders is an important, but neglected, aspect of research and services. This study evaluated the effects of choice-making opportunities, embedded within activity schedules, and contingent praise on the engagement of three adults with autism in a community vocational setting. In the baseline condition, staff assigned the order of the tasks. In the Choice condition and Maintenance phases, the participants chose the order of tasks that supervisors assigned to them. They made their own activity schedules by writing down the order of their tasks for that morning. Social praise was provided contingent on the participant's task completion. The same tasks were used in baseline, intervention, and maintenance phases. During the Choice and Maintenance conditions, client engagement was substantially higher than baseline for all three participants. Increasing choice-making opportunities within activity schedules was an effective and socially acceptable way to increase choice and engagement in adults with autism. C1 CUNY Queens Coll, Dept Psychol, Flushing, NY 11367 USA. CUNY, Grad Ctr, Flushing, NY 11367 USA. RP Sturmey, P (reprint author), CUNY Queens Coll, Dept Psychol, 65-30 Kissena Blvd, Flushing, NY 11367 USA. CR Anderson MD, 1997, RES DEV DISABIL, V18, P231, DOI 10.1016/S0891-4222(97)00006-1 Dunlap G, 1994, J Appl Behav Anal, V27, P505, DOI 10.1901/jaba.1994.27-505 Guess D., 1985, J ASSOC PERS SEVERE, V10, P79 MACDUFF GS, 1993, J APPL BEHAV ANAL, V26, P89, DOI 10.1901/jaba.1993.26-89 MCCLANNAHAN LE, 1999, TOPICS AUTISM Moes DR, 1998, J ASSOC PERS SEVERE, V23, P319, DOI 10.2511/rpsd.23.4.319 PARSONS MB, 1990, J APPL BEHAV ANAL, V23, P253, DOI 10.1901/jaba.1990.23-253 NR 7 TC 16 Z9 16 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 2003 VL 33 IS 5 BP 535 EP 538 DI 10.1023/A:1025835729718 PG 4 WC Psychology, Developmental SC Psychology GA 725HT UT WOS:000185538700007 PM 14594333 ER PT J AU Escalante-Mead, PR Minshew, NJ Sweeney, JA AF Escalante-Mead, PR Minshew, NJ Sweeney, JA TI Abnormal brain lateralization in high-functioning autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger's disorder; pervasive developmental disorders; brain lateralization; handedness; neuropsychology ID CORPUS-CALLOSUM; INFANTILE-AUTISM; CHILDHOOD AUTISM; HAND PREFERENCE; HANDEDNESS; CHILDREN; INDIVIDUALS; SKILL; SIZE AB Disturbances in lateral preference in autism are of interest because of their potential to shed light on brain maturational processes in this disorder. Forty-seven autistic individuals with a history of disordered early language development and 22 autistic individuals with normal early language acquisition were matched with 112 healthy individuals and compared on a standardized measure of lateral preference, the Edinburgh Handedness Inventory. Autistic individuals with a history of early language disturbance showed more atypical cerebral dominance than both healthy participants and autistic individuals with normal early language skills. The data indicated maturational disturbances in establishing lateral preference rather than increased rates of left handedness. Atypical establishment of cerebral dominance may be one cause of disordered language development in autism. C1 Univ Illinois, Ctr Cognit Med, Chicago, IL 60612 USA. Univ Pittsburgh, Pittsburgh, PA USA. RP Sweeney, JA (reprint author), Univ Illinois, Ctr Cognit Med, Chicago, IL 60612 USA. 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RP Edelson, SM (reprint author), Autism Res Inst, 4182 Adams Ave, San Diego, CA 92116 USA. CR Edelson SM, 1999, AM J OCCUP THER, V53, P145 Edelson SM, 1999, FOCUS AUTISM OTHER D, V14, P73, DOI 10.1177/108835769901400202 Goldstein H, 2000, J AUTISM DEV DISORD, V30, P423, DOI 10.1023/A:1005599406819 Rimland B., 1994, AM J SPEECH-LANG PAT, V3, P16 RIMLAND B, 1994, AM J SPEECH-LANG PAT, V5, P38 RIMLAND B, 1995, J AUTISM DEV DISORD, V25, P61, DOI 10.1007/BF02178168 NR 6 TC 0 Z9 0 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 2003 VL 33 IS 5 BP 551 EP 552 DI 10.1023/A:1025843931535 PG 2 WC Psychology, Developmental SC Psychology GA 725HT UT WOS:000185538700011 PM 14594336 ER PT J AU Goldstein, H AF Goldstein, H TI Interventions to facilitate auditory, visual, and motor integration: "Show me the data" - Response SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Editorial Material ID 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 EDELSON SM, 1999, AM J OCCUPATIONAL TH, V53, P143 Lonigan CJ, 1998, J CLIN CHILD PSYCHOL, V27, P138, DOI 10.1207/s15374424jccp2702_1 McGee J. 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PD OCT PY 2003 VL 33 IS 5 BP 557 EP 557 DI 10.1023/A:1025848032444 PG 1 WC Psychology, Developmental SC Psychology GA 725HT UT WOS:000185538700013 PM 14594337 ER PT J AU Gourion, D Pelissolo, A Orain-Pelissolo, S Lepine, JP AF Gourion, D Pelissolo, A Orain-Pelissolo, S Lepine, JP TI Neonatal tuberculous meningitis in a patient with Asperger's syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID AUTISM; CHILDREN; BRAIN C1 INSERM, E0117, F-75014 Paris, France. RP Gourion, D (reprint author), INSERM, E0117, 2 Ter Rue Alesia, F-75014 Paris, France. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bradford WZ, 1996, LANCET, V348, P928, DOI 10.1016/S0140-6736(96)03027-9 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 Happe F, 1996, BRAIN, V119, P1377, DOI 10.1093/brain/119.4.1377 Haznedar MM, 2000, AM J PSYCHIAT, V157, P1994, DOI 10.1176/appi.ajp.157.12.1994 Hosoglu S, 1998, INT J TUBERC LUNG D, V2, P553 McAlonan GM, 2002, BRAIN, V125, P1594, DOI 10.1093/brain/awf150 Oktem F, 2001, J CHILD NEUROL, V16, P253, DOI 10.1177/088307380101600404 Ozates M, 2000, ACTA RADIOL, V41, P13 Schoeman CJ, 1997, S AFR MED J, V87, P70 Starke J R, 1999, Semin Pediatr Neurol, V6, P318, DOI 10.1016/S1071-9091(99)80029-1 NR 11 TC 0 Z9 0 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 2003 VL 33 IS 5 BP 559 EP 560 DI 10.1023/A:1025800116514 PG 2 WC Psychology, Developmental SC Psychology GA 725HT UT WOS:000185538700014 PM 14594338 ER PT J AU Riikonen, R AF Riikonen, R TI Neurotrophic factors in the pathogenesis of Rett syndrome SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT Meeting of the International-Child-Neurology-Society/Rett Syndrome Satellite Symposium CY SEP 20, 2002 CL BEIJING, PEOPLES R CHINA SP Int Child Neurol Soc ID NERVE-GROWTH-FACTOR; CEREBROSPINAL-FLUID; FACTOR-I; BASAL FOREBRAIN; AUTISM; CHILDREN; SEROTONIN; EXCITOTOXICITY; DEGENERATION; NEUROBIOLOGY AB Rett syndrome is characterized by disruption of a period of vigorous brain growth with synapse development. Neurotrophic factors are important regulators of neuronal growth, differentiation, and survival during early brain development. The aims of this study were to study the role of neurotrophic factors in Rett syndrome, specifically whether Rett syndrome has abnormal levels of specific neurotrophic factors in serum and cerebrospinal fluid and whether the changes differ from other neuropediatric patients, for example, those with infantile autism. Four neurotrophic factors were measured: nerve growth factor, brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, and insulin-like growth factor I from the frozen cerebrospinal fluid and from serum (except glial cell line-derived neurotrophic factor) by enzyme-linked immunosorbent assay and cerebrospinal fluid glutamate and aspartate by high-performance liquid chromatography (HPLC) method in patients with Rett syndrome. Insulin-like growth factor 1 was measured from the cerebrospinal fluid of patients with infantile autism. We found low concentrations of cerebrospinal fluid nerve growth factor in patients with Rett syndrome compared with control patients. The serum levels and other cerebrospinal fluid neurotrophic factor levels of the patients did not differ from the controls. Patients with Rett syndrome had high cerebrospinal fluid glutamate levels. Patients with infantile autism had low cerebrospinal fluid insulin-like growth factor 1 levels. Nerve growth factor acts especially on cholinergic neurons of the basal forebrain, whereas insulin-like growth factor I acts on cerebellar neurons. In Rett syndrome, the forebrain is more severely affected than the other cortical areas. In autism, many studies show hippocampal or cerebellar pathology. Our findings are in agreement with the different morphologic and neurochemical findings (brain growth, affected brain areas, neurotransmitter metabolism) in the two syndromes. Impairment in dendritic development in Rett syndrome could be the consequence of cholinergic deficiency and of neurotrophic factor/glutamate imbalance. Cholinergic gene expression might be influenced by the Rett syndrome gene directly or via the neurotrophic factor system. C1 Univ Kuopio, Childrens Hosp, FIN-70211 Kuopio, Finland. RP Riikonen, R (reprint author), Univ Kuopio, Childrens Hosp, PL 1627, FIN-70211 Kuopio, Finland. 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PD OCT PY 2003 VL 24 IS 5 BP 393 EP 393 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 734FT UT WOS:000186044900022 ER PT J AU Shastry, BS AF Shastry, BS TI Molecular genetics of autism spectrum disorders SO JOURNAL OF HUMAN GENETICS LA English DT Review DE linkage; gene; cytogenetic; chromosome ID PERVASIVE DEVELOPMENTAL DISORDERS; AFFECTED SIBLING PAIRS; SUSCEPTIBILITY GENE; INFANTILE-AUTISM; SEROTONIN TRANSPORTER; MULTIPLEX FAMILIES; GENOMEWIDE SCREEN; CANDIDATE GENES; GENOMIC SCREEN; RECIPROCAL TRANSLOCATION AB Autistic disorder belongs to a broad spectrum of pervasive developmental disorders. Autism is a clinically and genetically heterogeneous condition. It is characterized by impairment in a broad range of social interactions, communication, and repetitive patterns of behavior and interest. Although the exact etiology of the condition is not known, family and twin studies strongly support genetic factors in autism. Genome-wide scans suggest several susceptibility loci that may contain one or more predisposing genes. However, no such genes have been identified so far that predispose patients to autism. The condition is over 90% heritable, but the mode of inheritance is not clear. Moreover, it does not seem to be a single gene disorder. There is no cure for autism. Individualized structured education, family support services, and antipsychotic drugs are recommended. These may alleviate some behavioral problems. The identification of autism genes, an understanding of the neurobiology of the condition, and additional clinical studies may help to develop pharmacological interventions in the future. C1 Oakland Univ, Dept Biol Sci, Rochester, MI 48309 USA. RP Shastry, BS (reprint author), Oakland Univ, Dept Biol Sci, Rochester, MI 48309 USA. 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Hum. Genet. PD OCT PY 2003 VL 48 IS 10 BP 495 EP 501 DI 10.1007/s10038-003-0064-9 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 737QG UT WOS:000186242800001 PM 13680297 ER PT J AU Irwin, JR Carter, AS Briggs-Gowan, MJ AF Irwin, JR Carter, AS Briggs-Gowan, MJ TI Depression and suicidality in preschoolers - Reply SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Letter ID AUTISM C1 Haskins Labs Inc, New Haven, CT 06511 USA. Univ Massachusetts, Boston, MA 02125 USA. Yale Univ, Dept Epidemiol & Publ Hlth, New Haven, CT 06520 USA. RP Irwin, JR (reprint author), Haskins Labs Inc, 270 Crown St, New Haven, CT 06511 USA. CR Carter A. 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R., 2003, MIND TREE MIRACULOUS 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 OCT 1 PY 2003 VL 128 IS 16 BP 101 EP 101 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 724AP UT WOS:000185464300158 ER PT J AU Krauss, MW Gulley, S Sciegaj, M Wells, N AF Krauss, MW Gulley, S Sciegaj, M Wells, N TI Access to specialty medical care for children with mental retardation, autism, and other special health care needs SO MENTAL RETARDATION LA English DT Article ID MANAGED CARE; MAINTENANCE ORGANIZATIONS; CHRONIC ILLNESS; DISABILITIES; INSURANCE; QUALITY; IMPACT AB Access to specialty medical care among children with mental retardation, autism, or other types of special health care needs was examined. Results from a national survey indicate that over a third of the children with autism, over a fifth with mental retardation, and over a fifth with other types of special health care needs had problems obtaining needed care from specialty doctors in the preceding year. The most common problems included getting referrals and finding providers with appropriate training. Children with unstable health conditions, autism, or those whose parent was in poor health were at greater risk for problems. Primary Medicaid coverage and public secondary health coverage were associated with fewer access problems. Implications for health services for children with special health care needs are discussed. 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Retard. PD OCT PY 2003 VL 41 IS 5 BP 329 EP 339 DI 10.1352/0047-6765(2003)41<329:ATSMCF>2.0.CO;2 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 723LV UT WOS:000185434600002 PM 12962535 ER PT J AU Somogyi, L Ross, SO Cintron, M Toskes, PP AF Somogyi, L Ross, SO Cintron, M Toskes, PP TI Comparison of biologic porcine secretin, synthetic porcine secretin, and synthetic human secretin in pancreatic function testing SO PANCREAS LA English DT Article DE chronic pancreatitis; biologic porcine secretin; bicarbonate; synthetic porcine secretin; synthetic human secretin ID HISTOLOGICAL-CHANGES; EXOCRINE FUNCTION; AUTISM; DIAGNOSIS AB Background and Aims: Due to the unavailability of biologic porcine secretin (BPS), 2 synthetic forms of secretin were developed. Our aim is to determine the bioequivalency of the 3 forms of secretin in pancreatic function testing. Methods: In a randomized, crossover design, synthetic porcine (SPS) and synthetic human secretin (SHS) were compared in a group of 12 subjects with chronic pancreatitis undergoing secretin stimulation test (SST). The 2 synthetic forms of secretin were then compared with BPS in 12 subjects utilizing a similar design. Finally, 18 healthy subjects underwent secretin stimulation testing with SHS. Results: There was excellent correlation of peak bicarbonate measurements in the comparison of SPS to SHS (R = 0.967) as well as in the comparison of all 3 forms of secretin (P = 0.08, ANOVA for correlated samples). In the SST, each of the synthetic forms of secretin were 100% accurate in diagnosing chronic pancreatitis in disease subjects and in excluding chronic pancreatitis in normal controls. The synthetic forms of secretin were associated with fewer side effects when compared with BPS with the exception of transient tachycardia which occurred in up to 19% of subjects. 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PD OCT PY 2003 VL 32 IS 10 BP 677 EP 684 PG 8 WC Pediatrics SC Pediatrics GA 733AN UT WOS:000185977900007 PM 14606218 ER PT J AU Levy, SE Hyman, SL AF Levy, SE Hyman, SL TI Use of complementary and alternative treatments for children with autistic spectrum disorders is increasing SO PEDIATRIC ANNALS LA English DT Article ID DOUBLE-BLIND; ONSET AUTISM; PLACEBO; MAGNESIUM; TRIAL; SECRETIN; ACID C1 Childrens Hosp Philadelphia, Childrens Seashore House, Div Child Dev & Rehabil, Philadelphia, PA USA. Univ Penn, Sch Med, Philadelphia, PA 19104 USA. Univ Rochester, Sch Med, Rochester, NY USA. RP Levy, SE (reprint author), 3405 Civ Ctr Blvd, Philadelphia, PA 19003 USA. 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Annu. PD OCT PY 2003 VL 32 IS 10 BP 685 EP 691 PG 7 WC Pediatrics SC Pediatrics GA 733AN UT WOS:000185977900008 PM 14606219 ER PT J AU Afzal, N Murch, S Thirrupathy, K Berger, L Fagbemi, A Heuschkel, R AF Afzal, N Murch, S Thirrupathy, K Berger, L Fagbemi, A Heuschkel, R TI Constipation with acquired megarectum in children with autism SO PEDIATRICS LA English DT Article DE autism; neurodisability; constipation; child; abdominal radiographs ID DISORDERS; INFLAMMATION; CHILDHOOD; EOTAXIN; ALLERGY; GLUTEN AB Objective. Recent evidence suggests that autistic children may have significant gastrointestinal symptoms. Although constipation occurs in 2% to 5% of healthy children, its clinical diagnosis is often difficult in children with behavioral disorders. We thus aimed to assess the prevalence of fecal loading in autistic children with gastrointestinal symptoms and to identify possible predictors of constipation. Methods. We studied abdominal radiographs of 103 autistic children (87 boys) who were referred for gastroenterological assessment, in comparison with 29 control radiographs from children who were referred to the emergency department, most with abdominal pain. Radiographs were scored independently, in blinded manner, by 4 pediatric gastroenterologists and a radiologist. The severity of constipation was determined using a validated index. Details of stool habit, abdominal pain, dietary history, and laxative use were obtained from case notes. Results. The incidence of constipation in the control subjects with abdominal pain was higher than reported for normal children. Despite this, moderate or severe constipation was more frequent in the autistic group than in the control subjects (36% vs 10%). Analysis of rectosigmoid loading showed more striking differences (54.4% of autistic children had moderate/severe loading or acquired megarectum compared with 24.1% of control subjects). Multivariate regression analysis showed consumption of milk to be the strongest predictor of constipation in the autistic group, whereas stool frequency, gluten consumption, soiling, and abdominal pain were not predictive of constipation. Conclusions. Constipation is a frequent finding in children with gastrointestinal symptoms and autism, particularly in the rectosigmoid colon, often with acquired megarectum. The absence of any correlation between the clinical history and the degree of fecal impaction in autistic children confirms the importance of an abdominal radiograph in the assessment of their degree of constipation. C1 Royal Free Hosp, Ctr Pediat Gastroenterol, London NW3 2QG, England. Royal Free Hosp, Dept Radiol, London NW3 2QG, England. RP Heuschkel, R (reprint author), Royal Free Hosp, Ctr Pediat Gastroenterol, Pond St, London NW3 2QG, England. 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PD OCT-DEC PY 2003 VL 23 IS 4 BP 269 EP 270 PG 2 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 736LE UT WOS:000186171600002 ER PT J AU Mirenda, P AF Mirenda, P TI "He's not really a reader ...": Perspectives on supporting literacy development in individuals with autism SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE augmentative and alternative communication; autism; literacy ID FACILITATED COMMUNICATION; SEVERE DISABILITIES; MULTILEVEL INSTRUCTION; WORD RECOGNITION; CHILDREN; CLASSROOM; STUDENTS; MODERATE; PROGRAM; ABILITY AB Although many individuals with autism are able to demonstrate skills that are directly related to literacy, they are often seen as "too cognitively impaired" or "not ready for" instruction in this important area. This article provides suggestions for strategies that can be used to promote literacy learning across the five stages of word reading development described by Ehri. 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PD OCT-DEC PY 2003 VL 23 IS 4 BP 271 EP 282 PG 12 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 736LE UT WOS:000186171600003 ER PT J AU Koppenhaver, DA Erickson, KA AF Koppenhaver, DA Erickson, KA TI Natural emergent literacy supports for preschoolers with autism and severe communication impairments SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE autism; autism spectrum disorders; computers; emergent literacy; emergent reading; emergent writing; severe communication disorders ID CHILDREN; INTERVENTION; LANGUAGE; INSTRUCTION; PRECURSORS AB Print materials, experiences, and writing technologies were introduced into a preschool classroom for children with autism spectrum disorders, including three 3-year-olds with severe communication impairments. The goal was to increase natural literacy learning opportunities and to explore the effects on children's emergent literacy behaviors and understandings. 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PD OCT-DEC PY 2003 VL 23 IS 4 BP 283 EP 292 PG 10 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 736LE UT WOS:000186171600004 ER PT J AU Blischak, DM Schlosser, RW AF Blischak, DM Schlosser, RW TI Use of technology to support independent spelling by students with autism SO TOPICS IN LANGUAGE DISORDERS LA English DT Article; Proceedings Paper CT Annual Convention of the American-Speech-Language-Hearing-Association CY NOV, 2002 CL NEW ORLEANS, LOUISIANA SP Amer Speech language Hear Assoc DE augmentative and alternative communication; autism; computers; literacy; speech-generating devices; spelling; talking word processing software ID YOUNG-CHILDREN; COMMUNICATION; INSTRUCTION; STRATEGIES; PROGRAM; ISSUES AB For individuals with little or no functional speech, the ability to spell is critical in generating spontaneous, novel utterances. 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PD OCT-DEC PY 2003 VL 23 IS 4 BP 293 EP 303 PG 11 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 736LE UT WOS:000186171600005 ER PT J AU Bedrosian, J Lasker, J Speidel, K Politsch, A AF Bedrosian, J Lasker, J Speidel, K Politsch, A TI Enhancing the written narrative skills of an AAC student with autism: Evidence-based research issues SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE augmentative and alternative communication; children with autism; literacy; written narrative skills ID SUBJECT EXPERIMENTAL-DESIGNS; FLEXIBILITY AB This article describes an intervention study designed to enhance the skills needed in the planning and writing of stories by an adolescent student with autism working with a typically speaking peer as a partner. Also described is the decision-making process used with respect to several evidence-based research issues. 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PD OCT-DEC PY 2003 VL 23 IS 4 BP 305 EP 324 PG 20 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 736LE UT WOS:000186171600006 ER PT J AU Foley, BE Staples, AH AF Foley, BE Staples, AH TI Developing augmentative and alternative communication (AAC) and literacy interventions in a supported employment setting SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE AAC intervention; autism; literacy intervention; supported employment ID AUTISM AB This article describes an integrated augmentative and alternative communication (AAC) and literacy intervention program developed for five adults with autism in a supported employment facility. Specific assessment and intervention strategies as well as general outcomes of the program are discussed. Three detailed case studies describe approaches used with project participants who had emerging, beginning, and more advanced levels of communication and literacy skill. C1 Utah State Univ, Dept Communicat Disorders & Deaf Educ, Logan, UT 84322 USA. Univ No Iowa, Dept Special Educ, Cedar Falls, IA 50614 USA. RP Foley, BE (reprint author), Utah State Univ, Dept Communicat Disorders & Deaf Educ, UMC 1000, Logan, UT 84322 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bear D. R., 1999, WORDS THEIR WAY WORD Beukelman D. R., 1998, AUGMENTATIVE ALTERNA Clay M. M., 1993, OBSERVATION SURVEY E Colasent R, 1998, READ TEACH, V51, P414 Coyne P., 1999, FOCUS AUTISM OTHER D, V14, P42, DOI DOI 10.1177/108835769901400106 CUNNINGHAM P, 1998, READ TEACH, V44, P566 CUNNINGHAM PM, 1995, PHONICS USE WORDS RE CUNNINGHAM PM, 2002, CLASSROOMS WORK CAN *D JOHNS INC, 1999, WRIT OUTL COMP SOFTW ELDER P, 1996, COMMUNICATION OVER L ERICKSON KA, 1994, TR9415 NCAL Flannery K. 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PD OCT-DEC PY 2003 VL 23 IS 4 BP 325 EP 343 PG 19 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 736LE UT WOS:000186171600007 ER PT J AU Bellaby, P AF Bellaby, P TI Communication and miscommunication of risk: understanding UK parents' attitudes to combined MMR vaccination SO BRITISH MEDICAL JOURNAL LA English DT Article ID CREUTZFELDT-JAKOB-DISEASE; RUBELLA VACCINE; TREND ANALYSIS; MEASLES; MUMPS; IMMUNIZATION; CHILDREN; ENGLAND; AUTISM; POLICY AB In this article on the public perception of risks Paul Bellaby considers three examples of risks to children in the UK-an insignificant risk (autism caused by MMR vaccine), a real but probably small risk (vCJD from BSE), and a real and demonstrably larger risk (injuries from road crashes) and contrasts the perceptions of the risks by parents. C1 Univ Salford, Inst Publ Hlth Res & Policy, Salford M5 4QA, Greater Manches, England. RP Bellaby, P (reprint author), Univ Salford, Inst Publ Hlth Res & Policy, Salford M5 4QA, Greater Manches, England. 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Med. J. PD SEP 27 PY 2003 VL 327 IS 7417 BP 725 EP 728 DI 10.1136/bmj.327.7417.725 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 728FZ UT WOS:000185708300022 PM 14512482 ER PT J AU Plon, M AF Plon, M TI Recognizing autism SO QUINZAINE LITTERAIRE LA French DT Book Review CR LEFORT R, DISTINCTION AUTISME NR 1 TC 0 Z9 0 PU QUINZAINE LITTERAIRE PI PARIS PA 135 RUE SAINT-MARTIN, 75194 PARIS, FRANCE SN 0048-6493 J9 QUINZAINE LITTERAIRE JI Quinz. Litt. PD SEP 16 PY 2003 IS 861 BP 30 EP 30 PG 1 WC Literature SC Literature GA 725VD UT WOS:000185562300028 ER PT J AU Tecchio, F Benassi, F Zappasodi, F Gialloreti, LE Palermo, M Seri, S Rossini, PM AF Tecchio, F Benassi, F Zappasodi, F Gialloreti, LE Palermo, M Seri, S Rossini, PM TI Auditory sensory processing in autism: A magnetoencephalographic study SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; cortical discrimination ability; magnetoencephalography; mismatch field; automatic neural mismatch; sensory impairment ID DEVELOPMENTAL LANGUAGE DISORDER; BRAIN POTENTIAL EVIDENCE; MISMATCH NEGATIVITY MMN; TUBEROUS SCLEROSIS; RETARDED-CHILDREN; RESPONSES; GENERATORS; CHILDHOOD; ATTENTION; DEFECTS AB Background: Patients with autism show clinical features suggestive of abnormal processing of auditory and other sensory information. We hypothesized that low-functioning autistic subjects present abnormalities in discriminating simple auditory stimuli at sensory system preconscious stages of cortical processing. Methods: To verify our hypothesis, we used magnetoencephalographic measurements of mismatch field (MMF), which reflects the detection of a change in the physical characteristics of a repetitive sound. Fourteen patients (aged 8-32 Years) who met DSM-IV diagnostic criteria for autistic disorder participated in an auditory oddball experiment. Ten healthy participants matched for age and gender acted as control subjects. Results: Significant differences in cerebral responses between patients and control subjects were recorded. Whereas control subjects showed a clearly identifiable MMF, with distinct generators in the M100 brain wave with regard to latency, position, and strength, no identifiable MMF was present in the autistic group. 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We previously observed that the OMgp gene locus on chromosome 17 could be associated with autism, a developmental disorder. The aim of the present study was to characterise the developmental expression of OMgp mRNA in the central nervous system. First we determined the rat OMgp gene sequence and compared it with the human and mouse sequences. Several regions, putative sites for the fixation of transcription factors, are conserved between these three species in the unique intron of this gene. Using quantitative and semi-quantitative RT-PCR, we studied OMgp gene expression in rat brain during post-natal development. We found that OM-p mRNA expression was developmentally regulated, with a peak of expression in the late stages of myelination. We observed a similar profile in oligodendrocyte cultures, in absence of neurones, suggesting that OM-p mRNA expression by oligodendrocytes was independent of axonal influence. Our observations suggest that OMgp is a late marker of myelination, which could be implicated in the arrest of oligodendrocyte proliferation, arrest of myelination or compaction of myelin. (C) 2003 Elsevier B.V. All rights reserved. C1 INSERM, U 316, F-37032 Tours, France. RP Andres, C (reprint author), INSERM, U 316, 2 Bis Blvd Tonnelle, F-37032 Tours, France. 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Brain Res. PD SEP 10 PY 2003 VL 144 IS 2 BP 159 EP 168 DI 10.1016/S0165-3806(03)00167-6 PG 10 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 723QU UT WOS:000185443700004 ER PT J AU Gage, NM Siegel, B Roberts, TPL AF Gage, NM Siegel, B Roberts, TPL TI Cortical auditory system maturational abnormalities in children with autism disorder: an MEG investigation SO DEVELOPMENTAL BRAIN RESEARCH LA English DT Article DE autism; magnetoencephalography; maturation; auditory cortex; language ID POTENTIALS N1 WAVE; EVOKED-POTENTIALS; DEVELOPMENTAL-CHANGES; TUBEROUS SCLEROSIS; HEALTHY-CHILDREN; RESPONSES; TIME; COMPONENTS; TOPOGRAPHY; CHILDHOOD AB Latency of electric (e.g., PI and NI) and magnetic (e.g., M100) auditory evoked components depends on age in typically developing children, with longer latencies for younger (4-6 years) and shorter, adult-like latencies for older (14-16 years) children. Age-related changes in evoked components provide indirect measures of auditory system maturation and reflect changes that occur during development. We use magnetoencephalography (MEG) to investigate maturational changes in cortical auditory systems in left (LH) and right (RH) hemispheres in children with autism disorder (AD) and Controls. We recorded auditory evoked responses over left and right temporal lobes in 17 Control and 15 AD children in the age range 8-16 years and measured M100 latency as a function of age, subject group and hemisphere. Linear regression analyses of age and M100 latency provided an estimate of the rate of latency change (ms/year) by hemisphere and subject group. Controls: M100 latency for the group ranged from 100.8 to 166.1 ms and varied linearly in both hemispheres, decreasing at a rate of -4 ms/year (LH) and -4.5 ms/year (RH). AD: M100 latency ranged from 116.2 to 186.2 ins. Slopes of regression lines did not differ from zero in either LH or RH. M100 latency showed a tendency to vary with age in LH, decreasing at a rate of -4.6 ms/year. M100 latency in RH increased slightly (at a rate of 0.8 ms/year) with age. Results provide evidence for a differential auditory system development in AD children which may reflect abnormalities in cortical maturational processes in AD. (C) 2003 Elsevier B.V. All rights reserved. C1 Biomagnet Imaging Lab, San Francisco, CA USA. Univ Calif San Francisco, Pervas Dev Disorders Clin, San Francisco, CA 94143 USA. RP Gage, NM (reprint author), Univ Calif Irvine, Dept Cognit Sci, Mail Code 5100,3151 Social Sci Plaza A, Irvine, CA 92697 USA. 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Brain Res. PD SEP 10 PY 2003 VL 144 IS 2 BP 201 EP 209 DI 10.1016/S0165-3806(03)00172-X PG 9 WC Developmental Biology; Neurosciences SC Developmental Biology; Neurosciences & Neurology GA 723QU UT WOS:000185443700008 ER PT J AU Jefferson, T Price, D Demicheli, V Bianco, E AF Jefferson, T Price, D Demicheli, V Bianco, E CA European Res Program Improved Vacc TI Unintended events following immunization with MMR: a systematic review SO VACCINE LA English DT Article DE measles; mumps and rubella (MMR); randomized controlled trials (RCTs); CCTs ID MEASLES-MUMPS-RUBELLA; ASEPTIC-MENINGITIS; COMBINED TRIVALENT; CONTROLLED TRIAL; LIVE MEASLES; VACCINE; CHILDREN; POPULATION; VIRUS; SYMPTOMS AB Public debate over the safety of the trivalent measles, mumps and rubella (MMR) vaccine and the drop in vaccination rates in several countries persists despite its almost universal use and accepted effectiveness. We carried out a systematic review to assess the evidence of unintended effects (beneficial or harmful) associated with MMR and the applicability of systematic reviewing methods to the field of safety evaluation. Eligible studies were comparative prospective or retrospective on healthy individuals up to 15 years of age, carried out or published by 2003. We identified 120 articles satisfying our inclusion criteria and included 22. MMR is associated with a lower incidence of upper respiratory tract infections, a higher incidence of irritability, similar incidence of other adverse effects compared to placebo and is likely to be associated with benign thrombocytopenic purpura (TP), parotitis, joint and limb complaints and aseptic meningitis (mumps Urabe strain-containing MMR). Exposure to MMR is unlikely to be associated with Crohn's disease, ulcerative colitis, autism or aseptic meningitis (mumps Jeryl-Lynn strain-containing MMR). The design and reporting of safety outcomes in MMR vaccine studies, both pre- and post-marketing, are largely inadequate. The evidence of adverse events following immunization with MMR cannot be separated from its role in preventing the target diseases. (C) 2003 Elsevier Ltd. All rights reserved. C1 Ist Super Sanita, Reparto Epidemiol Clin, I-00161 Rome, Italy. RP Jefferson, T (reprint author), Ist Super Sanita, Reparto Epidemiol Clin, Viale Regina Elena 299, I-00161 Rome, Italy. 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Public backlash against this vaccine not only took place earlier in Britain than the United States, but also was so widespread that a series of whooping cough epidemics soon followed. As with the more recent dispute involving measles-mumps-rubella (MMR) vaccine and autism, the United Kingdom played a primary role in defining, promoting, and ultimately exporting this controversy. This essay seeks to explain this phenomenon by situating it in Britain's long history of suspicion regarding vaccines evident among both the public and the medical profession, a theme dating back to the compulsory vaccination laws of the 19th century. It argues that anti-vaccinationism, far front being simply a new development related to the public's lack of awareness of childhood vaccine-preventable illness, actually represents a revival of a much older movement. Elsevier Ltd. All rights reserved. C1 Duke Univ, Ctr Study Med Eth & Humanities, Durham, NC 27706 USA. RP Baker, JP (reprint author), Duke Univ, Ctr Study Med Eth & Humanities, Box 3040 DUMC, Durham, NC 27706 USA. 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PD SEP 6 PY 2003 VL 179 IS 2411 BP 17 EP 17 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 719AF UT WOS:000185180300016 ER PT J AU Schmitz, C Martineau, J Barthelemy, C Assaiante, C AF Schmitz, C Martineau, J Barthelemy, C Assaiante, C TI Motor control and children with autism: deficit of anticipatory function? SO NEUROSCIENCE LETTERS LA English DT Article DE autism; anticipation; motor development; electromyographic; kinematics ID HUMAN PRECISION GRIP; POSTURAL ADJUSTMENT; COORDINATION; MOVEMENT; LIFE AB This study aims at investigating how do anticipatory postural adjustments develop in children with autism, during a bimanual load-lifting task that required maintaining the stabilisation of the forearm despite imposed or voluntary unloading. Elbow angle and electromyographic were recorded on the child forearm supporting the load. The forearm stabilisation was as good in children with autism as in the control group. However, in children with autism, the latencies for both kinematics and muscular events indicated an increase of the duration of unloading. These results indicate the use of a feedback rather than a feed-forward mode of control. Impairments in both the building of internal representations and the mastering of timing parameters, could explain the deficient postural anticipation reported in children with autism. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved. C1 CNRS, Inst Neurosci Physiol & Cognit, F-13402 Marseille 20, France. CHU Bretonneau, INSERM U316, Tours, France. RP Schmitz, C (reprint author), CNRS, Inst Neurosci Physiol & Cognit, 31 Chemin J Aiguier, F-13402 Marseille 20, France. 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10.1054/plef.2000.0198 NR 82 TC 7 Z9 7 PU INNOVISION COMMUNICATIONS PI ALISO VIEJO PA 101 COLUMBIA, ALISO VIEJO, CA 92656 USA SN 1078-6791 J9 ALTERN THER HEALTH M JI Altern. Ther. Health Med. PD SEP-OCT PY 2003 VL 9 IS 5 BP 22 EP 31 PG 10 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 720ZE UT WOS:000185291900005 PM 14526708 ER PT J AU Niedermeyer, E Ebaugh, K AF Niedermeyer, E Ebaugh, K TI Sleep spindles mixed with spikes. Any clinical significance? SO AMERICAN JOURNAL OF ELECTRONEURODIAGNOSTIC TECHNOLOGY LA English DT Article DE extreme spindles; frontal lobe epilepsy; prematurity encephalopathy; spikes and spindles; spindles ID EPILEPSY AB Spikes are commonly found in association with K complexes in patients with primary generalized epilepsy. A mixture of spikes and (unusually abundant) sleep spindles, however, is rather unique in clinical EEG. Such a blend of spikes and spindles was the hallmark of a sleep tracing in a 10-year-old boy with recent onset Of seizures. Seizure type and the waking EEG suggested frontal (especially left frontal) origin of the seizures. The history and clinical findings revealed a mild encephalopathy, presumably caused by prematurity and associated with a moderate type of autism. Computed tomography (CT) findings were unremarkable. The combination of frontal lobe epilepsy with mixed spindles and spikes is not readily understood and deserves attention. The overabundance of spindles could be related to the pattern known as "extreme spindles.". C1 Sinai Hosp, Dept Med, Div Neurol, Baltimore, MD USA. RP Niedermeyer, E (reprint author), 305 Colonial Court, Towson, MD 21204 USA. 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J. Electroneurodiagn. Technol. PD SEP PY 2003 VL 43 IS 3 BP 123 EP 129 PG 7 WC Medical Laboratory Technology; Neurosciences SC Medical Laboratory Technology; Neurosciences & Neurology GA 743CG UT WOS:000186554400001 ER PT J AU Sweeten, TL Posey, DJ McDougle, CJ AF Sweeten, TL Posey, DJ McDougle, CJ TI High blood monocyte counts and neopterin levels in children with autistic disorder SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID URINARY LEVELS; BIOPTERIN; PTERINS AB Objective: Leukocyte counts and plasma neopterin levels were determined in autistic children and matched healthy comparison subjects. Method: Blood from 31 autistic children and 28 age- and gender-matched healthy comparison subjects was analyzed for numbers of neutrophils, eosinophils, basophils, lymphocytes, monocytes, and total leukocytes and for plasma neopterin levels. Results: The monocyte count and neopterin level were significantly higher in the autistic children than in the comparison subjects. Conclusions: These results suggest that the immune system may be activated in some children with autism. C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. RP McDougle, CJ (reprint author), Indiana Univ, Sch Med, Dept Psychiat, Psychiat Bldg,A305,1111 W 10th St, Indianapolis, IN 46202 USA. 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J. Psychiat. PD SEP PY 2003 VL 160 IS 9 BP 1691 EP 1693 DI 10.1176/appi.ajp.160.9.1691 PG 3 WC Psychiatry SC Psychiatry GA 718PV UT WOS:000185156400022 PM 12944347 ER PT J AU Demark, JL Feldman, MA Holden, JJA AF Demark, JL Feldman, MA Holden, JJA TI Behavioral relationship between autism and fragile X syndrome SO AMERICAN JOURNAL ON MENTAL RETARDATION LA English DT Article ID DSM-III-R; MENTAL-RETARDATION; INFANTILE-AUTISM; DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; RATING-SCALE; CHILDREN; MALES; INDIVIDUALS; PREVALENCE AB Previous researchers have reported autistic features in children with fragile X syndrome. We compared 21 children with pervasive developmental disorders (autism group) to 15 with fragile X syndrome on the Childhood Autism Rating Scale and the Reiss Scales for Children's Dual Diagnosis. The 7 children (47%) with fragile X who scored above the Childhood Autism Rating Scale cut-off (fragile X-autism group) were more impaired than the remaining children (fragile X-no autism) on Childhood Autism Rating Scale subscales related to emotion, visual and listening responses, and communication. The autism group's Reiss scores were higher than fragile X-no autism group, but not fragile X-autism group. Although the Childhood Autism Rating Scale identified almost 50% of children with fragile X as having autism, qualitative differences may exist in specific autistic-like behaviors between children with autism and children with fragile X. C1 Queens Univ, Kingston, ON K7L 3N6, Canada. Brock Univ, Dept Child & Youth Studies, St Catharines, ON 12S 3A1, Canada. RP Feldman, MA (reprint author), Brock Univ, Dept Child & Youth Studies, 455 Acad S, St Catharines, ON 12S 3A1, Canada. 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J. Ment. Retard. PD SEP PY 2003 VL 108 IS 5 BP 314 EP 326 DI 10.1352/0895-8017(2003)108<314:BRBAAF>2.0.CO;2 PG 13 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 714XK UT WOS:000184939400004 PM 12901707 ER PT J AU Roper, L Arnold, P Monteiro, B AF Roper, L Arnold, P Monteiro, B TI Co-occurrence of autism and deafness - Diagnostic considerations SO AUTISM LA English DT Article DE autism; deafness ID CHILDREN AB Autism spectrum disorders are particularly difficult to diagnose in the presence of early profound deafness because of communication related issues. Two parts of the Autism Screening Instrument were administered to 13 deaf individuals with autism and two comparison groups: hearing autistic and deaf learning disabled. A parental questionnaire was also used. No differences in autistic symptomatology were found between the deaf autistic and the hearing autistic group. However, the deaf autistic group was diagnosed later than the hearing autistic group. It is concluded that autism can be diagnosed in the deaf., that it resembles autism in the hearing; and that it is not a consequence of deafness per se. Learning disabled deaf individuals who are not autistic do not resemble people with autism in behavioural terms. The findings have implications for remediation, education, and the emergence and management of challenging behaviours. C1 Univ Manchester, Dept Psychol, Manchester M13 9PL, Lancs, England. Natl Ctr Mental Hlth & Deafness, Manchester, Lancs, England. RP Arnold, P (reprint author), Univ Manchester, Dept Psychol, Oxford Rd, Manchester M13 9PL, Lancs, England. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th COLEMAN ML, 1993, EUR CHILD ADOLES PSY, V2, P161 DENMARK JC, 1994, DEAFNESS MENTAL HLTH GARREAU B, 1984, J AUTISM DEV DISORD, V14, P105, DOI 10.1007/BF02408559 GORDON AG, 1991, AM J PSYCHIAT, V148, P1615 Happe F., 1994, AUTISM INTRO PSYCHOL Hiskey M., 1966, HISKEY NEBRASKA TEST Jordan R. R., 1995, UNDERSTANDING TEACHI JURE R, 1991, DEV MED CHILD NEUROL, V33, P1062 KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x Krug DA, 1993, AUTISM SCREENING INS Lewis V., 1987, DEV HANDICAP RAPIN I, 1991, PEDIATRICS, V87, P751 NR 13 TC 32 Z9 33 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2003 VL 7 IS 3 BP 245 EP 253 DI 10.1177/1362361303007003002 PG 9 WC Psychology, Developmental SC Psychology GA 716JK UT WOS:000185024900002 PM 14516058 ER PT J AU Fecteau, S Mottron, L Berthiaume, C Burack, JA AF Fecteau, S Mottron, L Berthiaume, C Burack, JA TI Developmental changes of autistic symptoms SO AUTISM LA English DT Article DE ADI-R; autism; developmental changes; repetitive behaviors; restricted interests ID DIAGNOSTIC OBSERVATION SCHEDULE; SELF-INJURIOUS-BEHAVIOR; FOLLOW-UP; INFANTILE-AUTISM; CHILDREN; ADULTS; ADOLESCENTS; POPULATION; INTERVIEW; SPECTRUM AB The study examined developmental changes in autistic symptoms retrospectively in a sample of 28 verbal children and adolescents with autism. Individuals with Asperger syndrome, PDD-NOS, and related medical conditions were not included in the study. We compared autistic symptoms present at the retrospective assessment and during the 4- to 5-year age period using the ADI-R. Our findings revealed a significant improvement in the three domains relevant for the diagnosis of autism, independent of age or IQ level. Improvement occurred in more symptoms from the social than the communication domain, and for more symptoms from the latter than the restricted interest and repetitive behavior domains. The finding that improvement was not linked to level of functioning and was found in individuals still positive for a diagnosis of autism suggests that improvement belongs to the 'natural history' of the handicap. C1 Hop Riviere des Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. RP Mottron, L (reprint author), Hop Riviere des Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. CR ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th American Psychiatric Association, 1985, DIAGN STAT MAN MENT BallabanGil K, 1996, PEDIATR NEUROL, V15, P217, DOI 10.1016/S0887-8994(96)00219-6 BARTAK L, 1976, J AUTISM CHILD SCHIZ, V6, P109, DOI 10.1007/BF01538054 Boelte S., 2000, AUTISM, V4, P382, DOI [10.1177/1362361300004004004, DOI 10.1177/1362361300004004004] Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Church C C, 1995, J Pediatr Health Care, V9, P22, DOI 10.1016/S0891-5245(05)80043-4 Collacott RA, 1998, BRIT J PSYCHIAT, V173, P428, DOI 10.1192/bjp.173.5.428 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 GILLBERG C, 1987, J AUTISM DEV DISORD, V17, P273, DOI 10.1007/BF01495061 GILLBERG C, 1984, DEV MED CHILD NEUROL, V26, P125 JACOBSON JW, 1990, J AUTISM DEV DISORD, V20, P205, DOI 10.1007/BF02284719 KOBAYASHI R, 1992, J AUTISM DEV DISORD, V22, P395, DOI 10.1007/BF01048242 LAINHART JE, 1994, J AUTISM DEV DISORD, V24, P587, DOI 10.1007/BF02172140 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 Lord C, 1997, J AUTISM DEV DISORD, V27, P501, DOI 10.1023/A:1025873925661 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 Lord C., 1994, J AUTISM DEV DISORD, V24, P569 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Loveland K. A., 1997, HDB AUTISM PERVASIVE, P283 LOVELAND KA, 1991, AM J MENT RETARDATIO, V96, P1 MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 Mottron L, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P131 Mottron L, 2000, DEVELOPMENTAL SCI, V3, P29 Murphy G, 1999, J INTELL DISABIL RES, V43, P149, DOI 10.1046/j.1365-2788.1999.00183.x Oliver A, 2000, DEVELOPMENTAL SCI, V3, P1, DOI 10.1111/1467-7687.00094 Piven J, 1996, J AM ACAD CHILD PSY, V35, P523, DOI 10.1097/00004583-199604000-00019 PLUMET MH, 1993, COMMUNICATION Poustka F, 1993, Acta Paedopsychiatr, V56, P69 PRIZANT BM, 1983, J SPEECH HEAR DISORD, V48, P296 RASMUSSEN P, 1983, ACTA PAEDIATR SCAND, V72, P125, DOI 10.1111/j.1651-2227.1983.tb09676.x RITVO ER, 1994, COMPR PSYCHIAT, V35, P149, DOI 10.1016/0010-440X(94)90061-L ROBBINS LC, 1963, J ABNORM PSYCHOL, V66, P261, DOI 10.1037/h0049084 RUMSEY JM, 1985, J AM ACAD CHILD PSY, V24, P465, DOI 10.1016/S0002-7138(09)60566-5 RUTTER M, 1967, BRIT J PSYCHIAT, V113, P1169, DOI 10.1192/bjp.113.504.1169 RUTTER M, 1967, BRIT J PSYCHIAT, V113, P1187 Szatmari P., 2000, ASPERGER SYNDROME, P403 SZATMARI P, 1989, J AUTISM DEV DISORD, V19, P213, DOI 10.1007/BF02211842 Towbin KE, 1997, HDB AUTISM PERVASIVE, P123 Turner M. A., 1997, AUTISM EXECUTIVE DIS, P57 VOLKMAR FR, 1986, J AM ACAD CHILD PSY, V25, P190, DOI 10.1016/S0002-7138(09)60226-0 Von Knorring A.-L., 1993, EUROPEAN CHILD ADOLE, V2, P91, DOI 10.1007/BF02098864 Wechsler D, 1974, WECHSLER INTELLIGENC WECHSLER D, 1981, WECHSLER PRESCHOOL P *WHO, 1993, CLASS MENT BEH DIS C Wing Lorna, 1988, DIAGNOSIS ASSESSMENT, P91 NR 49 TC 60 Z9 61 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2003 VL 7 IS 3 BP 255 EP 268 DI 10.1177/1362361303007003003 PG 14 WC Psychology, Developmental SC Psychology GA 716JK UT WOS:000185024900003 PM 14516059 ER PT J AU Fenton, G D'Ardia, C Valente, D Del Vecchio, I Fabrizi, A Bernabei, P AF Fenton, G D'Ardia, C Valente, D Del Vecchio, I Fabrizi, A Bernabei, P TI Vineland adaptive behavior profiles in children with autism and moderate to severe developmental delay SO AUTISM LA English DT Article DE autism; developmental delay; Vineland Adaptive Behavior scales ID DOWN-SYNDROME; STABILITY; AGE; ADOLESCENTS; SCALES; SAMPLE AB The purpose of this study was to examine adaptive behaviour profiles in children with autism and moderate to severe developmental delay. Previous research has found that children with autism present a characteristic pattern of adaptive behaviour, as measured by the Vineland Adaptive Behavior Scales (VABS) (deficit in the domain of socialization, relative deficit in the domain of communication and relative strength in the domain of daily living). In this study VABS were administered (as part of a comprehensive evaluation of abilities) to a sample of 50 children with moderate to severe developmental delay (2 3 children with autism and 2 7 chronological and developmental age matched non-autistic children). Contrary to initial predictions, the sample presented fairly homogeneous adaptive behaviour profiles. Results are discussed with respect to the effectiveness of adaptive behaviour profiles in the detection of autism and the importance of employing limited chronological and developmental age ranges in the study of autism in infancy. C1 Univ Roma La Sapienza, Dept Child & Adolescent Neuropsychiat, I-00185 Rome, Italy. RP Bernabei, P (reprint author), Univ Roma La Sapienza, Dept Child & Adolescent Neuropsychiat, Via Sabelli 108, I-00185 Rome, Italy. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BAYLEY N, 1969, BAILEY SCALES INFANT BURACK JA, 1992, J CHILD PSYCHOL PSYC, V33, P607, DOI 10.1111/j.1469-7610.1992.tb00894.x Carpentieri S, 1996, J AUTISM DEV DISORD, V26, P611, DOI 10.1007/BF02172350 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 FERRI R, 2000, QUANDO BOMBINI CRESC FOMBONNE E, 1992, J AUTISM DEV DISORD, V22, P563, DOI 10.1007/BF01046328 FOMBONNE E, 1993, J CHILD PSYCHOL PSYC, V34, P1051, DOI 10.1111/j.1469-7610.1993.tb01108.x FREEMAN BJ, 1991, J AM ACAD CHILD PSY, V30, P479, DOI 10.1097/00004583-199105000-00020 Kraijer D, 2000, J AUTISM DEV DISORD, V30, P39, DOI 10.1023/A:1005460027636 Liss M, 2001, J AUTISM DEV DISORD, V31, P219, DOI 10.1023/A:1010707417274 LORD C, 1989, J AUTISM DEV DISORD, V19, P483, DOI 10.1007/BF02212853 LORD C, 1989, J CHILD PSYCHOL PSYC, V30, P575, DOI 10.1111/j.1469-7610.1989.tb00269.x LOVELAND KA, 1991, AM J MENT RETARD, V96, P13 RODRIGUE JR, 1991, J AUTISM DEV DISORD, V21, P187, DOI 10.1007/BF02284759 Rutter M., 1983, HDB CHILD PSYCHOL, V4, P775 SCHATZ J, 1995, J AUTISM DEV DISORD, V25, P51, DOI 10.1007/BF02178167 Schopler E., 1988, CHILDHOOD AUTISM RAT SEXTON M, 1984, INFANT PERFORMANCE E, P230 Sparrow S, 1984, VINELAND ADAPTIVE BE UZGIRIS IC, 1975, UZGIRIS HUNT ORDINAL VINTER A, 1993, SVILUPPO SENSOMOTRIO VOLKMAR FR, 1990, ISSUES DEV APPROACH, P246 VOLKMAR FR, 1993, J AM ACAD CHILD PSY, V32, P627, DOI 10.1097/00004583-199305000-00020 VOLKMAR FR, 1987, J AM ACAD CHILD PSY, V26, P156, DOI 10.1097/00004583-198703000-00005 WACHS TD, 1984, INFANT PERFORMANCE E, P208 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 27 TC 30 Z9 31 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2003 VL 7 IS 3 BP 269 EP 287 DI 10.1177/1362361303007003004 PG 19 WC Psychology, Developmental SC Psychology GA 716JK UT WOS:000185024900004 PM 14516060 ER PT J AU Bledsoe, R Myles, BS Simpson, RL AF Bledsoe, R Myles, BS Simpson, RL TI Use of a Social Story intervention to improve mealtime skills of an adolescent with Asperger syndrome SO AUTISM LA English DT Article DE Asperger syndrome; eating behaviour; mealtime skills; Social Stories ID AUTISM AB This study assessed the utility of a Social Story intervention to improve the lunchtime eating behaviors of an adolescent diagnosed with Asperger syndrome. Using an ABAB design, the Social Story program appeared to result in a decrease in the number of food and drink spills and an increase in the frequency of appropriate mouth-wiping during lunch at school. C1 Univ Kansas, Dept Special Educ, Lawrence, KS 66045 USA. Univ Kansas, Lawrence, KS 66045 USA. RP Myles, BS (reprint author), Univ Kansas, Dept Special Educ, 1122 W Campus Rd, Lawrence, KS 66045 USA. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Barnhill G., 2000, DIAGNOSTIQUE, V25, P147 Barnhill G. P., 2001, FOCUS AUTISM OTHER D, V16, P46, DOI 10.1177/108835760101600112 CESARONI L, 1991, J AUTISM DEV DISORD, V21, P303, DOI 10.1007/BF02207327 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P279 Gray C. A., 1993, FOCUS AUTISTIC BEHAV, V8, P1, DOI DOI 10.1177/108835769300800101 GRAY CA, 1997, BUILD BRIDG BETT TOM Gray C.A., 1995, SOCIAL STORIES UNLIM Kuttler S., 1998, FOCUS AUTISM OTHER D, V13, P176, DOI DOI 10.1177/108835769801300306 Lorimer PA, 2002, J POSIT BEHAV INTERV, V4, P53, DOI 10.1177/109830070200400109 Myles B. S., 1999, FOCUS AUTISM OTHER D, V14, P82, DOI 10.1177/108835769901400203 Myles BS, 2001, FOCUS EXCEPT CHILD, V34, P1 National Research Council, 2001, ED CHILD AUT Norris C, 1999, FOCUS AUTISM OTHER D, V14, P180, DOI DOI 10.1177/108835769901400307 Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Volkmar F. R., 2000, ASPERGER SYNDROME, P25 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WETHERBY AM, 2000, T DEV PERSPECTIVE, V9 Woodcock R. W., 1989, WOODCOCK JOHNSON PSY NR 19 TC 34 Z9 34 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2003 VL 7 IS 3 BP 289 EP 295 DI 10.1177/1362361303007003005 PG 7 WC Psychology, Developmental SC Psychology GA 716JK UT WOS:000185024900005 PM 14516061 ER PT J AU Martin, NT Bibby, P Mudford, OC Eikeseth, S AF Martin, NT Bibby, P Mudford, OC Eikeseth, S TI Toward the use of a standardized assessment for young children with autism - Current assessment practices in the UK SO AUTISM LA English DT Article DE assessment protocols; autism; monitoring; statements ID ADAPTIVE-BEHAVIOR SCALES; EARLY INTERVENTION; STABILITY; PROGRESS; OUTCOMES; SCORES AB Little is known about the progress of autistic children following specific interventions in England. Nor do we know how frequently standardized assessments are used to monitor progress or to evaluate specific educational interventions. The reports of 75 children with autism, for whom special educational provision had been determined by a local education authority, were reviewed. Parents were interviewed and educational psychologists were contacted for details of any norm-referenced assessments. Of these children, 3 9 percent had no standardized assessments before education authorities determined their provision, and only 9 percent had follow-up assessments that could be used to evaluate progress. Children with autism in the UK rarely have sufficient assessments to allow an objective evaluation of their progress. There is currently no standardized assessment protocol to prescribe a specific educational intervention, to evaluate the progress of children or to make comparisons between interventions. We recommend the development of such a protocol. C1 Univ Kent, Canterbury, Kent, England. Univ Keele, Keele ST5 5BG, Staffs, England. Akershus Coll, Bekkestua, Norway. RP Martin, NT (reprint author), TreeHouse Trust, 49 Mecklenburg Sq, London WC1N 2NY, England. CR Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 Bayley N, 1993, MANUAL BAYLEY SCALES Bibby P, 2001, RES DEV DISABIL, V22, P425, DOI 10.1016/S0891-4222(01)00082-8 Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 Carpentieri S, 1996, J AUTISM DEV DISORD, V26, P611, DOI 10.1007/BF02172350 Carter AS, 1998, J AUTISM DEV DISORD, V28, P287, DOI 10.1023/A:1026056518470 Connor M., 1998, ED PSYCHOL PRACTICE, V14, P109, DOI 10.1080/0266736980140206 *DFES, 1999, NAT CURR KEY STAG 1 *DFES, 2001, SPEC ED NEEDS DIS AC, pCH10 Edwards S, 1997, REYNELL DEV LANGUAGE FREEMAN BJ, 1991, J AM ACAD CHILD PSY, V30, P479, DOI 10.1097/00004583-199105000-00020 FREEMAN BJ, 1988, J AM ACAD CHILD PSY, V27, P428, DOI 10.1097/00004583-198807000-00008 Greenspan S. 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RP Minshew, NJ (reprint author), Western Psychiat Inst & Clin, 3811 OHara St, Pittsburgh, PA 15213 USA. CR MESIBOV GB, 2002, UNDERSTANDING ASPERG NR 1 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2003 VL 7 IS 3 BP 331 EP 333 PG 3 WC Psychology, Developmental SC Psychology GA 716JK UT WOS:000185024900008 ER PT J AU Kern, JK AF Kern, JK TI Purkinje cell vulnerability and autism: a possible etiological connection SO BRAIN & DEVELOPMENT LA English DT Review DE autism; onset; Purkinje cell; insult; etiology; heterogeneity; gliosis; vulnerability ID VOLATILE ORGANIC-COMPOUNDS; POSITRON-EMISSION-TOMOGRAPHY; WEAVER MUTANT MICE/; DEVELOPMENTAL DISORDERS; SELECTIVE VULNERABILITY; GLUTAMATE RECEPTORS; SPECTRUM DISORDERS; CEREBELLAR CORTEX; PARENTS CONCERNS; MERCURY-VAPOR AB Autism is a neurological disorder of unknown etiology. The onset of the abnormal growth and development within the brain is also not known. Current thought by experts in autism is that the time of onset is prenatal, occurring prior to 30 weeks gestation. However, autism comprises a heterogeneous population in that parents report either that their child was abnormal from birth, or that their child was developmentally normal until sometime after birth, at which time the child began to regress or deteriorate. Anecdotal reports suggest that some children with autism have significant illness or clinical events prior to the development of autistic symptoms. Conceivably, these children may become autistic from neuronal cell death or brain damage sometime after birth as result of insult. To support this theory is that marked Purkinje cell loss, the most consistent finding in the autistic disorder, can result from insult. Evidence suggests that the Purkinje cell is selectively vulnerable. This article discusses a theory that the selective vulnerability of the Purkinje cell may play a role in the etiology of autism, and suggests that a future direction in autism research may be to investigate the possibility of neuronal cell loss from insult as a cause of autism. Results of a small pilot survey are also discussed. (C) 2003 Elsevier Science B.V. All rights reserved. C1 Univ Texas, SW Med Ctr Dallas, Dept Psychiat, Dallas, TX 75390 USA. RP Kern, JK (reprint author), Univ Texas, SW Med Ctr Dallas, Dept Psychiat, St Paul Profess Bldg 1,5959 Harry Hines Blvd,Suit, Dallas, TX 75390 USA. 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PD SEP PY 2003 VL 25 IS 6 BP 377 EP 382 DI 10.1016/S0387-7604(03)00056-1 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 713MV UT WOS:000184862800001 PM 12907269 ER PT J AU Abu-Akel, A AF Abu-Akel, A TI A neurobiological mapping of theory of mind SO BRAIN RESEARCH REVIEWS LA English DT Review DE autism; neurobiology; schizophrenia; theory of mind; mental representation/attribution; simulation/theory theory ID MEDIAL PREFRONTAL CORTEX; HIGH-FUNCTIONING AUTISM; SCHIZOPHRENIC-PATIENTS; NEURAL REPRESENTATION; EXECUTIVE FUNCTIONS; ASPERGERS SYNDROME; CINGULATE CORTEX; BIOLOGICAL BASIS; BRAIN; AMYGDALA AB This paper attempts, based on a review of a wide range of clinical, biobehavioral and neuroanatomical studies, to account for the various theory of mind impairments observed in psychiatric and developmental disorders in a single neurobiological model. The proposed model is composed of a representational component subserved by posterior brain regions (temporal and parietal) and an application/execution component subserved by prefrontal regions. Information processed in posterior regions is relayed through a limbic-paralimbic system, which is essential for the implementation of theory of mind processes. In addition to its clinical implications, the proposed model accounts for (1) the ability to mentalize about both the self and others, (2) the nature of the anatomic connections of the various brain regions and their functional correlates, and (3) theories pertaining to the inferencing mechanisms used during mental representation/attribution. (C) 2003 Elsevier B.V. All rights reserved. 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We can infer from these findings that individuals who have difficulty representing mental states, such as those with autism, may also have difficulty reversing ambiguous figures. The results from our study, however, showed that a majority of those with autism easily succeeded in making alternative interpretations despite many making errors in tests of false belief. Many also had difficulty acknowledging that a less informed person would interpret a non-descript portion of a drawing differently than themselves. Comparison participants with moderate learning disabilities, who had a similar intellectual profile, generally performed well on the theory of mind tests and a majority made alternative interpretations of ambiguous figures. Typically developing children aged 7 and 8 years performed well on all tests. The ambiguity test does not require participants to understand that representations are open to revision, unlike theory of mind tests, and this might explain their good performance. 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J. Psychiat.-Rev. Can. Psychiat. PD SEP PY 2003 VL 48 IS 8 BP 503 EP 505 PG 3 WC Psychiatry SC Psychiatry GA 003UE UT WOS:000234706300001 PM 14574825 ER PT J AU Bryson, SE Rogers, SJ Fombonne, E AF Bryson, SE Rogers, SJ Fombonne, E TI Autism spectrum disorders: Early detection, intervention, education, and psychopharmacological management SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Review DE autism; autistic spectrum disorders; early detection; early screening; early intervention; intensive behavioural intervention; education; psychopharmacological management ID PERVASIVE DEVELOPMENTAL DISORDERS; INTENSIVE BEHAVIORAL TREATMENT; PLACEBO-CONTROLLED TRIAL; DOUBLE-BLIND; YOUNG-CHILDREN; PRESCHOOL-CHILDREN; FOLLOW-UP; AGE; HALOPERIDOL; SYMPTOMS AB Our understanding and treatment of children with autism have changed dramatically since Leo Kanner first formally documented the disorder in 1943. With reference to the historical context, this paper reviews recent research addressing 4 major issues: early detection, intervention, education, and psychopharmacological management of children with autism and related (autistic) spectrum disorders (hereafter, "autism"). We conclude from our review of the evidence that, in the absence of additional, more compelling data, the clinical usefulness of existing screening instruments remains questionable. However, the potential importance of such research is underscored by the clear benefits of early behavioural intervention: despite differences in orientation, outcomes for children with autism can be significantly enhanced with early intensive intervention. Although many questions remain (notably, What are the critical therapeutic components? For whom? For what domains of development? For what level of intensity and duration?), interventions shown to be effective are all carefully planned, engineered, monitored, and designed to target specific skill domains. Including children with autism in regular classes within the public school system poses several challenges, the most pressing of which is the large number of school personnel who need to be trained in evidence-based teaching and behavioural management practices. Finally, psychotropic drugs may help to reduce some symptoms, but they are neither curative nor a substitute for other forms of support and intervention. C1 Dalhousie Univ, Dept Pediat, IWK Hlth Ctr, Halifax, NS B3J 3G9, Canada. Dalhousie Univ, Dept Psychol, IWK Hlth Ctr, Halifax, NS B3J 3G9, Canada. Univ Calif Davis, Med Ctr, MIND Inst, Sacramento, CA 95817 USA. McGill Univ, Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3H 1P3, Canada. 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PD SEP PY 2003 VL 48 IS 8 BP 506 EP 516 PG 11 WC Psychiatry SC Psychiatry GA 003UE UT WOS:000234706300002 PM 14574826 ER PT J AU Tidmarsh, L Volkmar, FR AF Tidmarsh, L Volkmar, FR TI Diagnosis and epidemiology of autism spectrum disorders SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Review DE autism; diagnosis; epidemiology; assessment; prognosis ID PERVASIVE DEVELOPMENTAL DISORDERS; RUBELLA VACCINATION; ASPERGER-SYNDROME; RETT-SYNDROME; CHILDREN; MEASLES; MUMPS; ASSOCIATION; CHILDHOOD; SCHIZOPHRENIA AB In this paper, we give an overview of the diagnostic categories of autism and other pervasive developmental disorders (PDDs) and discuss the changes in the DSM classification system over the past 20 years. We describe each subtype of PDD, along with comorbid psychiatric conditions, assessment guidelines, and tools for diagnosis. The epidemiology of autism has generated much discussion and research; we report the most recent data, as well as recent findings about controversial issues purporting to cause the increased prevalence rate observed in the past decade. Finally, we discuss the prognosis for individuals with autism, indicating the challenges faced by patients, families, and professionals aiming to optimize their outcome. C1 McGill Univ, Ctr Hosp, Montreal, PQ, Canada. Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Tidmarsh, L (reprint author), Montreal Childrens Hosp, Dept Psychiat, 4018 Ste Catherine St W, Montreal, PQ H3Z 1P2, Canada. 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PD SEP PY 2003 VL 48 IS 8 BP 517 EP 525 PG 9 WC Psychiatry SC Psychiatry GA 003UE UT WOS:000234706300003 PM 14574827 ER PT J AU Nicolson, R Szatmari, P AF Nicolson, R Szatmari, P TI Genetic and neurodevelopmental influences in autistic disorder SO CANADIAN JOURNAL OF PSYCHIATRY-REVUE CANADIENNE DE PSYCHIATRIE LA English DT Review DE autism; genetics; phenotype expression; neurodevelopment; magnetic resonance imaging ID QUANTITATIVE-TRAIT-LOCUS; AFFECTED-SIB-PAIR; CORPUS-CALLOSUM; SUSCEPTIBILITY GENE; MULTIPLEX FAMILIES; GENOMEWIDE SCAN; GENOMIC SCREEN; LINKAGE DISEQUILIBRIUM; LANGUAGE IMPAIRMENT; MENTAL-RETARDATION AB Objective: In the past, autism was considered to be largely psychogenic. However, research in the last 2 decades indicates that autism is largely caused by genetic factors that lead to abnormal brain development. This article reviews research into the genetic and neurodevelopmental factors underlying autism. Methods: We review the findings from genetic and brain-imaging studies of autism over the past 15 years and synthesize these findings as a guide for future research. Results: Genome scans and association studies have suggested potential genomic regions and genes, respectively, that may be involved in the etiology of autism, and there have been some replications of these results. Similarly, the findings that brain volume is exaggerated in autism and corpus callosum. size is reduced have also been independently replicated. Unfortunately, studies of other subcortical structures remain inconclusive or contradictory. Conclusions: Overwhelming evidence now supports a neurobiological basis for autism. However, further refinements will be needed to guide future studies, particularly to identify the most informative phenotypes to investigate. Additionally, studies examining the role of genetic factors in the brain abnormalities underlying autism will likely lead to further findings that will enhance our understanding of autism's causes. C1 Univ Western Ontario, Dept Psychiat, London, ON N6A 3K7, Canada. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON, Canada. RP Nicolson, R (reprint author), 800 Commissioners Rd E 6110, London, ON N6C 2V5, Canada. 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J. Psychiat.-Rev. Can. Psychiat. PD SEP PY 2003 VL 48 IS 8 BP 526 EP 537 PG 12 WC Psychiatry SC Psychiatry GA 003UE UT WOS:000234706300004 PM 14574828 ER PT J AU Zaffanello, M Zamboni, G Fontana, E Zoccante, L Tato, L AF Zaffanello, M Zamboni, G Fontana, E Zoccante, L Tato, L TI A case of partial biotinidase deficiency associated with autism SO CHILD NEUROPSYCHOLOGY LA English DT Article ID DISORDERS; CHILDREN AB We report the case of a child with partial biotinidase deficiency and autistic developmental disorder. We arrived at the diagnosis of biotinidase deficiency when the child was almost 4 years of age. Consequently, he began cofactor biotin treatment (10 mg daily) which did not resolve his autistic behavior. His younger brother was affected by partial biotinidase deficiency diagnosed at birth through our neonatal screening program. He was precociously treated with cofactor biotin therapy (10 mg daily) and did not show any behavioral abnormality or developmental delay. Since the brain is quite vulnerable to biotin deficiency, delayed biotin therapy could result in neurological damage. Our patient is the first case of partial biotinidase deficiency associated with autism. We hypothesize that the low biotinidase activity could have caused biotin deficiency in his brain and cerebrospinal fluids and consequently serious neurological problems, such as stereotyped and autistic behaviors, which were irreversible in spite of biotin supplementation. C1 Univ Verona, Dept Pediat, I-37134 Verona, Italy. Univ Verona, Reg Ctr Neonatal Congenital Errors Metab, I-37134 Verona, Italy. RP Zaffanello, M (reprint author), Univ Verona, Dept Pediat, Piazzale L Scuro, I-37134 Verona, Italy. 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PD SEP PY 2003 VL 9 IS 3 BP 184 EP 188 DI 10.1076/chin.9.3.184.16457 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 733ZR UT WOS:000186031200004 PM 13680408 ER PT J AU Cuccaro, ML Shao, YJ Grubber, J Slifer, M Wolpert, CM Donnelly, SL Abramson, RK Ravan, SA Wright, HH DeLong, GR Pericak-Vance, MA AF Cuccaro, ML Shao, YJ Grubber, J Slifer, M Wolpert, CM Donnelly, SL Abramson, RK Ravan, SA Wright, HH DeLong, GR Pericak-Vance, MA TI Factor analysis of restricted and repetitive behaviors in autism using the Autism Diagnostic Interview-R SO CHILD PSYCHIATRY & HUMAN DEVELOPMENT LA English DT Article DE autism; repetitive behaviors; factor analysis ID COMPULSIVE-LIKE BEHAVIOR; DEVELOPMENTAL DISORDERS; MENTAL-RETARDATION; SPECTRUM DISORDER; BASAL GANGLIA; INDIVIDUALS; PREVALENCE; CHILDREN; DOMAINS; ADULTS AB The current study examined the factor structure of restricted and repetitive behaviors (RRB) in children with autism. Factor extraction procedures of 12 items from the Autism Diagnostic Interview-Revised (ADI-R) were applied in N = 207 individuals with autism. Two interpretable factors were identified: Factor 1-repetitive sensory motor actions and Factor 2-resistance to change. There was a significant negative correlation between an index of level of adaptive functioning and Factor 1. Intraclass correlations were not significant for either factor in a subset of families with two or more siblings with autism (multiplex). No differences in scores were apparent for either factor when multiplex families and families containing only one affected individual with autism (singleton) were compared. RRB in autism are represented by two distinct factors which may reflect two separate groups within autism. Defining subgroups within autism will allow for reduction of clinical heterogeneity and enhance our ability to dissect the genetic etiology of this complex disorder. 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Hum. Dev. PD FAL PY 2003 VL 34 IS 1 BP 3 EP 17 DI 10.1023/A:1025321707947 PG 15 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 722GV UT WOS:000185367800001 PM 14518620 ER PT J AU Suganthy, J Raghuram, L Antonisamy, B Vettivel, S Madhavi, C Koshi, R AF Suganthy, J Raghuram, L Antonisamy, B Vettivel, S Madhavi, C Koshi, R TI Gender- and age-related differences in the morphology of the corpus callosum SO CLINICAL ANATOMY LA English DT Article DE area; corpus callosum; genu; length; magnetic resonance imaging; trunk; splenium; width ID SEX-RELATED DIFFERENCES; MORPHOMETRIC ANALYSIS; CHRONIC-SCHIZOPHRENIA; PREDICT GENDER; SIZE; DIMORPHISM; AUTISM; MRI; HANDEDNESS; ISTHMUS AB The size and shape of the adult corpus callosum may vary with gender and age. There is, however, little data on the morphology of the corpus callosum in the Indian population. The purpose of this study was to measure the size of the corpus callosum in normal adult Indian males and females, and to identify gender- and age-related differences. The size of the corpus callosum on midsagittal section was measured in 100 (50 males, 50 females) normal adult Indians using magnetic resonance imaging. The length of the corpus callosum, the width of the genu, trunk, and splenium, the area of the splenium, and the total area of the corpus callosum were measured. The length of the brain also was measured. Means were compared for significant difference by gender using the Student's unpaired t-test and by age using ANOVA followed by Duncan's multiple range test. Gender was estimated by discriminant function analysis and age was estimated by regression analysis from significant parameters. The corpus callosum was longer in males and the discriminant score to differentiate gender was determined with an accuracy of 66%. The length of the corpus callosum increased with age and regression equations for predicting age was derived from the length of the corpus callosum. The width of the trunk and genu decreased with age in males but not in females. (C) 2003 Wiley-Liss, Inc. C1 Christian Med Coll & Hosp, Dept Anat, Vellore 632002, Tamil Nadu, India. Christian Med Coll & Hosp, Dept Radiodiag, Vellore 632002, Tamil Nadu, India. Christian Med Coll & Hosp, Dept Biostat, Vellore 632002, Tamil Nadu, India. RP Suganthy, J (reprint author), Christian Med Coll & Hosp, Dept Anat, Vellore 632002, Tamil Nadu, India. 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We examined the relation between MAOA-uVNTR alleles and the phenotypic expression of autism in 41 males younger than 12.6 years of age. Children with the low-activity MAOA allele had both lower intelligence quotients (IQ) and more severe autistic behavior than children with the high-activity allele. In follow-up testing of 34 of the males at the 1-year time-point, those with the low-activity allele showed a worsening in IQ but no change in the severity of their autistic behavior. We conclude that functional MAOA-uVNTR alleles may act as a genetic modifier of the severity of autism in males. C1 New York State Inst Basic Res Dev Disabil, Dept Psychol, Staten Isl, NY 10314 USA. New York State Inst Basic Res Dev Disabil, Dept Cytogenet, Staten Isl, NY 10314 USA. New York State Inst Basic Res Dev Disabil, Dept Human Genet, Staten Isl, NY 10314 USA. Queens Univ, Dept Psychiat, Kingston, ON K7L 3N6, Canada. Queens Univ, Dept Physiol, Kingston, ON K7L 3N6, Canada. 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PD SEP PY 2003 VL 64 IS 3 BP 190 EP 197 DI 10.1034/j.1399-0004.2003.00115.x PG 8 WC Genetics & Heredity SC Genetics & Heredity GA 711LQ UT WOS:000184742600002 PM 12919132 ER PT J AU Ferri, R Elia, M Agarwal, N Lanuzza, B Musumeci, SA Pennisi, G AF Ferri, R Elia, M Agarwal, N Lanuzza, B Musumeci, SA Pennisi, G TI The mismatch negativity and the P3a components of the auditory event-related potentials in autistic low-functioning subjects SO CLINICAL NEUROPHYSIOLOGY LA English DT Article DE autism; mental retardation; event-related potentials; mismatch negativity; P3a ID DEVELOPMENTAL LANGUAGE DISORDER; BRAIN POTENTIALS; PRESCHOOL-CHILDREN; CHILDHOOD AUTISM; ATTENTION; MMN; STIMULI; GENERATORS; DEFICIT; NOVELTY AB Objective: In order to understand better the psychophysiological basis of auditory processing abnormalities in autism, we decided to study two automatic components of the auditory event-related potentials (ERPs): the mismatch negativity (MMN)-a component of the ERP which is recorded when, during repetitive auditory stimulation, rare changes are introduced-and the novelty-related P3a which is recorded as a response to unexpected novel events occurring in a sequence of repetitive stimuli. Methods: Ten male subjects, mean age 12.3 years (SD 4.95), affected by autism and mental retardation were admitted to this study. All patients were also mentally retarded. Ten normal male subjects, mean age 12.2 years (SD 3.94), were used as controls. Auditory evoked potentials were recorded from 19 scalp electrodes (10-20 system), and stimuli were presented in sequences consisting of 2000 tones (70 dB, ISI = 800 ms). Three types of stimuli were presented: (1) standard stimuli (1000 Hz tones, 80% of total stimuli), (2) deviant stimuli (1300 Hz tones, 10% of total stimuli), and (3) novel stimuli (complex and non-monotonal, 10% of total stimuli). To quantify the MMN, the evoked response to the standard tones was subtracted from the corresponding deviant stimulus response and its amplitude and latency at peak were measured over Fz, Cz and Pz; similarly, the P3a component of the ERP was obtained by subtracting the response to the standard tone from that to the novel stimuli and its amplitude and latency at peak were measured over Fz, Cz and Pz. Also, the amplitude and latency at peak for the NI component of the auditory evoked potential obtained with the standard stimuli were measured over Fz, Cz and Pz. The correlation between age and MMN and P3a amplitude was also analyzed. Results: NI showed significantly shorter latencies in the autistic groups. MMN elicited by deviant stimuli, but not that elicited by novel stimuli, was found to be significantly larger in autistic children than in normal controls. P3a showed higher amplitude in autistic subjects than in normal controls during childhood; the opposite was observed during young adulthood. Discussion: Our findings indicate that significant changes in ERPs can also be seen in non-cooperative individuals with autism and mental retardation, which might be different from the changes already reported for high-functioning autistic subjects and deserve further insight. These changes show developmental modifications that should be taken into consideration when analyzing data from autistic subjects. (C) 2003 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved. C1 IRCCS, Dept Neurol, Oasi Inst Res Mental Retardat & Brain Aging, I-94018 Troina, Italy. Univ Catania, Dept Neurol Sci, I-95124 Catania, Italy. RP Ferri, R (reprint author), IRCCS, Dept Neurol, Oasi Inst Res Mental Retardat & Brain Aging, Via Conte Ruggero 73, I-94018 Troina, Italy. 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We consider literature reviews, program descriptions, and empirical studies in two broad areas of early intervention: for children with developmental disabilities, and for children considered at-risk for developmental problems. Recent findings This year's empirical studies utilized a broad array of outcome variables, going beyond cognitive factors to include children's socio-emotional development and family functioning as well. The 'at-risk' studies made contributions in three areas: predictors of outcome, parent-child relationships, and comparisons and replications of programs. The developmental disability reviews and studies were concentrated on autism, with a methodological focus. Their conclusion was that despite much encouraging evidence for early intervention effectiveness with autism, there is still no one approach that meets accepted criteria for an empirically validated treatment. Summary Comprehensive early intervention programs can be quite effective for young children with developmental disabilities, as well as for children who are at risk due to biological or environmental factors. There is a need for additional development and evaluation of evidence-based treatments, as well as a further understanding of mediators and moderators of treatment outcome. C1 Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. RP Baker, BL (reprint author), Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. CR Baker B. 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P., 2000, HDB EARLY CHILDHOOD Smith T, 2002, BEHAV INTERVENT, V17, P129, DOI 10.1002/bin.114 Stormshak Elizabeth A, 2002, Prev Sci, V3, P223, DOI 10.1023/A:1019998601210 *TASK FORC PSYCH I, 1995, TEMPL DEV GUID INT M *UD DEP ED, 2000, 22 ANN REM C IMPL IN Vogler SD, 2002, J DEV BEHAV PEDIATR, V23 Weiss SJ, 2002, CHILD PSYCHIAT HUM D, V33, P3, DOI 10.1023/A:1016583904918 Whalen C, 2003, J CHILD PSYCHOL PSYC, V44, P456, DOI 10.1111/1469-7610.00135 Wolery M, 2002, J AUTISM DEV DISORD, V32, P463, DOI 10.1023/A:1020598023809 NR 59 TC 2 Z9 2 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0951-7367 J9 CURR OPIN PSYCHIATR JI Curr. Opin. Psychiatr. PD SEP PY 2003 VL 16 IS 5 BP 503 EP 509 DI 10.1097/01.yco.0000087255.35258.d6 PG 7 WC Psychiatry SC Psychiatry GA 714DV UT WOS:000184897800003 ER PT J AU Kwok, HWM AF Kwok, HWM TI Psychopharmacology in autism spectrum disorders SO CURRENT OPINION IN PSYCHIATRY LA English DT Article DE autism; challenging behaviors; pharmacotherapy ID PERVASIVE DEVELOPMENTAL DISORDERS; PLACEBO-CONTROLLED TRIAL; ALZHEIMERS-DISEASE; OPEN-LABEL; DOUBLE-BLIND; OLANZAPINE TREATMENT; BEHAVIORAL SYMPTOMS; WEIGHT CHANGE; CHILDREN; RISPERIDONE AB Purpose of review This review is intended to provide an update of recent advances in psychopharmacology to support evidence-based prescription of psychotropic medications for autism spectrum disorders. Recent findings Pharmacotherapy continues to be an important component of a comprehensive treatment program for autism spectrum disorders. Evidence is accumulating supporting the use of second-generation antipsychotic medications and selective serotonin reuptake inhibitors. Recent studies suggest that they are effective and relatively well tolerated, not only in the adult population but also in children with this disorder. Other approaches, such as the use of acetylcholinesterase inhibitors, anticonvulsants and dietary enzymes, may also be potentially useful, but further research on these compounds is needed. Summary One of the intriguing aspects of autism spectrum disorders is the unclear pathogenesis. In the absence of any definite evidence of neurochemical abnormalities, there is currently no medication that can be used for the curative treatment of this disorder, However, many distressing symptoms and aberrant behaviors, such as severe tantrums, aggression, hyperactivity and self-injurious behaviors, can be targeted by pharmacotherapy. Amelioration of these symptoms will enhance the individual's ability to participate in educational and community programs, as well as reducing the stress experienced by the carers. C1 Kwai Chung Hosp, Psychiat Unit Learning Disabil, Hong Kong, Hong Kong, Peoples R China. RP Kwok, HWM (reprint author), Kwai Chung Hosp, Psychiat Unit Learning Disabil, 3-15 Kwai Chung Hosp Rd, Hong Kong, Hong Kong, Peoples R China. 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Opin. Psychiatr. PD SEP PY 2003 VL 16 IS 5 BP 529 EP 534 DI 10.1097/01.yco.0000087259.35258.e9 PG 6 WC Psychiatry SC Psychiatry GA 714DV UT WOS:000184897800007 ER PT J AU Blacher, J Kraemer, B Schalow, M AF Blacher, J Kraemer, B Schalow, M TI Asperger syndrome and high functioning autism: research concerns and emerging foci SO CURRENT OPINION IN PSYCHIATRY LA English DT Article DE high functioning autism; Asperger syndrome; social communication; theory of mind ID PERVASIVE DEVELOPMENTAL DISORDER; LANGUAGE IMPAIRMENT; CHILDREN; ADOLESCENTS; RISPERIDONE; INDIVIDUALS; BEHAVIOR; ADULTS; COMMUNICATION; MANAGEMENT AB Purpose of review This review focuses on papers that pertain to recent work on Asperger syndrome or high functioning autism. We noted areas in which there was a preponderance of research published over the last year, including: social communication, sensory characteristics, eye gaze, neurocognitive aspects, comorbidity, and treatment and intervention studies. Recent findings Children, adolescents, and even adults with Asperger syndrome/high functioning autism appear to be deficient in social skills that involve self-referencing, empathy, determination of emotions in others or inferring the thoughts of others. Some neurocognitive studies suggest that Asperger syndrome and high functioning autism are distinct disorders. A variety of social-behavioral interventions appeared in the literature, with generally positive outcomes. Comorbidity of Asperger syndrome and other psychiatric conditions (e.g. attention-deficit hyperactivity disorder or depression) continues to be identified. Summary Studies focusing on descriptions and specific sequelae of social deficits in Asperger syndrome/high functioning autism dominated the literature of the past year. With the decoding of the human genome it is also likely that the search for genetic pathways to Asperger syndrome/high functioning autism will continue. Finally, based on the almost total lack of information in this area, there is a clear need to develop better understanding of the experience of families raising children with high functioning autism or Asperger syndrome. C1 Univ Calif Riverside, Grad Sch Educ, Riverside, CA 92521 USA. RP Blacher, J (reprint author), Univ Calif Riverside, Grad Sch Educ, Riverside, CA 92521 USA. 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Opin. Psychiatr. PD SEP PY 2003 VL 16 IS 5 BP 535 EP 542 DI 10.1097/01.yco.0000087260.35258.64 PG 8 WC Psychiatry SC Psychiatry GA 714DV UT WOS:000184897800008 ER PT J AU Herbert, MR Ziegler, DA Makris, N Bakardjiev, A Hodgson, J Adrien, KT Kennedy, DN Filipek, PA Caviness, VS AF Herbert, MR Ziegler, DA Makris, N Bakardjiev, A Hodgson, J Adrien, KT Kennedy, DN Filipek, PA Caviness, VS TI Larger brain and white matter volumes in children with developmental language disorder SO DEVELOPMENTAL SCIENCE LA English DT Article ID HIGH-LEVEL AUTISM; EARLY ADULT LIFE; IMPAIRED CHILDREN; TOPOGRAPHIC PARCELLATION; PROCESSING ABILITIES; IDENTIFYING CHILDREN; INHERITED SPEECH; SOCIAL COGNITION; CEREBRAL-CORTEX; FOLLOW-UP AB Developmental language disorder (DLD) is predominantly a language disorder, but children with DLD also manifest non-language impairments, and neuroanatomical abnormalities have been found in multiple areas of the brain, not all language-associated We therefore performed a whole brain general segmentation analysis of all major brain regions on MRI scans of 24 DID subjects (16M 8F) and 30 controls (15M, 15F), ages 5.7 to 11.3 years. Children with DID showed increased total brain volume, driven predominantly by a substantial increase in the volume of cerebral white matter Cerebral cortex and caudate were relatively but not absolutely smaller in DID. These findings are discussed in relation to issues of specificity vs. generality as they arise in debates about (1) modular vs. general processing deficits and connectionist modeling in DID, (2) language-specific vs. pervasive, non-specific deficits in DLD and (3) specificity of the disorder vs. overlap with other disorders, notably autism. C1 Harvard Univ, Massachusetts Gen Hosp, Sch Med, Ctr Morphometr Anal Pediat Neurol,Dept Neurol, Boston, MA 02114 USA. Harvard Univ, Massachusetts Gen Hosp, Sch Med, Dept Radiol, Boston, MA 02114 USA. Childrens Hosp Oakland, Dept Infect Dis, Oakland, CA 94609 USA. Augsburg Coll, Ctr Learning, Minneapolis, MN USA. Augsburg Coll, Adapt Student Serv, Minneapolis, MN USA. New England Coll Optometry, Boston, MA USA. 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Charles Univ, Dept Imaging Methods, CR-11636 Prague, Czech Republic. Charles Univ, Dept Child Neurol, CR-11636 Prague 1, Czech Republic. Charles Univ, Inst Biol & Med Genet, CR-11636 Prague 1, Czech Republic. Acad Sci, Inst Psychol, Brno, Czech Republic. RI Urbanek, Tomas/G-9427-2014; Blatny, Marek/H-4293-2014 OI Urbanek, Tomas/0000-0002-8807-4869; Blatny, Marek/0000-0001-9831-0637 CR Beglinger LJ, 2001, J AUTISM DEV DISORD, V31, P411, DOI 10.1023/A:1010616719877 NR 1 TC 0 Z9 0 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0924-977X J9 EUR NEUROPSYCHOPHARM JI Eur. Neuropsychopharmacol. PD SEP PY 2003 VL 13 SU 4 BP S431 EP S432 DI 10.1016/S0924-977X(03)92310-8 PG 2 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 723BJ UT WOS:000185412300716 ER PT J AU Hill, JM Ades, AM McCune, SK Sahir, N Moody, EM Abebe, DT Crnic, LS Brenneman, DE AF Hill, JM Ades, AM McCune, SK Sahir, N Moody, EM Abebe, DT Crnic, LS Brenneman, DE TI Vasoactive intestinal peptide in the brain of a mouse model for Down syndrome SO EXPERIMENTAL NEUROLOGY LA English DT Article DE Down syndrome; Ts65Dn segmental trisomy; vasoactive intestinal peptide; VIP binding sites; VIP mRNA; immunocytochemistry; GTP-insensitive binding ID EMBRYONIC GROWTH; TS65DN MICE; NEURONAL DEATH; BINDING-SITES; RAT-BRAIN; VIP; POLYPEPTIDE; EXPRESSION; RECEPTORS; BLOCKADE AB The most common genetic cause of mental retardation is Down syndrome, trisomy of chromosome 21, which is accompanied by small stature, developmental delays, and mental retardation. In the Ts65Dn segmental trisomy mouse model of Down syndrome, the section of mouse chromosome 16 most homologous to human chromosome 21 is trisomic. This model exhibits aspects of Down syndrome including growth restriction, delay in achieving developmental milestones, and cognitive dysfunction. Recent data link vasoactive intestinal peptide malfunction with developmental delays and cognitive deficits. Blockage of vasoactive intestinal peptide during rodent development results in growth and developmental delays, neuronal dystrophy, and, in adults, cognitive dysfunction. Also, vasoactive intestinal peptide is elevated in the blood of newborn children with autism and Down syndrome. In the current experiments, vasoactive intestinal peptide binding sites were significantly increased in several brain areas of the segmental trisomy mouse, including the olfactory bulb, hippocampus, cortex, caudate/putamen, and cerebellum, compared with wild-type littermates. In situ hybridization for VIP mRNA revealed significantly more dense vasoactive intestinal peptide mRNA in the hippocampus, cortex, raphe nuclei, and vestibular nuclei in the segmental trisomy mouse compared with wild-type littermates. In the segmental trisomy mouse cortex and hippocampus, over three times as many vasoactive intestinal peptide-immunopositive cells were visible than in wild-type mouse cortex. These abnormalities in vasoactive intestinal peptide parameters in the segmental trisomy model of Down syndrome suggest that vasoactive intestinal peptide may have a role in the neuropathology of Down-like cognitive dysfunction. (C) 2003 Elsevier Science (USA). All rights reserved. C1 NICHD, Sect Dev & Mol Pharmacol, NIH, Bethesda, MD 20892 USA. Childrens Natl Med Ctr, Dept Neonatol, Washington, DC 20010 USA. Univ Colorado, Sch Med, Dept Pediat, Denver, CO 80262 USA. Univ Colorado, Sch Med, Dept Psychiat, Denver, CO 80262 USA. 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Neurol. PD SEP PY 2003 VL 183 IS 1 BP 56 EP 65 DI 10.1016/S0014-4886(03)00164-X PG 10 WC Neurosciences SC Neurosciences & Neurology GA 718VG UT WOS:000185166700008 PM 12957488 ER PT J AU Vojdani, A Pangborn, JB Vojdani, E Cooper, EL AF Vojdani, A Pangborn, JB Vojdani, E Cooper, EL TI Infections, toxic chemicals and dietary peptides binding to lymphocyte receptors and tissue enzymes are major instigators of autoimmunity in autism SO INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY LA English DT Article DE chemotaxis; atherosclerosis; innate immunity; adaptive immunity; thrombin ID FLUID T-CELLS; CHLAMYDIA-PNEUMONIAE; SPECTRUM DISORDERS; ACTIVATION ANTIGEN; CELIAC-DISEASE; CROSS-REACT; CHILDREN; ANTIBODIES; CD26; EXPRESSION AB Similar to many complex autoimmune diseases, genetic and environmental factors including diet, infection and xenobiotics play a critical role in the development of autism. In this study, we postulated that infectious agent antigens such as streptokinase, dietary peptides (gliadin and casein) and ethyl mercury (xenobiotic) bind to different lymphocyte receptors and tissue enzyme (DPP IV or CD26). We assessed this hypothesis first by measuring IgG, IgM and IgA antibodies against CD26, CD69, streptokinase (SK), gliadin and casein peptides and against ethyl mercury bound to human serum albumin in patients with autism. A significant percentage of children with autism developed anti-SK, anti-gliadin and casein peptides and anti-ethyl mercury antibodies, concomitant with the appearance of anti-CD26 and anti-CD69 autoantibodies. These antibodies are synthesized as a result of SK, gliadin, casein and ethyl mercury binding to CD26 and CD69, indicating that they are specific. Immune absorption demonstrated that only specific antigens, like CD26, were capable of significantly reducing serum anti-CD26 levels. However, for direct demonstration of SK, gliadin, casein and ethyl mercury to CD26 or CD69, microtiter wells were coated with CD26 or CD69 alone or in combination with SK, gliadin, casein or ethyl mercury and then reacted with enzyme labeled rabbit anti-CD26 or anti-CD69. Adding these molecules to CD26 or CD69 resulted in 28-86% inhibition of CD26 or CD69 binding to anti-CD26 or anti-CD69 antibodies. The highest % binding of these antigens or peptides to CD26 or CD69 was attributed to SK and the lowest to casein peptides. We, therefore, propose that bacterial antigens (SK), dietary peptides (gliadin, casein) and Thimerosal (ethyl mercury) in individuals with pre-disposing HLA molecules bind to CD26 or CD69 and induce antibodies against these molecules. In conclusion, this study is apparently the first to demonstrate that dietary peptides, bacterial toxins and xenobiotics bind to lymphocyte receptors and/or tissue enzymes, resulting in autoimmune reaction in children with autism. 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J. Immunopathol. Pharmacol. PD SEP-DEC PY 2003 VL 16 IS 3 BP 189 EP 199 PG 11 WC Immunology; Pathology; Pharmacology & Pharmacy SC Immunology; Pathology; Pharmacology & Pharmacy GA 750DC UT WOS:000186975200002 PM 14611720 ER PT J AU Cooper, EL AF Cooper, EL TI Neuroimmunology of autism: A multifaceted hypothesis SO INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY LA English DT Letter ID UVB IRRADIATION; CYTOKINE; INNATE C1 Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Lab Comparat Neuroimmunol, Los Angeles, CA 90095 USA. RP Cooper, EL (reprint author), Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Lab Comparat Neuroimmunol, Los Angeles, CA 90095 USA. 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PD SEP-DEC PY 2003 VL 16 IS 3 BP 289 EP 292 PG 4 WC Immunology; Pathology; Pharmacology & Pharmacy SC Immunology; Pathology; Pharmacology & Pharmacy GA 750DC UT WOS:000186975200016 PM 14611734 ER PT J AU Williams, G Perez-Gonzalez, LA Vogt, K AF Williams, G Perez-Gonzalez, LA Vogt, K TI The role of specific consequences in the maintenance of three types of questions SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE question asking; verbalizations; autism; language acquisition; verbal behavior; establishing operations ID TEACHING-CHILDREN; AUTISM AB This research replicated and extended a study by Williams, Donley, and Keller (2000). In that study, children with autism received a box with an object inside and learned to ask "What's that?," "Can I see it?," and "Can I have it?" to have the name of the object, to see the object, and to get the object, respectively. The purpose of the present research was to determine if the three questions (a) were three independent repertoires of behavior, (b) constituted three instances of a single functional response class, or (c) belonged to a chain of behavior. The 3 boys with autism who participated responded independently to each question when the consequences for each question were altered. This indicates that the three target responses were three independent repertoires of behavior, each one reinforced and maintained with its specific consequences. Thus, this procedure serves to teach children with autism to ask questions with flexibility according to a variable context. C1 Appl Behav Consultant Serv, Englewood, NJ 07631 USA. Univ Oviedo, Oviedo, Spain. David Gregory Sch, Paramus, NJ USA. RP Williams, G (reprint author), Appl Behav Consultant Serv, 66 Regency Circle, Englewood, NJ 07631 USA. RI Perez-Gonzalez, Luis/L-2338-2014 CR Donahoe J. W., 1994, LEARNING COMPLEX BEH Koegel LK, 1998, AM J MENT RETARD, V102, P346 Shabani DB, 2002, J APPL BEHAV ANAL, V35, P79, DOI 10.1901/jaba.2002.35-79 Skinner BF, 1934, P NATL ACAD SCI USA, V20, P532, DOI 10.1073/pnas.20.9.532 SUNDBERG M, 2000, 26 ANN C ASS BEH AN TAYLOR BA, 1995, J APPL BEHAV ANAL, V28, P3, DOI 10.1901/jaba.1995.28-3 Williams G, 2000, J APPL BEHAV ANAL, V33, P627, DOI 10.1901/jaba.2000.33-627 NR 7 TC 10 Z9 10 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 2003 VL 36 IS 3 BP 285 EP 296 DI 10.1901/jaba.2003.36-285 PG 12 WC Psychology, Clinical SC Psychology GA 727WJ UT WOS:000185683600001 PM 14596570 ER PT J AU Ahearn, WH AF Ahearn, WH TI Using simultaneous presentation to increase vegetable consumption in a mildly selective child with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article; Proceedings Paper CT 20th Annual Meeting of the California-Association-for-Behavior-Analysis CY FEB, 2002 CL SAN FRANCISCO, CALIFORNIA SP Calif Assoc Behav Anal DE antecedent manipulation; conditioned food preferences; establishing operations; food selectivity; preference assessment ID FOOD SELECTIVITY AB A multiple baseline design was used to evaluate the effects of adding condiments on the consumption of previously rejected foods (vegetables). Adding condiments produced increased food acceptance across three food items. Data are discussed in relation to conditioned food preferences and establishing operations. C1 New England Ctr Children, Southborough, MA 01772 USA. RP Ahearn, WH (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. CR Ahearn WH, 1996, J APPL BEHAV ANAL, V29, P321, DOI 10.1901/jaba.1996.29-321 Ahearn WH, 2001, J AUTISM DEV DISORD, V31, P505, DOI 10.1023/A:1012221026124 FISHER W, 1992, J APPL BEHAV ANAL, V25, P491, DOI 10.1901/jaba.1992.25-491 Kern L, 1996, J APPL BEHAV ANAL, V29, P243, DOI 10.1901/jaba.1996.29-243 Piazza CC, 2002, J APPL BEHAV ANAL, V35, P259, DOI 10.1901/jaba.2002.35-259 NR 5 TC 33 Z9 33 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 2003 VL 36 IS 3 BP 361 EP 365 DI 10.1901/jaba.2003.36-361 PG 5 WC Psychology, Clinical SC Psychology GA 727WJ UT WOS:000185683600008 PM 14596577 ER PT J AU Arntzen, E Halstadtro, AM Halstadtro, M AF Arntzen, E Halstadtro, AM Halstadtro, M TI Training play behavior in a 5-year-old boy with developmental disabilities SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE children; developmental disabilities; play behavior ID AUTISM AB The purpose of the current study was twofold: (a) to investigate if it was possible to train three different games (both as a leader and as a participant) to a child with developmental disabilities through interaction with 4 typically developing peers, and (b) to examine if correct responding would be maintained after the training was faded. A multiple probe design across three games was used. The results showed that the child learned both skills as a leader and as a participant in all three games, and that skills were maintained for a period of 3 weeks after the training had stopped. C1 Akerhus Univ Coll, N-1301 Sandvika, Norway. RP Arntzen, E (reprint author), Akerhus Univ Coll, POB 372, N-1301 Sandvika, Norway. CR BIJOU SW, 1976, CHILD DEV BASIC STAG GOLDSTEIN H, 1992, J APPL BEHAV ANAL, V25, P289, DOI 10.1901/jaba.1992.25-289 Thiemann KS, 2001, J APPL BEHAV ANAL, V34, P425, DOI 10.1901/jaba.2001.34-425 NR 3 TC 2 Z9 2 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 2003 VL 36 IS 3 BP 367 EP 370 DI 10.1901/jaba.2003.36-367 PG 4 WC Psychology, Clinical SC Psychology GA 727WJ UT WOS:000185683600009 PM 14596578 ER PT J AU Najdowski, AC Wallace, MD Doney, JK Ghezzi, PM AF Najdowski, AC Wallace, MD Doney, JK Ghezzi, PM TI Parental assessment and treatment of food selectivity in natural settings SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; demand fading; differential reinforcement; escape extinction; food selectivity; functional analysis AB This study evaluated the effects of a parent-conducted functional analysis and treatment consisting of differential reinforcement of an alternative behavior, escape extinction, and demand fading on food selectivity in a young child with autism. Increases in food acceptance at home and in a restaurant were obtained. C1 Univ Nevada, Dept Psychol 296, Reno, NV 89557 USA. RP Wallace, MD (reprint author), Univ Nevada, Dept Psychol 296, Reno, NV 89557 USA. CR Anderson CM, 2001, J APPL BEHAV ANAL, V34, P511, DOI 10.1901/jaba.2001.34-511 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P197, DOI 10.1901/jaba.1994.27-197 Piazza CC, 2002, J APPL BEHAV ANAL, V35, P259, DOI 10.1901/jaba.2002.35-259 NR 3 TC 33 Z9 33 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 2003 VL 36 IS 3 BP 383 EP 386 DI 10.1901/jaba.2003.36-383 PG 4 WC Psychology, Clinical SC Psychology GA 727WJ UT WOS:000185683600013 PM 14596582 ER PT J AU Mundy, P AF Mundy, P TI Annotation: The neural basis of social impairments in autism: the role of the dorsal medial-frontal cortex and anterior cingulate system SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Review DE brain imaging; frontal cortex; anterior cingulate; joint attention; social orienting; social cognition; autism ID POSITRON-EMISSION-TOMOGRAPHY; SUPPLEMENTARY EYE FIELD; HIGH-FUNCTIONING AUTISM; CEREBRAL-BLOOD-FLOW; JOINT ATTENTION; NONVERBAL-COMMUNICATION; MENTAL-RETARDATION; SPECTRUM DISORDER; ASPERGER-SYNDROME; CHILDHOOD AUTISM AB Background: The fundamental social disturbance of autism is characterized, in part, by problems in the acquisition of joint attention skills in the first years of life, followed by impairments in the development of social cognition, as assessed on theory of mind (ToM) measures. Recently, studies have indicated that a system involving the dorsal medial-frontal cortex (DMFC), and the anterior cingulate (AC), may contribute to the development of the tendency to initiate joint attention in infancy. Similarly, research has implicated the DMFC/AC system in ToM performance in typical and atypical individuals. These data suggest it may be useful to consider the functions associated with this system in the developmental psychopathology of autism. Method: A review of the studies of the connections between the DMFC/AC system, joint attention and ToM task performance. Results and conclusions: This review raises the hypothesis that the DMFC/AC may be involved in the basic disturbance in social orienting in autism. The DMFAC/AC may also play a role in the capacity to monitor proprioceptive information concerning self-action and integrate this self-related information with exteroceptive perceptual information about the behavior of other people. 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PD SEP PY 2003 VL 44 IS 6 BP 793 EP 809 DI 10.1111/1469-7610.00165 PG 17 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 715WN UT WOS:000184996200002 PM 12959489 ER PT J AU Mottron, L Burack, JA Iarocci, G Belleville, S Enns, JT AF Mottron, L Burack, JA Iarocci, G Belleville, S Enns, JT TI Locally oriented perception with intact global processing among adolescents with high-functioning autism: evidence from multiple paradigms SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE Asperger's disorder; autistic disorder; neuropsychology; perception; visuo-spatial functioning ID VISUAL-SEARCH; ENHANCED DISCRIMINATION; INDIVIDUALS; TASK; CHILDREN; PATTERNS; DEFICIT; STIMULI; ABILITY; SET AB Background: According to predictions from the Weak Central Coherence (WCC) theory for perceptual processing, persons with autism should display a tendency to focus on minute details rather than on a more general picture (Frith & Happe, 1994). However, the evidence for this theory is not consistent with findings of an enhanced detection of local targets (Plaisted, O'Riordan, & Baron-Cohen, 1998b; Plaisted, Swettenham, & Rees, 1999), but a typical global bias (Mottron, Burack, Stauder, Robaey, 1999; Ozonoff, Strayer, McMahon, & Filloux, 1994). Method: Adolescents with high-functioning autism and CA- (approximately 15 years) and IQ- (approximately 105-110) matched typically developing adolescents were administered a series of global-local visual tasks, including a traditional task of hierarchical processing, three tasks of configural processing, and a disembedding task that involved rapid perceptual processing. Results: No group differences were found on either the traditional task of hierarchical processing or on tasks of configural processing. However, group differences were found on the disembedding task as the search for embedded, in relation to isolated stimuli, was slower for the typically developing adolescents but similar for the participants with autism. Conclusions: These findings are consistent with other reports of superior performance in detecting embedded figures (Jolliffe & Baron-Cohen, 1997; Shah & Frith, 1983), but typical performance in global and configural processing (Mottron, Burack et al., 1999; Ozonoff et al., 1994) among persons with high-functioning autism. Thus, the notions of local bias and global impairment that are part of WCC may need to be reexamined. C1 Hop Riviere Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ, Canada. McGill Univ, Dept Educ & Counseling Psychol, Montreal, PQ H3A 2T5, Canada. Simon Fraser Univ, Dept Psychol, Burnaby, BC V5A 1S6, Canada. Univ Montreal, Grp Rech & Neuropsychol Expt, Montreal, PQ H3C 3J7, Canada. Univ Geriatrie Montreal, Ctr Rech Inst, Montreal, PQ, Canada. Univ British Columbia, Dept Psychol, Vancouver, BC V5Z 1M9, Canada. RP Mottron, L (reprint author), Hop Riviere Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. CR Bonnel A, 2003, J COGNITIVE NEUROSCI, V15, P226, DOI 10.1162/089892903321208169 Burack JA, 2000, DEV PSYCHOL, V36, P731, DOI 10.1037//0012-1649.36.6.731 ENNS JT, 1991, BEHAV RES METH INSTR, V23, P265, DOI 10.3758/BF03203376 ENNS JT, 1995, PSYCHOL SCI, V6, P283, DOI 10.1111/j.1467-9280.1995.tb00512.x Frith U., 1989, AUTISM EXPLAINING EN FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 GOODALE MA, 1992, TRENDS NEUROSCI, V15, P20, DOI 10.1016/0166-2236(92)90344-8 Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Humphreys G. W., 1987, VISUAL OBJECT PROCES, P281 IAROCCI G, 2001, SOC RES CHILD DEV MI Jolliffe T, 1997, J CHILD PSYCHOL PSYC, V38, P527, DOI 10.1111/j.1469-7610.1997.tb01539.x KINCHLA RA, 1979, PERCEPT PSYCHOPHYS, V25, P225, DOI 10.3758/BF03202991 LAMB MR, 1990, PERCEPT PSYCHOPHYS, V47, P489, DOI 10.3758/BF03208182 LAMB MR, 1990, J EXP PSYCHOL LEARN, V16, P471, DOI 10.1037/0278-7393.16.3.471 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 LORD C, 1997, AUTISM DIAGNOSIS OBS LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 LORD C, 1993, INFANT MENTAL HLTH J, V14, P235 Mottron L, 1999, J CHILD PSYCHOL PSYC, V40, P743, DOI 10.1017/S0021963098003795 Mottron L, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P131 Mottron L, 1999, J CHILD PSYCHOL PSYC, V40, P203, DOI 10.1017/S0021963098003333 Mottron L, 2000, J CHILD PSYCHOL PSYC, V41, P1057, DOI 10.1017/S0021963099006253 OLDFIELD RC, 1971, NEUROPSYCHOLOGIA, V9, P97, DOI 10.1016/0028-3932(71)90067-4 O'Riordan M, 2001, Q J EXP PSYCHOL-A, V54, P961, DOI 10.1080/02724980042000543 O'Riordan MA, 2001, J EXP PSYCHOL HUMAN, V27, P719, DOI 10.1037//0096-1523.27.3.719 OZONOFF S, 1994, J CHILD PSYCHOL PSYC, V35, P1015, DOI 10.1111/j.1469-7610.1994.tb01807.x Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P765, DOI 10.1017/S0021963098002601 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 Plaisted KC, 2001, DEVELOPMENT OF AUTISM: PERSPECTIVES FROM THEORY AND RESEARCH, P149 Rinehart NJ, 2000, J CHILD PSYCHOL PSYC, V41, P769, DOI 10.1017/S002196309900596X 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 SNODGRASS JG, 1980, J EXP PSYCHOL-HUM L, V6, P174, DOI 10.1037/0278-7393.6.2.174 TYMCHUK AJ, 1977, J MENT DEFIC RES, V21, P133 Witkin HA, 1971, MANUAL EMBEDDED FIGU NR 36 TC 140 Z9 144 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD SEP PY 2003 VL 44 IS 6 BP 904 EP 913 DI 10.1111/1469-7610.00174 PG 10 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 715WN UT WOS:000184996200011 PM 12959498 ER PT J AU Pilowsky, T Yirmiya, N Shalev, RS Gross-Tsur, V AF Pilowsky, T Yirmiya, N Shalev, RS Gross-Tsur, V TI Language abilities of siblings of children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY AND ALLIED DISCIPLINES LA English DT Article DE autistic disorder; behavioral genetics; family history; individual differences; language disorder; siblings ID FAMILY HISTORY; COGNITIVE DISABILITIES; BROADER PHENOTYPE; INFANTILE-AUTISM; INDIVIDUALS; DISORDERS; RELATIVES; PARENTS; TWIN; EXPRESSION AB Background: Language abilities of siblings of children with autism were examined to explore the possibility that language abilities are behavioral markers specific to the genetic liability for autism, as part of the broader phenotype. Method: Language abilities were compared among 27 siblings of children with autism, 23 siblings of children with mental retardation of unknown etiology (MR), and 22 siblings of children with developmental language disorders (DLD). Groups were matched by siblings' age, gender, birth order, family size, ethnicity, family income and by probands' gender and mental age. Results: Siblings of children with autism achieved higher scores than siblings of children with DLD on receptive, expressive, and total language scales of the Children's Evaluation of Language Fundamentals and on verbal IQ. Moreover, within the DLD group, school problems in the domains of reading and arithmetic were more prevalent than within the other two groups. Only 2 siblings of children with autism received clinical diagnoses based on DSM-IV criteria compared to 3 siblings of children with MR and 7 siblings of children with DLD. Conclusions: After excluding data of the diagnosed siblings, no differences in language abilities could be discerned among the groups, except that more siblings in the DLD group were identified as having language difficulties. In summary, although language deficits characterize autism, siblings of children with autism were not found to demonstrate deficits in language skills assessed by formal language tests, IQ, or academic skills. C1 Hebrew Univ Jerusalem, Jerusalem, Israel. Shaare Zedek Med Ctr, Neuropediat Unit, Jerusalem, Israel. RP Yirmiya, N (reprint author), Hebrew Univ Jerusalem, Jerusalem, Israel. CR Achenbach T. M., 1983, MANUAL CHILD BEHAV C Achenbach T. M., 1991, MANUAL CBCL 4 18 199 Achenbach T. M., 1981, MONOGRAPHS SOC RES C, V46 *AM GUID SERV, 1984, MULL SCAL EARL LEARN American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th AUERBACH JG, 1991, J CHILD PSYCHOL PSYC, V32, P1017, DOI 10.1111/j.1469-7610.1991.tb01926.x AUGUST GJ, 1981, BRIT J PSYCHIAT, V138, P416, DOI 10.1192/bjp.138.5.416 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x BAILEY A, 1995, PSYCHOL MED, V25, P63 BAIRD TD, 1985, J AUTISM DEV DISORD, V15, P315, DOI 10.1007/BF01531501 Baltaxe CA, 1977, J PEDIATR PSYCHOL, V2, P176, DOI DOI 10.1093/JPEPSY/2.4.176 Bayley N, 1993, MANUAL BAYLEY SCALES BEBKO JM, 1987, J AUTISM DEV DISORD, V17, P565, DOI 10.1007/BF01486971 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 BISHOP DVM, 1995, DEV MED CHILD NEUROL, V37, P56 Bishop DVM, 2001, PHILOS T R SOC B, V356, P369, DOI 10.1098/rstb.2000.0770 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Boutin P, 1997, J AUTISM DEV DISORD, V27, P165, DOI 10.1023/A:1025891824269 CATTELL P, 1960, MEASUREMENT INTELLIG CREAK M, 1960, J CHILD PSYCHOL PSYC, V1, P156, DOI 10.1111/j.1469-7610.1960.tb01990.x Dale PS, 1998, NAT NEUROSCI, V1, P324 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 EALES MJ, 1993, J AUTISM DEV DISORD, V23, P593, DOI 10.1007/BF01046104 Fisher SE, 1998, NAT GENET, V18, P168, DOI 10.1038/ng0298-168 FOLSTEIN S, 1987, J AUTISM DEV DISORD, V18, P3 FOLSTEIN S, 1977, J CHILD PSYCHOL PSYC, V18, P297, DOI 10.1111/j.1469-7610.1977.tb00443.x Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 FRITH U, 1994, PHILOS T ROY SOC B, V346, P97, DOI 10.1098/rstb.1994.0133 GILLBERG C, 1992, DEV MED CHILD NEUROL, V34, P389 Happe F, 2001, J CHILD PSYCHOL PSYC, V42, P299, DOI 10.1111/1469-7610.00723 Hughes C, 1999, J CHILD PSYCHOL PSYC, V40, P705, DOI 10.1017/S0021963099004023 KAUFMAN A, 1983, MANUAL KAUFMAN ASSES LANDA R, 1992, PSYCHOL MED, V22, P245 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 LEBOYER M, 1995, DEV NEUROPSYCHOL, V11, P139 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 NARAYAN S, 1990, J AUTISM DEV DISORD, V20, P523, DOI 10.1007/BF02216057 ORVASHEL H, 1997, SCHEDULE AFFECTIVE D OZONOFF S, 1996, BRAIN LANG, V52, P434 Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 PIVEN J, 1995, COMMUNICATON Piven J, 1997, J CHILD PSYCHOL PSYC, V38, P1011, DOI 10.1111/j.1469-7610.1997.tb01618.x Piven J, 1997, AM J PSYCHIAT, V154, P185 PIVEN J, 1990, J AM ACAD CHILD PSY, V29, P177, DOI 10.1097/00004583-199003000-00004 Piven J, 1999, INT REV PSYCHIATR, V11, P299, DOI 10.1080/09540269974186 Plumet MH, 1995, CORTEX, V31, P723 Reynell J, 1987, REYNELL DEV LANGUAGE RITVO ER, 1985, AM J PSYCHIAT, V142, P74 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 Semel E, 1995, CLIN EVALUATION LANG, V3rd Shields J, 1996, DEV MED CHILD NEUROL, V38, P473 SIMMONS JQ, 1975, J AUTISM CHILD SCHIZ, V5, P333, DOI 10.1007/BF01540680 SMALLEY SL, 1988, ARCH GEN PSYCHIAT, V45, P935 SMALLEY SL, 1990, J AUTISM DEV DISORD, V20, P271, DOI 10.1007/BF02284724 SMALLEY SL, 1991, PSYCHIAT CLIN N AM, V14, P125 Sparrow S, 1984, VINELAND ADAPTIVE BE STEFFENBURG S, 1989, J CHILD PSYCHOL PSYC, V30, P405, DOI 10.1111/j.1469-7610.1989.tb00254.x *STOELT CO, 1948, LEIT INT PERF SCAL Stutsman R., 1948, MERRILLPALMER SCALE Thorndike R. L., 1986, STANFORDBINET INTELL VARGHAKHADEM F, 1995, P NATL ACAD SCI USA, V92, P930, DOI 10.1073/pnas.92.3.930 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd Wiig E. H., 1992, CLIN EVALUATION LANG Yirmiya N, 2001, RESEARCH BASIS FOR AUTISM INTERVENTION, P59 YIRMIYA N, 1991, CLIN PSYCHOL REV, V11, P669, DOI 10.1016/0272-7358(91)90125-E NR 65 TC 26 Z9 26 PU BLACKWELL PUBL LTD PI OXFORD PA 108 COWLEY RD, OXFORD OX4 1JF, OXON, ENGLAND SN 0021-9630 J9 J CHILD PSYCHOL PSYC JI J. Child Psychol. Psychiatry Allied Discip. PD SEP PY 2003 VL 44 IS 6 BP 914 EP 925 DI 10.1111/1469-7610.00175 PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 715WN UT WOS:000184996200012 PM 12959499 ER PT J AU Masi, G Cosenza, A Mucci, M Brovedani, P AF Masi, G Cosenza, A Mucci, M Brovedani, P TI A 3-year naturalistic study of 53 preschool children with pervasive developmental disorders treated with risperidone SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID AUTISM RATING-SCALE; YOUNG-CHILDREN; CHILDHOOD AUTISM; PEDIATRIC PSYCHOPHARMACOLOGY; INFANTILE-AUTISM; OPEN TRIAL; FOLLOW-UP; ADOLESCENTS; HALOPERIDOL; SCHIZOPHRENIA AB Background: Only sparse and short-term data are available on pharmacologic treatments in very young children with pervasive developmental disorders (PDD). The purpose of this 3-year naturalistic study (March 1999-April 2002) is to describe the clinical outcome of a consecutive sample of preschool children with PDD treated with risperidone monotherapy. Method: The sample consisted of 45 boys and 8 girls aged 3.6 to 6.6 years (mean +/- SD age = 4.6 +/- 0.7 years) with a DSM-IV diagnosis of autistic disorder or PDD, not otherwise specified. Outcome measures included the Children's Psychiatric Rating Scale (CPRS), Clinical Global Impressions-Improvement scale (CGI-I), Children's Global Assessment Scale (CGAS), and a checklist for risperidone side effects. Results: Patients received risperidone for a period ranging from I to 32 months (7.9 +/- 6.8 months). Twenty-five patients (47.2%) continued to receive risperidone after the study was completed, while 28 (52.8%) discontinued due to side effects (22.6% [N = 12]), parents' choice (18.9% [N = 10]), lack of efficacy (5.7% [N = 3]), and decision of the treating psychiatrist (5.7% [N = 3]). The optimal dose was 0.55 +/- 0.2 mg/day. Significant improvement at the last observation was found in CPRS (p < .0001) and CGAS (p < .0001) scores. On the basis of both an improvement of 25% in CPRS score and a score of I or 2 on the CGI-I, 46.8% (N = 22) of subjects were considered responders. Behavioral disorders and affect dysregulation were more sensitive to treatment than was interpersonal functioning. Responders received higher doses of medication for a longer period and had a greater weight gain than did nonresponders. Increased prolactin levels without clinical signs (65% [24 of 37]) and increased appetite (15% [8 of 53]) were the most frequent side effects. Conclusion: These findings suggest that low-dose risperidone may positively affect the clinical outcome in young children with PDD not only in the short-term, but also in the long-term period. C1 IRCCS Stella Maris, Sci Inst Child Neurol & Psychiat, I-56018 Pisa, Italy. RP Masi, G (reprint author), IRCCS Stella Maris, Sci Inst Child Neurol & Psychiat, Via Giacinti 2, I-56018 Pisa, Italy. 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Clin. Psychiatry PD SEP PY 2003 VL 64 IS 9 BP 1039 EP 1047 PG 9 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 723XV UT WOS:000185457600009 PM 14628979 ER PT J AU Zahavi, D Parnas, J AF Zahavi, D Parnas, J TI Conceptual problems in infantile autism research - Why cognitive science needs phenomenology SO JOURNAL OF CONSCIOUSNESS STUDIES LA English DT Article ID MIND AB Until recently, cognitive research in infantile autism primarily focussed on the ability of autistic subjects to understand and predict the actions of others. Currently, researchers are also considering the capacity of autists to understand their own minds. In this article we discuss selected recent contributions to the theory of mind debate and the study of infantile autism, and provide an analysis of intersubjectivity and self-awareness that is informed both by empirical research and by work in the phenomenological tradition. 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Conscious. Stud. PD SEP-OCT PY 2003 VL 10 IS 9-10 BP 53 EP 71 PG 19 WC Philosophy; Social Sciences, Interdisciplinary SC Philosophy; Social Sciences - Other Topics GA 733HR UT WOS:000185994600005 ER PT J AU Nelson, C Huefner, DS AF Nelson, C Huefner, DS TI Young children with autism: Judicial responses to the Lovaas and discrete trial training debates SO JOURNAL OF EARLY INTERVENTION LA English DT Article ID INTENSIVE BEHAVIORAL TREATMENT; INTERVENTION; PROJECT AB In the last decade, parents have filed an increasing number of due process hearings and court cases requesting the Lovaas method, an intensive discrete trial training based on select principles of applied behavior analysis, for their young children with autism. This article examines provisions of the Individuals with Disabilities Education Act (IDEA) that relate to these cases, the Lovaas method and research issues surrounding it, published federal cases decided since the revisions to IDEA in 1997, and public policy issues that have surfaced as a result of the controversial cases. Recommendations for addressing these issues are offered. C1 Univ Utah, Dept Special Educ, Salt Lake City, UT 84112 USA. RP Nelson, C (reprint author), Univ Utah, Dept Special Educ, 1705 E Campus Ctr Dr Room 221, Salt Lake City, UT 84112 USA. CR BAER DM, 1968, J APPL BEHAV ANAL, V1, P91, DOI 10.1901/jaba.1968.1-91 Bayley N., 1969, BAYLEY SCALES INFANT BERKMAN M, 1997, HDB AUTISM PERVASIVE, P808 BIRD R, 2002, REPORT LEGISLATURE P Bryson S. E., 1997, HDB AUTISM PERVASIVE, P41 Cohen D. J, 1997, HDB AUTISM PERVASIVE Dawson G., 1997, EFFECTIVENESS EARLY, P307 *DIV EARL CHILDH C, 2000, DEV DEL EL CAT POS P FEINBERG E, 1998, INFANTS YOUNG CHILDR, V10, P51 Green G, 1996, BEHAV INTERVENTION Y, P29 Greenspan S. I., 1998, CHILD SPECIAL NEEDS Gresham FM, 1997, BEHAV DISORDERS, V22, P185 Gresham FM, 1997, BEHAV DISORDERS, V22, P219 HARRIS SL, 1998, RIGHT START BEHAV IN Harris SL, 2000, PRESCHOOL ED PROGRAM, P233 Hehir T., 1999, LAW SCH REFORM, P205 HEWARD WL, 1987, APPL BEHAV ANAL, P14 Huefner D. S., 2000, GETTING COMFORTABLE HUEFNER DS, 1997, ISSUES ED STUDENTS D, P343 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Marcus LM, 2001, RESEARCH BASIS FOR AUTISM INTERVENTION, P171 MARCUS LM, 2000, PRESCHOOL ED PROGRAM, P631 MCBRIDE SL, 1993, J EARLY INTERVENTION, V17, P414 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 MCGEE GG, 1994, PRESCHOOL ED PROGRAM, P127 MCGONIGAL MJ, 1991, GUIDELINES RECOMMEND National Research Council, 2001, ED CHILDR AUT Schopler E., 1995, LEARNING COGNITION A, P243 Schopler E., 1997, HDB AUTISM PERVASIVE, P767 Smith T, 1998, INFANT YOUNG CHILD, V10, P67 Smith T, 1997, AM J MENT RETARD, V102, P238, DOI 10.1352/0895-8017(1997)102<0238:IBTFPW>2.0.CO;2 STRAIN PS, 1994, PRESCHOOL ED PROGRAM, P127 *US DEP ED, 1999, FED REGISTER, V64, P12552 *US DEP ED, 1996, 18 US DEP ED *US DEP ED, 1999, FED REGISTER, V64, P12406 *US DEP ED, 2001, NUMB CHILDR 6 21 S B Volkmar F. R., 1997, HDB AUTISM PERVASIVE, P5 Wing L, 1993, Eur Child Adolesc Psychiatry, V2, P61, DOI 10.1007/BF02098832 Yell ML, 2000, J SPEC EDUC, V33, P205, DOI 10.1177/002246690003300403 NR 39 TC 5 Z9 5 PU COUNCIL EXCEPTIONAL CHILDREN PI RESTON PA 1920 ASSOCIATION DR, RESTON, VA 22091-1589 USA SN 1053-8151 J9 J EARLY INTERVENTION JI J. Early Interv. PD FAL PY 2003 VL 26 IS 1 BP 1 EP 19 DI 10.1177/105381510302600101 PG 19 WC Education, Special; Psychology, Educational; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 742UZ UT WOS:000186537600001 ER PT J AU Matthews, B AF Matthews, B TI A picture's worth: PECS and other visual communication strategies in autism SO JOURNAL OF INTELLECTUAL & DEVELOPMENTAL DISABILITY LA English DT Book Review C1 Flinders Univ S Australia, Dept Disabil Studies, Adelaide, SA 5001, Australia. RP Matthews, B (reprint author), Flinders Univ S Australia, Dept Disabil Studies, Adelaide, SA 5001, Australia. CR Bondy Andy, 2002, PICTURES WORTH PECS NR 1 TC 1 Z9 1 PU TAYLOR & FRANCIS LTD PI ABINGDON PA 4 PARK SQUARE, MILTON PARK, ABINGDON OX14 4RN, OXON, ENGLAND SN 1366-8250 J9 J INTELLECT DEV DIS JI J. Intellect. Dev. Dis. PD SEP PY 2003 VL 28 IS 3 BP 311 EP 312 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 714VP UT WOS:000184934400009 ER PT J AU McClintock, K Hall, S Oliver, C AF McClintock, K Hall, S Oliver, C TI Risk markers associated with challenging behaviours in people with intellectual disabilities: a meta-analytic study SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article ID SELF-INJURIOUS-BEHAVIOR; MENTALLY-RETARDED CHILDREN; MALADAPTIVE BEHAVIORS; LEARNING-DISABILITIES; STIMULATORY BEHAVIOR; SKILL LEVELS; PREVALENCE; EPIDEMIOLOGY; INDIVIDUALS; RETARDATION AB A meta-analysis of prevalence and cohort studies conducted over the last 30 years was carried out to identify risk markers for challenging behaviour shown by individuals with intellectual disabilities (IDS). A total of 86 potential studies was identified from the review, with 22 (25.6%) containing sufficient data to enable a statistical analysis to be conducted. Results indicated that males were significantly more likely to show aggression than females, and that individuals with a severe/profound degree of ID were significantly more likely to show self-injury and stereotypy than individuals with a mild/moderate degree of ID. Individuals with a diagnosis of autism were significantly more likely to show self-injury, aggression and disruption to the environment whilst individuals with deficits in receptive and expressive communication were significantly more likely to show self-injury. In most cases, tests for heterogeneity were statistically significant, as expected. The meta-analysis highlighted the paucity of methodologically robust studies of risk markers for challenging behaviours and the lack of data on incidence, prevalence and chronicity of challenging behaviour in this population. C1 Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England. RP Oliver, C (reprint author), Univ Birmingham, Sch Psychol, Birmingham B15 2TT, W Midlands, England. CR Abramson JH, 1994, MAKING SENSE DATA SE ANDO H, 1979, CHILD PSYCHIAT HUM D, V9, P131, DOI 10.1007/BF01433475 ANDO H, 1979, CHILD PSYCHIAT HUM D, V10, P85, DOI 10.1007/BF01433500 BALLINGE.BR, 1971, BRIT J PSYCHIAT, V118, P535, DOI 10.1192/bjp.118.546.535 BERKSON G, 1985, MENT RETARD, V23, P31 Bhaumik S, 1997, BRIT J PSYCHIAT, V170, P502, DOI 10.1192/bjp.170.6.502 Blettner M, 1999, INT J EPIDEMIOL, V28, P1, DOI 10.1093/ije/28.1.1 Borthwick-Duffy S. 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R., 2002, SELF INJURIOUS BEHAV, P41, DOI 10.1037/10457-003 Schroeder S. R., 1986, ADV LEARNING BEHAV D, V5, P63 SHODELL MJ, 1968, ARCH GEN PSYCHIAT, V19, P453 THOMPSON SG, 1994, BRIT MED J, V309, P1351 WINDAHL S, 1988, 8 IASSMD C DUBL NR 48 TC 199 Z9 199 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD SEP PY 2003 VL 47 BP 405 EP 416 DI 10.1046/j.1365-2788.2003.00517.x PN 6 PG 12 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 719LA UT WOS:000185203500001 PM 12919191 ER PT J AU Kwok, H AF Kwok, H TI Autism and related disorders SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Book Review CR HOLT G, 2002, AUTISM RELATED DISOR NR 1 TC 0 Z9 0 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0964-2633 J9 J INTELL DISABIL RES JI J. Intell. Disabil. Res. PD SEP PY 2003 VL 47 BP 495 EP 495 DI 10.1046/j.1365-2788.2003.00520.x PN 6 PG 1 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 719LA UT WOS:000185203500012 ER PT J AU Freeman, RL Grzymala-Busse, JW Harvey, M AF Freeman, RL Grzymala-Busse, JW Harvey, M TI Functional behavioral assessment using the LERS data mining system - Strategies for understanding complex physiological and behavioral patterns SO JOURNAL OF INTELLIGENT INFORMATION SYSTEMS LA English DT Article DE self-injurious behavior; data mining; LERS; LEM2 algorithm ID SELF-INJURY AB Many individuals with mental retardation, autism, and other related disabilities lead lives that are significantly restricted because of problem behaviors such as self-injury and aggression. We processed two data sets, one describing heart rate patterns and the other describing the behavioral events of one subject diagnosed with severe mental retardation, visual impairments, and severe problem behavior. From these data sets the LERS data mining system induced certain and possible rule sets. In our research these rule sets were successfully used for interpretation, or, more specifically, to discover mechanisms of triggering specific physiological and behavioral patterns. C1 Univ Kansas, Bur Child Res, Inst Life Span Studies, Lawrence, KS 66045 USA. Univ Kansas, Dept Elect Engn & Comp Sci, Lawrence, KS 66045 USA. Vanderbilt Univ, John F Kennedy Ctr, Peabody Coll, Nashville, TN USA. RP Grzymala-Busse, JW (reprint author), Univ Kansas, Bur Child Res, Inst Life Span Studies, Lawrence, KS 66045 USA. EM jerzy@lightning.eecs.ku.edu CR Bakeman R., 1986, OBSERVING INTERACTIO Boccia ML, 2000, BEHAVIORAL OBSERVATION, P83 Booker L., 1990, MACHINE LEARNING PAR, P235 DERBY KM, 1992, J APPL BEHAV ANAL, V25, P713, DOI 10.1901/jaba.1992.25-713 FOSTER B, 1993, AM LAB, V25, P44 FREEMAN RL, 2001, LECT NOTES COMPUTER, V2253, P395 Freeman RL, 2001, COMP MED SY, P11 FREEMAN RL, 2001, JSAI JAP SOC ART INT, P195 Freeman RL, 1999, AM J MENT RETARD, V104, P330, DOI 10.1352/0895-8017(1999)104<0330:RBHRAP>2.0.CO;2 Gottman JM, 1981, TIME SERIES ANAL COM Grzymala-Busse J. W., 1997, Fundamenta Informaticae, V31 Grzymala-Busse J. W., 1992, HDB APPL ADV ROUGH S, P3 Grzymala-Busse J.W., 1991, MANAGING UNCERTAINTY Guess D., 1991, AM J MENT RETARD, V96, P335 Holland J. H., 1986, INDUCTION PROCESSES HORNER RH, 1990, J ASSOC PERS SEVERE, V15, P91 IWATA BA, 1994, J APPL BEHAV ANAL, V27, P215, DOI 10.1901/jaba.1994.27-215 IWATA BA, 1982, ANAL INTERVEN DEVEL, V2, P3, DOI 10.1016/0270-4684(82)90003-9 KARSH KG, 1989, PORTABLE COMPUTER SY MACE FC, 1991, J APPL BEHAV ANAL, V24, P553, DOI 10.1901/jaba.1991.24-553 O'Neill R. E., 1997, FUNCTIONAL ASSESSMEN, V2nd Pawlak Z., 1991, ROUGH SETS THEORETIC PAWLAK Z, 1982, INT J COMPUT INF SCI, V11, P341, DOI 10.1007/BF01001956 REICHLE J, 1993, TOP LANG DISORD, V13, P61 Romanczyk R. G., 1992, SELF INJURIOUS BEHAV, P93 Schroeder Sr, 1999, CHALLENGING BEHAVIOR OF PERSONS WITH MENTAL HEALTH DISORDERS AND SEVERE DEVELOPMENTAL DISABILITIES, P65 SHORES RE, 1999, FUNCTIONAL ANAL PROB, P219 Thompson T, 1999, CHALLENGING BEHAVIOR OF PERSONS WITH MENTAL HEALTH DISORDERS AND SEVERE DEVELOPMENTAL DISABILITIES, P125 Thompson T., 1994, DESTRUCTIVE BEHAV DE, P83 VOLLMER TR, 1994, J APPL BEHAV ANAL, V27, P331, DOI 10.1901/jaba.1994.27-331 NR 30 TC 2 Z9 2 PU SPRINGER PI DORDRECHT PA VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS SN 0925-9902 J9 J INTELL INF SYST JI J. Intell. Inf. Syst. PD SEP PY 2003 VL 21 IS 2 BP 173 EP 181 DI 10.1023/A:1024762516786 PG 9 WC Computer Science, Artificial Intelligence; Computer Science, Information Systems SC Computer Science GA 700QM UT WOS:000184122700006 ER PT J AU King, B Zwi, K Nunn, K Longworth, J Dossetor, D AF King, B Zwi, K Nunn, K Longworth, J Dossetor, D TI Use of risperidone in a paediatric population: An observational study SO JOURNAL OF PAEDIATRICS AND CHILD HEALTH LA English DT Article DE behaviour; complications; efficacy; risperidone ID PERVASIVE DEVELOPMENTAL DISORDERS; DOUBLE-BLIND; SCHIZOPHRENIC-PATIENTS; AGGRESSIVE-BEHAVIOR; CHILDREN; HALOPERIDOL; ADOLESCENTS; EFFICACY; METAANALYSIS; AUTISM AB Objective: To evaluate the impact of risperidone on functional impairment in a paediatric sample and to document the range of adverse drug reactions. Methods: Risperidone treatment in children and adolescents (n = 51) with severe behavioural disturbances was assessed retrospectively to determine clinical response and adverse events. The change in patient functional performance during treatment was assessed using the Royal Alexandra Hospital for Children Measure of Function (MOF) score. Changes in target behaviours ( such as severe aggression) were also assessed. Results: The average duration of follow up was 9 months. Clinical improvement was demonstrated in 76% of the sample. There was a statistically significant improvement in the mean MOF with risperidone therapy (10.61 with 99% confidence interval 6.6 - 14.6). Risperidone appeared to be particularly useful in patients with autistic spectrum disorders. Twenty-five of the 51 patients (49%) experienced side-effects including sedation (27%), weight gain (20%), anticholinergic (10%) and extrapyramidal (8%) side-effects. Conclusions: This study suggests that risperidone is an effective agent in severely behaviourally disturbed paediatric patients. However, risperidone use is limited by the high frequency of side-effects. Randomized controlled trial data are required to determine the safety and efficacy of risperidone. C1 Childrens Hosp Westmead, Dept Psychol Med, Westmead, NSW 2145, Australia. RP Dossetor, D (reprint author), Childrens Hosp Westmead, Dept Psychol Med, Locked Bag 4001, Westmead, NSW 2145, Australia. 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Paediatr. Child Health PD SEP-OCT PY 2003 VL 39 IS 7 BP 523 EP 527 DI 10.1046/j.1440-1754.2003.00205.x PG 5 WC Pediatrics SC Pediatrics GA 720FY UT WOS:000185251800008 PM 12969207 ER PT J AU Brookman, L Boettcher, M Klein, E Openden, D Koegel, RL Koegel, LK AF Brookman, L Boettcher, M Klein, E Openden, D Koegel, RL Koegel, LK TI Facilitating social interactions in a community summer camp setting for children with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Editorial Material ID SEVERE DISABILITIES AB This article describes a program developed to support the participation of children with autism in a full-inclusion summer day camp program with their typically developing peers. The goal of the program was to support the children in inclusive summer recreational settings and specifically target their social development with typically developing peers. The program contained the following elements: recruiting appropriate aides, providing the aides with ongoing training and support, creating individualized social and behavioral goals for the campers, developing interventions that were contextually appropriate to the camp settings, and communicating with the families during their participation in the program. This article discusses the relevant child, family, agency, and community issues relevant to the implementation of this program. C1 Univ Calif Santa Barbara, Gevirtz Grad Sch Educ, Santa Barbara, CA 93106 USA. RP Brookman, L (reprint author), Univ Calif Santa Barbara, Gevirtz Grad Sch Educ, CCSP Phelps 1110, Santa Barbara, CA 93106 USA. 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PD FAL PY 2003 VL 5 IS 4 BP 249 EP 252 DI 10.1177/10983007030050040801 PG 4 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 725YC UT WOS:000185569100008 ER PT J AU Staufenberg, EFA Kemeney, A Graydon, M Verma, NK AF Staufenberg, EFA Kemeney, A Graydon, M Verma, NK TI Vagus nerve stimulation (VNS) temporal lobe epilepsy & autism: A case of seizure reduction alternating with neurobehavioural changes SO JOURNAL OF PSYCHOPHARMACOLOGY LA English DT Meeting Abstract CT Summer Meeting of the British-Association-for-Psychopharmacology CY JUL 20-23, 2003 CL CAMBRIDGE, ENGLAND SP British Assoc Psychopharmacol C1 Norfolk & Norwich Univ Hosp, Norwich Epilepsy Clin, Norwich, Norfolk, England. Royal Hallamshire Hosp, Sheffield S10 2JF, S Yorkshire, England. NR 0 TC 0 Z9 0 PU SAGE PUBLICATIONS LTD PI LONDON PA 6 BONHILL STREET, LONDON EC2A 4PU, ENGLAND SN 0269-8811 J9 J PSYCHOPHARMACOL JI J. Psychopharmacol. PD SEP PY 2003 VL 17 IS 3 SU S BP A59 EP A59 PG 1 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 726WC UT WOS:000185623500236 ER PT J AU Sadowsky, J AF Sadowsky, J TI Autism in history: The case of Hugh Blair of borgue. SO JOURNAL OF THE HISTORY OF THE BEHAVIORAL SCIENCES LA English DT Book Review C1 Case Western Reserve Univ, Cleveland, OH 44106 USA. RP Sadowsky, J (reprint author), Case Western Reserve Univ, Cleveland, OH 44106 USA. CR Houston Rab, 2000, AUTISM HIST CASE HUG NR 1 TC 0 Z9 0 PU JOHN WILEY & SONS INC PI HOBOKEN PA 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0022-5061 J9 J HIST BEHAV SCI JI J. Hist. Behav. Sci. 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This article gives a brief review of the cumulative evidence in favor of the model: Prevalence of absolute pitch is increased (a) in the congenitally and early blind, (b) among musicians in Japan, a country with a special tradition of early music training, and (c) in different types of genetically based cognitive deficit syndromes; (d) latent forms of absolute pitch are widespread, (e) there are remarkable parallels to first language acquisition, and (f) strong correlations are consistently found between early music training and the manifestation of AP in adolescence. Apart from atypical cases, early tonal training during a sensitive period and up to a "hard" age limit seems to be a necessary condition for the development of absolute pitch. The question of sufficiency of adequate early training methods (i.e., acquisition without hypothetical distinctive genetic priming factors) is not yet sufficiently settled. C1 Univ Klagenfurt, Dept Psychol, CPU, A-9020 Klagenfurt, Austria. 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PD FAL PY 2003 VL 21 IS 1 BP 111 EP 117 DI 10.1525/mp.2003.21.1.111 PG 7 WC Music; Psychology, Experimental SC Music; Psychology GA 721WR UT WOS:000185341900007 ER PT J AU Jentsch, JD Arguello, PA Anzivino, LA AF Jentsch, JD Arguello, PA Anzivino, LA TI Null mutation of the arginine-vasopressin gene in rats slows attentional engagement and facilitates response accuracy in a lateralized reaction time task SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE attention; vasopressin; catecholamines; cognition; animal models ID STRIATAL DOPAMINE DEPLETION; BRATTLEBORO RAT; DESGLYCINAMIDE-VASOPRESSIN; DIABETES-INSIPIDUS; SENSORY ATTENTION; BRAIN-DEVELOPMENT; FRONTAL-CORTEX; MESSENGER-RNA; PERFORMANCE; NORADRENALINE AB The neurophysin vasopressin is thought to play an important role in emotional behavior and aspects of cognition in the rat, and the pathophysiology of this system has been implicated in two neurodevelopmental disorders, namely autism and schizophrenia. Genetic deficiency of vasopressin in rats, resulting from a null mutation of the vasopressin gene, causes alterations of brain development with resulting behavioral and neurochemical phenotypes in adulthood. We previously demonstrated that partial vasopressin deficiency ( rats heterozygous for the null mutation) produces enhanced visuospatial attention and motor speeding. Here, the results of studies of homozygous Brattleboro rats that are fully vasopressin deficient are reported. We trained subjects to perform a lateralized reaction time task that measures visuospatial divided attention; in task conditions in which the duration of target stimuli was varied from trial to trial, homozygous Brattleboro rats showed a performance phenotype that consisted of more accurate responding for longer duration, and less accurate responding for briefer duration, target stimuli. No differences in response times were measured. Further experiments revealed that two separate processes produced this complex phenotype: a relatively slowed period of attentional engagement ( resulting in compromised detection of fast onset-fast offset stimuli) that only partially masks a generally more accurate pattern of responding. These results, taken with earlier data, indicate that vasopressin plays a critical role in regulating visual attention and cognition, either directly, or via early alterations in neurodevelopment. C1 Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA. RP Jentsch, JD (reprint author), Univ Calif Los Angeles, Dept Psychol, POB 951563, Los Angeles, CA 90095 USA. 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It has been suggested that thimerosal, a mercury-containing preservative in vaccines, is a risk factor for the development of autism. We examined whether discontinuing the use of thimerosal-containing vaccines in Denmark led to a decrease in the incidence of autism. Design. Analysis of data from the Danish Psychiatric Central Research Register recording all psychiatric admissions since 1971, and all outpatient contacts in psychiatric departments in Denmark since 1995. Patients. All children between 2 and 10 years old who were diagnosed with autism during the period from 1971-2000. Outcome Measures. Annual and age-specific incidence for first day of first recorded admission with a diagnosis of autism in children between 2 and 10 years old. Results. A total of 956 children with a male-to-female ratio of 3.5:1 had been diagnosed with autism during the period from 1971-2000. There was no trend toward an increase in the incidence of autism during that period when thimerosal was used in Denmark, up through 1990. From 1991 until 2000 the incidence increased and continued to rise after the removal of thimerosal from vaccines, including increases among children born after the discontinuation of thimerosal. Conclusions. The discontinuation of thimerosal-containing vaccines in Denmark in 1992 was followed by an increase in the incidence of autism. Our ecological data do not support a correlation between thimerosal-containing vaccines and the incidence of autism. C1 Aarhus Univ, Dept Epidemiol & Social Med, Danish Epidemiol Sci Ctr, DK-8000 Aarhus, Denmark. Psychiat Hosp Aarhus, Dept Psychiat demog, Inst Basic Psychiat Res, Risskov, Denmark. Univ Aarhus, Natl Ctr Register Based Res, Aarhus, Denmark. State Serum Inst, Dept Med, Copenhagen, Denmark. RP Madsen, KM (reprint author), Aarhus Univ, Dept Epidemiol & Social Med, Danish Epidemiol Sci Ctr, DK-8000 Aarhus, Denmark. 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Based on these findings a psychoeducational group parent training, which, focused on (1) addressing issues of nature, etiology, treatment and family-related consequences of autism (2) teaching child management and education skills was developed, and the training outcomes were evaluated within a 3-months-follow-up design. A total of 24 parents of 23 autistic children (mean age: 9 yrs.) participated in the center-based training program which was performed in three small groups in different areas of Germany in 3 one-day sessions succeeding in 1-month-intervals. The outcome variables included: (a) group training assessments by parents; they evaluated quality of trainer variables, curriculum, and, group atmosphere using a questionnaire format of-bipolar rating scale-items (b) parental,3-months-follow-up assessments of the-effects of group training on parent-child interactions and family adaptation, using a questionnaire based on rating scales, and a semi-structured questionnaire on training-related child and parent behaviors in the family. The parent training resulted in (a) a high degree of parent satisfaction with the training format and (b) positive effects on daily parent-child interactions from the perspective of parents. These findings provide some evidence for both clinical and social validity:of the parent training procedure examined in this study. C1 Univ Hamburg, Fachbereich Psychol, D-20146 Hamburg, Germany. RP Probst, P (reprint author), Univ Hamburg, Fachbereich Psychol, Von Melle Pk 5, D-20146 Hamburg, Germany. 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Kinderpsychol. Kinderpsychiatr. PD SEP PY 2003 VL 52 IS 7 BP 473 EP 490 PG 18 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 720VQ UT WOS:000185280900001 PM 14526758 ER PT J AU Mowry, BJ AF Mowry, BJ TI Psychiatric genetics in Australia SO PSYCHIATRIC GENETICS LA English DT Review DE Australia; alcoholism; anxiety; attention deficit hyperactivity disorder; autism; bipolar disorder; dementia; depression; schizophrenia ID BIPOLAR AFFECTIVE-DISORDER; DEFICIT-HYPERACTIVITY DISORDER; AMYLOID PRECURSOR PROTEIN; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; SEROTONIN TRANSPORTER GENE; ONSET ALZHEIMERS-DISEASE; SUSCEPTIBILITY LOCUS; RECEPTOR GENE; CLOSE LINKAGE; TWIN SAMPLE AB Australian research in psychiatric genetics covers molecular genetic studies of depression, anxiety, alcohol dependence, Alzheimer's disease, bipolar disorder, schizophrenia, autism, and attention deficit hyperactivity disorder. For each disorder, a variety of clinical cohorts have been recruited including affected sib pair families, trios, case/controls, and twins from a large population-based twin registry. These studies are taking place both independently and in collaboration with international groups. Microarray studies now complement DNA investigations, while animal models are in development An Australian government genome facility provides a high throughput genotyping and mutation detection service to the Australian scientific community, enhancing the contribution of Australian psychiatric genetics groups to gene discovery. (C) 2003 Lippincott Williams Wilkins. C1 Univ Queensland, Dept Psychiat, Queensland Ctr Schizophrenia Res, Ctr Mental Hlth, Wacol, Qld 4076, Australia. 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RP Newschaffer, CJ (reprint author), Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Epidemiol, Ctr Autism & Dev Disabil Epidemiol, 615 N Wolfe St,Rm E6142, Baltimore, MD 21205 USA. 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PD SEP-OCT PY 2003 VL 118 IS 5 BP 393 EP 399 DI 10.1016/S0033-3549(04)50270-4 PG 7 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 754AQ UT WOS:000187280900001 PM 12941851 ER PT J AU Rehfeldt, RA Latimore, D Stromer, R AF Rehfeldt, RA Latimore, D Stromer, R TI Observational learning and the formation of classes of reading skills by individuals with autism and other developmental disabilities SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE observational learning; stimulus classes; peer modeling; autism; developmental disabilities ID PEER MODELS; ACQUISITION; CHILDREN; INSTRUCTION; BEHAVIOR AB We investigated whether individuals with developmental disabilities will demonstrate stimulus classes after observing another individual demonstrate the prerequisite conditional discriminations. In Experiment 1, participants learned conditional discriminations among dictated words, pictures, and printed words. They also observed a model without disabilities demonstrate conditional discriminations among a different set of dictated words, pictures, and printed words. The classes assigned to each participant belonged to a larger superordinate category, as did the classes assigned to each model. The superordinate categories were different for participants and models. All participants subsequently demonstrated full stimulus classes with the stimuli involved in direct training: They named pictures, read printed words, and matched pictures and words to one another. However, based on observing a model, none of the participants demonstrated full stimulus classes. In Experiment 2, participants learned conditional discriminations among the stimuli in three sets, and observed a model's training with the stimuli in three different sets. The classes assigned to each participant belonged to the same larger superordinate category as did those assigned to their respective model. All participants subsequently demonstrated full stimulus classes with the stimuli involved in direct training. They also demonstrated full classes with at least one of their model's sets of training stimuli. When full stimulus classes did not occur from observing a model, participants named the model's pictures, read the model's printed words, or matched the model's pictures and words. Stimulus class technology, coupled with the opportunity to observe another individual perform a skill, may be an economical and efficient means of teaching persons with developmental disabilities. (C) 2003 Elsevier Ltd. All rights reserved. C1 So Illinois Univ, Inst Rehabil, Rehabil Serv Program, Carbondale, IL 62901 USA. Univ Nevada, Reno, NV 89557 USA. Trin Serv, Reno, NV USA. Univ Massachusetts, Sch Med, Shriver Ctr, Worcester, MA 01605 USA. RP Rehfeldt, RA (reprint author), So Illinois Univ, Inst Rehabil, Rehabil Serv Program, Mailcode 4609, Carbondale, IL 62901 USA. 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Dev. Disabil. PD SEP-OCT PY 2003 VL 24 IS 5 BP 333 EP 358 DI 10.1016/S0891-4222(03)00059-3 PG 26 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 722BW UT WOS:000185356200002 PM 12951131 ER PT J AU Siegal, M Blades, M AF Siegal, M Blades, M TI Language and auditory processing in autism SO TRENDS IN COGNITIVE SCIENCES LA English DT Review ID INFANTILE-AUTISM; MIND; MECHANISMS; INSIGHTS; CHILDREN AB Autism is characterized by varying degrees of disorders in language, communication and imagination. What are the prospects for making sense of this heterogeneous condition? Advances in identifying phenotypes in relation to subgroups within autism, based on disproportionate language impairment, have been recently reported by Tager-Flusberg and Joseph. The symptom severity of these subgroups requires investigation for underlying deficits, such as in auditory processing. Other recent reports support the view that a deficit in auditory processing might be a key factor in autism. C1 Univ Sheffield, Western Bank, Dept Psychol, Sheffield S10 2TP, S Yorkshire, England. RP Siegal, M (reprint author), Univ Sheffield, Western Bank, Dept Psychol, Sheffield S10 2TP, S Yorkshire, England. 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SCI. PD SEP PY 2003 VL 7 IS 9 BP 378 EP 380 DI 10.1016/S1364-6613(03)00194-3 PG 3 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 722KW UT WOS:000185374800002 ER PT J AU Baron-Cohen, S AF Baron-Cohen, S TI Autism: Explaining the enigma SO TRENDS IN COGNITIVE SCIENCES LA English DT Book Review C1 Univ Cambridge, Autism Res Ctr, Cambridge CB2 3EB, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Autism Res Ctr, Downing St, Cambridge CB2 3EB, England. CR Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Frith U., 2003, AUTISM EXPLAINING EN NR 3 TC 4 Z9 4 PU ELSEVIER SCIENCE LONDON PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1364-6613 J9 TRENDS COGN SCI JI TRENDS COGN. SCI. PD SEP PY 2003 VL 7 IS 9 BP 380 EP 383 DI 10.1016/S1364-6613(03)00188-8 PG 4 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 722KW UT WOS:000185374800003 ER PT J AU Baird, G Cass, H Slonims, V AF Baird, G Cass, H Slonims, V TI Diagnosis of autism SO BRITISH MEDICAL JOURNAL LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; EARLY RECOGNITION; CHILDREN; INTERVIEW; GENETICS C1 Guys & St Thomas NHS Trust, Newcomen Ctr, London SE1 9RT, England. Great Ormond St Hosp Children, London WC1N 3JH, England. RP Baird, G (reprint author), Guys & St Thomas NHS Trust, Newcomen Ctr, London SE1 9RT, England. CR ATTWOOD T, 1988, ASPERGERS SYNDROME G Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Baron-Cohen S., 1993, AUTISM FACTS Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bryson S. 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Med. J. PD AUG 30 PY 2003 VL 327 IS 7413 BP 488 EP 493 DI 10.1136/bmj.327.7413.488 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 717LA UT WOS:000185088900020 PM 12946972 ER PT J AU Hollander, E Phillips, AT Yeh, CC AF Hollander, E Phillips, AT Yeh, CC TI Targeted treatments for symptom domains in child and adolescent autism SO LANCET LA English DT Review ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; OPEN-LABEL; OPEN TRIAL; ADULTS; RISPERIDONE; STRATEGIES AB Context The number of people with autism spectrum disorders has dramatically increased over the past decade, and problem behaviours in autism are an increasing challenge to families, schools, physicians, and other health-care professionals. Pharmacological treatments can effectively target problem behaviours associated with autism. Starting point Recently, L Namerow and colleagues (J Dev Behav Pediatr 2003;, 24: 104-08) presented preliminary data in children and adolescents with autism treated with citalopram, which suggested that selective serotonin-reuptake inhibitors are useful in the reduction of symptom domains such as repetitive behaviours and mood disorders. J McCracken and colleagues (N Engl J Med 2000; 347: 314-21) showed that the atypical antipsychotic risperidone reduced serious behavioural problems, such as tantrums, aggression, or self-injury in children with autism and in children with below-average intelligence quotients. These and other studies show how 1 developments in study, design, selection of patients, and outcome measures have allowed treatment trials in autism to progress beyond anecdotal reports and case observations, and show reduction in the severity of specific symptom domains within these disorders. Where next? In therapeutic intervention the risk of treatment toxicity must be balanced against the benefits of improved symptom severity. The newer methods enable informed decisions about which patients will benefit from which treatments. Other symptom domains within autism and effects on development need to be evaluated in adequately designed clinical trials. Future strategies include extending treatment to children as young as the preschool years. C1 Mt Sinai Sch Med, Dept Psychiat, Seaver & New York Autism Ctr Excellence, New York, NY 10029 USA. RP Hollander, E (reprint author), Mt Sinai Sch Med, Dept Psychiat, Seaver & New York Autism Ctr Excellence, Box 1230,1 Gustave Levy Pl, New York, NY 10029 USA. 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Reported clinical features and genetic findings were used in cytogenetic screenings to estimate the prevalence of the fragile X (fra X) and other chromosomal aberrations in 120 patients with mental retardation, language disorders, attention deficit hyperactivity, or developmental delay, in comparison with 30 healthy children. Data on the clinical, intellectual and behavioral findings in 14 fra X positive children (11.7%) is presented. Ten of the 120 patients (8.3%) had enlargement of the heterochromatin region of chromosome 9. Other chromosomal aberrations and autosomal fragile sites (FS) were also observed. There was a statistically significant difference in the autosomal and X-linked FS between the study and control groups (p<0.05). The tests for the fra X chromosome are likely to be of diagnostic benefit in young children with autism or developmental delay, particularly in speech, and who have large and prominent ears. 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J. PD AUG 30 PY 2003 VL 44 IS 4 BP 583 EP 592 PG 10 WC Medicine, General & Internal SC General & Internal Medicine GA 720ZQ UT WOS:000185292900004 PM 12950112 ER PT J AU Lauritsen, MB Nyegaard, M Betancur, C Colineaux, C Josiassen, TL Kruse, TA Leboyer, M Ewald, H AF Lauritsen, MB Nyegaard, M Betancur, C Colineaux, C Josiassen, TL Kruse, TA Leboyer, M Ewald, H TI Analysis of transmission of novel polymorphisms in the somatostatin receptor 5 (SSTR5) gene in patients with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; polymorphisms; SSTR5; association; TDT ID PERVASIVE DEVELOPMENTAL DISORDERS; GROWTH-HORMONE RESPONSE; TRANSMISSION/DISEQUILIBRIUM TEST; SUMATRIPTAN CHALLENGE; TUBEROUS-SCLEROSIS; GENOMEWIDE SCREEN; FAMILY HISTORY; DOPAMINE; ASSOCIATION; ETIOLOGY AB Infantile autism is a pervasive developmental disorder with a strong genetic component. The mode of inheritance appears to be complex and no specific susceptibility genes have yet been identified. Chromosome 16p13.3 may contain a susceptibility gene based on findings from genome scans and reports of chromosome abnormalities in individuals with autism. The somatostatin receptor 5 (SSTR5) gene is located on chromosome 16p13.3 and is thus a positional candidate gene for autism. SSTR5 may also be a functional candidate gene for autism because somatostatin inhibits growth hormone secretion, and increased growth hormone response has been reported in some individuals with autism. Moreover, the somatostatinergic system interacts with the dopaminergic system, which has been hypothesized to be involved in the etiology of autism; in particular, somatostatin secretion is regulated by dopamine, and the dopamine D2 receptor and the SSTR5 receptor interact to form a receptor complex with enhanced functional activity. In the present study, we tested whether the alleles of twelve new single nucleotide polymorphisms (SNPs) in the SSTR5 gene were preferentially transmitted, using the transmission disequilibrium test (TDT) in a sample of 79 trios with autism (18 from Denmark and 61 from France). Furthermore, we combined four missense SNPs into haplotypes and searched for preferential transmission using the program TRANSMIT. No significant preferential transmission of the alleles and haplotypes of the twelve SNPs was found. Our results do not suggest the SSTR5 gene as a susceptibility gene for autism. (C) 2003 Wiley-Liss, Inc. C1 Aarhus Univ Hosp, Dept Psychiat Demog, Inst Basic Psychiat Res, Psychiat Hosp Aarhus, DK-8240 Risskov, Denmark. Odense Univ Hosp, Dept Clin Biochem & Genet, DK-5000 Odense, Denmark. Fac Med, INSERM, U513, Creteil, France. Hop Robert Debre, Dept Child & Adolescent Psychiat, F-75019 Paris, France. Assistance Publ Hop Paris, Dept Psychiat, Hop Albert Chenevier & Henri Mondor, Creteil, France. Psychiat Hosp Aarhus, Dept Biol Psychiat, Inst Basic Psychiat Res, Risskov, Denmark. RP Lauritsen, MB (reprint author), Aarhus Univ Hosp, Dept Psychiat Demog, Inst Basic Psychiat Res, Psychiat Hosp Aarhus, DK-8240 Risskov, Denmark. 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These species were employed for isotope dilution GC-ICPMS to study uptake and biotransformation of ethylmercury in mice treated with thimerosal, (sodium ethylmercurithiosalicylate) 10 mg L-1 in drinking water ad libitum for 1, 2.5, 6, or 14 days. Prior to analysis, samples were spiked with aqueous solutions of (CH3Hg+)-Hg-200, (C2H5Hg+)-Hg-199, and Hg-201(2+) and then digested in 20% tetramethylammonium hydroxide and extracted at pH 9 with DDTC/toluene. Extracted mercury species were reacted with butylmagnesium chloride to form butylated derivatives. Absolute detection limits for CH3Hg+, C2H5Hg+, and Hg2+ were 0.4, 0.2, and 0.6 pg on the basis of 3sigma of five separate blanks. Up to 9% of the C2H5Hg+ was decomposed to Hg2+ during sample preparation, and it is therefore crucial to use a species-specific internal standard when determining ethylmercury. No demethylation, methylation, or ethylation during sample preparation was detected. The ethylmercury component of thimerosal was rapidly taken up in the organs of the mice (kidney, liver, and mesenterial lymph nodes), and concentrations of C2H5Hg+ as well as Hg2+ increased over the 14 days of thimerosal treatment. This shows that C2H5Hg+ in mice to a large degree is degraded to Hg2+. Increased concentrations of CH3Hg+ were also observed, which was found to be due to impurities in the thimerosal. C1 Umea Univ, Dept Chem, S-90187 Umea, Sweden. Umea Univ, Umea Marine Sci Ctr, S-91020 Hornefors, Sweden. Linkoping Univ, Dept Mol & Clin Med, S-58185 Linkoping, Sweden. RP Qvarnstrom, J (reprint author), Umea Univ, Dept Chem, S-90187 Umea, Sweden. 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PD AUG 5 PY 2003 VL 169 IS 3 BP 224 EP 224 PG 1 WC Medicine, General & Internal SC General & Internal Medicine GA 710TZ UT WOS:000184698700023 ER PT J AU Granon, S Faure, P Changeux, JP AF Granon, S Faure, P Changeux, JP TI Executive and social behaviors under nicotinic receptor regulation SO PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA LA English DT Article ID MEDIAL PREFRONTAL LESIONS; ANTERIOR CINGULATE CORTEX; WORKING-MEMORY; RESPONSE SELECTION; BETA-2 SUBUNIT; RAT; BRAIN; ATTENTION; DEMENTIA; FLEXIBILITY AB Nicotine enhances several cognitive and psychomotor behaviors, and nicotinic antagonists cause impairments in tasks requiring cognitive effort. To explore the contribution of nicotinic receptors to complex cognitive functions, we developed an automated method to investigate sequential locomotor behavior in the mouse and an analysis of social behavior. We show that, in the beta2(-/-)mutant, the high-order spatiotemporal organization of locomotor behavior, together with conflict resolution and social interaction, is selectively dissociated from low-level, more automatic motor behaviors. Such deficits in executive functions resemble the rigid and asocial behavior found in some psychopathological disorders such as autism and attention deficit hyperactivity disorder. C1 Inst Pasteur, CNRS, Dept Neurosci Receptors & Cognit, F-75724 Paris 15, France. RP Changeux, JP (reprint author), Inst Pasteur, CNRS, Dept Neurosci Receptors & Cognit, 25 Rue Dr Roux, F-75724 Paris 15, France. 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PD AUG 5 PY 2003 VL 100 IS 16 BP 9596 EP 9601 DI 10.1073/pnas.1533498100 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 709HP UT WOS:000184620000088 PM 12876201 ER PT J AU DeFelice, ML Ruchelli, ED Markowitz, JE Strogatz, M Reddy, KP Kadivar, K Mulbert, AE Brown, KA AF DeFelice, ML Ruchelli, ED Markowitz, JE Strogatz, M Reddy, KP Kadivar, K Mulbert, AE Brown, KA TI Intestinal cytokines in children with pervasive developmental disorders SO AMERICAN JOURNAL OF GASTROENTEROLOGY LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; LYMPHONODULAR HYPERPLASIA; AUTISM; CELLS; INTERLEUKIN-8; COLON; DIFFERENTIATION; PROTEIN; COLITIS; MUCOSA AB OBJECTIVE: A relationship between autism and gastrointestinal (GI) immune dysregulation has been postulated based on incidence of GI complaints as well as macroscopically observed lymphonodular hyperplasia and microscopically determined enterocolitis in pediatric patients with autism. To evaluate GI immunity, we quantitatively assessed levels of proinflammatory cytokines, interleukin (IL)-6, IL-8, and IL-1beta, produced by intestinal biopsies of children with pervasive developmental disorders. METHODS: Fifteen patients, six with pervasive developmental disorders and nine age-matched controls, presenting for C, diagnostic colonoscopy were enrolled. Endoscopic biopsies were organ cultured, supernatants were harvested, and IL-6, IL-8, and IL-1beta levels were quantified by ELISA. Tissue histology was evaluated by blinded pathologists. RESULTS: Concentrations of IL-6 from intestinal organ culture supernatants of patients with pervasive developmental disorders (median 318.5 pg/ml, interquartile range 282.0-393.0 pg/ml) when compared with controls (median 436.9 pg/ml, interquartile range 312.6-602.5 pg/ml) were not significantly different (p = 0.0987). Concentrations of IL-8 (median 84,000 pg/ml, interquartile range 16,000-143,000 pg/ml) when compared with controls (median 177,000 pg/ ml, interquartile range 114,000-244,000 pg/ml) were not significantly different (p = 0.0707). Concentrations of IL-1beta (median 0.0 pg/ml, interquartile range 0.0-94.7 pg/ ml) when compared with controls (median 0.0 pg/ml, interquartile range 0.0-60.2 pg/ml) were not significantly different (p = 0.8826). Tissue histology was nonpathological for all patients. CONCLUSIONS: We have demonstrated no significant difference in production of IL-6, IL-8, and IL-1beta between patients with pervasive developmental disorders and age-matched controls. In general, intestinal levels of IL-6 and IL-8 were lower in patients with pervasive developmental disorders than in age-matched controls. These data fail to support an association between autism and GI inflammation. C1 Childrens Hosp Philadelphia, Div Gastroenterol & Nutr, Philadelphia, PA 19104 USA. 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RI Steiner, Carlos/B-9319-2014 OI Steiner, Carlos/0000-0001-5148-3063 CR Fidler DJ, 2000, DEV MED CHILD NEUROL, V42, P737, DOI 10.1017/S0012162200001365 GILLBERG C, 1988, J CHILD PSYCHOL PSYC, V29, P257, DOI 10.1111/j.1469-7610.1988.tb00714.x MINSHEW NJ, 1991, PEDIATRICS, V87, P774 Orstavik KH, 1997, J MED GENET, V34, P849, DOI 10.1136/jmg.34.10.849 NR 4 TC 4 Z9 4 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 A JI Am. J. Med. Genet. A PD AUG 1 PY 2003 VL 120A IS 4 BP 564 EP 565 DI 10.1002/ajmg.a.20032 PG 2 WC Genetics & Heredity SC Genetics & Heredity GA 707NG UT WOS:000184516300021 PM 12884441 ER PT J AU Thomas, NS Roberts, SE Browne, CE AF Thomas, NS Roberts, SE Browne, CE TI Estimate of the prevalence of chromosome 15q11-q13 duplications SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Letter ID PROXIMAL 15Q DUPLICATION; INTERSTITIAL DUPLICATIONS; TRIPLICATIONS; PROBANDS; AUTISM C1 Salisbury Dist Hosp, Wessex Reg Genet Lab, Salisbury SP2 8BJ, Wilts, England. Univ Southampton, Southampton, Hants, England. Salisbury Dist Hosp, Wessex Reg Genet Lab, Salisbury, Wilts, England. RP Thomas, NS (reprint author), Salisbury Dist Hosp, Wessex Reg Genet Lab, Salisbury SP2 8BJ, Wilts, England. CR Barber JCK, 1998, HUM GENET, V103, P600, DOI 10.1007/s004390050875 BLENNOW E, 1995, AM J MED GENET, V55, P85, DOI 10.1002/ajmg.1320550122 Bolton PF, 2001, AM J MED GENET, V105, P675, DOI 10.1002/ajmg.1551 Browne CE, 1997, AM J HUM GENET, V61, P1342, DOI 10.1086/301624 BUCKTON KE, 1985, HUM GENET, V69, P353, DOI 10.1007/BF00291656 Cook EH, 1997, AM J HUM GENET, V60, P928 Jacobsen J, 1998, J MED GENET, V35, P534, DOI 10.1136/jmg.35.7.534 Moeschler JB, 2002, AM J MED GENET, V111, P440, DOI 10.1002/ajmg.10419 Roberts SE, 2002, HUM GENET, V110, P227, DOI 10.1007/s00439-001-0678-6 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 Torrisi L, 2001, AM J MED GENET, V106, P125, DOI 10.1002/ajmg.1570 WANG CH, 1998, AM J HUM GENET, V63, pA344 NR 12 TC 8 Z9 8 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 A JI Am. J. Med. Genet. A PD AUG 1 PY 2003 VL 120A IS 4 BP 596 EP 598 DI 10.1002/ajmg.a.20140 PG 3 WC Genetics & Heredity SC Genetics & Heredity GA 707NG UT WOS:000184516300027 PM 12884447 ER PT J AU Stehr-Green, P Tull, P Stellfeld, M Mortenson, PB Simpson, D AF Stehr-Green, P Tull, P Stellfeld, M Mortenson, PB Simpson, D TI Autism and thimerosal-containing vaccines - Lack of consistent evidence for an association SO AMERICAN JOURNAL OF PREVENTIVE MEDICINE LA English DT Article ID CHILDREN AB Background: In 1999, concerns were raised that vaccines containing the preservative Thimerosal(TM) might increase the risk of autism and/or other neurodevelopmental disorders. Methods: Between the mid-1980s through the late-1990s, we compared the prevalence/incidence of autism in California, Sweden, and Denmark with average exposures to Thimerosal-containing vaccines. Graphic ecologic analyses were used to examine population-based data from the United States (national immunization coverage surveys and counts of children diagnosed with autism-like disorders seeking special education services in California); Sweden (national inpatient data on autism cases, national vaccination coverage levels, and information on use of all vaccines and vaccine-specific amounts of Thimerosal); and Denmark (national registry of inpatient/ outpatient-diagnosed autism cases, national vaccination coverage levels, and information on use of all vaccines and vaccine-specific amounts of Thimerosal). Results: In all three countries, the incidence and prevalence of autism-like disorders began to rise in the 1985-1989 period, and the rate of increase accelerated in the early 1990s. However, in contrast to the situation in the United States, where the average Thimerosal dose from vaccines increased throughout the 1990s, Thimerosal exposures from vaccines in both Sweden and Denmark-already low throughout the 1970s and 1980s-began to decrease in the late 1980s and were eliminated in the early 1990s. Conclusions: The body of existing data, including the ecologic data presented herein, is not consistent with the hypothesis that increased exposure to Thimerosal-containing vaccines is responsible for the apparent increase in the rates of autism in young children being observed worldwide. C1 Univ Washington, Dept Epidemiol, Sch Publ Hlth & Community Med, Seattle, WA 98195 USA. Natl Board Hlth & Welf, Stockholm, Sweden. Natl Ctr Register Based Res, Aarhus, Denmark. Statens Serum Inst, DK-2300 Copenhagen, Denmark. Ctr Dis Control & Prevent, Natl Immunizat Program, Atlanta, GA 30333 USA. RP Simpson, D (reprint author), Ctr Dis Control & Prevent, Natl Immunizat Program, 1600 Clifton Rd,Mailstop E-62, Atlanta, GA 30333 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Ball LK, 2001, PEDIATRICS, V107, P1147, DOI 10.1542/peds.107.5.1147 BLAXILL M, 2001, I MED THIMEROSAL COU, P49 *CAL DEP DEV SERV, 1999, CHANG POP PERS AUT P GILLBERG C, 1984, J CHILD PSYCHOL PSYC, V25, P35, DOI 10.1111/j.1469-7610.1984.tb01717.x GILLBERG C, 1991, BRIT J PSYCHIAT, V158, P403, DOI 10.1192/bjp.158.3.403 Grandjean P, 1997, NEUROTOXICOL TERATOL, V19, P417, DOI 10.1016/S0892-0362(97)00097-4 Institute of Medicine, 2001, THIM CONT VACC NEUR MADSEN KM, 2003, IN PRESS PEDIATRICS MORGENSTERN H, 1982, AM J PUBLIC HEALTH, V72, P1336, DOI 10.2105/AJPH.72.12.1336 Nordin V, 1996, DEV MED CHILD NEUROL, V38, P297 NR 11 TC 85 Z9 90 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0749-3797 J9 AM J PREV MED JI Am. J. Prev. Med. PD AUG PY 2003 VL 25 IS 2 BP 101 EP 106 DI 10.1016/S0749-3797(03)00113-2 PG 6 WC Public, Environmental & Occupational Health; Medicine, General & Internal SC Public, Environmental & Occupational Health; General & Internal Medicine GA 703TC UT WOS:000184296200004 PM 12880876 ER PT J AU Hall, GBC Szechtman, H Nahmias, C AF Hall, GBC Szechtman, H Nahmias, C TI Enhanced salience and emotion recognition in autism: A PET study SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID CROSSMODAL BINDING; CHILDREN; EXPRESSIONS; BEHAVIOR; CORTEX; FACE AB objective: This study examined neural activation of facial stimuli in autism when the salience of emotional cues was increased by prosodic information. Method: Regional cerebral blood flow (rCBF) was measured while eight high-functioning men with autism and eight men without autism performed an emotion-recognition task in which facial emotion stimuli were matched with prosodic voices and a baseline gender-recognition task. Results: Emotion processing in autistic subjects, compared to that in comparison subjects, resulted in lower rCBF in the inferior frontal and fusiform areas and higher rCBF in the right anterior temporal pole, the anterior cingulate, and the thalamus. Conclusions: Even with the enhanced emotional salience of facial stimuli, adults with autism showed lower activity in the fusiform cortex and differed from the comparison subjects in activation of other brain regions. The authors suggested that the recognition of emotion by adults with autism is achieved through recruitment of brain regions concerned with allocation of attention, sensory gating, the referencing of perceptual knowledge, and categorization. C1 St Josephs Healthcare Hamilton, Brain Body Inst, Hamilton, ON L8N 4A6, Canada. McMaster Univ, Dept Psychiat & Behav Neurosci, Hamilton, ON L8S 4L8, Canada. RP Hall, GBC (reprint author), St Josephs Healthcare Hamilton, Brain Body Inst, 314 Martha Wing,50 Charlton Ave E, Hamilton, ON L8N 4A6, Canada. RI Szechtman, Henry/A-4706-2009 OI Szechtman, Henry/0000-0003-3986-4482 CR Anderson AK, 1998, NEUROREPORT, V9, P3607 Baron-Cohen S, 1999, EUR J NEUROSCI, V11, P1891, DOI 10.1046/j.1460-9568.1999.00621.x Brown L., 1990, TEST NONVERBAL INTEL Calvert GA, 2000, CURR BIOL, V10, P649, DOI 10.1016/S0960-9822(00)00513-3 Calvert GA, 1999, NEUROREPORT, V10, P2619, DOI 10.1097/00001756-199908200-00033 CAPPS L, 1992, J CHILD PSYCHOL PSYC, V33, P1169, DOI 10.1111/j.1469-7610.1992.tb00936.x Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 DEVINSKY O, 1995, BRAIN, V118, P279, DOI 10.1093/brain/118.1.279 Dubois S, 1999, NEUROIMAGE, V9, P278, DOI 10.1006/nimg.1998.0409 Ekman P., 1976, PICTURES FACIAL AFFE HOBSON RP, 1988, BRIT J PSYCHOL, V79, P441 Moore CJ, 1999, BRAIN, V122, P943, DOI 10.1093/brain/122.5.943 OLDFIELD RC, 1971, NEUROPSYCHOLOGIA, V9, P97, DOI 10.1016/0028-3932(71)90067-4 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 *SPM, 1999, 99 SPM U COLL I NEUR *U CALG DEP PSYCH, 1992, SAINSB BUTL FAC REC VANLANCKER D, 1989, DEV NEUROPSYCHOL, V5, P207 WEEKS SJ, 1987, J CHILD PSYCHOL PSYC, V28, P137, DOI 10.1111/j.1469-7610.1987.tb00658.x Woods R. P., 1996, NEUROIMAGE, V4, P84 NR 19 TC 98 Z9 101 PU AMER PSYCHIATRIC PRESS, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD AUG PY 2003 VL 160 IS 8 BP 1439 EP 1441 DI 10.1176/appi.ajp.160.8.1439 PG 3 WC Psychiatry SC Psychiatry GA 708AK UT WOS:000184543700013 PM 12900306 ER PT J AU Condouris, K Meyer, E Tager-Flusberg, H AF Condouris, K Meyer, E Tager-Flusberg, H TI The relationship between standardized measures of language and measures of spontaneous speech in children with autism SO AMERICAN JOURNAL OF SPEECH-LANGUAGE PATHOLOGY LA English DT Article DE autism; spontaneous speech measures; standardized language tests; MLU; NDWR ID UTTERANCE LENGTH; PRESCHOOL-CHILDREN; IMPAIRMENT; AGE; SUBGROUPS; DISORDERS; VALIDITY; OUTCOMES; DEFICITS; SYNTAX AB This study investigated the relationship between scores on standardized tests (Clinical Evaluation of Language Fundamentals [CELF], Peabody Picture Vocabulary Test-Third Edition [PPVT-III], and Expressive Vocabulary Test) and measures of spontaneous speech (mean length of utterance [MLU], Index of Productive Syntax, and number of different word roots [NDWR]) derived from-natural language samples obtained from 44 children with autism between the ages of 4 and 14 years old. The children with autism were impaired across both groups of measures. The two groups of measures were significantly correlated, and specific relationships were found between lexical-semantic measures (NDWR, vocabulary tests; and the CELF lexical-semantic subtests) and grammatical measures (MLU, and CELF grammar subtests), suggesting that both standardized and spontaneous speech measures tap the same underlying linguistic abilities in children with autism. These findings have important implications for clinicians and researchers who depend on these types of language measures for diagnostic purposes, assessment, and investigations of language impairments in autism. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. Univ N Carolina, Div TEACH, Chapel Hill, NC 27515 USA. RP Tager-Flusberg, H (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St,L-814, Boston, MA 02118 USA. RI Tager-Flusberg, Helen/D-5265-2009 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bornstein MH, 1998, CHILD DEV, V69, P654, DOI 10.2307/1132196 Botting N, 1997, EUR J DISORDER COMM, V32, P317 BROWN R, 1973, 1 LANGUAGE EARLY CANTWELL D, 1978, J CHILD PSYCHOL PSYC, V19, P351, DOI 10.1111/j.1469-7610.1978.tb00481.x Chapman R., 2000, SYSTEMATIC ANAL LANG Conti-Ramsden G, 2001, INT J LANG COMM DIS, V36, P207, DOI 10.1080/13682820010019883 Craig HK, 2000, J SPEECH LANG HEAR R, V43, P366 Dollaghan CA, 1999, J SPEECH LANG HEAR R, V42, P1432 Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd Dunn M, 1996, J SPEECH HEAR RES, V39, P643 Elliott C. D., 1990, DIFFERENTIAL ABILITY Evans JL, 1996, J SPEECH HEAR RES, V39, P655 Goffman L, 2000, AM J SPEECH-LANG PAT, V9, P151 Kjelgaard MM, 2001, LANG COGNITIVE PROC, V16, P287 KLEE T, 1989, J SPEECH HEAR DISORD, V54, P226 KLEE T, 1992, TOP LANG DISORD, V12, P28 Koegel LK, 1997, J AUTISM DEV DISORD, V27, P233, DOI 10.1023/A:1025894213424 Lord C., 1997, HDB AUTISM PERVASIVE, P195 Lord C, 1996, J AM ACAD CHILD PSY, V35, P1542, DOI 10.1097/00004583-199611000-00024 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 MILLER JF, 1991, RESEARCH ON CHILD LANGUAGE DISORDERS : A DECADE OF PROGRESS, P211 PAUL R, 1985, J SPEECH HEAR RES, V28, P475 Rescorla L, 1997, J SPEECH LANG HEAR R, V40, P556 Restrepo MA, 1998, J SPEECH LANG HEAR R, V41, P1398 Rollins P. R., 1996, 1 LANGUAGE, V16, P243, DOI 10.1177/014272379601604705 RONDAL JA, 1988, AM J MENT RETARD, V93, P64 RONDAL JA, 1987, J CHILD LANG, V14, P433 SCARBOROUGH H, 1986, J SPEECH HEAR RES, V29, P394 SCARBOROUGH HS, 1990, APPL PSYCHOLINGUIST, V11, P1, DOI 10.1017/S0142716400008262 SCARBOROUGH HS, 1991, APPL PSYCHOLINGUIST, V12, P23, DOI 10.1017/S014271640000936X Semel E, 1995, CLIN EVALUATION LANG, V3rd Sparrow SS, 1997, HDB AUTISM PERVASIVE, P411 Stevens MC, 2000, J AM ACAD CHILD PSY, V39, P346, DOI 10.1097/00004583-200003000-00017 TAGERFLUSBERG H, 1991, J CHILD PSYCHOL PSYC, V32, P1123, DOI 10.1111/j.1469-7610.1991.tb00353.x Tager-Flusberg H, 2000, METHODS FOR STUDYING LANGUAGE PRODUCTION, P313 TAGERFLUSBERG H, 1994, CONSTRAINTS LANGUAGE Tager-Flusberg Helen, 2000, INT REV RES MENT RET, P185 Ukrainetz T. A., 2002, CHILD LANG TEACH THE, V18, P59, DOI DOI 10.1191/0265659002CT227OA WATKINS RV, 1995, J SPEECH HEAR RES, V38, P1349 Wiig E. H., 1992, CLIN EVALUATION LANG Wilkinson KM, 1998, MENT RETARD DEV D R, V4, P73, DOI 10.1002/(SICI)1098-2779(1998)4:2<73::AID-MRDD3>3.0.CO;2-Y Williams K. T., 1997, EXPRESSIVE VOCABULAR NR 44 TC 48 Z9 52 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 1058-0360 J9 AM J SPEECH-LANG PAT JI Am. J. Speech-Lang. Pathol. PD AUG PY 2003 VL 12 IS 3 BP 349 EP 358 DI 10.1044/1058-0360(2003/080) PG 10 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 714HF UT WOS:000184906700010 PM 12971823 ER PT J AU Lingam, R Simmons, A Andrews, N Miller, E Stowe, J Taylor, B AF Lingam, R Simmons, A Andrews, N Miller, E Stowe, J Taylor, B TI Prevalence of autism and parentally reported triggers in a north east London population SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID DEVELOPMENTAL REGRESSION; CHILDREN; VACCINATION; DISORDER; MEASLES; MUMPS; MMR AB Background: The recorded prevalence of autistic spectrum disorders has risen over recent decades. Measles, mumps and rubella (MMR) vaccine has been blamed, by causing a "new variant" form of "regressive autism" associated with "autistic enterocolitis". Aims: To estimate the prevalence of autism and to assess any changes in parental perception regarding the onset or causes of autism. Methods and Results: A total of 567 children with autistic spectrum disorder in five districts in north east London were identified, born 1979 - 98. Reported autism, excluding the 94 cases of Asperger's syndrome, increased by year of birth until 1992, since when prevalence has plateaued. This flattening off persisted after allowing for expected delay in diagnosis in more recent birth cohorts. The age at diagnosis of autistic spectrum disorder was estimated to have decreased per five year period since 1983, by 8.7% for childhood autism and by 11.0% for atypical autism. There was some evidence that MMR was more likely to be mentioned as a trigger after August 1997 than before. Conclusions: The prevalence of autism, which was apparently rising from 1979 to 1992, reached a plateau from 1992 to 1996 at a rate of some 2.6 per 1000 live births. This levelling off, together with the reducing age at diagnosis, suggests that the earlier recorded rise in prevalence was not a real increase but was likely due to factors such as increased recognition, a greater willingness on the part of educationalists and families to accept the diagnostic label, and better recording systems. The proportion of parents attributing their child's autism to MMR appears to have increased since August 1997. C1 UCL, Royal Free & Univ Coll Med Sch, Dept Paediat & Child Hlth, Ctr Community Child Hlth, London NW3 2PF, England. Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Immunisat Div, London NW9 5EQ, England. Publ Hlth Lab Serv, Stat Unit, London NW9 5EQ, England. RP Taylor, B (reprint author), UCL, Royal Free & Univ Coll Med Sch, Dept Paediat & Child Hlth, Ctr Community Child Hlth, Royal Free Campus, London NW3 2PF, England. EM b.taylor@rfc.ucl.ac.uk CR Andrews N, 2002, ARCH DIS CHILD, V87, P493, DOI 10.1136/adc.87.6.493 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Committee on Safety of Medicines, 1999, CURRENT PROBLEMS PHA, V25, P9 Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 FOMBONNE E, 2001, PEDIATRICS, V108, DOI UNSP E582001A Fombonne E, 2001, PEDIATRICS, V107, P411, DOI 10.1542/peds.107.2.411 Gillberg C, 1999, ACTA PSYCHIAT SCAND, V99, P399, DOI 10.1111/j.1600-0447.1999.tb00984.x GILLBERG C, 2000, AUTISM, V4, P1 Halsey NA, 2001, PEDIATRICS, V107, P1 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 Taylor B, 1999, LANCET, V354, P950 Taylor B, 2002, BRIT MED J, V324, P393, DOI 10.1136/bmj.324.7334.393 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 1997, PULSE 0802 NR 16 TC 66 Z9 69 PU B M J PUBLISHING GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD AUG 1 PY 2003 VL 88 IS 8 BP 666 EP 670 DI 10.1136/adc.88.8.666 PG 5 WC Pediatrics SC Pediatrics GA 704BC UT WOS:000184317000007 PM 12876158 ER PT J AU Levy, SE Souders, MC Wray, J Jawad, AF Gallagher, PR Coplan, J Belchic, JK Gerdes, M Mitchell, R Mulberg, AE AF Levy, SE Souders, MC Wray, J Jawad, AF Gallagher, PR Coplan, J Belchic, JK Gerdes, M Mitchell, R Mulberg, AE TI Children with autistic spectrum disorders. I: Comparison of placebo and single dose of human synthetic secretin SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID CONTROLLED TRIAL; YOUNG-CHILDREN; DOUBLE-BLIND; RAT AB Aims: To examine the effect of a single dose of human synthetic secretin (HSS) on behaviour and communication in children with autism spectrum disorder (ASD) using an objective measure of communication and social reciprocity and standardised rating scales. Methods: Randomised, crossover, double blind, and placebo controlled trial of a single intravenous dose of human synthetic secretin (HSS) 2 CU/kg. The 62 subjects ( 3 - 8 years) were assigned to group 1 ( saline placebo/HSS) or group 2 (HSS/saline placebo). Diagnosis was confirmed by ADI-R ( Autism Diagnostic Interview - Revised) algorithm. Severity of symptoms was rated using the CARS ( Childhood Autism Rating Scale). Outcome measures included Communication and Symbolic Behavior Scale ( CSBS), Ritvo Real-life Rating Scale, weekly Global Rating Scale ( GBRS) by parents and teachers, and daily log of gastrointestinal symptoms. The communication subscale of the CSBS, specifying communication function, reciprocity, and social-affective signalling was videotaped and scored by a blinded, trained observer. Results: Sixty one children completed the study. After randomisation, there were no significant differences in gender, race, age, and parent and teacher GBRS and Ritvo Scale between the two groups. Compared with placebo, secretin treatment was not associated with significant improvement of CSBS standard scores from baseline to 2 or 4 weeks post-infusion. Five children showed clinical improvement in standard scores: two after HSS and three after placebo. There were no significant changes in gastrointestinal symptoms after HSS or saline placebo. Conclusions: A single dose of intravenous human secretin is not effective in changing behaviour and communication in children with ASD when compared to placebo. C1 Childrens Hosp Philadelphia, Childrens Seashore House, Div Child Dev & Rehabil, Philadelphia, PA 19104 USA. Princess Margaret Hosp, State Child Dev Ctr, Perth, Australia. Childrens Hosp Philadelphia, Div Biostat & Epidemiol, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Div Gen Pediat, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Div Gastroenterol & Nutr, Philadelphia, PA 19104 USA. RP Levy, SE (reprint author), Childrens Hosp Philadelphia, Childrens Seashore House, Div Child Dev & Rehabil, 3405 Civic Ctr Blvd, Philadelphia, PA 19104 USA. CR [Anonymous], 1994, DIAGNOSTIC STAT MANU Barton M, 1998, J AUTISM DEV DISORD, V28, P273, DOI 10.1023/A:1026052417561 Bristol MM, 1996, J AUTISM DEV DISORD, V26, P121, DOI 10.1007/BF02172002 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 Coniglio SJ, 2001, J PEDIATR-US, V138, P649, DOI 10.1067/mpd.2001.112474 Coplan J, 2003, ARCH DIS CHILD, V88, P737, DOI 10.1136/adc.88.8.737 Corbett B, 2001, CLIN PEDIATR, V40, P327, DOI 10.1177/000992280104000604 Dunn-Geier J, 2000, DEV MED CHILD NEUROL, V42, P796 Elliott GR, 2001, PEDIATRICS, V108, pE90, DOI 10.1542/peds.108.5.e90 Fombonne E, 1999, PSYCHOL MED, V29, P769, DOI 10.1017/S0033291799008508 FREEMAN BJ, 1986, J AM ACAD CHILD PSY, V25, P130, DOI 10.1016/S0002-7138(09)60610-5 Gillberg C, 1996, DEV MED CHILD NEUROL, V38, P191 Herlihy WC, 2000, NEW ENGL J MED, V342, P1217 Horvath K, 1999, J PEDIATR-US, V135, P559, DOI 10.1016/S0022-3476(99)70052-1 HORVATH K, 1998, J ASS ACAD MINOR PHY, V1, P9 Horvath K, 2000, NEW ENGL J MED, V342, P1216 Hurth J, 1999, INFANT YOUNG CHILD, V12, P17 Krug DA, 1993, AUTISM SCREENING INS LAMERS CB, 1981, J CLIN GASTROENTEROL, V3, P255, DOI 10.1097/00004836-198109000-00009 Lamson D W, 2001, Altern Med Rev, V6, P311 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 OWLEY T, 1999, DOUBLE BLIND PLACEBO Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 Rimland B, 2000, J AUTISM DEV DISORD, V30, P95, DOI 10.1023/A:1005447203394 Roberts W., 2001, PEDIATRICS, V107, P71 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 Sandler AD, 2000, J DEV BEHAV PEDIATR, V21, P347 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 SAS Publishing, 2000, SAS STAT USERS GUIDE Schopler E., 1988, CHILDHOOD AUTISM RAT SCHUTT C, 1998, NEWSLETT NAT ALLIANC, V4, P21 Sparrow S, 1984, VINELAND ADAPTIVE BE Wetherby A., 1993, COMMUNICATION SYMBOL 1908, ED CHILDREN AUTISM NR 38 TC 25 Z9 25 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD AUG 1 PY 2003 VL 88 IS 8 BP 731 EP 736 DI 10.1136/adc.88.8.731 PG 6 WC Pediatrics SC Pediatrics GA 704BC UT WOS:000184317000024 PM 12876177 ER PT J AU Coplan, J Souders, MC Mulberg, AE Belchic, JK Wray, J Jawad, AF Gallagher, PR Mitchell, R Gerdes, M Levy, SE AF Coplan, J Souders, MC Mulberg, AE Belchic, JK Wray, J Jawad, AF Gallagher, PR Mitchell, R Gerdes, M Levy, SE TI Children with autistic spectrum disorders. II: Parents are unable to distinguish secretin from placebo under double-blind conditions SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article AB Background: Standardised measures of behaviour have failed to detect short term improvement in children with autism following treatment with secretin. However, it is possible that standardised measures are insensitive to dimensions of child behaviour that are nonetheless detectable by parents. Aim: To determine the ability of parents of children with autism to guess, under double blind conditions, whether their child had received secretin or placebo. Methods: 2 x 2 crossover randomised blinded study, comparing the effect of synthetic human secretin 2 U/kg to placebo ( saline). Sixty two children with autism ( aged 43 - 103 months) were randomly allocated to two groups: group 1 received placebo, followed six weeks later by secretin, and group 2 received secretin followed by placebo. At the conclusion of the study, parents were asked to guess their child's group assignment. Results: Twenty seven families guessed their child's group assignment correctly and 27 guessed incorrectly. In 48 instances, parents based their guess on perceived improvement; in six cases, parents based their guess on perceived deterioration. Six families saw no difference after either infusion, and offered no guess. One family dropped out after the first infusion, and one family was lost to follow up after the second infusion. Conclusion: In a controlled setting, parents of young children with autism are unable to distinguish the short term behavioural effects of secretin from placebo. C1 Childrens Hosp Philadelphia, Childrens Seashore House, Div Child Dev & Rehabil, Philadelphia, PA 19104 USA. Princess Margaret Hosp, State Child Dev Ctr, Perth, Australia. Childrens Hosp Philadelphia, Div Biostat & Epidemiol, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Div Gen Pediat, Philadelphia, PA 19104 USA. Childrens Hosp Philadelphia, Div Gastroenterol & Nutr, Philadelphia, PA 19104 USA. RP Levy, SE (reprint author), Childrens Hosp Philadelphia, Childrens Seashore House, Div Child Dev & Rehabil, 3405 Civic Ctr Blvd, Philadelphia, PA 19104 USA. CR COPLAN J, 2000, PEDIATRICS, V105, P65 Levy SE, 2003, ARCH DIS CHILD, V88, P731, DOI 10.1136/adc.88.8.731 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 NR 3 TC 17 Z9 17 PU BRITISH MED JOURNAL PUBL GROUP PI LONDON PA BRITISH MED ASSOC HOUSE, TAVISTOCK SQUARE, LONDON WC1H 9JR, ENGLAND SN 0003-9888 J9 ARCH DIS CHILD JI Arch. Dis. Child. PD AUG 1 PY 2003 VL 88 IS 8 BP 737 EP 739 DI 10.1136/adc.88.8.737 PG 3 WC Pediatrics SC Pediatrics GA 704BC UT WOS:000184317000025 PM 12876178 ER PT J AU Brosius, J AF Brosius, J TI From Eden to a hell of uniformity? Directed evolution in humans SO BIOESSAYS LA English DT Editorial Material ID COGNITIVE PHENOTYPE; HIV-1 INFECTION; NOVELTY SEEKING; KNOCKOUT MICE; GENE; AUTISM; GENOME; BEHAVIOR; DISEASE; SCHIZOPHRENIA AB For the first time during evolution of life on this planet, a species has acquired the ability to direct its own genetic destiny. Following 200,000 years of evolution, modern man now has the technologies not only to eradicate genetic disease but also to prolong life and enhance desired physical and mental traits. These technologies include preimplantation diagnosis, cloning, and gene therapy in the germline on native chromosomes or by adding artificial ones. At first glance, we should all be in favor of eliminating genetic diseases and enhancing genetic traits. Evolutionary considerations, however, uncover hidden dangers and suggest caution against the total embracement of such actions. The first major concern is that the genome will never be a completely reliable crystal ball for predicting human phenotypes. This is especially true for predictions concerning the performance of alleles in future generations whose populations might be subjected to different environmental and social challenges. The second, and perhaps more important, concern is that the end result of germline intervention and genetic enhancement will likely lead to the impoverishment of gene variants in the human population and deprive us of one of our most valued assets for survival in the future, our genetic diversity. (C) 2003 Wiley Periodicals, Inc. C1 Univ Munster, Inst Expt Pathol, ZMBE, D-4400 Munster, Germany. RP Brosius, J (reprint author), Univ Munster, Inst Expt Pathol, ZMBE, Von Esmarch Str 56, D-4400 Munster, Germany. 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Participants were 17 high-ability adolescents with autistic disorder (16-24 years), 24 typically developing children (9-10 years) and 16 adults (18-33 years). In Experiment 1, a normal inversion effect was found for the adolescents with autism in a standard face recognition paradigm with reduced memory demands, except for a subgroup with low social intelligence who were not better in recognizing upright relative to inverted photographs of faces. In Experiment 2, the group with autism did not show the composite effect like the adult group did: they recognized face halves as well in aligned composite faces as in non-aligned composite faces. The results on the inversion task suggest that most adolescents with autism form a normal configuration-based face representation, but the absence of the composite effect indicates that they are less prone to use the contextual information of the face in a visual-search task. (C) 2003 Elsevier Science (USA). All rights reserved. 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PD AUG PY 2003 VL 52 IS 3 BP 285 EP 294 DI 10.1016/S0278-2626(03)00042-3 PG 10 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 712MA UT WOS:000184800400001 PM 12907173 ER PT J AU Senju, A Yaguchi, K Tojo, Y Hasegawa, T AF Senju, A Yaguchi, K Tojo, Y Hasegawa, T TI Eye contact does not facilitate detection in children with autism SO COGNITION LA English DT Article DE eye gaze; direct gaze; face; autism; oddball task ID GAZE; FACE; ATTACHMENT; PERCEPTION; DIRECTION; BEHAVIOR; LOOKING AB Eye contact is crucial in achieving social communication. Deviant patterns of eye contact behavior are found in individuals with autism, who suffer from severe social and communicative deficits. This study used a visual oddball paradigm to investigate whether children with high functioning autism have difficulty in detecting mutual gaze under experimental conditions. The results revealed that children with autism were no better at detecting direct gaze than at detecting averted gaze, which is unlike normal children. This suggests that whereas typically developing children have the ability to detect direct gaze, children with autism do not. This might result in altered eye-contact behavior, which hampers subsequent development of social and communicative skills. (C) 2003 Elsevier Science B.V. All rights reserved. C1 Univ Tokyo, Grad Sch Arts & Sci, Dept Cognit & Behav Sci, Meguro Ku, Tokyo 1538902, Japan. Jikei Univ, Tokyo, Japan. Natl Inst Special Educ, Tokyo, Japan. RP Senju, A (reprint author), Univ Tokyo, Grad Sch Arts & Sci, Dept Cognit & Behav Sci, Meguro Ku, 3-8-1 Komaba, Tokyo 1538902, Japan. RI Senju, Atsushi/C-4097-2008 OI Senju, Atsushi/0000-0002-8081-7170 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BARONCOHEN S, 1995, BRIT J DEV PSYCHOL, V13, P379 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Batki A, 2000, INFANT BEHAV DEV, V23, P223, DOI 10.1016/S0163-6383(01)00037-6 BUITELAAR JK, 1995, BEHAVIOUR, V132, P319, DOI 10.1163/156853995X00595 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 Farroni T, 2002, P NATL ACAD SCI USA, V99, P9602, DOI 10.1073/pnas.152159999 GARCIALARREA L, 1992, NEUROPSYCHOLOGIA, V30, P723, DOI 10.1016/0028-3932(92)90042-K GIBSON JJ, 1963, AM J PSYCHOL, V76, P386, DOI 10.2307/1419779 Kampe KKW, 2001, NATURE, V413, P589, DOI 10.1038/35098149 KLEINKE CL, 1986, PSYCHOL BULL, V100, P78, DOI 10.1037//0033-2909.100.1.78 Leekam S, 1997, BRIT J DEV PSYCHOL, V15, P77 Macrae CN, 2002, PSYCHOL SCI, V13, P460, DOI 10.1111/1467-9280.00481 NEELY J, 2001, THESIS U DURHAM OKADA T, 2002, SEISHIN IGAKU, V44, P893 PERRETT DI, 1994, CAH PSYCHOL COGN, V13, P683 Pierce K, 2001, BRAIN, V124, P2059, DOI 10.1093/brain/124.10.2059 Raven J.C., 1956, COLOURED PROGRESSIVE ROBSON KS, 1967, J CHILD PSYCHOL PSYC, V8, P13, DOI 10.1111/j.1469-7610.1967.tb02176.x Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 SENJU A, 2001, HUM BEH EV SOC M YEA Sugishita M., 1993, JAPANESE RAVENS COLO SWETTENHAM J, 2000, J COGNITIVE NEURO SS, V53 Volkmar F. R., 1990, DEV PSYCHOPATHOL, V2, P61, DOI 10.1017/S0954579400000596 vonGrunau M, 1995, PERCEPTION, V24, P1297 Wicker B, 2003, NEUROPSYCHOLOGIA, V41, P139, DOI 10.1016/S0028-3932(02)00144-6 NR 26 TC 43 Z9 45 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0010-0277 J9 COGNITION JI Cognition PD AUG PY 2003 VL 89 IS 1 BP B43 EP B51 DI 10.1016/S0010-0277(03)00081-7 PG 9 WC Psychology, Experimental SC Psychology GA 708WN UT WOS:000184593200008 PM 12893128 ER PT J AU Milicic, J Petkovic, ZB Bozikov, J AF Milicic, J Petkovic, ZB Bozikov, J TI Dermatoglyphs of digito-palmar complex in autistic disorder: Family analysis SO CROATIAN MEDICAL JOURNAL LA English DT Article; Proceedings Paper CT Mayo Clinic Course in Advanced Cellular and Molecular Medicine CY SEP 01-05, 2003 CL ZAGREB, CROATIA ID FRAGILE-X-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; SEROTONIN TRANSPORTER; CHILDREN; CHROMOSOME; BEHAVIOR; GENE; LOCI AB Aim. To examine the role of the genetic component in the quantitative dermatoglyphic traits of autistic patients and their families, and the transmission of the autism. Methods. Finger and palm prints were taken from 120 autistic patients (92 males and 28 females), their parents (92 mothers and 70 fathers), 32 healthy brothers and 28 sisters, as well as 400 healthy controls (200 males and 200 females). An analysis of quantitative traits of dermatoglyphs on the fingers (FRC-finger ridge count) and palms (a-b, b-c, and c-d ridge count, and atd angle) was performed. Descriptive statistics, multivariate analysis of variance (MANOVA) with Tukey HSD post hoc test, and discriminant analysis were used to determine the differences among the groups. In addition, correlations among family members were analyzed. Results. Multivariate analysis showed significant differences among examined groups of autistic patients and their family members and healthy volunteers regarding both group membership and sex. Autistic male patients differed significantly from the healthy controls in the ridge count (RC) on the fourth and fifth finger, and in a-b RC and atd angle of both hands. Healthy fathers of autistic patients differed in atd angle, and brothers of autistic patients differed in all palmar variables from the healthy control group. Mothers of autistic patients differed significantly from the healthy female controls in the RC of the first, fourth, and fifth finger, in a-b and c-l RC on the palms, and atd angle of both hands. The first two discriminant functions explained 85.4% of variance and separated groups clearly in two ways: the first function separated healthy controls from family members of autistic patients, and the second one males from females. Interfamilial analysis showed significant interclass correlations between autistic sons and their mothers or fathers in practically all variables. However, the correlation between parents and their autistic daughters was lower. Both mothers and fathers of autistic patients correlated with their healthy children only in palmar variables. Conclusions. We found significant differences in ridge counts on the fingers and palms between the affected patients and their healthy controls, but these differences also existed between family members of autistic patients and healthy controls. Particularly pronounced were the differences between healthy female controls and female family members, including not only autistic female patients, but also their healthy mothers and sisters. Since the mothers and their autistic sons showed higher statistically significant correlation in most of the examined variables, unlike the mothers and their autistic or healthy daughters, it is possible that there is a connection between a recessive X-chromosome linkage, as a genetic component in the etiology of autistic disorders, and the influence of the inactivation of the affected X-chromosome in the females. C1 Inst Anthropol Res, Zagreb 10000, Croatia. Jankomir Psychiat Hosp, Zagreb, Croatia. Univ Zagreb, Andrija Stampar Sch Publ Hlth, Zagreb, Croatia. RP Milicic, J (reprint author), Inst Anthropol Res, Amruseva 8,POB 290, Zagreb 10000, Croatia. 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Med. J. PD AUG PY 2003 VL 44 IS 4 BP 469 EP 476 PG 8 WC Medicine, General & Internal SC General & Internal Medicine GA 718HB UT WOS:000185138100014 PM 12950152 ER PT J AU Coleman, M AF Coleman, M TI Autism: known and unknown SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID CHILDREN RP Coleman, M (reprint author), 929 Route 9W, Upper Grandview, NY 10960 USA. CR BAHU S, 2002, LANCET, V359, P310 COLEMAN M, 1981, NEONATOL NEUROLOGY DeLong GR, 1998, DEV MED CHILD NEUROL, V40, P551 Felicetti T, 1981, MILIEU THERAPY, V1, P13 GILLBERG C, 1989, ACTA PAEDIATR SCAND, V78, P314, DOI 10.1111/j.1651-2227.1989.tb11076.x Gillberg C., 2000, BIOL AUTISTIC SYNDRO Hillis AE, 2002, ANN NEUROL, V51, P537, DOI 10.1002/ana.10211 Jamain S, 2002, MOL PSYCHIATR, V7, P217, DOI 10.1038/sj.mp.4000968 Licinio J, 2002, MOL PSYCHIATR, V7, P229, DOI 10.1038/sj/mp/4001088 MILES JH, 2000, AM J MED GENET, V91, P254 Murphy ML, 2002, ARCH PEDIAT ADOL MED, V156, P356 NELSON KB, 2000, NEUROLOGY S, V3, P247 WALKER HA, 1976, AUTISTIC SYNDROME WIEDEL L, 1976, AUTISTIC SYNDROME NR 14 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4221 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD AUG PY 2003 VL 45 SU 95 BP 31 EP 34 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 712FX UT WOS:000184788000012 ER PT J AU Wilson, S Djukic, A Shinnar, S Dharmani, C Rapin, I AF Wilson, S Djukic, A Shinnar, S Dharmani, C Rapin, I TI Clinical characteristics of language regression in children SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID LANDAU-KLEFFNER-SYNDROME; PERVASIVE DEVELOPMENTAL DISORDERS; ELECTRICAL STATUS EPILEPTICUS; VERBAL AUDITORY AGNOSIA; INFANTILE-AUTISM; ACQUIRED APHASIA; SPEECH LOSS; CONVULSIVE DISORDER; DYSPHASIC CHILDREN; FOLLOW-UP AB The spectrum of language regression in childhood is incompletely understood. To describe the features of this disorder more fully, we reviewed the records of 196 consecutive children (143 males and 53 females) with language regression or perceived plateau evaluated between 1988 and 1994 by a child neurologist. Mean age at regression was 21.2 months and the mean interval to referral was 34.8 months. A trigger for the regression was identified in 74 of the children (38%) and was associated with a more rapid regression. Mean age at follow-up was 64 months (SD 55). Seventy per cent of the children became nonverbal, and 75% were cognitively impaired. Language regression was associated with a more global autistic regression in 93% of children. There was a history of seizures in 15% of the children. Some recovery occurred in 61% but only one child recovered fully. Improvement was more likely in the 49% who were entirely developmentally normal before the regression. We conclude that language regression in childhood is a serious disorder with significant long-term morbidity. C1 Albert Einstein Coll Med, Saul R Korey Dept Neurol, Bronx, NY 10461 USA. RP Rapin, I (reprint author), Albert Einstein Coll Med, Saul R Korey Dept Neurol, K 807,1300 Morris Pk Ave, Bronx, NY 10461 USA. EM rapin@aecom.yu.edu CR American Psychiatric Association, 1987, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Aram DM, 1992, HDB NEUROPSYCHOLOGY, P73 ARAM DM, 1994, J SPEECH HEAR RES, V37, P824 BallabanGil K, 1996, PEDIATR NEUROL, V15, P217, DOI 10.1016/S0887-8994(96)00219-6 Bates E, 2001, BRAIN LANG, V79, P223, DOI 10.1006/brln.2001.2482 Beaumanoir Anne, 1992, P231 BISHOP DVM, 1985, DEV MED CHILD NEUROL, V27, P705 Commission on Epidemiology and Prognosis International League Against Epilepsy, 1993, EPILEPSIA, V34, P592 Dennis M, 1998, BRAIN LANG, V61, P305, DOI 10.1006/brln.1997.1881 DEONNA TW, 1991, J CLIN NEUROPHYSIOL, V8, P288, DOI 10.1097/00004691-199107010-00005 Dugas M, 1995, MARIANI F P, V3, P47 Eisele JA, 1998, BRAIN LANG, V61, P376, DOI 10.1006/brln.1997.1883 GILLBERG C, 1987, J AUTISM DEV DISORD, V17, P273, DOI 10.1007/BF01495061 Goldhaber-Gordon D, 1998, NATURE, V391, P156 Hall N E, 1997, Semin Pediatr Neurol, V4, P77, DOI 10.1016/S1071-9091(97)80023-X Howlin P, 1997, EUR CHILD ADOLES PSY, V6, P55 Howlin P, 1998, J CHILD PSYCHOL PSYC, V39, P307, DOI 10.1017/S0021963097002138 Klein SK, 2000, J CHILD NEUROL, V15, P36, DOI 10.1177/088307380001500109 KURITA H, 1992, J AUTISM DEV DISORD, V22, P175, DOI 10.1007/BF01058149 KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 Kurita H, 1996, PSYCHIAT CLIN NEUROS, V50, P181, DOI 10.1111/j.1440-1819.1996.tb02739.x BANCAUD J, 1981, EPILEPSIA, V22, P489 LANDAU WM, 1957, NEUROLOGY, V7, P523 Lewine JD, 1999, PEDIATRICS, V104, P405, DOI 10.1542/peds.104.3.405 VENTER A, 1992, J CHILD PSYCHOL PSYC, V33, P489, DOI 10.1111/j.1469-7610.1992.tb00887.x Mantovani JF, 2000, DEV MED CHILD NEUROL, V42, P349, DOI 10.1017/S0012162200210621 National Research Council, 2001, ED CHILDR AUT RAPIN I, 1977, DEV MED CHILD NEUROL, V19, P192 Rossi PG, 1999, BRAIN DEV-JPN, V21, P90 Shinn AP, 2001, J FISH DIS, V24, P83, DOI 10.1046/j.1365-2761.2001.00272.x Tassinari CA, 2000, CLIN NEUROPHYSIOL, V111, pS94, DOI 10.1016/S1388-2457(00)00408-9 TUCHMAN RF, 1991, PEDIATRICS, V88, P1211 TUCHMAN RF, 1991, PEDIATRICS, V88, P1219 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 vanGent T, 1997, J CHILD PSYCHOL PSYC, V38, P337 VANHOUT A, 2003, HDB NEUROPSYCHOLOGY, V8, P631 NR 37 TC 30 Z9 32 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD AUG PY 2003 VL 45 IS 8 BP 508 EP 514 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 704LT UT WOS:000184341700002 PM 12882529 ER PT J AU Botting, N Conti-Ramsden, G AF Botting, N Conti-Ramsden, G TI Autism, primary pragmatic difficulties, and specific language impairment: can we distinguish them using psycholinguistic markers? SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID DIAGNOSTIC INTERVIEW; SPECTRUM DISORDERS; GENETIC INFLUENCES; MEMORY DEFICITS; FOLLOW-UP; CHILDREN; INDIVIDUALS; CLASSIFICATION; PRODUCTIVITY; MORPHOLOGY AB Three groups of children with communication disorders were examined using a series of psycholinguistic markers to explore whether the tasks could identify children with impairments other than specific language impairment (SLI), and to examine whether the different groups within this clinical population could be distinguished reliably from one another. The groups comprised children with autistic spectrum disorders (ASD; n=13, all males; mean age 10 years 10 months, range 10 years 2 months to 12 years 6 months); children with primary pragmatic language impairment (PLI) but who did not have definite ASD diagnoses (n=25,22 males, three females; mean age 11 years 3 months, range 10 years 2 months to 12 years 5 months); and children with specific language impairment (SLI) without marked pragmatic language difficulties (n=29, 25 males, 4 females; mean age 10 years 10 months, range 10 years 2 months to 11 years 9 months). Clinical markers examined were: the Children's Non-Word Repetition (CNRep), the Past Tense Task (PTT), and the Clinical Evaluation of Language Fundamentals, Recalling Sentences. First, it was found that the a priori groupings were not sufficiently defined and that four groups were actually present. The PLI group was in fact two separate samples: those with PLI pure and those with some autistic-like behaviours (referred to here as PLI plus, following Bishop 1998). Second, group comparisons indicated that CNRep was significantly lower for children with SLI than all other groups (although this measure was not such a good discriminator using a specificity analysis). Third, the markers were able to discriminate between all types of communication impairment in normal control participants (n=100; 51 females, 49 males; mean age 11 years, range 10 years 5 months to 11 years 6 months) with sensitivity levels of at least 75% and specificity of 80%. Recalling Sentences was the most efficient marker for all groups. Finally, analysis showed that children with PLI plus could be accurately distinguished from all others, scoring most favourably overall on communication markers and on performance IQ scores. C1 Univ Manchester, Sch Educ, Manchester M13 9PL, Lancs, England. RP Botting, N (reprint author), Univ Manchester, Sch Educ, Oxford Rd, Manchester M13 9PL, Lancs, England. CR Adams AM, 2000, INT J LANG COMM DIS, V35, P95 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th GATHERCOLE SE, 1990, J MEM LANG, V29, P336, DOI 10.1016/0749-596X(90)90004-J Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Bishop D. V. 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Med. Child Neurol. PD AUG PY 2003 VL 45 IS 8 BP 515 EP 524 PG 10 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 704LT UT WOS:000184341700003 PM 12882530 ER PT J AU Sabaratnam, M Murthy, NV Wijeratne, A Buckingham, A Payne, S AF Sabaratnam, M Murthy, NV Wijeratne, A Buckingham, A Payne, S TI Autistic-like behaviour profile and psychiatric morbidity in Fragile X Syndrome - A prospective ten-year follow-up study SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE Fragile X Syndrome; autistic-like behaviour; autism; follow-up; psychiatric morbidity; prevalence ID DSM-III-R; MALES; TRAJECTORIES; SCHEDULE AB In subjects with Fragile X Syndrome (FXS), the mutation of Fragile X Mental Retardation Type 1 (FMR-1) gene at Xq27.3 predisposes to Mental Retardation (MR), autistic-like behaviour and to a variety of psychiatric syndromes. However, the longitudinal course of autistic-like behaviour profile and psychiatric morbidity is untested. In this study, we followed up people with FXS for 10 years to establish the stability of their autistic-like behaviour profile and psychiatric morbidity. The autistic-like behaviour profile was assessed using Brief Disability Assessment Schedule (B-DAS) and relevant items from Handicaps, Behaviour and Skills (HBS) Schedule. The psychiatric morbidity was assessed using data from the case notes, Mini Psychiatric Assessment Schedule for Adults with Developmental Disability (Mini PAS-ADD) and clinical interview. Our findings suggest that the autistic-like behaviour pattern is a stable phenotypic feature of FXS, but for increase in resistance to change over time. There is a tenfold increase in the prevalence of psychiatric morbidity in FXS compared to the general population, which does not increase significantly over time. C1 Univ London Imperial Coll Sci Technol & Med, London, England. Northwick Pk & St Marks NHS Trust, Harrow, Middx, England. 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