FN Thomson Reuters Web of Science™ VR 1.0 PT J AU Scahill, L AF Scahill, L TI Diagnosis and evaluation of pervasive developmental disorders SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID ABERRANT BEHAVIOR CHECKLIST; SEVERE RETARDATION MESSIER; MATSON EVALUATION; SOCIAL-SKILLS; RATING-SCALE; AUTISM; INDIVIDUALS; RELIABILITY; RISPERIDONE; CHILDREN AB Accurate diagnosis and appropriate treatment of pervasive developmental disorders (PDDs), including autistic disorder, Asperger's disorder, and pervasive developmental disorder not otherwise specified, are necessary to ensure the best possible outcomes for children with these disorders. In the past, it was not uncommon for children with PDDs to wait several years from the time of parental recognition of developmental delay to the determination of the correct diagnosis and initiation of treatment. Increased awareness of PDDs and the availability of better assessment tools have improved the detection of these conditions in children. A wide variety of standardized diagnostic checklists, interviews, and observational measures are available to assist the clinician in making an accurate PDD diagnosis. A comprehensive evaluation also establishes a baseline of adaptive functioning and problematic behavior, which is essential for subsequent assessment of progress. This article discusses the differential diagnosis and evaluation of PDDs, focusing on the various assessment tools. The elements of a contemporary diagnostic evaluation and behavioral assessment are presented. The application of discretionary evaluations for special situations are also introduced. C1 Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06520 USA. Yale Univ, Sch Nursing, New Haven, CT 06520 USA. RP Scahill, L (reprint author), Yale Univ, Sch Med, Ctr Child Study, 230 S Frontage Rd,POB 207900, New Haven, CT 06520 USA. 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Psychiatry PY 2005 VL 66 SU 10 BP 19 EP 25 PG 7 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 001TG UT WOS:000234558800003 PM 16401146 ER PT J AU Findling, RL AF Findling, RL TI Pharmacologic treatment of behavioral symptoms in autism and pervasive developmental disorders SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID PLACEBO-CONTROLLED CROSSOVER; DOUBLE-BLIND; OPEN-LABEL; OPEN TRIAL; SPECTRUM DISORDERS; SCHIZOPHRENIC CHILDREN; RETROSPECTIVE ANALYSIS; FLUOXETINE TREATMENT; MENTAL-RETARDATION; YOUNG-CHILDREN AB Autism and other pervasive. developmental disorders (PDDs) are associated with various dysfunctional and problematic behaviors, in addition to the core features of language and social skills dysfunction that define these conditions. Although there is-currently no pharmacologic cure for the core features of PDDs, some of the behavioral symptoms may be treated pharmacologically. In addition to relieving some of the daily stress in the lives of patients and their families, improvement of these behavioral symptoms, which include hyperactivity, aggression, tantrums, and self-injury, removes some of the hindrances to other rehabilitative efforts. This article discusses the efficacy and tolerability of various medications and alternative interventions in addressing the symptoms of autism and other PDDs. C1 Univ Hosp Cleveland, Div Child & Adolescent Psychiat, Cleveland, OH 44106 USA. Case Western Reserve Univ, Dept Psychiat, Cleveland, OH 44106 USA. RP Findling, RL (reprint author), Univ Hosp Cleveland, Div Child & Adolescent Psychiat, 11100 Euclid Ave, Cleveland, OH 44106 USA. 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Psychiatry PY 2005 VL 66 SU 10 BP 26 EP 31 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 001TG UT WOS:000234558800004 PM 16401147 ER PT J AU Findling, RL Steiner, H Weller, EB AF Findling, RL Steiner, H Weller, EB TI Use of antipsychotics in children and adolescents SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article; Proceedings Paper CT Symposium on Developmental Neurobiology and Psychiatry - Challenges and Best Practices for Studies in Children and Adolescents CY OCT 03-04, 2003 CL Henderson, NV SP Otsuka Pharmaceut Inc, Abbott, Amer Fdn Suicide Prevent, AstraZeneca, Bristol-Mayers Squibb Co, Forest, GlaxoSmithKline, Janssen, Natl Alliance Res Schizophrenia & Depress, Natl Inst Mental Hlth, Pfizer Inc, Stanley Fdn/Natl Alliance Mentally III, Wyeth-Ayerst ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDHOOD-ONSET SCHIZOPHRENIA; HOSPITALIZED AGGRESSIVE-CHILDREN; DISRUPTIVE BEHAVIOR DISORDERS; ACUTE BIPOLAR MANIA; LONG-TERM SAFETY; OPEN-LABEL TRIAL; RANDOMIZED CONTROLLED-TRIAL; DOUBLE-BLIND; CONDUCT DISORDER AB The comparable efficacy and improved safety of the atypical antipsychotics compared with the traditional antipsychotic agents in the treatment of schizophrenia and other disorders in adults have prompted the use of these agents in children and adolescents. The atypical antipsychotics are increasingly being used in children and adolescents with a variety of different psychiatric diagnoses, including schizophrenia, bipolar disorder, autism/pervasive developmental disorders, conduct disorder, depression, anxiety disorders, tic disorders, delirium, and eating disorders. Unfortunately, clinical use of these agents in pediatric patients has far exceeded the limited evidence from randomized controlled trials. This article reviews the available evidence from the published literature on the use of the atypical antipsychotics in children and adolescents with schizophrenia, bipolar disorder, and maladaptive aggression associated with autism/pervasive developmental disorders and conduct disorder/disruptive behavior disorders. C1 Case Western Reserve Univ, Univ Hosp Cleveland, Div Child & Adolescent Psychiat, Dept Psychiat, Cleveland, OH 44106 USA. Stanford Univ, Sch Med, Stanford, CA 94305 USA. Univ Penn, Philadelphia, PA 19104 USA. 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Clin. Psychiatry PY 2005 VL 66 SU 7 BP 29 EP 40 PG 12 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 966HV UT WOS:000232011600005 PM 16124839 ER PT J AU McCracken, JT AF McCracken, JT TI Safety issues with drug therapies for autism spectrum disorders SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; DEFICIT HYPERACTIVITY DISORDER; OPEN-LABEL; PSYCHOACTIVE MEDICINES; DISRUPTIVE BEHAVIORS; CHILDREN; RISPERIDONE; PATTERNS; METHYLPHENIDATE; INDIVIDUALS AB Although currently no medication has been approved to treat autism spectrum disorders, survey data show that community practitioners are prescribing a broad range of medication treatments, including, but not limited to, antidepressants, stimulants, antipsychotics, alpha agonists, and anticonvulsants. Patients with autism spectrum disorders are also taking alternative treatments, including herbal remedies, immunologic treatments, and vitamin therapies, which may themselves produce side effects and/or create drug interactions with traditional medications. Although short-term data on the efficacy and safety of commonly prescribed treatments for autism spectrum disorders are increasing, few data are currently available on long-term treatment for autism spectrum disorders, but available studies and clinical experience can offer preliminary recommendations on the safety of and monitoring needs for the medications currently used for these disorders. Monitoring the safety and tolerability of drugs used in patients with these disorders should minimize the burden of side effects and optimize treatment outcome. C1 Univ Calif Los Angeles, Inst Neuropsychiat, Los Angeles, CA 90024 USA. RP McCracken, JT (reprint author), 760 Westwood Plaza,48-270, Los Angeles, CA 90024 USA. 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Clin. Psychiatry PY 2005 VL 66 SU 10 BP 32 EP 37 PG 6 WC Psychology, Clinical; Psychiatry SC Psychology; Psychiatry GA 001TG UT WOS:000234558800005 PM 16401148 ER PT J AU Aman, MG AF Aman, MG TI Treatment planning for patients with autism spectrum disorders SO JOURNAL OF CLINICAL PSYCHIATRY LA English DT Article ID QUALITY-STANDARDS-SUBCOMMITTEE; CHILD-NEUROLOGY-SOCIETY; FACILITATED COMMUNICATION; PEDIATRICIANS ROLE; PRACTICE PARAMETER; AMERICAN-ACADEMY; DOUBLE-BLIND; DIAGNOSIS; INTERVENTION; MANAGEMENT AB Patients with autism spectrum disorders (ASDs) can present with extremely heterogeneous issues, and, therefore, their treatment,can be very challenging. Most patients with ASDs will,benefit from contact with a multitude of disciplines. In,this article, treatment planning is structured in terms of the patient's life stages. Early on, assessment of. developmental milestones, metabolic conditions, and hearing; making the diagnosis of ASD; and providing genetic counseling are salient. As the child grows, speech and language therapy, early intensive intervention, special education, parent training, and neurologic assessment become important. With greater age, behavior therapy, pharmacotherapy, occupational therapy, and sexuality issues are often in ascendancy. As the patient approaches and proceeds through adulthood, transition training, housing options, and guardianship issues may be priorities. Advocacy is relevant throughout the life span. Professionals have an obligation to familiarize parents with interventions likely to be fruitful or unhelpful. There is growing evidence that early intensive behavior intervention, though expensive, may produce lifelong gains in functioning. A variety of experimental and/or unproven treatments are. identified; mental health professionals can help families with members who have ASDs by guiding them toward effective treatments and away from therapies of unknown value but with potential risks and/or costs. 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PY 2005 SU S BP 63 EP 63 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878700250 ER PT J AU Boser, K AF Boser, K TI Number representation and interhemispheric connectivity in autism SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Johns Hopkins Univ, Sch Med, Baltimore, MD USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 68 EP 69 PG 2 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878700275 ER PT J AU Thomas, C Behrmann, M Kimchi, R MInshew, N AF Thomas, C Behrmann, M Kimchi, R MInshew, N TI Global and local visual processing in autism: Insights from heterogeneous hierarchical letter stimuli. SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Carnegie Mellon Univ, Pittsburgh, PA 15213 USA. Univ Haifa, IL-31999 Haifa, Israel. Univ Pittsburgh, Pittsburgh, PA 15260 USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 111 EP 111 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878700470 ER PT J AU Walenski, M Mostofsky, SH Larson, J Ullman, MT AF Walenski, M Mostofsky, SH Larson, J Ullman, MT TI Fast grammatical computation in autism SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Georgetown Univ, Washington, DC 20057 USA. Kennedy Krieger Inst, Baltimore, MD USA. Johns Hopkins Sch Med, Baltimore, MD USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 117 EP 117 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878700498 ER PT J AU Webb, SJ Keil, A McPartland, J Shook, J Dawson, G AF Webb, SJ Keil, A McPartland, J Shook, J Dawson, G TI Gamma activation during object perception and memory in teens with autism and typical development SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Univ Washington, Seattle, WA 98195 USA. Univ Konstanz, D-7750 Constance, Germany. Univ Denver, Denver, CO 80208 USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 117 EP 117 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878700497 ER PT J AU Beal, P Reed, C Kopelioff, L Hepburn, S Pulham, D AF Beal, P Reed, C Kopelioff, L Hepburn, S Pulham, D TI Body posture: What individuals with autism spectrum disorder might be missing. SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Univ Denver, Dept Psychol, Denver, CO 80208 USA. Univ Colorado, Hlth Sci Ctr, Boulder, CO USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 118 EP 118 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878700503 ER PT J AU Scherf, KS Behrmann, M Minshew, N Luna, B AF Scherf, KS Behrmann, M Minshew, N Luna, B TI Face recognition deficits in autism: A failure to develop second-order configural processing skills SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Univ Pittsburgh, Ctr Neural Basis Cognit, Pittsburgh, PA 15260 USA. Carnegie Mellon Univ, Ctr Neural Basis Cognit, Pittsburgh, PA 15213 USA. RI Luna, Beatriz/F-1201-2010 NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 156 EP 156 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878701049 ER PT J AU Cornew, L Carver, L AF Cornew, L Carver, L TI Neural correlates of social referencing in infants at risk for autism SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Univ Calif San Diego, San Diego, CA 92103 USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 192 EP 192 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878701210 ER PT J AU Lewis, J Elman, J Courchesne, E AF Lewis, J Elman, J Courchesne, E TI Increased corpus callosum size in young children with autism SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Univ Calif San Diego, San Diego, CA 92103 USA. RI Elman, Jeffrey/A-9858-2008 NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 194 EP 194 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878701218 ER PT J AU Gage, N Isenberg, AL Fillmore, P Spence, MA AF Gage, N Isenberg, AL Fillmore, P Spence, MA TI MEG and behavioral measures of speech perception in children with autism disorder SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Univ Calif Irvine, Irvine, CA 92717 USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 212 EP 213 PG 2 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878701305 ER PT J AU Vaidya, C Kaplan, L Kenworthy, L Gilotty, L Girton, L Fos, J Lacey, E Gaillard, W AF Vaidya, C Kaplan, L Kenworthy, L Gilotty, L Girton, L Fos, J Lacey, E Gaillard, W TI Altered neural basis of controlling interference from social and non-social information in childhood autism: A functional magnetic resonance study SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Georgetown Univ, Washington, DC 20057 USA. Columbia Univ, New York, NY 10027 USA. NIH, Bethesda, MD 20892 USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 222 EP 222 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878701344 ER PT J AU Koldewyn, K Henry, M Solomon, M Rivera, S AF Koldewyn, K Henry, M Solomon, M Rivera, S TI Children with autism show functional activation differences on a response inhibition task SO JOURNAL OF COGNITIVE NEUROSCIENCE LA English DT Meeting Abstract CT 12th Annnual Meeting of the Cognitive-Neuroscience-Society CY APR 09-12, 2005 CL New York, NY SP Cognit Neurosci Soc C1 Univ Calif Davis, MIND Inst, Davis, CA 95616 USA. NR 0 TC 0 Z9 0 PU M I T PRESS PI CAMBRIDGE PA FIVE CAMBRIDGE CENTER, CAMBRIDGE, MA 02142 USA SN 0898-929X J9 J COGNITIVE NEUROSCI JI J. Cogn. Neurosci. PY 2005 SU S BP 224 EP 224 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 909RP UT WOS:000227878701353 ER PT J AU Ghaziuddin, M Quinlan, P Ghaziuddin, N AF Ghaziuddin, M Quinlan, P Ghaziuddin, N TI Catatonia in autism: a distinct subtype? SO JOURNAL OF INTELLECTUAL DISABILITY RESEARCH LA English DT Article DE Asperger syndrome; autism; catatonia; comorbidity; depression; ECT ID DISORDERS AB Catatonia is a life-threatening disorder characterized by motor abnormalities, mutism, and disturbances of behaviour, which is increasingly being diagnosed in persons with autism. In this report, we describe the presentation and course of catatonia in an adolescent with autism who responded to electroconvulsive therapy (ECT). The illness started with depressive symptoms, but the predominant feature was one of extreme obsessive slowing and immobility. We propose that catatonia should be ruled out as a cause of regression sometimes seen in adolescents with autism, and that catatonia of autism may index a distinct subtype with a particularly poor outcome. C1 Univ Michigan, Med Ctr, Ann Arbor, MI 48109 USA. RP Ghaziuddin, M (reprint author), Univ Michigan, Med Ctr, POB 0277, Ann Arbor, MI 48109 USA. 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PD JAN PY 2005 VL 49 BP 102 EP 105 DI 10.1111/j.1365-2788.2005.00666.x PN 1 PG 4 WC Education, Special; Genetics & Heredity; Clinical Neurology; Psychiatry; Rehabilitation SC Education & Educational Research; Genetics & Heredity; Neurosciences & Neurology; Psychiatry; Rehabilitation GA 882PG UT WOS:000225950200012 PM 15634317 ER PT J AU Farzin, F Perry, H Hessl, D Loesch, DZ Cohen, J Gane, LW Kradin, M Hagerman, RJ AF Farzin, F Perry, H Hessl, D Loesch, DZ Cohen, J Gane, LW Kradin, M Hagerman, RJ TI Autism spectrum disorders in boys with the fragile X premutation. SO JOURNAL OF INVESTIGATIVE MEDICINE LA English DT Meeting Abstract C1 Univ Calif Davis, Sacramento, CA 95817 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 2005 VL 53 IS 1 SU S MA 93 BP S93 EP S94 PG 2 WC Medicine, General & Internal; Medicine, Research & Experimental SC General & Internal Medicine; Research & Experimental Medicine GA 890VR UT WOS:000226539700107 ER PT J AU Welch, MG Welch-Horan, TB Anwar, M Anwar, N Ludwig, RJ Ruggiero, DA AF Welch, MG Welch-Horan, TB Anwar, M Anwar, N Ludwig, RJ Ruggiero, DA TI Brain effects of chronic IBD in areas abnormal in autism and treatment by single neuropeptides secretin and oxytocin SO JOURNAL OF MOLECULAR NEUROSCIENCE LA English DT Review DE treatment; autism; IBD; peptides; oxytocin; secretin; inflammation; amygdala; hypothalamic stress axis conditioning ID INFLAMMATORY-BOWEL-DISEASE; HIGH-FUNCTIONING CHILDREN; PLACEBO-CONTROLLED TRIAL; HAPTEN-INDUCED COLITIS; MATERNAL-BEHAVIOR; CROHNS-DISEASE; NERVOUS-SYSTEM; DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; PORCINE SECRETIN AB Recent research points to the connection between behavioral and gut disorders. Early adverse events are associated with inflammatory bowel disease (IBD). In animal models, maternal deprivation and social isolation predispose to gastric erosion and brain pathology. This study examined (1) brain effects of chronic gastrointestinal inflammation in a rat model of acquired IBD and (2) whether such changes are resolved by individual secretin (S) or oxytocin (OT) peptide treatment. Neurological manifestations of IBD were mapped by c-fos gene expression in male Sprague-Dawley rats (n = 10) with trinitrobenzene sulfonic acid (TNBS)-induced IBD vs controls (n = 11). IBD was characterized by moderate/severe infiltration of inflammatory cells 10 d after TNBS infusion. Age-matched pairs were processed for immunocytochemical detection of Fos, expressed when neurons are stimulated. S or OT (100 μ g/250 μ L saline) or equivolume saline was administered iv by Alzet pump for 20 d after disease onset. Degree of resolution of colitis-induced brain activation was assessed by c-fos expression, and mean numbers of Fos-immunoreactive nuclei for each group were compared using Independent Samples T-test. Chronic IBD activated periventricular gray, hypothalamic/visceral thalamic stress axes and cortical domains, and septal/preoptic/amygdala, brain areas abnormal in autism. Single peptide treatment with S or OT did not alter the effects of inflammation on the brain. Brain areas concomitantly activated by visceral inflammation are those often abnormal in autism, suggesting that IBD could be a model for testing treatments of autism. Other single and combined peptide treatments of IBD should be tested. The clinical implications for treating autism, IBD, and concomitant sickness behaviors with peptide therapy, with or without maternal nurturing as a natural equivalent, are presented. C1 Columbia Univ Coll Phys & Surg, Dept Psychiat, Div Neurosci, New York, NY 10032 USA. 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Mol. Neurosci. PY 2005 VL 25 IS 3 BP 259 EP 273 DI 10.1385/JMN:25:3:259 PG 15 WC Biochemistry & Molecular Biology; Neurosciences SC Biochemistry & Molecular Biology; Neurosciences & Neurology GA 924UA UT WOS:000229004700007 PM 15800379 ER PT J AU Howlin, P AF Howlin, P TI The effectiveness of interventions for children with autism SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Review ID EXCHANGE COMMUNICATION-SYSTEM; SPECTRUM DISORDERS; YOUNG-CHILDREN; FOLLOW-UP; ASPERGER-SYNDROME; PROGRAM; ADULTS; ADOLESCENTS; OUTCOMES; ACQUISITION AB Over the past 50 years very many different treatments have been promoted as bringing about significant improvements, or even cures, for children with autism. However, few interventions involve controlled studies of any kind; randomised control trials are virtually non-existent and when appropriate research methodology has been applied the results are generally far from positive. 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P., 1965, CASE STUDIES BEHAV M Welch M, 1988, HOLDING TIME WING L, 1981, PSYCHOL MED, V11, P115 ZAPPELLA M, 1988, TERAPIE AUTISMO 2000, TIMES 0726 NR 128 TC 16 Z9 17 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0303-6995 J9 J NEURAL TRANSM-SUPP JI J. Neural Transm.-Suppl. PY 2005 IS 69 BP 101 EP 119 PG 19 WC Neurosciences SC Neurosciences & Neurology GA 993OE UT WOS:000233962600007 PM 16355605 ER PT J AU Remschmidt, H Theisen, FM AF Remschmidt, H Theisen, FM TI Schizophrenia and related disorders in children and adolescents SO JOURNAL OF NEURAL TRANSMISSION-SUPPLEMENT LA English DT Article ID CHILDHOOD-ONSET SCHIZOPHRENIA; DEVELOPMENTAL DISORDER; PSYCHOSES; PERSONALITY; PSYCHIATRY; PSYCHOLOGY; SYMPTOMS; RISK AB This paper reviews the concept and recent studies on childhood and adolescent psychoses with special reference to schizophrenia. After a short historical introduction, the definition, classification, and epidemiology of child- and adolescent-onset psychoses are described, pointing out that some early-onset psychotic states seem to be related to schizophrenia (such as infantile catatonia) and others not (such as desintegrative disorder). The frequency of childhood schizophrenia is less than 1 in 10,000 children, but there is a remarkable increase in frequency between 13 and 18 years of age. Currently, schizophrenia is diagnosed according to ICD-10 and DSM-IV criteria. The differential diagnosis includes autism, desintegrative disorder, multiplex complex developmental disorder (MCDD) respectively multiple developmental impairment (MDI), affective psychoses, Asperger syndrome, drug-induced psychosis and psychotic states caused by organic disorders. With regard to etiology, there is strong evidence for the importance of genetic factors and for neurointegrative deficits preceding the onset of the disorder. Treatment is based upon a multimodal approach including antipsychotic medication (mainly by atypical neuroleptics), psychotherapeutic measures, family-oriented measures, and specific measures of rehabilitation applied in about 30% of the patients after completion of inpatient treatment. The long-term course of childhood- and adolescent-onset schizophrenia is worse than in adulthood schizophrenia, and the patients with manifestation of the disorder below the age of 14 have a very poor prognosis. C1 Univ Marburg, Dept Child & Adolescent Psychiat, D-35033 Marburg, Germany. RP Remschmidt, H (reprint author), Univ Marburg, Dept Child & Adolescent Psychiat, Hans Sachs Str 6, D-35033 Marburg, Germany. 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Neural Transm.-Suppl. PY 2005 IS 69 BP 121 EP 141 PG 21 WC Neurosciences SC Neurosciences & Neurology GA 993OE UT WOS:000233962600008 PM 16355606 ER PT J AU Bourre, JM AF Bourre, JM TI Dietary omega-3 fatty acids and psychiatry: Mood, behaviour, stress, depression, dementia and aging SO JOURNAL OF NUTRITION HEALTH & AGING LA English DT Review DE fatty acids; omega-3; brain; psychiatry; depression; dementia; stress; mood ID POLYUNSATURATED FATTY-ACIDS; PLACEBO-CONTROLLED TRIAL; ALPHA-LINOLENIC ACID; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PRELIMINARY DOUBLE-BLIND; ETHYL-EICOSAPENTAENOIC ACID; INCIDENT ALZHEIMER-DISEASE; STRUCTURAL BRAIN CHANGES; BLOOD-CELL MEMBRANES; DOCOSAHEXAENOIC ACID AB In view of the high omega-3 polyunsaturated fatty acid content of the brain, it is evident that these fats are involved in brain biochemistry, physiology and functionning; and thus in some neuropsychiatric diseases and in the cognitive decline of ageing. Though omega-3 fatty acids (from fatty fish in the human diet) appear effective in the prevention of stress, their role as regulator of mood and of libido is a matter for discussion pending experimental proof in animal and human models. Dietary omega-3 fatty acids play a role in the prevention of some disorders including depression, as well as in dementia, particularly Alzheimer's disease. Their direct role in major depression, bipolar disorder (manic-depressive disease) and schizophrenia is not yet established. Their deficiency can prevent the renewal of membranes, and thus accelerate cerebral ageing; nonetheless, the respective roles of the vascular component on one hand (where the omega-3's are active) and the cerebral parenchyma itself on the other, have not yet been clearly resolved. The role of omega-3 in certain diseases such as dyslexia and autism is suggested. In fact, omega-3 fatty acids participated in the first coherent experimental demonstration of the effect of dietary substances (nutrients) on the structure and function of the brain. Experiments were first of all carried out on ex-vivo cultured brain cells (1), then on in vivo brain cells (2), finally on physiochemical, biochemical, physiological, neurosensory, and behavioural parameters (3). These findings indicated that the nature of polyunsaturated fatty acids (in particular omega-3) present in formula milks for infants (both premature and term) determines the visual, cerebral, and intellectual abilities, as described in a recent review (4). Indeed, the insufficient dietary supply of omega-3 fatty acids in today's French and occidental diet raises the problem of how to correct dietary habits so that the consumer will select foods that are genuinely rich in omega-3/the omega-3 family; mainly rapeseed, (canola) and walnut oils on one hand and fatty fish on the other. 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PY 2005 VL 14 IS 4 BP 257 EP 257 DI 10.1026/0942-5403.14.4.257 PG 1 WC Psychology, Developmental SC Psychology GA 974OU UT WOS:000232602100009 ER PT S AU Sebrechts, MM AF Sebrechts, MM BE Tergan, SO Keller, T TI Visualizing information in virtual space: Prospects and pitfalls SO KNOWLEDGE AND INFORMATION VISUALIZATION: SEARCHING FOR SYNERGIES SE Lecture Notes in Computer Science LA English DT Article; Proceedings Paper CT International Workshop on Visual Artefacts for the Organization of Information and Knowledge, Searching for Synergies CY MAY, 2004 CL Tubingen, GERMANY HO Knowledge Media Res Ctr ID ENVIRONMENTS; RETRIEVAL; AUTISM AB This paper suggests how virtual reality (VR) may be a fruitful means to analyze potential synergies of information visualization and knowledge visualization in a learning context. Emphasis is placed on VR as a spatial context and as an interaction model. 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R., 2001, VISUAL DISPLAY QUANT, V2nd TULVING E, 1973, PSYCHOL REV, V80, P352, DOI 10.1037/h0020071 Tulving Endel, 1983, ELEMENTS EPISODIC ME VASILAKIS J, 2000, THESIS CATHOLIC U AM Ware C, 2000, INFORMATION VISUALIZ WICKENS C, 1992, P IEEE INT C SYST MA, P842, DOI 10.1109/ICSMC.1992.271688 Witmer BG, 1996, INT J HUM-COMPUT ST, V45, P413, DOI 10.1006/ijhc.1996.0060 YATES FA, 1966, ART MONEY NR 73 TC 1 Z9 1 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-26921-5 J9 LECT NOTES COMPUT SC PY 2005 VL 3426 BP 136 EP 166 PG 31 WC Computer Science, Information Systems; Computer Science, Theory & Methods SC Computer Science GA BCR01 UT WOS:000230860800008 ER PT J AU Farrington, CP Miller, E AF Farrington, CP Miller, E TI Informed choice, balance, and the MMR-autism saga SO LANCET INFECTIOUS DISEASES LA English DT Letter ID IMMUNIZATION; VACCINE; EVENTS C1 Open Univ, Dept Stat, Milton Keynes MK7 6AA, Bucks, England. Hlth Protect Agcy, Immunisat Dept, Commun Dis Surveillance Ctr, London, England. RP Farrington, CP (reprint author), Open Univ, Dept Stat, Walton Hall, Milton Keynes MK7 6AA, Bucks, England. EM c.p.farrington@open.ac.uk CR FARRINGTON CP, 1995, BIOMETRICS, V51, P228, DOI 10.2307/2533328 FARRINGTON P, 1995, LANCET, V345, P567, DOI 10.1016/S0140-6736(95)90471-9 GRIFFIN MR, 1991, PEDIATRICS, V88, P881 Jefferson T, 2004, LANCET INFECT DIS, V4, P135, DOI 10.1016/S1473-3099(04)00934-X Jefferson T, 2003, VACCINE, V21, P3954, DOI 10.1016/S0264-410X(03)00271-8 Kramarz P, 2000, ARCH FAM MED, V9, P617, DOI 10.1001/archfami.9.7.617 Miller Elizabeth, 2003, Semin Pediatr Infect Dis, V14, P199, DOI 10.1016/S1045-1870(03)00034-7 Murphy TV, 2001, NEW ENGL J MED, V344, P564, DOI 10.1056/NEJM200102223440804 NR 8 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1473-3099 J9 LANCET INFECT DIS JI Lancet Infect. Dis. PD JAN PY 2005 VL 5 IS 1 BP 2 EP 3 DI 10.1016/S1473-3099(04)01230-7 PG 2 WC Infectious Diseases SC Infectious Diseases GA 882UD UT WOS:000225963100003 PM 15620548 ER PT J AU Jefferson, T Price, D Demicheli, V AF Jefferson, T Price, D Demicheli, V TI Informed choice, balance, and the MMR-autism saga - Reply SO LANCET INFECTIOUS DISEASES LA English DT Letter ID IMMUNIZATION; EVENTS RP Jefferson, T (reprint author), Via Adige 28A, I-00061 Anguillara Sabazia, Italy. EM toj1@aol.com CR BIANCO E, 2004, COCHRANE LIB FARRINGTON P, 1995, LANCET, V345, P567, DOI 10.1016/S0140-6736(95)90471-9 GRIFFIN MR, 1991, PEDIATRICS, V88, P881 Jefferson T, 2004, LANCET INFECT DIS, V4, P135, DOI 10.1016/S1473-3099(04)00934-X Jefferson T, 2003, VACCINE, V21, P3954, DOI 10.1016/S0264-410X(03)00271-8 Miller Elizabeth, 2003, Semin Pediatr Infect Dis, V14, P199, DOI 10.1016/S1045-1870(03)00034-7 NR 6 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1473-3099 J9 LANCET INFECT DIS JI Lancet Infect. Dis. PD JAN PY 2005 VL 5 IS 1 BP 3 EP 4 DI 10.1016/S1473-3099(04)01231-9 PG 2 WC Infectious Diseases SC Infectious Diseases GA 882UD UT WOS:000225963100004 ER PT J AU Forsyth, R AF Forsyth, R TI Paediatrics: genetic insights and long-term follow-up SO LANCET NEUROLOGY LA English DT Editorial Material ID EPILEPSY; CHILDREN; AUTISM C1 Royal Victoria Infirm, Sch Clin Med Sci, Sir James Spence Inst Child Hlth, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England. RP Forsyth, R (reprint author), Royal Victoria Infirm, Sch Clin Med Sci, Sir James Spence Inst Child Hlth, Newcastle Upon Tyne NE1 4LP, Tyne & Wear, England. EM r.j.forsyth@newcastle.ac.uk RI Forsyth, Rob/I-9226-2012 CR Adab N, 2004, J NEUROL NEUROSUR PS, V75, P1575, DOI 10.1136/jnnp.2003.029132 Hammal D, 2004, DEV MED CHILD NEUROL, V46, P292, DOI 10.1017/S0012162204000489 Hunter LC, 2003, DEV MED CHILD NEUROL, V45, P121, DOI 10.1017/S0012162203000227 Jiang YH, 2004, AM J MED GENET A, V131A, P1, DOI 10.1002/ajmg.a.30297 Rhodes TH, 2004, P NATL ACAD SCI USA, V101, P11147, DOI 10.1073/pnas.0402482101 NR 5 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1474-4422 J9 LANCET NEUROL JI Lancet Neurol. PD JAN PY 2005 VL 4 IS 1 BP 8 EP 8 DI 10.1016/S1474-4422(04)00947-0 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 886SZ UT WOS:000226250200007 PM 15620849 ER PT J AU Young, EC Diehl, JJ Morris, D Hyman, SL Bennetto, L AF Young, EC Diehl, JJ Morris, D Hyman, SL Bennetto, L TI The use of two language tests to identify pragmatic language problems in children with autism spectrum disorders SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Article DE pragmatic language disorders; pragmatic language testing; autism spectrum disorders; test of pragmatic language; strong narrative assessment procedure; clinical evaluation of language fundamentals ID PERVASIVE DEVELOPMENTAL DISORDERS; ASPERGERS SYNDROME; INDIVIDUALS; MIND; IMPAIRMENT; COMPETENCE; SPEECH AB Purpose: Pragmatic language disorders (PLDs) are difficult to diagnose in a cost-effective manner, and there are few assessment tools that yield quantitative data. This investigation was designed to determine whether two formal assessment tools would differentiate PLDs in children with autism spectrum disorders (ASDs) from controls matched on verbal IQ and language fundamentals. Method: Thirty-four matched participants were given the Test of Pragmatic Language (TOPL; D. Phelps-Terasaki & T. Phelps-Gunn, 1992) and the Strong Narrative Assessment Procedure (SNAP; C. J. Strong, 1998). Results: Participants with ASDs had significantly poorer scores than controls on the TOPL. On the SNAP, the children with ASDs performed similarly to controls on syntax, cohesion, story grammar, and completeness of episodes. The controls performed significantly better only on the ability to answer inferential questions. Clinical Implications: The TOPL was effective in differentiating PLDs in children with ASDs when performance was compared to matched controls. The SNAP did not clearly differentiate language problems in these two groups. Research is needed to develop formal assessment tools that target the unique language disabilities of high-functioning individuals with ASDs. C1 Univ Rochester, Med Ctr, Rochester, NY 14642 USA. RP Young, EC (reprint author), Univ Rochester, Med Ctr, Box 627,601 Elmwood Ave, Rochester, NY 14642 USA. EM edna_young@URMC.Rochester.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT, V4 ARAM DM, 1993, J SPEECH HEAR RES, V36, P580 Baron-Cohen S., 2000, UNDERSTANDING OTHER, P3 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BISHOP DVM, 1989, BRIT J DISORD COMMUN, V24, P107 Capps I, 2000, J ABNORM CHILD PSYCH, V28, P193 Carrow-Woolfolk E, 1999, COMPREHENSIVE ASSESS GALLAGHER TM, 1983, PRAGMATIC ASSESSMENT Ghaziuddin M, 2000, J AUTISM DEV DISORD, V30, P67, DOI 10.1023/A:1005416212615 Grice H. 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M., 1989, SEMINARS SPEECH LANG, V10, P77, DOI 10.1055/s-0028-1082491 Wetherby AM, 1998, AM J SPEECH-LANG PAT, V7, P79 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1981, PSYCHOL MED, V11, P115 Yeargin-Allsopp M, 2003, JAMA-J AM MED ASSOC, V289, P49, DOI 10.1001/jama.289.1.49 Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 NR 45 TC 42 Z9 44 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 0161-1461 J9 LANG SPEECH HEAR SER JI Lang. Speech Hear. Serv. Sch. PD JAN PY 2005 VL 36 IS 1 BP 62 EP 72 DI 10.1044/0161-1461(2005/006) PG 11 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 892GO UT WOS:000226638300006 PM 15801508 ER PT J AU Timler, GR Olswang, LB Coggins, TE AF Timler, GR Olswang, LB Coggins, TE TI "Do I know what I need to do?" A social communication intervention for children with complex clinical profiles SO LANGUAGE SPEECH AND HEARING SERVICES IN SCHOOLS LA English DT Article DE social communication; intervention fetal alcohol spectrum disorder; elementary students ID FETAL ALCOHOL SYNDROME; SCHOOL-AGE-CHILDREN; FALSE BELIEF; NARRATIVE DISCOURSE; TEACHING THEORY; MIND; AUTISM; LANGUAGE; SKILLS; PERFORMANCE AB Purpose: Speech-language pathologists frequently address social communication difficulties in children with diverse clinical profiles. The purpose of this study was to investigate the feasibility of a social communication intervention for a school-age child with a complex cognitive and behavioral profile secondary to diagnosis of a fetal alcohol spectrum disorder. Method: A case study is presented to describe the implementation of the intervention targeting mental state verb production and social cognitive skills. The intervention included group role play of social scripts and a checklist to elicit the participant's statements about others' perspectives and strategies for completing the social script. Treatment data monitored the participant's responses to the checklist questions. Probe sessions, consisting of theory of mind false belief tasks, were used to examine mental state verb use. Results: Treatment data demonstrated that the participant stated more strategies in response to checklist questions. The participant did not produce any mental state verbs during baseline probes, but did produce mental state verbs during the treatment phase. Clinical Implications: The results support use of this intervention to change children's linguistic and social cognitive skills. Suggestions for extending this intervention to include a generalization plan targeting classroom social communication interactions are provided. C1 SUNY Buffalo, Dept Commun Disorders & Sci, Buffalo, NY 14214 USA. Washburn Univ, Seattle, WA USA. RP Timler, GR (reprint author), SUNY Buffalo, Dept Commun Disorders & Sci, 3455 Main St,122 Cary Hall, Buffalo, NY 14214 USA. 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R., 2000, THESIS U WASHINGTON TOMLER G, 2001, J POSIT BEHAV INTERV, V3, P48 Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd NR 53 TC 26 Z9 26 PU AMER SPEECH-LANGUAGE-HEARING ASSOC PI ROCKVILLE PA 10801 ROCKVILLE PIKE, ROCKVILLE, MD 20852-3279 USA SN 0161-1461 J9 LANG SPEECH HEAR SER JI Lang. Speech Hear. Serv. Sch. PD JAN PY 2005 VL 36 IS 1 BP 73 EP 85 DI 10.1044/0161-1461(2005/007) PG 13 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 892GO UT WOS:000226638300007 PM 15801509 ER PT J AU Huotilainen, M AF Huotilainen, M TI Magnetoencephalography in studies of infants and children SO MAGNETOENCEPHALOGRAPHY SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID NEURONAL CEROID-LIPOFUSCINOSIS; EVOKED MAGNETIC-FIELDS; MISMATCH NEGATIVITY; HUMAN-BRAIN; EPILEPTIFORM ACTIVITY; DYSLEXIC-CHILDREN; AUDITORY-CORTEX; AUTISM DISORDER; MEG; RESPONSES AB In this chapter, the use of MEG is discussed mainly in healthy children and infants. 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10.1016/0013-4694(95)00064-6 Uusitalo MA, 1997, MED BIOL ENG COMPUT, V35, P135, DOI 10.1007/BF02534144 Uutela K, 2001, NEUROIMAGE, V14, P1424, DOI 10.1006/nimg.2001.0915 Wakai RT, 1996, AM J OBSTET GYNECOL, V174, P1484, DOI 10.1016/S0002-9378(96)70592-6 Xiang J, 2003, PEDIATR RADIOL, V33, P321, DOI 10.1007/s00247-003-0883-z NR 89 TC 3 Z9 3 PU ELSEVIER ACADEMIC PRESS INC PI SAN DIEGO PA 525 B STREET, SUITE 1900, SAN DIEGO, CA 92101-4495 USA SN 0074-7742 J9 INT REV NEUROBIOL PY 2005 VL 68 BP 25 EP 50 DI 10.1016/S0074-7742(05)68002-6 PG 26 WC Engineering, Biomedical; Clinical Neurology; Neurosciences; Radiology, Nuclear Medicine & Medical Imaging SC Engineering; Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA BDP67 UT WOS:000234799300002 PM 16443009 ER PT J AU Tsai, SJ AF Tsai, SJ TI Is autism caused by early hyperactivity of brain-derived neurotrophic factor? SO MEDICAL HYPOTHESES LA English DT Article ID MENTAL-RETARDATION PROTEIN; FRAGILE-X; BDNF; HIPPOCAMPUS; POPULATION; EXPRESSION; DISORDER; GENETICS; CORTEX; LIFE AB Autism, a childhood-onset neurodevelopmental disorder, is characterized by disturbances in socialization and language skills, as welt as in perception. Several studies indicate the importance of both genetic and environmental factors in the development of idiopathic autism, but the underlying pathogenesis of this disorder is stilt unknown. Brain-derived neurotrophic factor (BDNF) is important for normal neuronal development. Early BDNF hyperactivity may play an etiological role in autism early in life. This hypothesis is supported by the finding that serum and brain tissue BDNF Levels are increased in autism compared with normal controls. Furthermore, BDNF hyperactivity may be associated with early brain outgrowth, increased prevalence of seizures in autism, and similar behaviors observed in autism and fragile X syndrome. Further studies of serum BDNF levels and genetic studies of the BDNF signaling pathway may help to clarify the rote of BDNF in the pathogenesis of autism. Attempts to prove the BDNF hyperactivity hypothesis may Lead investigators in a new direction for the study of the pathogenesis of autism and the development of an effective intervention of this disorder. © 2005 Elsevier Ltd. All rights reserved. C1 Vet Gen Hosp, Dept Psychiat, Taipei 11217, Taiwan. RP Tsai, SJ (reprint author), Vet Gen Hosp, Dept Psychiat, 201 Shin Pai Rd,Sec 2, Taipei 11217, Taiwan. 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Hypotheses PY 2005 VL 65 IS 1 BP 79 EP 82 DI 10.1016/j.mehy.2005.01.034 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 932DW UT WOS:000229535400015 PM 15893122 ER PT J AU Bayly, MB AF Bayly, MB TI Concept-matching in the brain depends on serotonin and gamma-frequency shifts SO MEDICAL HYPOTHESES LA English DT Article ID RECOGNITION; HUMANS AB A Eureka moment has three components - puzzle, solution and hedonic response (elation etc.). Puzzle and solution come together in the association cortex and are immensely variable from instance to instance. By contrast, the hedonic response is subcortical. and almost one-dimensional; how is it triggered? It is triggered by the relation between puzzle and solution, a good fit or good match, like the relation between two words that rhyme. In 1999 J.W. Fost proposed that serotonin is a crucial agent; here it is proposed that a frequency-jump initiates the serotonin causal chain, as energy shifts from 20 to 40 Hz or some such jump. The hypothesis assumes that any discrete idea is embodied in a time-course of electrical and chemical changes in a network of neurons, and that keeping the idea in mind involves repeating more or less the same time-course over and over. If observed frequencies in the gamma range result from such repetition, the period for running the time-course once is of the order of 25 ms. Also accepted is the suggestion that, although the brain runs many processes simultaneously, in the conscious mind attention focuses on only one idea at a time; an attempt to "think of two things at once" actually results only in giving them attention alternately, with a repeat-time of the order of 50 ms and frequency 20 Hz. Only if the two time-courses have certain elements in common will there be any repetition at 40 Hz. Now suppose a thinker takes up a problem and makes a succession of attempts at solution. As tong as he thinks of wrong answers, he generates activity only at 20 Hz, but when he hits upon the right answer, activity at 40 Hz shows up. This is a highly oversimplified scenario but its essential features might carry over to the vastly more complicated workings of a real brain. The virtue of the proposed mechanism is its generality. Under the proposal, any ideas in mind that do not match give no result but as soon as two ideas match, results ensue. This behavior in the model, wholly general except in one specific respect, is needed for conformity with real human brains' behavior. In normal people, production of this "link-joy" is an important reward mechanism and malfunction of this system may contribute to Capgras syndrome and some varieties of autism. © 2005 Elsevier Ltd. All rights reserved. C1 Rensselaer Polytech Inst, Troy, NY 12180 USA. RP Bayly, MB (reprint author), Rensselaer Polytech Inst, 415 Winter St, Troy, NY 12180 USA. EM baylym@rpi.edu CR ARNHEIM R, 1980, ART PSYCHOTHER, V7, P79, DOI 10.1016/0197-4556(80)90013-1 Cohen D. 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Hypotheses PY 2005 VL 65 IS 1 BP 149 EP 151 DI 10.1016/j.mehy.2005.01.019 PG 3 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 932DW UT WOS:000229535400025 PM 15893132 ER PT J AU Fabian, KJ AF Fabian, KJ TI Deep-feeling development gives autistics abstractions: When a young person has no abstractions, his or her thoughts or behaviors frequently seem autistic SO MEDICAL HYPOTHESES LA English DT Article AB The heart of autism is existence by oneself. It is being, talking and acting by oneself. Talking by oneself is not talking to oneself but talking at others. Its purpose is not exchanging or hearing words. Its purpose is sending words to another person. If being completely by themselves is autistics ' experience of their existence, then they may have no need for language. And there is no language development in about half of all autistics. For autistics who do have Language, if they are mostly sending out words and are only sometimes exchanging or hearing words, then another person ' s language has little or no effect on them. Without language from outside persons as a guide, autistics ' language becomes strange and free from the normal body motions (gestures) that come with language. So strange language and uncommon body motions with that language are two of autism ' s chief signs. Autistics are unnerved by change. So they keep their behaviors in a narrow range and do them over and over with no connection to other persons ' purposes. A narrow range of behaviors done over and over for no seeming purpose is another chief sign of autism. Because young boys and girls get to being, talking and acting by themselves when they come down with autism, they no longer seem to have any idea of what is going on between themselves and other persons. So when boys and girls get autism, they frequently do or say strange and surprising things with other persons. The knowledge of what to do and say with other persons comes as abstractions. This paper ' s one hypothesis is that autistic persons have no abstractions because the development of their deep feelings has not gone far enough to let abstractions come into existence. By acting or talking without the support of abstractions, autistic persons have a hard time with language, learning, living and loving in relation to other persons or to society. Autism comes from stopping the development of a baby ' s deep feelings within the first six months after birth. The development of deep feelings may be started again by a special operation named deep-feeling contact. (Body-to-body touching is never necessary for making deep-feeling contact.) As the development of his or her deep feelings goes forward, the autistic person ' s abstractions come into existence. Then language, learning, living and Loving become much simpler for him or her. (c) 2005 Elsevier Ltd. All rights reserved. RP Fabian, KJ (reprint author), POB 71565, Reno, NV 89570 USA. EM kenfabian@gbis.com CR EDWARDS B, 1999, NEW DRAWING RIGHT SI, P17 GRANDIN T, 1995, THINKING PICTURES OT, P28 GREENSPAN SI, 1997, GROWTH MIND ENDANGER, P1 HAPPE F, 1994, AUTISM INTRO PSYCHOL, P37 KANNER L, 1973, CHILDHOOD PSYCHOSIS, P63 LOVAAS OI, 1981, TEACHING DEV DISABLE, P110 STOLOROW RD, 2002, WORLDS EXPERIENCE IN, P13 NR 7 TC 0 Z9 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PY 2005 VL 65 IS 4 BP 694 EP 698 DI 10.1016/j.mehy.2005.04.039 PG 5 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 961IB UT WOS:000231654200009 PM 16019156 ER PT J AU Vakalopoulos, C AF Vakalopoulos, C TI A scientific paradigm for consciousness: Theory of premotor relations SO MEDICAL HYPOTHESES LA English DT Article ID PARKINSONS-DISEASE; BASAL GANGLIA; EXTERNAL PALLIDUM; DIRECT PERCEPTION; SCHIZOPHRENIA; AUTISM; ADAPTATION; NUCLEUS; VISION; ATTENTION AB Consciousness has become a holy grail for scientific research only in the last few decades. In spite of the extensive recent research in the field agreement on a correct approach to a theory has been elusive. We all have an intuitive idea of what we mean by the term and at the very least relate awareness to a descriptive phenomenology. I present a theory of consciousness based on motor capacity. An organism may exert control through movement and any action it performs on its surroundings results in a reaction. This type of reafference generated by movement provides the organism with a unique opportunity to compare perceptual information, for example, a retinal. image of a ball with what the body is telling the agent about the object. In other words, limb movements will describe a certain physical distance to the object and the shape will be conveyed by the arc described around it by any part of the body that comes into contact with it. The reafference, also called motor efference copy, can modulate neocortical networks strictly associated with concurrent perceptual information via input to thalamocortical projections. Concurrent perceptual and motor reafferent input provide the critical organizing principles bestowing on a neural assembly the capacity of conscious awareness. The cortical neural coding represents an interactive history and is what I call a premotor relation. It avoids the trap of behaviorism by emphasizing a developmental causality such that, once the networks are established no further motoric component is required. Supportive evidence for this position comes from the classic psychological studies of perceptual adaptation to distorting tenses facilitated by movement and elegant animal experiments dissociating sensorimotor development from visual exposure. One of the most innovative and useful conceptions advanced in the paper is a component theory of motor efference copy analyzing the two key parameters of any action namely force and proprioceptive change. There is massive neocortical input to the basal ganglia and cerebellum and recent research has implicated cognitive roles for these structures. I propose they serve the respective component parameters of motor efference copy. Finally, a theory of premotor relations provides a model for understanding how dysfunction in the basal ganglia and cerebellum relates to cognitive features of schizophrenia and autism, respectively. Motor dysfunction figures prominently in the early literature on these syndromes and I make the case for a fundamental causal connection between motor and cognitive symptoms. (c) 2005 Elsevier Ltd. All rights reserved. RP Vakalopoulos, C (reprint author), 171 McKean St, Melbourne, Vic 3068, Australia. 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Hypotheses PY 2005 VL 65 IS 4 BP 766 EP 784 DI 10.1016/j.mehy.2005.04.016 PG 19 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 961IB UT WOS:000231654200022 PM 15953692 ER PT J AU Datta, SS AF Datta, SS TI ECT treatment for autism: a viable alternative for a subgroup of patients? SO MEDICAL HYPOTHESES LA English DT Letter ID SCHIZOPHRENIA C1 Royal Cornhill Hosp, Dept Psychiat, Aberdeen AB25 2ZH, Scotland. RP Datta, SS (reprint author), Royal Cornhill Hosp, Dept Psychiat, Cornhill Rd, Aberdeen AB25 2ZH, Scotland. EM sdatta@nhs.net RI Datta, Soumitra /K-9408-2013 OI Datta, Soumitra /0000-0003-1674-5093 CR Dhossche DM, 2004, MED HYPOTHESES, V63, P371, DOI 10.1016/j.mehy.2004.03.023 Duman RS, 1998, J ECT, V14, P181 Miyazaki K, 2004, BRAIN DEV-JPN, V26, P292, DOI 10.1016/S0387-7604(03)00168-2 Riikonen R, 2003, J CHILD NEUROL, V18, P693, DOI 10.1177/08830738030180101101 Stahlberg O, 2004, J NEURAL TRANSM, V111, P891, DOI 10.1007/s00702-004-0115-1 WERRY JS, 1992, J AUTISM DEV DISORD, V22, P601, DOI 10.1007/BF01046330 NR 6 TC 0 Z9 0 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PY 2005 VL 64 IS 1 BP 219 EP 219 DI 10.1016/j.mehy.2004.08.014 PG 1 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 876FH UT WOS:000225481400048 PM 15533648 ER PT J AU Fallon, J AF Fallon, J TI Could one of the most widely precribed antibiotics amoxicillin/clavulanate "augmentin (TM)" be a risk factor for autism? SO MEDICAL HYPOTHESES LA English DT Article ID SPECTRUM DISORDERS; OTITIS-MEDIA; AMOXICILLIN; CLAVULANATE; PHARMACOKINETICS; EPIDEMIOLOGY; COMBINATION; CHILDREN; ACID AB Autism is an ever increasing problem in the United States. Characterized by multiple deficits in the areas of communication, development, and behavior; autistic children are found in every community in this country and abroad. Recent findings point to a significant increase in autism which can not be accounted for by means such as misclassification. The state of California recently reported a 273% increase in the number of cases between 1987 and 1998. Many possible causes have been proposed which range from genetics to environment, with a combination of the two most likely. Since the introduction of clavulanate/amoxicillin in the 1980s there has been the increase in numbers of cases of autism. In this study 206 children under the age of three years with autism were screened by means of a detailed case history. A significant commonality was discerned and that being the level of chronic otitis media. These children were found to have a mean number 9.96 bouts of otitis media (with a standard error of the mean of +/-1.83). This represents a sum total for all 206 children of 2052 bouts of otitis media. These children received a mean number of 12.04 courses of antibiotics (standard error of the mean of +/-.125). The sum total number of courses of antibiotics given to all 206 children was 2480. Of those 893 courses were Augmentin. with 362 of these Augmentin courses administered under the age of one year. A proposed mechanism whereby the production of clavulanate may yield high levels of urea/ammonia in the child is presented. Further an examination of this mechanism needs to be undertaken to determine if a subset of children are at risk for neurotoxicity from the use of clavulanic acid in pharmaceutical preparations. (C) 2004 Elsevier Ltd. All rights reserved. RP Fallon, J (reprint author), 1234 Cent Ave,Suite 1B, Yonkers, NY 10704 USA. 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Hypotheses PY 2005 VL 64 IS 2 BP 312 EP 315 DI 10.1016/j.mehy.2004.06.023 PG 4 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 886UP UT WOS:000226258500019 PM 15607562 ER PT J AU Janusonis, S AF Janusonis, S TI Serotonergic paradoxes of autism replicated in a simple mathematical model SO MEDICAL HYPOTHESES LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; WHOLE-BLOOD SEROTONIN; DORSAL RAPHE NUCLEUS; 5-HYDROXYINDOLEACETIC ACID; PLATELET SEROTONIN; PROMOTER VARIANTS; RETARDED-CHILDREN; 5-HT1A RECEPTORS; RAT-BRAIN; IN-VITRO AB The biological causes of autism are unknown. Since the early 1960s, the most consistent pathophysiological finding in autistic individuals has been their statistically elevated blood 5-hydroxytryptamine (5-HT, serotonin) levels. However, many autistic individuals have normal blood 5-HT levels, so this finding has been difficult to interpret. The serotonin transporter (SERT) controls 5-HT uptake by blood platelets and has been implicated in autism, but recent studies have found no correlation between SERT polymorphisms and autism. Finally, autism is considered a brain disorder, but studies have so far failed to find consistent serotonergic abnormalities in autistic brains. A simple mathematical model may account for these paradoxes, if one assumes that autism is associated with the failure of a molecular mechanism that both regulates 5-HT release from gut enterochromaffin cells and mediates 5-HT signaling in the brain. Some 5-HT receptors may play such a dual rote. White the failure of such a mechanism may lead to consistent abnormalities of synaptic transmission with no alteration of brain 5-HT levels, its effects on blood 5-HT levels may appear paradoxical. (c) 2004 Elsevier Ltd. All rights reserved. C1 Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA. RP Janusonis, S (reprint author), Yale Univ, Sch Med, Dept Neurobiol, POB 208001, New Haven, CT 06520 USA. 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Hypotheses PY 2005 VL 64 IS 4 BP 742 EP 750 DI 10.1016/j.mehy.2004.09.020 PG 9 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 906SP UT WOS:000227663500012 PM 15694691 ER PT J AU Geier, MR Geier, DA AF Geier, MR Geier, DA TI The potential importance of steroids in the treatment of autistic spectrum disorders and other disorders involving mercury toxicity SO MEDICAL HYPOTHESES LA English DT Article ID THIMEROSAL; CHILDREN; HYPOTHALAMUS; PREVALENCE; PITUITARY; VACCINES; HORMONE; AREA; RAT; 2ND AB Autism is a neurodevelopmentat disorder that according to the Centers for Disease Control and Prevention (CDC) affects 1 in 150 children in the United States. Autism is characterized by impairments in social relatedness and communication, repetitive behaviors, abnormal movements, and sensory dysfunction. Recently emerging evidence suggests that mercury, especially from childhood vaccines, appears to be a factor in the development of the autistic disorders, and that autistic children have higher than normal body-burdens of mercury. In considering mercury toxicity, it has previously been shown that testosterone significantly potentates mercury toxicity, whereas estrogen is protective. Examination of autistic children has shown that the severity of autistic disorders correlates with the amount of testosterone present in the amniotic fluid, and an examination of a case-series of autistic children has shown that some have plasma testosterone levels that were significantly elevated in comparison neurotypical control children. A review of some of the current biomedical therapies for autistics, such as glutathione and cysteine, chelation, secretin, and growth hormone, suggests that they may in fact lower testosterone levels. We put forward the medical hypothesis that autistic disorders, in fact, represents a form of testosterone mercury toxicity, and based upon this observation, one can design novel treatments for autistics directed towards higher testosterone levels in autistic children. We suggest a series of experiments that need to be conducted in order to evaluate the exact mechanisms for mercury-testosterone toxicity, and various types of clinical manipulations that may be employed to control testosterone levels. It is hoped by devising therapies that address the steroid hormone pathways, in addition to the current treatments that successful tower heavy metal. body-burdens of mercury, will work synergistically to improve clinical outcomes. In light of the fact that there are a number of other diseases that may have a chronic mercury toxicity component, such as Alzheimer's disease, heart disease, obesity, ALS, asthma, and other various forms of autoimmune disorders, it is imperative that further research should be conducted to understand mercury-testosterone toxicity. (c) 2004 Elsevier Ltd. All rights reserved. C1 MedCon Inc, Silver Spring, MD 20905 USA. Genet Ctr Amer, Silver Spring, MD 20905 USA. RP Geier, DA (reprint author), MedCon Inc, Silver Spring, MD 20905 USA. 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EM sjtsai@vghtpe.gov.tw CR Chugani DC, 2004, MENT RETARD DEV D R, V10, P112, DOI 10.1002/mrdd.20021 Dhossche Dirk, 2002, Med Sci Monit, V8, pPR1 Dhossche DM, 2004, MED HYPOTHESES, V63, P371, DOI 10.1016/j.mehy.2004.03.023 Grisaru N, 1998, AM J PSYCHIAT, V155, P1630 Gur E, 2000, NEUROREPORT, V11, P2925, DOI 10.1097/00001756-200009110-00019 Huber TJ, 2003, PSYCHIAT RES, V120, P103, DOI 10.1016/S0165-1781(03)00170-7 Lisanby SH, 2002, J CLIN NEUROPHYSIOL, V19, P344, DOI 10.1097/00004691-200208000-00007 Saba G, 2002, AM J PSYCHIAT, V159, P1794, DOI 10.1176/appi.ajp.159.10.1794 Sanacora G, 2003, AM J PSYCHIAT, V160, P577, DOI 10.1176/appi.ajp.160.3.577 NR 9 TC 6 Z9 7 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0306-9877 J9 MED HYPOTHESES JI Med. Hypotheses PY 2005 VL 64 IS 5 BP 1070 EP 1071 DI 10.1016/j.mehy.2004.11.025 PG 2 WC Medicine, Research & Experimental SC Research & Experimental Medicine GA 912VH UT WOS:000228107500041 PM 15780521 ER PT J AU Mandell, DS Novak, M AF Mandell, DS Novak, M TI The role of culture in families' treatment decisions for children with autism spectrum disorders SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; complementary and alternative medicine; culture; race; ethnicity; treatment ID MENTAL-HEALTH-CARE; ALTERNATIVE MEDICINE; DEVELOPMENTAL-DISABILITIES; YOUNG-CHILDREN; COMPLEMENTARY; DIAGNOSIS; PARENTS; RACE; SERVICES; IDENTIFICATION AB There is little information available about how and why parents of children with autism spectrum disorders (ASD) make decisions regarding which of the many available treatments to implement with their children. Given the lack of available information regarding treatment efficacy, it is likely that parents' beliefs about child development, interpretation of the symptoms of ASD, its etiology and course, and their experiences with the health system influence treatment decisions. This article addresses these issues within the context of cultural influences. We review the small body of existing literature regarding cultural influences on decisions regarding ASD and draw implications for the study and treatment of ASD from the larger body of literature on culture and other health conditions of childhood. In addition to examining the potential for differences in clinical presentation by culture and different experiences with the healthcare system, we use Kleinman's framework of questions for understanding the role of culture in the interpretation and treatment of ASD. These questions address interpretation of symptoms and beliefs about their cause, course, and treatment. Finally, we present specific language for clinicians to use in discussion with families with different cultural beliefs about the use of less traditional treatment strategies. (c) 2005 Wiley-Liss, Inc. C1 Univ Penn, Dept Psychiat, Sch Med, Ctr Mental Hlth Policy & Serv Res, Philadelphia, PA 19104 USA. Univ Penn, Dept Gen Pediat, Sch Med, Philadelphia, PA 19104 USA. Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA. RP Mandell, DS (reprint author), Univ Penn, Dept Psychiat, Sch Med, Ctr Mental Hlth Policy & Serv Res, 3535 Market St,3rd Floor, Philadelphia, PA 19104 USA. EM mandelld@mail.med.upenn.edu RI Mandelld, David/A-1044-2007; Mandell, David/H-2730-2012 OI Mandell, David/0000-0001-8240-820X CR Baer R. 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Retard. Dev. Disabil. Res. Rev. PY 2005 VL 11 IS 2 BP 110 EP 115 DI 10.1002/mrdd.20061 PG 6 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 940WV UT WOS:000230177500002 PM 15977313 ER PT J AU Levy, SE Hyman, SL AF Levy, SE Hyman, SL TI Novel treatments for autistic spectrum disorders SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE ASD; autism; complementary and alternative medical therapy (CAM) ID PERVASIVE DEVELOPMENTAL DISORDERS; PLACEBO-CONTROLLED TRIAL; SYNTHETIC HUMAN SECRETIN; DOUBLE-BLIND; INFANTILE-AUTISM; INTRAVENOUS IMMUNOGLOBULIN; MENTAL-RETARDATION; GASTROINTESTINAL DISORDERS; BEHAVIORAL TREATMENT; URINARY-EXCRETION AB In no area of developmental pediatric practice is there more controversy regarding the choice of treatment than related to children with autistic spectrum disorders (ASD). Complementary and alternative medical therapies (CAM) are often elected because they are perceived as treating the cause of symptoms rather than the symptoms themselves. CAM used for autism can be divided by proposed mechanism: immune modulation, gastrointestinal, supplements that affect neurotransmitter function, and nonbiologic intervention. Secretin as a therapy for autism is discussed as an example of how a clinical observation rapidly grew to a widespread treatment before well-designed studies demonstrated absence of effect. The plausibility for behavioral effect was not substantiated by clinical studies. CAM used for treatment of autism is examined in terms of rationale, evidence of efficacy, side effects, and additional commentary. Families and clinicians need access to well-designed clinical evidence to assist them in choice of therapies. (c) 2005 Wiley-Liss, Inc. C1 Univ Penn, Sch Med, Childrens Hosp, Philadelphia, PA 19104 USA. Univ Rochester, Strong Ctr Dev Disabil, Golisano Childrens Hosp, Rochester, NY USA. RP Levy, SE (reprint author), Univ Penn, Sch Med, Childrens Hosp, Childrens Seashore House, Philadelphia, PA 19104 USA. 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10.1023/B:CEMN.0000018618.59015.a2 Whitaker-Azmitia PM, 2005, INT J DEV NEUROSCI, V23, P75, DOI 10.1016/j.ijdevneu.2004.07.022 WILLIAMS K M, 1992, Biochemical Society Transactions, V20, p189S Winslow JT, 2002, NEUROPEPTIDES, V36, P221, DOI 10.1054/npep.2002.0909 Yang B., 2004, AM J PHYSIOL-REG I, V286, P927 Yung WH, 2001, J NEUROSCI, V21, P7063 YUWILER A, 1992, J AUTISM DEV DISORD, V22, P33, DOI 10.1007/BF01046401 NR 179 TC 78 Z9 79 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 1080-4013 J9 MENT RETARD DEV D R JI Ment. Retard. Dev. Disabil. Res. Rev. PY 2005 VL 11 IS 2 BP 131 EP 142 DI 10.1002/mrdd.20062 PG 12 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 940WV UT WOS:000230177500004 PM 15977319 ER PT J AU Schaaf, RC Miller, LJ AF Schaaf, RC Miller, LJ TI Occupational therapy using a sensory integrative approach for children with developmental disabilities SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE sensory integrative dysfunction; sensory processing ID LEARNING-DISABILITIES; AUTISTIC-CHILDREN; PERFORMANCE; MODULATION; DISORDERS; CRITIQUE; STIMULI; BRAIN AB This article provides an introduction and overview of sensory integration theory as it is used in occupational therapy practice for children with developmental disabilities. This review of the theoretical tenets of the theory, its historical foundations, and early research provides the reader with a basis for exploring current uses and applications. The key principles of the sensory integrative approach, including concepts such as "the just right challenge" and "the adaptive response" as conceptualized by A. Jean Ayres, the theory's founder, are presented to familiarize the reader with the approach. The state of research in this area is presented, including studies underway to further delineate the subtypes of sensory integrative dysfunction, the neurobiological mechanisms of poor sensory processing, advances in theory development, and the development of a fidelity measure for use in intervention studies. Finally, this article reviews the current state of the evidence to support this approach and suggests that consensual knowledge and empirical research are needed to further elucidate the theory and its utility for a variety of children, with developmental disabilities. This is especially critical given the public pressure by parents of children with autism and other developmental disabilities to obtain services and who have anecdotally noted the utility of sensory integration therapy for helping their children function more independently. Key limiting factors to research include lack of funding, paucity of doctorate trained clinicians and researchers in occupational therapy, and the inherent heterogeneity of the population of children affected by sensory integrative dysfunction. A call to action for occupational therapy researchers, funding agencies, and other professions is made to support ongoing efforts and to develop initiatives that will lead to better diagnoses and effective intervention for sensory integrative dysfunction, which will improve the lives of children and their families. (c) 2005 Wiley-Liss, Inc. C1 Thomas Jefferson Univ, Dept Occupat Therapy, Philadelphia, PA 19107 USA. Univ Colorado, Hlth Sci Ctr, Sensory Integrat Res & Treatment Ctr, Denver, CO 80202 USA. RP Schaaf, RC (reprint author), Thomas Jefferson Univ, Dept Occupat Therapy, 130 S 9th St,Edison 810, Philadelphia, PA 19107 USA. EM Roseann.schaaf@jefferson.edu CR Ahn RR, 2004, AM J OCCUP THER, V58, P287 Anzalone ME, 2000, COMM LANG INTERVEN, V9, P143 ARENDT RE, 1988, AM J MENT RETARD, V92, P401 Ayres A. J., 1989, SENSORY INTEGRATION Ayres A. 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PY 2005 VL 11 IS 2 BP 143 EP 148 DI 10.1002/mrdd.20067 PG 6 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 940WV UT WOS:000230177500005 PM 15977314 ER PT J AU Sandler, A AF Sandler, A TI Placebo effects in developmental disabilities: Implications for research and practice SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE placebo; research; disabilities; autism; ADHD; conditioning ID CONTROLLED-TRIALS; MAJOR DEPRESSION; CHILDREN; AUTISM; DISORDER; SECRETIN; CANCER AB Recent clinical trials of secretin in children with autism showed robust placebo effects and no benefit of secretin over placebo. This article explores the reasons for the observed placebo effects, focusing on the heightening of positive expectancy,by media attention and by the sensory experiences associated with intravenous injections. Comparisons are drawn with research involving other novel treatments and other clinical populations of children With developmental disabilities and neurobehavioral disorders. Research regarding mechanisms of placebo effects is reviewed, including patient and clinician attributes, expectancy effects, participation effects, changes in caregiver behavior, and conditioning. New evidence regarding the biological basis of placebo effects is briefly presented. Since placebo effects are ubiquitous and may operate by a variety of mechanisms, research design is critical in designing clinical trials and in evaluating other outcomes research. Measurement issues important for research in developmental disabilities are emphasized. Ethical concerns have been raised regarding the use of placebo in clinical research, but current analysis suggests that placebo controls are necessary and defensible on ethical grounds, if certain conditions are met. The study of placebo effects ("placebology") holds great promise as a new area of research in therapeutics. The author's research in the potential augmentation of stimulant effects in children with attention deficit/hyperactivity disorder (ADHD) by adding placebo in open label is briefly presented. The placebo has always been integral to the practice of medicine, but advances in scientific medicine and medical ethics have diminished the role and use of placebo in practice. An innovative,,approach to the ethical use of placebo is proposed. (c) 2005 Wiley-Liss, Inc. C1 Mission Childrens Hosp, Olson Huff Ctr, Asheville, NC 28801 USA. Univ N Carolina, Dept Pediat, Chapel Hill, NC USA. RP Sandler, A (reprint author), Mission Childrens Hosp, Olson Huff Ctr, 50 Doctors Dr,16 W Annex, Asheville, NC 28801 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2005 VL 11 IS 2 BP 164 EP 170 DI 10.1002/mrdd.20065 PG 7 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 940WV UT WOS:000230177500008 PM 15977316 ER PT J AU Landa, RJ AF Landa, RJ TI Assessment of social communication skills in preschoolers SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE social; communication; assessment; preschoolers ID LANGUAGE-DEVELOPMENT; AUTISTIC TRAITS; JOINT ATTENTION; YOUNG-CHILDREN; BEHAVIOR AB This paper orients the reader to social communication assessment and reviews methods for assessing social communication behavior in children from toddlerhood through the preschool years. Most standardized, normed tests of language in this age range focus on morpho-syntactic and semantic comprehension and production abilities. While social communication is perhaps one of the most important skills for peer acceptance, these skills are often overlooked in language evaluation with children. However, there are a number of caregiver questionnaires, interviews, or direct social-communication sampling methods that are available to assist clinicians or researchers in documenting social-communication skills or behaviors. Since assessment of social communication is essential in clinical work with children with an autism spectrum disorder, some of the tools described below are outgrowths of autism research or provide autism-related scores. While many children receiving social communication assessments do not have autism, the need to assess social communication skills in children with language impairment is highlighted by the growing literature documenting social and pragmatic difficulties in this population (Bishop [2000] Causes, Characteristics, Intervention, and Outcome. Hove, UK: Psychology press). 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PY 2005 VL 11 IS 3 BP 247 EP 252 DI 10.1002/mrdd.20079 PG 6 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 969FJ UT WOS:000232218900010 PM 16161095 ER PT J AU Dumont-Mathieu, T Fein, D AF Dumont-Mathieu, T Fein, D TI Screening for autism in young children: The modified checklist for autism in toddlers (M-CHAT) and other measures SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE autism; pediatric screening; early identification; early intervention ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDHOOD DISINTEGRATIVE DISORDER; INTENSIVE BEHAVIORAL TREATMENT; LANDAU-KLEFFNER-SYNDROME; 6-YEAR FOLLOW-UP; SPECTRUM DISORDERS; PARENTS CONCERNS; NATIONAL-SURVEY; EARLY IDENTIFICATION; MEDICAL HOME AB The literature on the importance of early identification and early intervention for children with developmental disabilities such as autism continues to grow. The increased prevalence of autistic spectrum disorders has fostered research efforts on the development and validation of autism-specific screening instruments for use with young children. There are currently several such autism-specific screening tools meant to be used with young children in various stages of development. Data from a few of these screening instruments have been published, and they include the Checklist for Autism in Toddlers (CHAT), Pervasive Developmental Disorders Screening Test (PDDST), Screening Tool for Autism in Two year olds (STAT), Checklist for Autism in Toddlers-23 (CHAT-23), and the Modified Checklist for Autism in Toddlers (M-CHAT). In this review, these five tools designed for use with children under three years old will be highlighted. In particular, the Modified Checklist for Autism in Toddlers (M-CHAT) will be discussed. (c) 2005 Wiley-Liss, Inc. C1 Univ Connecticut, Dept Psychol, Storrs, CT 06269 USA. Univ Connecticut, Dept Pediat, Sch Med, Storrs, CT 06269 USA. RP Dumont-Mathieu, T (reprint author), Univ Connecticut, Dept Psychol, 406 Babbidge Rd, Storrs, CT 06269 USA. 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Retard. Dev. Disabil. Res. Rev. PY 2005 VL 11 IS 3 BP 253 EP 262 DI 10.1002/mrdd.20072 PG 10 WC Clinical Neurology; Neurosciences; Pediatrics; Psychiatry SC Neurosciences & Neurology; Pediatrics; Psychiatry GA 969FJ UT WOS:000232218900011 PM 16161090 ER PT J AU Haydar, TF AF Haydar, TF TI Advanced microscopic imaging methods to investigate cortical development and the etiology of mental retardation SO MENTAL RETARDATION AND DEVELOPMENTAL DISABILITIES RESEARCH REVIEWS LA English DT Review DE live imaging; multi-photon; autism; fragile X syndrome; lissencephaly; Down syndrome ID DEVELOPING CEREBRAL-CORTEX; ASYMMETRIC CELL-DIVISION; NEURONAL MIGRATION DEFECTS; ORGANOTYPIC SLICE CULTURES; LASER-SCANNING MICROSCOPY; IN-VIVO ELECTROPORATION; RADIAL GLIAL-CELLS; TS65DN MOUSE MODEL; FRAGILE-X-SYNDROME; DOWN-SYNDROME AB Studies on human patients and animal models of disease have shown that disruptions in prenatal and early postnatal brain development are a root cause of mental retardation. Since proper brain development is achieved by a strict spatiotemporal control of neurogenesis, cell migration, and patterning of synapses, abnormalities in one or more of these events during prenatal development can lead to cognitive dysfunction after birth. Many of underlying causes of mental retardation must therefore be studied in developing brains. To aid in this research, live imaging using laser scanning microscopy (LSM) has recently allowed neuroscientists to delve deeply into the complex three-dimensional environment of the living brain to record dynamic cellular events over time. This review will highlight recent examples of how LSM is being applied to elucidate both normal and abnormal cortical development. (c) 2005 Wiley-Liss, Inc. C1 George Washington Univ, Sch Med, Neurosci Res Ctr, Childrens Res Inst,CNMC, Washington, DC 20010 USA. 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New strategies for the use of radiolabeled tracers hold potential for imaging gene expression in the brain during development and following interventions. In addition, PET may be key in identifying the physiological consequences of gene mutations associated with mental retardation. The development of high spatial resolution microPET scanners for imaging of rodents provides a means for longitudinal study of transgenic mouse models of genetic disorders associated with mental retardation, In this review, we describe PET methodology, illustrate how PET can be used to delineate biochemical changes during brain development, and provide examples of how PET has been applied to study brain glucose metabolism in Rett syndrome, serotonin synthesis in autism, and GABA(A) receptors in Angelman's syndrome and Prader-Willi syndrome. Future application of PET scanning in the study of mental retardation might include measurements of brain protein synthesis in fragile X syndrome and tuberous sclerosis complex, two common conditions associated with mental retardation in which cellular mechanisms involve dysregulation of protein synthesis. Mental retardation results in life-long disability, and application of new PET technologies holds promise for a better understanding of the biological underpinnings of mental retardation, with the potential to uncover new treatment options. (c) 2005 Wiley-Liss, Inc. C1 Wayne State Univ, Sch Med, Carman & Ann Adams Dept Pediat, Childrens Hosp Michigan, Detroit, MI USA. Wayne State Univ, Sch Med, Childrens Hosp Michigan, Dept Neurol, Detroit, MI USA. Wayne State Univ, Sch Med, Childrens Hosp Michigan, Dept Radiol, Detroit, MI USA. RP Chugani, DC (reprint author), Childrens Hosp Michigan, PET Ctr, 3901 Beaubian Blvd, Detroit, MI 48201 USA. 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Soc. Res. Child Dev. PY 2005 VL 70 IS 1 BP 133 EP 152 DI 10.1111/j.1540-5834.2005.00333.x PG 20 WC Psychology, Developmental SC Psychology GA 966VS UT WOS:000232051500002 PM 16156848 ER PT J AU El Mogharbel, C Sommer, G Deutsch, W Wenglorz, M Laufs, I AF El Mogharbel, C Sommer, G Deutsch, W Wenglorz, M Laufs, I TI The vocal development of a girl who sings but does not speak SO MUSICAE SCIENTIAE LA English DT Article; Proceedings Paper CT 1st Conference on Interdisciplinary Musicology (CIM04) CY APR 15-18, 2004 CL Graz, AUSTRIA HO Univ Graz, Dept Musicol ID SAVANT; AUTISM; MEMORY AB Background in music psychology. The development of singing involves not only the acquisition of melodies and words but also precise attunement to the timing structure and melodic features given by the social environment, which leads to a considerable conventionalization of performance. Background in linguistics. In the course of language development, children adapt their phonetic output to the sound patterns of the target language. In singing songs, the rendition of the lyrics naturally leans on these native language sound patterns, even if the semantic content of the lyrics plays little role. Aims. We report a long-term study of a child with infantile autism and severe mental handicap who sings songs but has no language. The only aspect of speech she produces is the phonetic realization of the songs she sings. This exceptional case in which musical development is dissociated from language development bears relevance to the question of the interrelationship of singing and speaking. Method. The material consists of two hours of audio data or 269 reproductions of familiar songs extracted from a long-term video documentation of the single case covering the period from age 3-15. Based on phonetic and musical transcriptions, the girl's musical abilities were qualitatively assessed by expert rating. Her phonetic repertoire was quantitatively assessed. Her vocal production (phonetic and musical) was examined longitudinally with respect to its approximation to the original songs. Results. At three years the autistic girl displays precocious musical competence in singing, which, however, does not grow further from this initial level. Musical creativity and expressiveness grow to a peak in middle childhood and then decline again in adolescence. The girl's phonetic inventory of sounds is highly restricted and shows no progression, but her articulation grows more and more deliberate and, within her bounds, nearer to the original words. The non-verbal girl apparently has a mental representation of the lyrics. Conclusion. 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PD JAN PY 2005 VL 6 IS 1 BP 9 EP 9 DI 10.1038/nrn1598 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 885KI UT WOS:000226155100010 ER PT J AU Seyffert, M Castellanos, FX AF Seyffert, M Castellanos, FX TI Functional MRI in pediatric neurobehavioral disorders SO NEUROIMAGING, PT B SE INTERNATIONAL REVIEW OF NEUROBIOLOGY LA English DT Review ID EVENT-RELATED FMRI; DEFICIT HYPERACTIVITY DISORDER; BODY-IMAGE DISTORTION; MAGNETIC-RESONANCE; RESPONSE-INHIBITION; FACIAL EXPRESSIONS; PREFRONTAL CORTEX; ANOREXIA-NERVOSA; WORKING-MEMORY; YOUNG-CHILDREN AB Pediatric functional neuroimaging has finally come into its own in this new century. In this brief review, we focus on functional magnetic resonance Imaging studies of typically developing children and adolescents that have examined executive function, language, and mood along with studies of autism and autism spectrum disorders, dyslexia, attention deficit hyperactivity disorder, conduct disorder, Tourette's disorder, anxiety disorders, anorexia, and juvenile bipolar disorder. Studies in autism, anxiety disorders, and dyslexia are beginning to provide replicated observations regarding the role of specific brain structures such as the amygdala, or posterior versus anterior language centers in respective models of pathophysiology. However, as is appropriate, the field is still in its infancy, and most studies cited are still exploratory. The increasing number of investigators and active pediatric imaging centers predicts that functional neuroimaging techniques will open an increasingly wider "window" into brain function of children and adolescents burdened with neuropsychiatric disorders. This may warrant the creation of large pediatric neuroimaging databases that will permit sharing of functional magnetic resonance imaging (fMRI) studies of normal and pathological human behavior. C1 NYU, Ctr Child Study, Inst Pediat Neurosci, New York, NY 10016 USA. RP Seyffert, M (reprint author), NYU, Ctr Child Study, Inst Pediat Neurosci, New York, NY 10016 USA. 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We describe several approaches for understanding developmental changes in brain structures based on MRI. Adas-based "parcellation" methods, for example, measure volumes of brain substructures, revealing how they change with age. Growth curves for different brain structures can be compiled, describing the expected trajectories of normal development. Additional computational anatomy techniques can be used to map spatial patterns of brain growth and tissue loss in individual children. Changes in cortical features, such as gray matter thickness, asymmetry, and complexity, can also be mapped. Individual maps can then be combined across subjects to make statistical maps or dynamic "time-lapse movies" that reveal systematic features of brain development in population subgroups while retaining information on their variance. We review several large-scale studies of brain development, including longitudinal studies in which children were scanned repeatedly with structural MRI at 2-year intervals for periods of up to 10 years. Image processing algorithms were then applied to recover detailed information from the resulting image databases. We describe the approaches necessary to compare brain MRI data across groups differing in age, covaried with gender, developmental disorders, or genotype. These methods reveal unsuspected links between development and cognition and can help discover genetic and environmental factors that affect development. These brain maps also chart the anatomical sequence of healthy brain maturation and visualize how it is derailed in neuropsychiatric disorders such as schizophrenia, autism, fetal alcohol syndrome, and Williams syndrome. C1 Univ Calif Los Angeles, Sch Med, Dept Neurol, Brain Mapping Div,Lab Neuro Imaging, Los Angeles, CA 90095 USA. 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Ruby, A Zimmerman-Bier, B AF Jyonouchi, H Geng, L Ruby, A Zimmerman-Bier, B TI Dysregulated innate immune responses in young children with autism spectrum disorders: Their relationship to gastrointestinal symptoms and dietary intervention SO NEUROPSYCHOBIOLOGY LA English DT Article DE tumor necrosis factor-alpha; interleukin-10; lipopolysaccharide; autism spectrum disorders; innate immunity ID TNF-ALPHA SECRETION; TOLL-LIKE RECEPTORS; CYTOKINE PRODUCTION; REGRESSIVE AUTISM; GENETICS; INFANTS; PROTEIN; HOST AB Objective: Our previous study indicated an association between cellular immune reactivity to common dietary proteins (DPs) and excessive proinflammatory cytokine production with endotoxin (lipopolysaccharide, LPS), a major stimulant of innate immunity in the gut mucosa, in a subset of autism spectrum disorder (ASD) children. However, it is unclear whether such abnormal LPS responses are intrinsic in these ASD children or the results of chronic gastrointestinal (GI) inflammation secondary to immune reactivity to DPs. This study further explored possible dysregulated production of proinflammatory and counter-regulatory cytokines with LPS in ASD children and its relationship to GI symptoms and the effects of dietary intervention measures. Methods: This study includes ASD children (median age 4.8 years) on the unrestricted (n = 100) or elimination (n = 77) diet appropriate with their immune reactivity. Controls include children with non-allergic food hypersensitivity (NFH; median age 2.9 years) on the unrestricted (n = 14) or elimination (n = 16) diet, and typically developing children (median age 4.5 years, n = 13). The innate immune responses were assessed by measuring production of proinflammatory (TNF-alpha, IL-1 beta, IL-6, and IL-12) and counter-regulatory (IL-1ra, IL-10, and sTNFRII) cytokines by peripheral blood mononuclear cells (PBMCs) with LPS. The results were also compared to T-cell responses with common DPs and control T-cell mitogens assessed by measuring T-cell cytokine production. Results: ASD and NFH PBMCs produced higher levels of TNF-alpha with LPS than controls regardless of dietary interventions. However, only in PBMCs from ASD children with positive gastrointestinal (GI(+)) symptoms, did we find a positive association between TNF-alpha levels produced with LPS and those with cow's milk protein (CMP) and its major components regardless of dietary interventions. In the unrestricted diet group, GI(+) ASD PBMCs produced higher IL-12 than controls and less IL-10 than GI(-) ASD PBMCs with LPS. GI(+) ASD but not GI(-) ASD or NFH PBMCs produced less counter-regulatory cytokines with LPS in the unrestricted diet group than in the elimination diet group. There was no significant difference among the study groups with regard to cytokine production in responses to T-cell mitogens and other recall antigens. Conclusion: Our results revealed that there are findings limited to GI(+) ASD PBMCs in both the unrestricted and elimination diet groups. Thus our findings indicate intrinsic defects of innate immune responses in GI(+) ASD children but not in NFH or GI(-) ASD children, suggesting a possible link between GI and behavioral symptoms mediated by innate immune abnormalities. Copyright (C) 2005 S. Karger AG, Basel. C1 Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Pediat, Div Pulm Allergy Immunol & Infect Dis, Newark, NJ 07101 USA. RP Jyonouchi, H (reprint author), Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Pediat, Div Pulm Allergy Immunol & Infect Dis, 85 S Orange Ave,POB 1709, Newark, NJ 07101 USA. 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In the current study, the season of birth in 472 Danish children with language disorder born between 1958 and 1976 was compared with the season of birth of all Danish live-born children in the same period. For some part of the period (1964-1969), an excess of boys born in November was found. Particular attention was given to the inconsistent findings also found in language-related disorders like infantile autism and dyslexia and the choice of statistical method to determine seasonality. Copyright (C) 2005 S. Karger AG, Basel. C1 Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. Borkop, Copenhagen, Denmark. Naestved Hosp, Dept Child & Adolescent Psychiat, Naestved, Denmark. RP Mouridsen, SE (reprint author), Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. 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Klin, Ami J. Gauthier, Isabel Skudlarski, Pawel Cohen, Donald J. Gore, John C. Volkmar, Fred R. Schultz, Robert T. TI fMRI activation of the fusiform gyrus and amygdala to cartoon characters but not to faces in a boy with autism SO NEUROPSYCHOLOGIA LA English DT Article DE face processing; social cognition; fusiform face area (FFA); Digimon/Pokemon; perceptual expertise; face module ID PERVASIVE DEVELOPMENTAL DISORDERS; EVENT-RELATED FMRI; FACIAL EXPRESSIONS; SPECTRUM DISORDER; ASPERGER-SYNDROME; CHILDS APPRAISAL; FUNCTIONAL MRI; BRAIN-AREAS; RECOGNITION; PERCEPTION AB Abnormal hypoactivation in the amygdala and fusiform gyrus, brain areas that participate in face processing and social cognition, has consistently been demonstrated in persons with autism. We investigated activity in these areas in a boy with autism, DD, who had a special interest in "Digimon" cartoon characters. DD individuates Digimon faster than familiar faces and objects, but he individuates familiar faces no faster than objects. In contrast, a typically developing boy with an interest in "Pokemon" cartoon characters is equally fast at individuating faces and Pokemon and faster at individuating faces and Pokemon than objects and Digimon. In addition, using functional magnetic resonance imaging (fMRI), we show that DD activates his amygdala and fusiform gyrus for perceptual discriminations involving Digimon but not for those involving familiar or unfamiliar faces. This pattern of activation is not seen in the typically developing control with an interest in Pokemon or in a second comparison case who has autism but no interest in Digimon. These results have important implications for our understanding of autism, cortical face specialization, and the possible role of the amygdala in the development of perceptual expertise. (c) 2004 Elsevier Ltd. All rights reserved. C1 Yale Univ, Sch Med, Child Study Ctr, New Haven, CT 06520 USA. Vanderbilt Univ, Dept Psychol, Nashville, TN 37203 USA. Yale Univ, Sch Med, Magnet Resonance Res Ctr, Dept Diagnost Radiol, New Haven, CT 06510 USA. Vanderbilt Univ, Inst Imaging Sci, Nashville, TN 37203 USA. RP Schultz, RT (reprint author), Yale Univ, Sch Med, Child Study Ctr, POB 207900, New Haven, CT 06520 USA. 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SO NEUROPSYCHOLOGIA LA English DT Article DE autism spectrum disorder; weak central coherence; visual perception ID MOTION PERCEPTION; PSYCHOPHYSICAL PERFORMANCE; CONTRAST SENSITIVITY; BIOLOGICAL MOTION; STREAM FUNCTION; CHILDREN; DEFICIT; DYSLEXIA; SYSTEM; RECOGNITION AB Frith and Happe (Frith, U., & Happe, F. (1994). Autism: Beyond theory of mind. Cognition, 50, 115-132) argue that individuals with autism exhibit 'weak central coherence': an inability to integrate elements of information into coherent wholes. Some authors have speculated that a high-level impairment might be present in the dorsal visual pathway in autism, and furthermore, that this might account for weak central coherence, at least at the visuospatial level. We assessed the integrity of the dorsal visual pathway in children diagnosed with an autism spectrum disorder (ASD), and in typically developing children, using two visual tasks, one examining functioning at higher levels of the dorsal cortical stream (Global Dot Motion (GDM)), and the other assessing lower-level dorsal stream functioning (Flicker Contrast Sensitivity (FCS)). Central coherence was tested using the Children's Embedded Figures Test (CEFT). Relative to the typically developing children, the children with ASD had shorter CEFT latencies and higher GDM thresholds but equivalent FCS thresholds. Additionally, CEFT latencies were inversely related to GDM thresholds in the ASD group. These outcomes indicate that the elevated global motion thresholds in autism are the result of high-level impairments in dorsal cortical regions. Weak vistiospatial coherence in autism may be in the form of abnormal cooperative mechanisms in extra-striate cortical areas, which might contribute to differential performance when processing stimuli as Gestalts, including both dynamic (i.e., global motion perception) and static (i.e., disembedding performance) stimuli. (c) 2004 Elsevier Ltd. All rights reserved. C1 Univ Western Australia, Sch Psychol, Perth, WA 6009, Australia. RP Pellicano, E (reprint author), Univ Sect Child & Adolescent Psychiat, Pk Hosp Children, Old Rd,Headington, Oxford OX3 7LQ, England. 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The detection of a change in eye direction elicited occipito-temporal negativity, which had two major differences between children with and without autism. First, while this occipito-temporal negativity predominated in the right hemisphere of typically developed children. it was distributed equally bilaterally in children with autism. Second, the amplitude of this negativity was more pronounced in typically developed children in response to the detection of direct gaze as compared to averted gaze, but was not sensitive to direct/averted gaze direction in children with autism, which converges with behavioral reports. The results concur with previous literature, suggesting the importance of the right hemisphere, especially the superior temporal sulcus, in gaze processing. Results indicate that deviant neural substrates might be involved in gaze processing in individuals with autism. (c) 2005 Elsevier Ltd. All rights reserved. C1 Univ Tokyo, Grad Sch Arts & Sci, Dept Cognit & Behav Sci, Meguro Ku, Tokyo 1538902, Japan. Natl Inst Special Educ, Sect Educ Children Autism, Tokyo, Japan. Jikei Univ, Dept Human Sci, 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. 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R., 1990, DEV PSYCHOPATHOL, V2, P61, DOI 10.1017/S0954579400000596 vonGrunau M, 1995, PERCEPTION, V24, P1297 Watanabe S, 2002, NEUROSCI LETT, V325, P163, DOI 10.1016/S0304-3940(02)00257-4 Watanabe S, 2003, NEUROSCIENCE, V116, P879, DOI 10.1016/S0306-4522(02)00752-2 Watanabe S, 2001, NEUROIMAGE, V13, P351, DOI 10.1006/nimg.2000.0682 NR 53 TC 68 Z9 69 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PY 2005 VL 43 IS 9 BP 1297 EP 1306 DI 10.1016/j.neuropsychologia.2004.12.002 PG 10 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 944XE UT WOS:000230463600008 PM 15949514 ER PT J AU Joseph, RM Steele, SD Meyer, E Tager-Flusberg, H AF Joseph, RM Steele, SD Meyer, E Tager-Flusberg, H TI Self-ordered pointing in children with autism: failure to use verbal mediation in the service of working memory? SO NEUROPSYCHOLOGIA LA English DT Article ID DORSOLATERAL PREFRONTAL CORTEX; LANGUAGE-ASSOCIATION CORTEX; LONG-TERM-MEMORY; EXECUTIVE FUNCTION; EPISODIC MEMORY; ASPERGERS-SYNDROME; INFANTILE-AUTISM; SEMANTIC MEMORY; FRONTAL-LOBE; PERFORMANCE AB This study tested the hypothesis that children with autism are impaired in using verbal encoding and rehearsal strategies in the service of working memory. Participants were 24 high-ability, school-age children with autism and a comparison group matched on verbal and non-verbal IQ, receptive and expressive vocabulary, and visual memory. Working memory was assessed using verbal and non-verbal variants of a nonspatial, self-ordered pointing test in which children had to point to a new stimulus in a set upon each presentation without repeating a previous choice. In the verbal condition, the stimuli were pictures of concrete, nameable objects, whereas in the non-verbal condition, the stimuli were not easily named or verbally encoded. Participants were also administered a verbal span task to assess non-executive verbal rehearsal skills. Although the two groups were equivalent in verbal rehearsal skills, the autism group performed significantly less well in the verbal, but not the non-verbal, self-ordered pointing test. These findings suggested that children with autism are deficient in the use of verbal mediation strategies to maintain and monitor goal-related information in working memory. The findings are discussed in terms of possible autistic impairments in episodic memory as well as working memory. (c) 2005 Elsevier Ltd. All rights reserved. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Joseph, RM (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St,L-814, Boston, MA 02118 USA. 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T., 1997, EXPRESSIVE VOCABULAR NR 82 TC 36 Z9 36 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0028-3932 J9 NEUROPSYCHOLOGIA JI Neuropsychologia PY 2005 VL 43 IS 10 BP 1400 EP 1411 DI 10.1016/j.neuropsychologia.2005.01.010 PG 12 WC Behavioral Sciences; Neurosciences; Psychology, Experimental SC Behavioral Sciences; Neurosciences & Neurology; Psychology GA 949ST UT WOS:000230809100002 PM 15989932 ER PT J AU Schneider, T Przewlocki, R AF Schneider, T Przewlocki, R TI Behavioral alterations in rats prenatally exposed to valproic acid: Animal model of autism SO NEUROPSYCHOPHARMACOLOGY LA English DT Article DE autism; rats; valproic acid; behavior ID EARLY INFANTILE-AUTISM; BRAIN-STEM; ADDITIONAL EVIDENCE; BETA-ENDORPHIN; CHILDREN; DIAGNOSIS; CEREBELLAR; ORIGIN; ASSOCIATION; INVOLVEMENT AB Autism is a severe behavioral disorder characterized by pervasive impairments in social interactions, deficits in verbal and nonverbal communication, and stereotyped, repetitive patterns of behaviors and interests. Recently, a new rodent model of autism was created by exposure of rat fetuses to valproic acid (VPA) on the 12.5th day of gestation (VPA rats). The model has striking anatomical, pathological, and etiological similarities to human data; however, it has not been characterized behaviorally. In order to determine if VPA rats present behavioral aberrations observed in autism, their behavior was extensively evaluated in a battery of tests. The results of the present experiments demonstrate that VPA rats exhibit: (1) lower sensitivity to pain and higher sensitivity to nonpainful stimuli, (2) diminished acoustic prepulse inhibition, (3) locomotor and repetitive/stereotypic-like hyperactivity combined with lower exploratory activity, and (4) decreased number of social behaviors and increased latency to social behaviors. In addition, VPA rats showed delayed maturation, lower body weight, delayed motor development, and attenuated integration of a coordinated series of reflexes, delayed nest-seeking response mediated by olfactory system, and normal negative geotaxis. Interestingly, all behavioral aberrations described in this paper appear before puberty, which could distinguish the VPA rat model of autism from other animal models of neurodevelopmental disorders, especially rodent models of schizophrenia. Our results bring further support to validity of the proposed VPA animal model of autism, suggesting similarities between the observed pattern of behavioral alterations in VPA rats and features of disturbed behavior in autistic patients. C1 Polish Acad Sci, Inst Pharmacol, Dept Mol Neuropharmacol, PL-31343 Krakow, Poland. Jagiellonian Univ, Inst Appl Psychol, Krakow, Poland. RP Przewlocki, R (reprint author), Polish Acad Sci, Inst Pharmacol, Dept Mol Neuropharmacol, 12 Smetna Str, PL-31343 Krakow, Poland. 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We have used intracellular recording and biocytin-labeling techniques in the in vitro hippocampal slice preparation to provide quantitative evaluation of the fundamental morphological and intrinsic electrophysiological characteristics of macaque monkey CA1 pyramidal neurons. These neurons have previously been studied in the rat in our laboratory. Monkey CA1 pyramidal neurons have an average soma volume of 3578 mu m(3), 4.71 basal dendrites with 53 terminal branches for a dendritic length of about 10,164 gm, 1.13 apical dendrites with 47 terminal branches for a dendritic length of about 10,678 mu m. In comparison, rat CA1 pyramidal neurons have an average soma volume of 2066 mu m(3), 3.35 basal dendrites with 29 terminal branches for a dendritic length of about 4,586 mu m, 1.43 apical dendrites with 62 terminal branches for a dendritic length of about 8,838 mu m. The basic intrinsic electrophysiological properties of CA1 pyramidal cells are similar in monkeys and rats. Monkey CA1 pyramidal neurons have a resting membrane potential of about -62 mV (rat: -62 mV), an input resistance of 35 M Omega (rat: 34-49 M Omega), a rheobase of 0.17 nA (rat: 0.12-0.20 nA) and an action potential amplitude of 83 mV (rat: 71-89 mV). Although morphological differences such as the increased dendritic length may translate into differences in neural processing between primates and rodents, the functional significance of these morphological differences is not yet clear. Quantitative studies of the primate brain are critical in order to extrapolate information derived from rodent studies into better understanding of the normal and pathological function of the human hippocampus. (c) 2005 Published by Elsevier Ltd on behalf of IBRO. C1 Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Tokyo Metropolitan Inst Neurosci, Dept Brain Struct, Tokyo 183, Japan. RP Amaral, DG (reprint author), Univ Calif Davis, MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. 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In the present report, we provide evidence for the endogenous release of secretin in the cerebellum and further characterize the actions of secretin in this brain area. First, to show that secretin is released endogenously, blocks of freshly dissected cerebella were challenged with a high concentration of KCI. Incubation with KCI almost doubled the rate of secretin release. This KCI-induced release was sensitive to tetrodotoxin and cadmium suggesting the involvement of voltage-gated sodium and calcium channels. The use of specific channel blockers further revealed that L-type and P/Q-type calcium channels underlie both basal and KCI-evoked secretin release. In support of this, depolarization of Purkinje neurons in the presence of NMDA, group II mGIuR and cannabinoid CB1 receptor blockers resulted in increased inhibitory postsynaptic current frequency. Second, we found that the previously reported facilitatory action of secretin on GABAergic inputs to Purkinje neurons is partly dependent on the release of endogenous glutamate. In the presence of CNQX, an AMPA/kainate receptor antagonist, the facilitatory effect of secretin on GABA release was significantly reduced. In support of this idea, application of AMPA, but not kainate receptor agonist, facilitated GABA release from inhibitory terminals, an action that was sensitive to AMPA receptor antagonists. These data indicate that a direct and an indirect pathway mediate the action of secretin in the basket cell-Purkinje neuron synapse. The results provide further and more solid evidence for the role of secretin as a neuropeptide in the mammalian CNS. (c) 2005 Published by Elsevier Ltd on behalf of IBRO. C1 Chinese Univ Hong Kong, Fac Med, Dept Physiol, Shatin, Hong Kong, Peoples R China. Univ Hong Kong, Dept Zool, Hong Kong, Hong Kong, Peoples R China. RP Yung, WH (reprint author), Chinese Univ Hong Kong, Fac Med, Dept Physiol, Shatin, Hong Kong, Peoples R China. 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This article presents moral arguments relating to conflicts between individual autonomy and collective responsibilities in vaccination decisions with a view to informing and advising health professionals and improving the effectiveness of education policies in avoiding resurgence of endemic measles. Lower population immunity, due to falling uptake, is hastening the need for greater public awareness of the consequences for the population. Vaccination refusals go hand in hand with responsibilities owed to future generations and society in not knowingly contributing to preventable harms. Issues such as parents' rights are considered and balanced against: collective responsibilities for public health; permissibility of 'free-riding'; conflicting duties of health professionals; and possible enforcement of vaccination. It is suggested that the arguments may form a persuasive tool for the practice of health professionals involved in informing and supporting parents' vaccination decisions. C1 Univ Salford, Sch Community Hlth Sci & Social Care, Manchester M6 6PU, England. RP Wood-Harper, J (reprint author), Univ Salford, Sch Community Hlth Sci & Social Care, Manchester M6 6PU, England. 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Ethics PD JAN PY 2005 VL 12 IS 1 BP 43 EP 58 DI 10.1191/0969733005ne757oa PG 16 WC Nursing SC Nursing GA 883OY UT WOS:000226024000008 PM 15685967 ER PT J AU Elder, JH Valcante, G Yarandi, H White, D Elder, TH AF Elder, JH Valcante, G Yarandi, H White, D Elder, TH TI Evaluating in-home training for fathers of children with autism using single-subject experimentation and group analysis methods SO NURSING RESEARCH LA English DT Article DE autism; father-child interactions; parent training; single-subject experimentation ID PERVASIVE DEVELOPMENTAL DISORDERS; FUNCTIONAL-ANALYSIS; SPECTRUM DISORDERS; INTERVENTIONS; PREVALENCE; CAREGIVERS AB Background: Autism, or the broader category of autistic spectrum disorder, is a complex developmental disability with uncertain etiologies that appears to be increasing in prevalence. Researchers have stated that training programs for children with autism are most effective when they are individualized, address communicative intent of child behaviors, and promote social reciprocity between children and individuals with whom they have regular contact. Yet, to date, most of what is known comes solely from studying mothers, who have traditionally been the most accessible parent. Objectives: In this study the mother-child in-home training program was modified and evaluated for its effects on the acquisition of training skills by fathers and on precommunication skills by the autistic children. Methods: Frequency counts of skills taught to fathers and targeted child behaviors were obtained from videotaped father-child play sessions. These data were analyzed for each father-child dyad by using graphs and visual analyses, which are integral parts of single-participant experimentation. This procedure was replicated across all of the father-child dyads. Data were then grouped and analyzed using the more traditional repeated measures analysis of variance. Results: The most significant findings were increases in father use of imitating with animation (p < .0001) and child initiating following training (p < .0004). Also noteworthy were significant increases in father responding (p < .0005) and child vocalizations (p < .05). Discussion: Results of the study indicate that the in-home training for fathers of children with autism was effective and valued by the participating families. C1 Univ Florida, Coll Nursing, Gainesville, FL 32611 USA. Univ Florida, Ctr Autism & Related Disabil, Gainesville, FL 32611 USA. Univ Florida, Coll Hlth & Human Performance, Gainesville, FL 32611 USA. RP Elder, JH (reprint author), Univ Florida, Coll Nursing, HPNP BLdg 101 Newell Rd,Box 100187, Gainesville, FL 32611 USA. 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PD JAN-FEB PY 2005 VL 54 IS 1 BP 22 EP 32 PG 11 WC Nursing SC Nursing GA 904CY UT WOS:000227474900004 PM 15695936 ER PT J AU Kerkhof, I Verbeke, E Peeters, W Bijttebier, P Steyaert, J Wagemans, J AF Kerkhof, I Verbeke, E Peeters, W Bijttebier, P Steyaert, J Wagemans, J TI The perception of facial expressions in children with autism spectrum disorders SO PERCEPTION LA English DT Meeting Abstract C1 Katholieke Univ Leuven, Lab Expt Psychol, B-3000 Louvain, Belgium. Katholieke Univ Leuven, Dept Psychol Psychodiagnost & Psychopathol, B-3000 Louvain, Belgium. Univ Leuven, Fac Med, B-3000 Louvain, Belgium. EM Inneke.Kerkhof@student.kuleuven.ac.be RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 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 2005 VL 34 SU S BP 169 EP 169 PG 1 WC Psychology; Psychology, Experimental SC Psychology GA 976IE UT WOS:000232726000417 ER PT J AU Austin, EJ AF Austin, EJ TI Personality correlates of the broader autism phenotype as assessed by the Autism Spectrum Quotient (AQ) SO PERSONALITY AND INDIVIDUAL DIFFERENCES LA English DT Article DE personality; autism; Asperger syndrome; AQ; autism phenotype; factor analysis ID 5-FACTOR MODEL; FAMILIES; EXTREME; PARENTS AB The main objective of this study was to characterise the five-factor personality model profile of the broader autism phenotype as assessed by the Autism Spectrum Quotient (AQ). Comparison data were also obtained for a brief Asperger syndrome screening measure. The psychometric properties and factor structure of the AQ were also assessed and group differences in AQ scores examined. The AQ and personality scale were completed by 201 undergraduates. A second group of 136 adults completed the personality scale and the Asperger screening measure. Examination of correlations showed that high scores on both 'autism' measures were associated with high neuroticisin and low extraversion and agreeableness. Three of the five proposed sub-scales of the AQ emerged from the factor analysis. The AQ and sub-scales had satisfactory or near-satisfactory reliabilities. Group differences were generally as expected: Mates had higher AQ scores than females, 'hard' science students had higher scores than other students and students with parent(s) in a scientific occupation had higher scores. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Edinburgh, Sch Philosophy Psychol & Language Sci, Edinburgh EH8 9JZ, Midlothian, Scotland. RP Austin, EJ (reprint author), Univ Edinburgh, Sch Philosophy Psychol & Language Sci, 7 George Sq, Edinburgh EH8 9JZ, Midlothian, Scotland. EM elizabeth.austin@ed.ac.uk RI Austin, Elizabeth/G-4746-2013 OI Austin, Elizabeth/0000-0002-0980-203X CR American Psychiatric Association, 1994, DSM 4 DIAGN STAT MAN, V4th Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S., 1998, AUTISM, V2, P296, DOI 10.1177/1362361398023008 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Baron-Cohen S, 1997, AUTISM INT J RES PRA, V1, P153 Costa P. 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L., 1992, PSYCHOL ASSESSMENT, V4, P47, DOI 10.1037//1040-3590.4.1.47 NR 19 TC 99 Z9 102 PU PERGAMON-ELSEVIER SCIENCE LTD PI OXFORD PA THE BOULEVARD, LANGFORD LANE, KIDLINGTON, OXFORD OX5 1GB, ENGLAND SN 0191-8869 J9 PERS INDIV DIFFER JI Pers. Individ. Differ. PD JAN PY 2005 VL 38 IS 2 BP 451 EP 460 DI 10.1016/j.paid.2004.04.022 PG 10 WC Psychology, Social SC Psychology GA 889FA UT WOS:000226427700017 ER PT J AU Mandell, DS Thompson, WW Weintraub, ES DeStefano, F Blank, MB AF Mandell, DS Thompson, WW Weintraub, ES DeStefano, F Blank, MB TI Trends in diagnosis rates for autism and ADHD at hospital discharge in the context of other psychiatric diagnoses SO PSYCHIATRIC SERVICES LA English DT Article ID DEFICIT-HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; DEVELOPMENTAL-DISABILITIES; RUBELLA VACCINATION; NATIONAL TRENDS; UNITED-STATES; HEALTH-CARE; CHILDREN; PREVALENCE; EPIDEMIOLOGY AB Objective: Concerns have been raised over observed increases in the number of children who are given a diagnosis of a neurodevelopmental disorder. The goal of this study was to examine trends by age and calendar year in the diagnosis of two of these disorders, autism and attention-deficit hyperactivity disorder (ADHD), in the context of other psychiatric disorders in a sample of hospitalized children. Methods: Data from the Healthcare Cost and Utilization Project (HCUP) were used for descriptive analyses of secular trends of diagnosed psychiatric disorders between 1989 and 2000. Changes over time in rates of diagnosis of autism, ADHD, affective disorders, and substance-related disorders were examined and compared. Results: Substance-related disorders were the most common mental disorders recorded at hospital discharge and increased by 39 percent between 1989 and 2000. Affective disorder was the next most common diagnosis and increased by 138 percent. Although autism and ADHD were far less common, their diagnosis rates nearly quadrupled over the course of the study. Although rates of diagnosis of affective and substance-related disorders generally increased over the lifespan, diagnosis of autism and ADHD followed a very different pattern, with peaks in rates at ages seven and 12. Conclusions: Increases in rates of diagnosis of etiologically unrelated mental disorders suggest that there have been changes in diagnostic practices over time, increases in community prevalence of these disorders, and increased likelihood of hospitalizations for different mental disorders. C1 Univ Penn, Ctr Mental Hlth Policy & Serv Res, Philadelphia, PA 19104 USA. Univ Penn, Leonard Davis Inst Hlth Econ, Philadelphia, PA 19104 USA. Ctr Dis Control & Prevent, Natl Immunizat Program, Atlanta, GA USA. RP Mandell, DS (reprint author), Univ Penn, Ctr Mental Hlth Policy & Serv Res, 3535 Market St,3rd Floor, Philadelphia, PA 19104 USA. 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PD JAN PY 2005 VL 56 IS 1 BP 56 EP 62 DI 10.1176/appi.ps.56.1.56 PG 7 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 886HJ UT WOS:000226217200010 PM 15637193 ER PT J AU Maestro, S Muratori, F Cesari, A Cavallaro, MC Paziente, A Pecini, C Grassi, C Manfredi, A Sommario, C AF Maestro, S Muratori, F Cesari, A Cavallaro, MC Paziente, A Pecini, C Grassi, C Manfredi, A Sommario, C TI Course of autism signs in the first year of life SO PSYCHOPATHOLOGY LA English DT Article DE autism spectrum disorders; home movies; behavioral summarized evaluation scale ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDER; HOME MOVIES; EARLY RECOGNITION; CHILDHOOD AUTISM; INFANTILE-AUTISM; FAMILY HISTORY; YOUNG-CHILDREN; AGE; ONSET AB Autism spectrum disorders (ASD) are thought to be present right from birth, even if a minority of children displays a normal course during infancy followed by a regression during the second year of life. However, established criteria are not yet available to differentiate these different courses of ASD, and data coming from different sources have not yet been organized into a clear definition. The aim of this study was to elucidate the time of onset, as well as type, frequency and stability of symptoms during the first year of life in ASD. The behavioral summarized evaluation scale, applied to 40 home movies of children later diagnosed as having ASD, showed that most of the subjects (87.5%) display symptoms within the first year of life, when only a small group (12.5%) is completely symptom free. A group of more rated symptoms was found, constituting a typical pattern characterized by being withdrawn, and displaying poor social initiative, hypoactivity, and lack of emotional modulation. The importance of these findings is discussed in relation to early diagnosis and treatment. Copyright (C) 2005 S. Karger AG, Basel. C1 Univ Pisa, Sci Inst Stella Maris, Div Child Neuropsychiat, Pisa, Italy. RP Muratori, F (reprint author), IRCCS Stella Maris, Via Giacinti 2, IT-56018 Calambrone Pisa, Italy. EM f.muratori@inpe.unipi.it CR ADRIEN J, 1992, J AUTISM DEV DISORD, V3, P375 ADRIEN JL, 1993, J AM ACAD CHILD PSY, V32, P617, DOI 10.1097/00004583-199305000-00019 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Amorosa H, 2002, Z KINDER JUG-PSYCH, V30, P211, DOI 10.1024//1422-4917.30.3.211 Baghdadli A, 2003, EUR CHILD ADOLES PSY, V12, P122, DOI 10.1007/s00787-003-0314-6 Bale JF, 2002, AM J MED GENET, V113, P229, DOI 10.1002/ajmg.10935 Baranek GT, 1999, J AUTISM DEV DISORD, V29, P213, DOI 10.1023/A:1023080005650 BARTHELEMY C, 1990, J AUTISM DEV DISORD, V20, P189, DOI 10.1007/BF02284718 Bristol MM, 1996, J AUTISM DEV DISORD, V26, P121, DOI 10.1007/BF02172002 Courchesne E, 2003, JAMA-J AM MED ASSOC, V290, P337, DOI 10.1001/jama.290.3.337 DAMASIO AR, 1978, ARCH NEUROL-CHICAGO, V35, P777 Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 DELONG GR, 1988, J AUTISM DEV DISORD, V18, P593 DELONG R, 1994, DEV MED CHILD NEUROL, V36, P674 HARPER J, 1975, J AUTISM CHILD SCHIZ, V5, P25, DOI 10.1007/BF01537970 HOSHINO Y, 1987, JPN J PSYCHIAT NEUR, V41, P237 KURITA H, 1992, J AUTISM DEV DISORD, V22, P175, DOI 10.1007/BF01058149 Maestro S, 2002, J AM ACAD CHILD PSY, V41, P1239, DOI 10.1097/01.CHI.0000020277.43550.02 Maestro S, 2001, PSYCHOPATHOLOGY, V34, P147, DOI 10.1159/000049298 Maestro S, 1999, PSYCHOPATHOLOGY, V32, P292, DOI 10.1159/000029102 MALVY J, 1997, NEUROPSYCHIAT ENFAN, V45, P749 Mari M, 2003, PHILOS T ROY SOC B, V358, P393, DOI 10.1098/rstb.2002.1205 MASSIE H, 1984, CHILDHOOD PSYCHOSIS Mundy P, 1997, J AUTISM DEV DISORD, V27, P653, DOI 10.1023/A:1025802832021 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 Osterling JA, 2002, DEV PSYCHOPATHOL, V14, P239 Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 ROGERS SJ, 1990, J AM ACAD CHILD PSY, V29, P863, DOI 10.1097/00004583-199011000-00004 ROSENTHAL J, 1980, J AUTISM DEV DISORD, V10, P433, DOI 10.1007/BF02414819 SAUVAGE D, 1988, ANN PSYCHIAT, V3, P418 Schopler E., 1986, CHILDHOOD AUTISM RAT SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 Teitelbaum P, 1998, P NATL ACAD SCI USA, V95, P13982, DOI 10.1073/pnas.95.23.13982 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 VILENSKY JA, 1981, ARCH NEUROL-CHICAGO, V38, P646 VOLKMAR FR, 1989, J CHILD PSYCHOL PSYC, V30, P717, DOI 10.1111/j.1469-7610.1989.tb00784.x Volkmar FR, 2003, LANCET, V362, P1133, DOI 10.1016/S0140-6736(03)14471-6 Volpe JJ, 2001, NEUROLOGY NEWBORN, p[45, 84, 87, 121, 134, 244, 296, 362, 365, 456, 523, 717, 775] Werner E, 2000, J AUTISM DEV DISORD, V30, P157, DOI 10.1023/A:1005463707029 NR 39 TC 46 Z9 48 PU KARGER PI BASEL PA ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND SN 0254-4962 J9 PSYCHOPATHOLOGY JI Psychopathology PY 2005 VL 38 IS 1 BP 26 EP 31 DI 10.1159/000083967 PG 6 WC Psychiatry SC Psychiatry GA 905HR UT WOS:000227559700004 PM 15731570 ER PT J AU Bolte, D Boschb, G AF Bolte, D Boschb, G TI The long-term outcome in two females with autism spectrum disorder SO PSYCHOPATHOLOGY LA English DT Article DE autism; schizoaffective disorder; anxiety disorder; follow-up; outcome ID PERVASIVE DEVELOPMENTAL DISORDERS; CHILDREN; SCHIZOPHRENIA; ASSOCIATION AB We describe the results of a long-term follow-up examination of two adult females diagnosed exhibiting an autism spectrum disorder in childhood. Over four decades after the initial diagnosis made by Gerhard Bosch, besides Leo Kanner and Hans Asperger, one of the first clinicians to describe cases of autistic behavior, the individuals had largely different psychiatric outcomes. Despite the fact that both females continuously showed definite autistic traits, one woman exhibited a generalized anxiety disorder, while the other was predominantly characterized by schizoaffective symptoms. The trajectories of the two cases are discussed in the light of research on possible associations and overlaps between autism spectrum disorders, psychosis and anxiety disorders. It is suggested that adult outcome studies in autism should consider a broader range of comorbidity. Copyright (C) 2005 S. Karger AG, Basel. C1 Univ Frankfurt Klinikum, Klin Psychiat & Psychotherapie Kindes & Jugendalt, DE-60528 Frankfurt, Germany. RP Bolte, D (reprint author), Univ Frankfurt Klinikum, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, DE-60528 Frankfurt, Germany. 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As evidence, decreased blood levels of omega-3 fatty acids have been associated with several neuropsychiatric conditions, including Attention Deficit ( Hyperactivity) Disorder, Alzheimer's Disease, Schizophrenia and Depression. Supplementation studies, using individual or combination omega-3 fatty acids, suggest the possibility for decreased symptoms associated with some of these conditions. Thus far, however, the benefits of supplementation, in terms of decreasing disease risk and/or aiding in symptom management, are not clear and more research is needed. The reasons for blood fatty acid alterations in these disorders are not known, nor are the potential mechanisms by which omega-3 fatty acids may function in normal neuronal activity and neuropsychiatric disease prevention and/or treatment. It is clear, however, that DHA is the predominant n-3 fatty acid found in the brain and that EPA plays an important role as an anti-inflammatory precursor. Both DHA and EPA can be linked with many aspects of neural function, including neurotransmission, membrane fluidity, ion channel and enzyme regulation and gene expression. This review summarizes the knowledge in terms of dietary omega-3 fatty acid intake and metabolism, as well as evidence pointing to potential mechanisms of omega-3 fatty acids in normal brain functioning, development of neuropsychiatric disorders and efficacy of omega-3 fatty acid supplementation in terms of symptom management. C1 Univ Guelph, Guelph, ON N1G 2W1, Canada. RGB Consulting, London, ON, Canada. RP Conquer, J (reprint author), Univ Guelph, Guelph, ON N1G 2W1, Canada. 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Nutr. Dev. PD JAN-FEB PY 2005 VL 45 IS 1 BP 1 EP 28 DI 10.1051/rnd:2005001 PG 28 WC Developmental Biology; Nutrition & Dietetics; Reproductive Biology; Zoology SC Developmental Biology; Nutrition & Dietetics; Reproductive Biology; Zoology GA 906ZK UT WOS:000227683700001 PM 15865053 ER PT J AU Buckley, SD Newchok, DK AF Buckley, SD Newchok, DK TI Differential impact of response effort within a response chain on use of mands in a student with autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE functional communication training; mands; positive reinforcement; response effort ID FUNCTIONAL COMMUNICATION; PROBLEM BEHAVIOR; SELF-INJURY; REINFORCEMENT; MAINTENANCE; ACQUISITION; EFFICIENCY AB We investigated the effects of response effort on the use of mands during functional communication training (FCT) in a participant with autism. The number of links in a picture exchange response chain determined two levels of response effort. Each level was paired with a fixed ratio (FR3) schedule of reinforcement for aggression in a reversal design. Responding to either schedule produced access to a preferred item. The participant opted for the low effort mand while aggression decreased significantly. However, the high effort mand did not compete with the FR3 schedule for aggression. Results are discussed in terms of response effort within a response chain of a picture exchange system and competing ratio schedules for problem behavior during mand training. (C) 2004 Elsevier Ltd. All rights reserved. C1 Allegro Sch Inc, Cedar Knolls, NJ 07927 USA. RP Buckley, SD (reprint author), Allegro Sch Inc, 125 Ridgedale Ave, Cedar Knolls, NJ 07927 USA. 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Dev. Disabil. PD JAN-FEB PY 2005 VL 26 IS 1 BP 77 EP 85 DI 10.1016/j.ridd.2004.07.004 PG 9 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 886FM UT WOS:000226212300008 PM 15590240 ER PT J AU Sturmey, P AF Sturmey, P TI Secretin is an ineffective treatment for pervasive developmental disabilities: a review of 15 double-blind randomized controlled trials SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE secretin; pervasive developmental disabilities; double-blind randomized controlled trials ID PLACEBO-CONTROLLED TRIAL; AUTISTIC SPECTRUM DISORDERS; SYNTHETIC HUMAN SECRETIN; PORCINE SECRETIN; CHILDREN; BENEFIT AB In 1998, Horvath et al. [Horvath, K., Stefanatos, G., Sokolski, K. N., Wachtel, R., Nabors, L., & Tildon, J. T. (1998). Improved social and language skills after secretin administration in patients with autism spectrum disorders. Journal of the Association of the Academy of Minority Physicians, 9, 9-15] reported an uncontrolled trial of secretin with three participants with autism, which apparently resulted in significant behavioral improvement. Subsequently, secretin was widely used. Sandler et al. [Sandler, A. D., Sutton, K. A., SeWeese, J., Girardi, M. A., Sheppard, V., & Bodfish, J. W. (1999). Lack of benefit of a single dose of synthetic human secretin in the treatment of autism and pervasive and developmental disorder. The New Frigland Journal of Medicine, 341, 1801-1806] reported the first double-blind trial of secretin with negative results. This article is a review of 15 double-blind trials of secretin. Almost none of the studies reported any significant effects and none concluded that secretin was effective. Transient effects of secretin, including both minor benefits and behavioral deterioration were reported, probably due to multiple statistical tests. Four papers reported data on differential responding in sub-groups of participants, including those with gastrointestinal symptoms. These effects were not replicable. At this time there is no robust evidence that secretin is an effective treatment for pervasive developmental disorders. (C) 2004 Elsevier Ltd. All rights reserved. C1 CUNY Queens Coll, Dept Psychol, Flushing, NY USA. CUNY Grad Ctr, Flushing, NY USA. RP Sturmey, P (reprint author), CUNY Queens Coll, Dept Psychol, 65-30 Kissena Blvd, Flushing, NY USA. EM psturmey@aol.com CR Carey T, 2002, J AUTISM DEV DISORD, V32, P161, DOI 10.1023/A:1015493412224 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 HERLIHY WC, 1999, NEW ENGL J MED, V342, P1217 Honomichl RD, 2002, CHILD PSYCHIAT HUM D, V33, P107, DOI 10.1023/A:1020778108068 Horvath K, 1998, J Assoc Acad Minor Phys, V9, P9 HORVATH K, 1999, NEW ENGL J MED, V342, P1216 Kern JK, 2002, J AUTISM DEV DISORD, V32, P153, DOI 10.1023/A:1015441428154 Levy SE, 2003, ARCH DIS CHILD, V88, P731, DOI 10.1136/adc.88.8.731 Molloy CA, 2002, J AUTISM DEV DISORD, V32, P545, DOI 10.1023/A:1021202930206 OWLEY T, 1999, MEDSCAPE GEN MED, V1, P2 Owley T, 2001, J AM ACAD CHILD PSY, V40, P1293, DOI 10.1097/00004583-200111000-00009 Roberts W., 2001, PEDIATRICS, V107, P71 SAID SI, 1999, NEW ENGL J MED, V342, P1217 Sandler AD, 1999, NEW ENGL J MED, V341, P1801, DOI 10.1056/NEJM199912093412404 Sponheim E, 2002, ACTA PAEDIATR, V91, P540, DOI 10.1080/080352502753711669 UNIS AS, 2002, J AM ACAD CHILD ADOL, V41, P1322 VOLKMAR FR, 1999, NEW ENGL J MED, V341, P1824 NR 21 TC 31 Z9 31 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 2005 VL 26 IS 1 BP 87 EP 97 DI 10.1016/j.ridd.2004.09.002 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 886FM UT WOS:000226212300009 PM 15590241 ER PT J AU Ben Shalom, D Bonneh, YS AF Ben Shalom, D Bonneh, YS TI Superior and not so superior visual search in autism: A case study SO REVIEWS IN THE NEUROSCIENCES LA English DT Meeting Abstract C1 Ben Gurion Univ Negev, Zlotowski Ctr Neurosci, IL-84105 Beer Sheva, Israel. Weizmann Inst Sci, IL-76100 Rehovot, Israel. NR 0 TC 0 Z9 0 PU FREUND & PETTMAN PUBLISHERS PI EAST YORKSHIRE PA ENHOLMES HALL, PATRINGTON, EAST YORKSHIRE HU12 OPR, ENGLAND SN 0334-1763 J9 REV NEUROSCIENCE JI Rev. Neurosci. PY 2005 VL 16 SU 1 BP S9 EP S9 PG 1 WC Neurosciences SC Neurosciences & Neurology GA 991HU UT WOS:000233804100037 ER PT J AU Bolduc, C Elyse, L Chevrier, E Mottron, L Godbout, R AF Bolduc, C Elyse, L Chevrier, E Mottron, L Godbout, R TI EEG activity during REM sleep in autism: Primary vs non-primary visual areas SO SLEEP LA English DT Meeting Abstract CT 19th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 18-23, 2005 CL Denver, CO SP Associated Profess Sleep Soc C1 Hop Riviere Des Prairies, Neurodev Disorders Program, Montreal, PQ, Canada. Hop Riviere Des 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 2005 VL 28 SU S MA 905 BP A306 EP A306 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 923JL UT WOS:000228906101413 ER PT J AU Liu, X Hubbard, J Ghosn, MB Adam, JB AF Liu, X Hubbard, J Ghosn, MB Adam, JB TI Parasomnias and correlates among children with autism spectrum disorders SO SLEEP LA English DT Meeting Abstract CT 19th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 18-23, 2005 CL Denver, CO SP Associated Profess Sleep Soc C1 Arizona State Univ, Prevent Res Ctr, Tempe, AZ 85287 USA. NR 0 TC 0 Z9 0 PU AMER ACADEMY SLEEP MEDICINE PI WESTCHESTER PA ONE WESTBROOK CORPORATE CENTER STE 920, WESTCHESTER, IL 60154 USA SN 0161-8105 J9 SLEEP JI Sleep PY 2005 VL 28 SU S MA 294 BP A99 EP A99 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 923JL UT WOS:000228906100295 ER PT J AU Malow, BA Henderson, L Stone, W McGrew, S MacDonald, L Babb, C AF Malow, BA Henderson, L Stone, W McGrew, S MacDonald, L Babb, C TI Insomnia in children with autism spectrum disorders SO SLEEP LA English DT Meeting Abstract CT 19th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 18-23, 2005 CL Denver, CO SP Associated Profess Sleep Soc C1 Vanderbilt Univ, Nashville, TN USA. NR 0 TC 0 Z9 0 PU AMER ACADEMY SLEEP MEDICINE PI WESTCHESTER PA ONE WESTBROOK CORPORATE CENTER STE 920, WESTCHESTER, IL 60154 USA SN 0161-8105 J9 SLEEP JI Sleep PY 2005 VL 28 SU S MA 279 BP A94 EP A95 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 923JL UT WOS:000228906100280 ER PT J AU Rowe, M Phipps, C Sweatland, L Lawson, A Medley, E AF Rowe, M Phipps, C Sweatland, L Lawson, A Medley, E TI Using technology to improve sleep in parents of children with autism SO SLEEP LA English DT Meeting Abstract CT 19th Annual Meeting of the Associated-Professional-Sleep-Societies CY JUN 18-23, 2005 CL Denver, CO SP Associated Profess Sleep Soc C1 Univ Florida, Coll Nursing, Gainesville, FL 32611 USA. NR 0 TC 0 Z9 0 PU AMER ACADEMY SLEEP MEDICINE PI WESTCHESTER PA ONE WESTBROOK CORPORATE CENTER STE 920, WESTCHESTER, IL 60154 USA SN 0161-8105 J9 SLEEP JI Sleep PY 2005 VL 28 SU S MA 230 BP A78 EP A78 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 923JL UT WOS:000228906100231 ER PT J AU Ronald, A Happe, F Hughes, C Plomin, R AF Ronald, A Happe, F Hughes, C Plomin, R TI Nice and nasty theory of mind in preschool children: Nature and nurture SO SOCIAL DEVELOPMENT LA English DT Article DE theory of mind; temperament; genetics; development ID THEORY-OF-MIND; INDIVIDUAL-DIFFERENCES; FALSE BELIEF; BEHAVIOR; LANGUAGE; AUTISM; BIAS; QUESTIONNAIRE; CHILDHOOD; DECEPTION AB Experimental research suggests the differentiation of 'nice' and 'nasty' theory of mind (ToM). Over 5000 parents from the Twins Early Development Study reported on nice (e.g., being considerate) and nasty (e.g., blaming others) behaviours following their twins' second, third, and fourth birthdays. Factor analyses yielded four factors and it was proposed that these related to prosocial behaviour necessitating ToM (Nice ToM), antisocial behaviour necessitating ToM (Nasty ToM), and prosocial and antisocial behaviour not necessitating ToM (Nice and Nasty). Interscale correlations, gender differences, and their relationship with language were consistent with this distinction. Both ToM scales showed moderate heritability and significant environmental influences (shared and nonshared). Bivariate analyses indicated somewhat distinct aetiological influences on Nice ToM versus Nasty ToM. However, further research is needed to confirm whether this distinction reflects interactions between ToM and temperament, or two underlying genetic and cognitively distinct ToM abilities. C1 Inst Psychiat, Social Genet & Dev Psychiat Ctr, London SE5 8AF, England. Univ Cambridge, Cambridge CB2 1TN, England. RP Ronald, A (reprint author), Inst Psychiat, Social Genet & Dev Psychiat Ctr, Box P083,De Crespigny Pk, London SE5 8AF, England. EM a.ronald@iop.kcl.ac.uk RI Happe, Francesca/D-5544-2012; Ronald, Angelica/C-7812-2009; Plomin, Robert/B-8911-2008 OI Ronald, Angelica/0000-0002-9576-2176; CR Argyle M., 1991, COOPERATION BASIS SO Astington JW, 1999, DEV PSYCHOL, V35, P1311, DOI 10.1037//0012-1649.35.5.1311 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 BEHAR L, 1974, DEV PSYCHOL, V10, P601, DOI 10.1037/h0037058 Byrne R. 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Dev. PY 2005 VL 14 IS 4 BP 664 EP 684 DI 10.1111/j.1467-9507.2005.00323.x PG 21 WC Psychology, Developmental SC Psychology GA 978CS UT WOS:000232850400007 ER PT J AU Janusonis, S AF Janusonis, Skirmantas TI Statistical distribution of blood serotonin as a predictor of early autistic brain abnormalities SO THEORETICAL BIOLOGY AND MEDICAL MODELLING LA English DT Article AB Background: A wide range of abnormalities has been reported in autistic brains, but these abnormalities may be the result of an earlier underlying developmental alteration that may no longer be evident by the time autism is diagnosed. The most consistent biological finding in autistic individuals has been their statistically elevated levels of 5-hydroxytryptamine (5-HT, serotonin) in blood platelets (platelet hyperserotonemia). The early developmental alteration of the autistic brain and the autistic platelet hyperserotonemia may be caused by the same biological factor expressed in the brain and outside the brain, respectively. Unlike the brain, blood platelets are short-lived and continue to be produced throughout the life span, suggesting that this factor may continue to operate outside the brain years after the brain is formed. The statistical distributions of the platelet 5-HT levels in normal and autistic groups have characteristic features and may contain information about the nature of this yet unidentified factor. Results: The identity of this factor was studied by using a novel, quantitative approach that was applied to published distributions of the platelet 5-HT levels in normal and autistic groups. It was shown that the published data are consistent with the hypothesis that a factor that interferes with brain development in autism may also regulate the release of 5-HT from gut enterochromaffin cells. Numerical analysis revealed that this factor may be non-functional in autistic individuals. Conclusion: At least some biological factors, the abnormal function of which leads to the development of the autistic brain, may regulate the release of 5-HT from the gut years after birth. If the present model is correct, it will allow future efforts to be focused on a limited number of gene candidates, some of which have not been suspected to be involved in autism (such as the 5-HT(4) receptor gene) based on currently available clinical and experimental studies. C1 Yale Univ, Sch Med, Dept Neurobiol, New Haven, CT 06520 USA. RP Janusonis, S (reprint author), Yale Univ, Sch Med, Dept Neurobiol, POB 208001, New Haven, CT 06520 USA. EM skirmantas.janusonis@yale.edu FU National Alliance for Autism Research (NAAR) FX I thank Dr. P. Rakic and the National Alliance for Autism Research (NAAR) for their financial support, the anonymous reviewers for their valuable suggestions, and Dr. G.M. Anderson, Dr. A.E. Ayoub and Michael Fischer for their comments on the revised manuscript. I also thank Vaiva, my inspiration. 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Biol. Med. Model. PY 2005 VL 2 AR 27 DI 10.1186/1742-4682-2-27 PG 16 WC Mathematical & Computational Biology SC Mathematical & Computational Biology GA V19EC UT WOS:000208054700027 PM 16029508 ER PT J AU Nation, K Norbury, CF AF Nation, K Norbury, CF TI Why reading comprehension fails - Insights from developmental disorders SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE autism; comprehension; language impairment; reading ID INDIVIDUAL-DIFFERENCES; LANGUAGE IMPAIRMENT; MEMORY SKILLS; FOLLOW-UP; CHILDREN; DIFFICULTIES; HYPERLEXIA; INFERENCE; ABILITY; DYSLEXIA AB Developmental difficulties with reading comprehension are not uncommon. This article examines the nature of reading comprehension deficits in three groups of children: children identified as having relatively specific impairments in reading comprehension, children with autism spectrum disorder, and children with specific language impairment. Our review emphasizes that in all three groups, poor reading comprehension is often associated with weaknesses in oral language. We conclude that a useful framework for understanding the complex relationship between language and reading in children with developmental disorders is provided by a model that sees variations in phonological and nonphonological language skills relating to different patterns of reading behavior. This framework also provides a useful basis for identifying children with poor reading comprehension, and for planning appropriately targeted interventions. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. RP Nation, K (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. 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PD JAN-MAR PY 2005 VL 25 IS 1 BP 21 EP 32 PG 12 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 917AY UT WOS:000228429400004 ER PT S AU Karbowniczek, M Henske, EP AF Karbowniczek, M Henske, EP BE ElDeiry, WS TI The role of tuberin in cellular differentiation: Are B-raf and MAPK involved? SO TUMOR PROGRESSION AND THERAPEUTIC RESISTANCE SE ANNALS OF THE NEW YORK ACADEMY OF SCIENCES LA English DT Article; Proceedings Paper CT Conference on Tumor Progression and Therapeutic Resistance CY NOV 08-09, 2004 CL Philadelphia, PA SP Univ Penn, Abramson Canc Ctr, Global Technol Comm LLC, Pfizer Inc, Fels Inst Canc Res, Thomas Jefferson Univ, Kimmel Canc Ctr, Wistar Inst DE TSC; tuberous sclerosis complex; mTOR; LAM; lymphangiomy-omatosis; TSC2; tuberin; TSC1; hamartin; Rheb; MAPK; B-Raf; C-Raf ID TUMOR-SUPPRESSOR GENE; S6 KINASE ACTIVATION; SCLEROSIS GENE; MAMMALIAN TARGET; PULMONARY LYMPHANGIOLEIOMYOMATOSIS; SOMATIC MUTATIONS; TSC1 GENE; A-RAF; RHEB; PRODUCT AB Tuberous sclerosis complex (TSC) is a tumor suppressor gene syndrome whose manifestations can include seizures, mental retardation, autism, and tumors in the brain, retina, kidney, heart, and skin. The products of the TSC1 and TSC2 genes, hamartin and tuberin, respectively, heterodimerize and inhibit the mammalian target of rapamycin (mTOR). This review focuses on the genetic and biochemical basis of the renal and pulmonary manifestations of TSC, angiomyolipomas, and lymphangiomyomatosis, respectively. Genetic analyses of sporadic angiomyolipomas revealed that all three components (smooth muscle, vessels, and fat) derive from a common progenitor cell, indicating the ability of cells lacking tuberin to differentiate into multiple lineages. Other genetic studies showed that the benign smooth muscle cells of pulmonary lymphangiomyomatosis have the ability to migrate to other organs. These findings suggest that tuberin and hamartin play a role in the regulation of cellular migration and differentiation. We have found that tuberin activates B-Raf kinase and p42/44 MAPK and that cells lacking tuberin have low levels of B-Raf activity. 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PY 2005 VL 1059 BP 168 EP 173 DI 10.1196/annals.1339.045 PG 6 WC Oncology; Multidisciplinary Sciences; Pharmacology & Pharmacy SC Oncology; Science & Technology - Other Topics; Pharmacology & Pharmacy GA BDZ00 UT WOS:000236279200016 PM 16382052 ER PT S AU Kientz, JA Boring, S Abowd, GD Hayes, GR AF Kientz, JA Boring, S Abowd, GD Hayes, GR BE Beigl, M Intille, S Rekimoto, J Tokuda, H TI Abaris: Evaluating automated capture applied to structured autism interventions SO UBICOMP 2005: UBIQUITOUS COMPUTING, PROCEEDINGS SE LECTURE NOTES IN COMPUTER SCIENCE LA English DT Article; Proceedings Paper CT 7th International Conference on Ubiquitous Computing CY SEP 11-14, 2005 CL Tokyo, JAPAN SP KDDI R&D Labs, NTT DoCoMo, NEC, Fuji Xerox, Fujitsu, Intel, Microsoft, Crossbow, IBM, Mistubishi Elect, Uchida, NTT, DNP, Ubitec, Panasonic, Toshiba, Hitachi, CiscoSystems, Ubiquitous Networking Forum AB We present an example of an automated capture application which provides access to details of discrete trial training, a highly structured intervention therapy often used with developmentally disabled children. This domain presents an interesting case study for capture technology, because of the well-defined practices and the tradition of manual recording and review of materials. There is a strong motivation for therapists to review the rich record of therapy sessions that is made possible by recorded video, but acceptance hinges on minimal intrusion upon the human activities. To achieve that, we leverage several perception technologies that fit with the natural activities of the live experience and allow the creation of meaningful indices. We also critically explore the contribution various perception technologies have on the overall utility of the capture system. C1 Georgia Inst Technol, Coll Comp, Atlanta, GA 30332 USA. Georgia Inst Technol, GVU Ctr, Atlanta, GA 30332 USA. Univ Munich, Munich, Germany. RP Kientz, JA (reprint author), Georgia Inst Technol, Coll Comp, Atlanta, GA 30332 USA. EM julie@cc.gatech.edu; boring@cip.ifi.lmu.de; abowd@cc.gatech.edu; gillian@cc.gatech.edu CR Alberto P. A., 2003, APPL BEHAV ANAL TEAC ARNSTEIN L, 2002, IEEE PERVASIVE COMPU BENFORD S, 2004, UBICOMP 2004 BROTHERTON JA, 2003, ACM T COMP HUM INT CHEVERST K, 2000, SIGCHI C HUM FACT CO CHIU PI, 1999, NACM MULTIMEDIA DAVIS RC, 1999, CHI 1999 GEMMELL J, 2002, ACM MULTIMEDIA 02 GRUDIN J, 1994, COMMUNICATIONS ACM HAYES GR, 2004, MOBILE HCI 2004 HAYES GR, 2004, UBICOMP 2004 Heflin L.J., 1998, FOCUS AUTISM OTHER D, V13, P194, DOI DOI 10.1177/108835769801300401 Lehman JF, 1998, 3 INT ACM C ASS TECH Lovaas O. I., 1981, TEACHING DEV DISABLE MACKAY WE, 1998, CHI 1998 PEDERSEN ER, 1993, ACM INTERCHI 1993 PHILIPOSE M, 2004, IEEE PERVASIVE C OCT, P50 RICHTER H, 2001, ACM C UB COMP ATL GA STIFELMAN LJ, 1997, MEDIA LAB TRUONG KN, 1999, CHI 1999 VEMURI S, 2004, UBICOMP 2004 NOTT UK 2002, MTRIALS NR 22 TC 4 Z9 5 PU SPRINGER-VERLAG BERLIN PI BERLIN PA HEIDELBERGER PLATZ 3, D-14197 BERLIN, GERMANY SN 0302-9743 BN 3-540-28760-4 J9 LECT NOTES COMPUT SC PY 2005 VL 3660 BP 323 EP 339 PG 17 WC Computer Science, Theory & Methods SC Computer Science GA BDA47 UT WOS:000232266200019 ER PT J AU Bolte, S Poustka, F AF Bolte, S Poustka, F TI Psychodiagnostic instruments for the assessment of autism spectrum disorders SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Review DE autism; diagnostics; early recognition; questionnaires; rating scales; interviews ID PERVASIVE DEVELOPMENTAL DISORDERS; BEHAVIORAL SUMMARIZED EVALUATION; HIGH-FUNCTIONING AUTISM; SCHOOL-AGE-CHILDREN; DIAGNOSTIC INTERVIEW; RATING-SCALE; ASPERGER-SYNDROME; YOUNG-CHILDREN; INTERRATER RELIABILITY; SCREENING INSTRUMENT AB Objectives: Established scales for the early detection and general diagnostics of autism will be reviewed with a focus on the instruments available in German. Methods: All questionnaires, observation scales and interviews for the assessment of autism and associated conditions found in a search of Medline, PsychInfo, Psyndex and Google up to May 2004 are quoted. Instruments adapted and developed for the German-speaking countries are presented in more depth. Results: An increasing number of reliable national and international scales for the assessment of disorders of the autism spectrum are available. Currently a combination of the Social Communication Questionnaire (SCQ), the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview-Revised (ADI-R) is regarded as the standard for a psychometrically based diagnosis of autism. Conclusions: For certain diagnostic groups and issues there continues to be a need for German-language instruments. Particularly scales for the assessment of the broader phenotype of autism, as well as instruments that are more sensitive to change would be desirable for Outcome measurement and intervention evaluation. C1 Goethe Univ Frankfurt, Klin Psychiat & Psychotherapie Kindes & Jugendalt, DE-60528 Frankfurt, Germany. RP Bolte, S (reprint author), Goethe Univ Frankfurt, Klin Psychiat & Psychotherapie Kindes & Jugendalt, Deutschordenstr 50, DE-60528 Frankfurt, Germany. EM Boelte@em.uni-frankfurt.de CR ADRIEN JL, 1992, J AUTISM DEV DISORD, V22, P375, DOI 10.1007/BF01048241 ATTWOOD T, 2000, ASPERGER SYNDROM RAT ATTWOOD T, 1998, ASPERGERS SYNDROME G, P16 Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 BARTHELEMY C, 1990, J AUTISM DEV DISORD, V20, P189, DOI 10.1007/BF02284718 Bishop DVM, 1998, J CHILD PSYCHOL PSYC, V39, P879, DOI 10.1017/S0021963098002832 Bolte S, 2004, Z KINDER JUG-PSYCH, V32, P45, DOI 10.1024/1422-4917.32.1.45 Bolte S, 2000, DIAGNOSTICA, V46, P149, DOI 10.1026//0012-1924.46.3.149 Brereton AV, 2002, J AM ACAD CHILD PSY, V41, P1369, DOI 10.1097/01.CHI.0000024838.94814.A5 CASTELLOE P, 1993, J AUTISM DEV DISORD, V23, P229, DOI 10.1007/BF01046217 COHEN IL, 1993, J AUTISM DEV DISORD, V23, P443, DOI 10.1007/BF01046050 Cohen IL, 2003, J AUTISM DEV DISORD, V33, P31, DOI 10.1023/A:1022226403878 Constantino JN, 2003, J AUTISM DEV DISORD, V33, P427, DOI 10.1023/A:1025014929212 DAHLGREN SO, 1989, EUR ARCH PSY CLIN N, V238, P169 de Bildt A, 2003, J AUTISM DEV DISORD, V33, P595, DOI 10.1023/B:JADD.0000005997.92287.a3 DOPFNER M, 1998, DIAGNOSTIK SYSTEM ST Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 FREEMAN BJ, 1986, J AM ACAD CHILD PSY, V25, P130, DOI 10.1016/S0002-7138(09)60610-5 Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 GILLIAM J, 2003, GILLIAM AUTISM RATIN GILLIAM J, 1995, GILLIAM ASPERGERS DI Hubl D, 2003, NEUROLOGY, V61, P1232 KAMPBECKER I, IN PRESS Z KINDER JU KEHRER H, 1995, AUTISMUS DIANGOSTISC KRAIJER D, 1992, AUTISME VERWANTE STO Kraijer D., 2003, SKALA ERFASSUNG AUTI KRUG DA, 1980, J CHILD PSYCHOL PSYC, V21, P221, DOI 10.1111/j.1469-7610.1980.tb01797.x Krug DA, 1993, AUTISM SCREENING INS KURSCHAT M, 1983, THESIS U MUNSTER 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., 2001, AUTISM DIAGNOSTIC OB Luteijn E, 2000, J AUTISM DEV DISORD, V30, P317, DOI 10.1023/A:1005527300247 Matson JL, 1996, RES DEV DISABIL, V17, P135, DOI 10.1016/0891-4222(95)00044-5 MESIBOV G, 2000, AAPEP ENTWICKLUNGS V Mesibov G. B., 1988, ADOLESCENT ADULT PSY Bolte S, 2001, Z KINDER JUG-PSYCH, V29, P221, DOI 10.1024//1422-4917.29.3.221 Myles B. S., 2001, ASPERGER SYNDROME DI Nylander L, 2001, ACTA PSYCHIAT SCAND, V103, P428, DOI 10.1034/j.1600-0447.2001.00175.x Poustka F, 1996, PSYCHOPATHOLOGY, V29, P145 POUSTKA F, 2004, AUTISTISCHE STORUNGE, V5 RIMLAND B, 1971, J AUTISM CHILD SCHIZ, V1, P161, DOI 10.1007/BF01537955 Robins DL, 2001, J AUTISM DEV DISORD, V31, P131, DOI 10.1023/A:1010738829569 Ruhl D, 2004, DIAGNOSTISCHE BEOBAC RUHL D, 1995, AUTISMUS DIAGNOSTISC RUTTENBE.BA, 1966, J AMER ACAD CHILD PS, V5, P453, DOI 10.1016/S0002-7138(09)62093-8 RUTTER M, 2003, AUTISM DIANGNOSTIC I Rutter M., 2003, SOCIAL COMMUNICATION Scambler D, 2001, J AM ACAD CHILD PSY, V40, P1457, DOI 10.1097/00004583-200112000-00017 SCHOPLER E, 1990, PSYCHOEDCATIONAL PRO SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 SCHOPLER E, 2000, PEP R ENTWICKLUNGS V Scott FJ, 2002, AUTISM, V6, P9, DOI 10.1177/1362361302006001003 SEIGEL B, 2004, PERVASIVE DEV DISORD Skuse D, 2004, J AM ACAD CHILD PSY, V43, P548, DOI 10.1097/00004583-200405000-00008 SQUIRES J, 2002, PARENT COMPLETED CHI STEINHAUSEN HC, 1996, PSYCHISCHE STORUNGEN STEINHAUSEN HC, 2002, PSYCHISCHE STORUNGEN Stone WL, 2003, AUTISM, V7, P9, DOI 10.1177/1362361303007001003 Stone WL, 2000, J AUTISM DEV DISORD, V30, P607, DOI 10.1023/A:1005647629002 Tobing LE, 2002, RES DEV DISABIL, V23, P211, DOI 10.1016/S0891-4222(02)00099-9 Van Bourgondien ME, 1998, RES DEV DISABIL, V19, P381 WILLEMSENSWINKE.SH, 2001, SOC RES CHILD DEV AP Wing L, 2002, J CHILD PSYCHOL PSYC, V43, P307, DOI 10.1111/1469-7610.00023 NR 66 TC 11 Z9 11 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD JAN PY 2005 VL 33 IS 1 BP 5 EP 14 DI 10.1024/1422-4917.33.1.5 PG 10 WC Psychiatry SC Psychiatry GA 891TG UT WOS:000226603300002 PM 15714836 ER PT J AU Kamp-Becker, I Mattejat, F Wolf-Ostermann, K Remschmidt, H AF Kamp-Becker, I Mattejat, F Wolf-Ostermann, K Remschmidt, H TI The Marburg Rating Scale for Aspergers syndrome (MBAS) - a screening instrument for high functioning autistic disorders SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE Asperger's Syndrome; high-functioning autism; diagnostics; screening ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; SPECTRUM; BEHAVIOR; CHILDREN AB Objectives: Asperger's Syndrome is a disorder of uncertain nosological validity, which is difficult to differentiate from high-functioning autism. Even today these disorders are unfortunately diagnosed very late, often in the wake of earlier, different diagnoses. The purpose of this study is to present a screening instrument (MBAS), which is sensitive to these disorders. Methods: The instrument was tested among a total of 91 probands (44 of whom had been diagnosed as autistic, and 47 of whom had been diagnosed with a non-autistic disorder). Results: The items on the WAS were of average difficulty; generally, the all item-total correlation was good. The total scale has an internal consistency of Cronbach's alpha = .91 and the convergent validity of the WAS and the ADI-R reached r = .61 (p = .001). The total score of the questionnaire discriminated highly significantly between the group with autism and that without. At a sensitivity of 95.5% and a specificity of 95.7% the number of misclassifications is low. False negative classifications occurred only in the case of very young children. Conclusions: The MBAS is a reliable and valid instrument for screening and generating tentative diagnoses of high-functioning autism. The questionnaire is well suited for the selection and generation of tentative diagnoses of autism on a high-functioning level. C1 Univ Marburg, Klin Psychiat & Psychotherapie Kines & Jugendalte, DE-35039 Marburg, Germany. RP Kamp-Becker, I (reprint author), Univ Marburg, Klin Psychiat & Psychotherapie Kines & Jugendalte, Hans Sachs Str 4 & 6, DE-35039 Marburg, Germany. EM kampbeck@med.uni-marburg.de CR Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 ATTWOOD T, 2000, ASPERGER SYNDROME RO Bolte S, 2000, DIAGNOSTICA, V46, P149, DOI 10.1026//0012-1924.46.3.149 Bonus B, 1997, FORTSCHR NEUROL PSYC, V65, P41, DOI 10.1055/s-2007-996308 CAMPBELL DT, 1959, PSYCHOL BULL, V103, P276 Fahrmeir L., 1996, MULTIVARIATE STAT VE Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Fombonne E., 2003, TRENDS EVIDENCE BASE, V5, P29 Gilchrist A, 2001, J CHILD PSYCHOL PSYC, V42, P227, DOI 10.1017/S0021963001006631 GILIAM JE, 2001, GILLIAM ASPERGERS DI Goldstein S, 2002, J AUTISM DEV DISORD, V32, P611, DOI 10.1023/A:1021215300163 Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 KAMPBECKER I, IN PRESS PRAXIS KIND KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Klin A., 2000, ASPERGER SYNDROME LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 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 LROD C, 1997, HDB AUTISM PERVASIVE Mayes SD, 2001, AUTISM, V5, P81, DOI 10.1177/1362361301005001008 Bolte S, 2001, Z KINDER JUG-PSYCH, V29, P221, DOI 10.1024//1422-4917.29.3.221 MYLES BS, 2001, ASPERGER SYNDROME DI Ozonoff S., 2000, AUTISM, V4, P29, DOI DOI 10.1177/1362361300041003 Poustka F, 1996, PSYCHOPATHOLOGY, V29, P145 REMSCHMIDT H, 2000, AUTISMUS ERSCHEINUNG Remschmidt H, 2001, Z KINDER JUG-PSYCH, V29, P59, DOI 10.1024//1422-4917.29.1.59 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 RUHL D, 2000, NERVENARZT, V72, P535 SZATMARI P, 1995, J AM ACAD CHILD PSY, V34, P1662, DOI 10.1097/00004583-199512000-00017 Tanguay PE, 2000, J AM ACAD CHILD PSY, V39, P1079, DOI 10.1097/00004583-200009000-00007 TANTAM D, 1988, J CHILD PSYCHOL PSYC, V29, P245, DOI 10.1111/j.1469-7610.1988.tb00713.x Tidmarsh L, 2003, CAN J PSYCHIAT, V48, P517 Tsatsanis KD, 2003, CHILD ADOL PSYCH CL, V12, P47, DOI 10.1016/S1056-4993(02)00056-1 VOLKMAR FR, 2000, DIANGOSTIC ISSUES AS NR 35 TC 12 Z9 12 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD JAN PY 2005 VL 33 IS 1 BP 15 EP 26 DI 10.1024/1422-4917.33.1.15 PG 12 WC Psychiatry SC Psychiatry GA 891TG UT WOS:000226603300003 PM 15714837 ER PT J AU Melfsen, S Walitza, S Attwood, A Warnke, A AF Melfsen, S Walitza, S Attwood, A Warnke, A TI Validation of the German version of the Australian Scale of Asperger's syndrome (ASAS) SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE Asperger's Syndrome; screening; children and adolescents ID TOTAL POPULATION; AUTISM; CHILDREN; EPIDEMIOLOGY AB Objectives: The aim of the study was to validate the German version of the Australian Scale for Asperger's Syndrome (ASAS). Furthermore, the scoring of the ASAS as applied by the Australian authors was verified. Methods: The mothers of 18 children with Asperger's Syndrome, those of 18 children referred for a possible diagnosis of Asperger's Syndrome, but who did not receive that diagnosis, and the mothers of 15 children with other mental disorders participated in the study. All of the children were inpatients at the University of Wuerzburg Hospital of Child and Adolescent Psychiatry. Results: According to an analysis of variance, the scale successfully differentiates among the three samples. A stepwise discriminant analysis was performed. Classification results show that the membership of the three groups could be labelled accurately (accuracy rate: 60.78%). The ASAS's scoring methodology appears to yield good results for German patients. Conclusions: The scale appears to be an adequate tool for screening purposes in that it correctly discriminates children and adolescents with Asperger's Syndrome. C1 Univ Wurzburg, Klin & Poliklin Kinder & Jugendpsychiat & Psychot, D-97070 Wurzburg, Germany. MacGregor Specialist Ctr, Brisbane, Qld, Australia. RP Melfsen, S (reprint author), Fuchsleinstr 15, DE-97080 Wurzburg, Germany. CR [Anonymous], 2001, DIAGNOSTISCHES STAT ATTWOOD T, 2000, ASPERGER SYNDROME RA BARONCOHEN S, 2000, UNDERSTANDING MINDS BARONCOHEN S, 1989, BRIT J CLIN PSYCHOL, V28, P193 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 CHAKRABARTI S, 2001, JAMA-J AM MED ASSOC, V285, P2093 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x GARNETT MS, 1995, AUSTR SCALE ASPERGER GILLIAM JE, 2001, GILLIAM ASPERGERS DI Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 JORGENSEN OS, 2002, ASPERGER SYNDROM ZWI Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 KAMPBECKER I, IN PRESS Z KINDER JU LROD C, 1994, CHIDL ADOLESCENT PSY Mayes SD, 2001, AUTISM, V5, P81, DOI 10.1177/1362361301005001008 MYELS BS, 2001, ASPERGER SYNDROME DI POUSTKA F, 2004, AUTISTISCHE STORUNGE, V5 Premack D., 1978, BEHAVIORAL BRAIN SCI, V4, P515, DOI [10.1017/S0140525X00076512, DOI 10.1017/S0140525X00076512] Remschmidt H, 2001, Z KINDER JUG-PSYCH, V29, P59, DOI 10.1024//1422-4917.29.1.59 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 SZATMARI P, 1989, CAN J PSYCHIAT, V34, P554 Tsatsanis KD, 2003, CHILD ADOL PSYCH CL, V12, P47, DOI 10.1016/S1056-4993(02)00056-1 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1981, PSYCHOL MED, V11, P115 World Health Organization, 1991, ICD 10 CLASS MENT BE NR 26 TC 4 Z9 4 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD JAN PY 2005 VL 33 IS 1 BP 27 EP 34 DI 10.1024/1422-4917.33.1.27 PG 8 WC Psychiatry SC Psychiatry GA 891TG UT WOS:000226603300004 PM 15714838 ER PT J AU Hippler, K Klicpera, C AF Hippler, K Klicpera, C TI Hans Asperger and his patients - a retrospective examination of the spectrum of Autistic disorders SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE Asperger's Syndrome; autistic psychopathy; autistic spectrum; autistic phenotype ID SYNDROME/HIGH-FUNCTIONING AUTISM AB Hans Asperger and His Patients - a Retrospective Examination of the Spectrum of Autistic Disorders In 1944 the Viennese paediatrician Hans Asperger described for the first time a number of boys with so-called "autistic psychopathy" but failed to give a detailed quantitative-descriptive phenomenology of the condition. The aim of this second part of a retrospective analysis of the clinical case records of children diagnosed by Asperger and his team is to provide a quantitative, in-depth description of these children, as well as to investigate Asperger's idea of a transition from autistic psychopathic personality traits towards "normality". We examined 181 case records of children seen between 1950 and 1986 who were either clearly diagnosed with autistic psychopathy (AP) or showed autistic features (AZ). Consequently, features common to both the AP and AZ groups and the differences between them are described and compared to the current ICD-10 criteria for Asperger's syndrome. Children with AZ shared the high intelligence, the social handicap and the impairment of "instincts", but showed less severe symptoms and more distinct skills, as well as fewer co-morbid disorders than children with AP. Results suggest that there is indeed something like an "autistic phenotype" with certain deficits and assets that can be found in less handicapped children with autistic impain-nents. The current ICD-10 criteria do not seem to fully capture Asperger's original account of the syndrome and should be discussed anew if Asperger's syndrome is reconsidered for inclusion into diagnostic criteria in the future. C1 Univ Klin & Kinder & Jugendheilkunde, Interdisziplinare Tagesklin Kinder & Jugendpsychia, A-1090 Vienna, Austria. Univ Vienna, Inst Psychol, Arbeitsbereich Klin Psychol, A-1010 Vienna, Austria. RP Hippler, K (reprint author), Univ Klin & Kinder & Jugendheilkunde, Interdisziplinare Tagesklin Kinder & Jugendpsychia, Wahringer Gurtel 18-20, A-1090 Vienna, Austria. EM kathrin.hippler@univie.ac.at CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ASPERGER H, 1974, DTSCH ARZTEBLATT, V14, P1010 Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 ASPERGER H, 1952, HEILPADAGOGIK EINFUH ATTWOOD T, 2000, ASPERGER SYNDROM RAT Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S, 2000, DEV PSYCHOPATHOL, V12, P489, DOI 10.1017/S0954579400003126 Frith U., 2003, AUTISM EXPLAINING EN GILLBERG C, 2001, J DEV LEARNING DISOR, V5, P79 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Hippler K, 2003, PHILOS T ROY SOC B, V358, P291, DOI 10.1098/rstb.2002.1197 Kanner L, 1943, NERV CHILD, V2, P217 Macintosh KE, 2004, J CHILD PSYCHOL PSYC, V45, P421, DOI 10.1111/j.1469-7610.2004.00234.x Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 RUHL D, 2001, NERVENARZT, V71, P535 SCHUBERT MT, 1982, Z KLIN PSYCHOL, V4, P253 SZATMARI P, 1989, DEV MED CHILD NEUROL, V31, P287 *WELTG, 2001, TASCH ICD 10 KLASS P Wing Lorna, 2000, ASPERGER SYNDROME, P418 NR 19 TC 4 Z9 4 PU VERLAG HANS HUBER PI BERN 9 PA LANGGASS-STRASSE 76, CH-3000 BERN 9, SWITZERLAND SN 1422-4917 J9 Z KINDER JUG-PSYCH JI Z. Kinder-und Jugendpsy. Psychother. PD JAN PY 2005 VL 33 IS 1 BP 35 EP 47 DI 10.1024/1422-4917.33.1.35 PG 13 WC Psychiatry SC Psychiatry GA 891TG UT WOS:000226603300005 PM 15714839 ER PT J AU Leppert, T Probst, P AF Leppert, T Probst, P TI Development and evaluation of a psychoeducational group training programme for teachers of autistic pupils with mental retardation SO ZEITSCHRIFT FUR KINDER-UND JUGENDPSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE autistic children; pervasive developmental disorders; mental retardation teacher training; TEACCH-method; treatment effectiveness evaluation AB Objectives: Teachers of autistic pupils show profiles of increased stress that are caused by the social, communicational, and cognitive deficits of these children. The aim of the present study was to develop and evaluate a psycho-educational group training programme for teachers. Methods: The curriculum covered theoretical issues of autism as well as educational skills focusing on "structured teaching" (TEACCH: Schopler, 1997). The training outcomes were evaluated within a pre-post (9 months) design. A total of 10 teachers working with 10 autistic children (mean age: 10 years) from schools for mentally retarded pupils participated in the training programme which included three one-day group sessions followed by six half-hour individual training sessions in the classroom (over a period of six months). The outcome variables were measured by means of teacher questionnaires assessing child behavioural symptoms, teachers' stress reactions, effects on the teachers' psychological adaptation, teacher-student-interaction and implementation of methods. Results: The training programme resulted in significant effects (p < 0.5) on child symptoms as well as on teachers' stress reactions. In addition, the teachers' psychological adaptation and teacher-student-interaction improved. On average, teachers implemented about two structured teaching methods. Conclusions: These findings indicate some evidence for the clinical validity of the teacher training procedure examined, taking into consideration some methodological limitations. C1 Univ Hamburg, Psychol Inst 2, DE-20146 Hamburg, Germany. Univ Hamburg, Fachbereich Psychol, DE-20146 Hamburg, Germany. RP Leppert, T (reprint author), Univ Hamburg, Psychol Inst 2, Von Melle Pk 5, DE-20146 Hamburg, Germany. 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PD JAN PY 2005 VL 33 IS 1 BP 49 EP 58 DI 10.1024/1422-4917.33.1.49 PG 10 WC Psychiatry SC Psychiatry GA 891TG UT WOS:000226603300006 PM 15714840 ER PT J AU Probst, P AF Probst, P TI "Communication unbound - or unfound"? - An integrative review on the effectiveness of Facilitated Communication (FC) in non-verbal persons with autism and mental retardation SO ZEITSCHRIFT FUR KLINISCHE PSYCHOLOGIE PSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Review DE Facilitated Communication; autism; mental retardation; treatment effectiveness evaluation; children; adults; metaanalysis ID SEXUAL-ABUSE; CHILDREN; VALIDITY; SCIENCE; ALLEGATIONS; VALIDATION; PSEUDOSCIENCE; PERSPECTIVE; DISORDER; PEOPLE AB The treatment method of Facilitated Communication (FC) has been propagated by Crossley and Biklen claiming to improve the communicative skills of nonverbal persons with autism and mental retardation significantly. In this paper an integrative review on the effectiveness of FC is presented. After outlining definition, concept, and some socio-cultural aspects of FC, the results of 37 controlled clinical studies drawn from a sample of 343 persons are reviewed. The main findings show that there is a highly influential facilitator guiding effect in FC, and that no case in the sample examined has been identified who demonstrates,unexpected communicative skills" under FC. Overall, FC has failed to show clinical validity, shows some features of pseudoscience, and bears severe risks of detrimental psychological side effects. Some socio-political consequences in the fields of education, health care, and law are suggested, in order to protect the vulnerable group of nonverbal persons and their families. 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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Klin. Psychol. Psychiatr. Psychother. PY 2005 VL 53 IS 2 BP 93 EP 128 PG 36 WC Psychology, Clinical SC Psychology GA 916OD UT WOS:000228394100001 ER PT J AU Gabriel, B Zeender, N Bodenmann, G AF Gabriel, B Zeender, N Bodenmann, G TI Stress and coping in parents of children with conduct problems, Down syndrome and normal development: What's the role of dyadic coping? SO ZEITSCHRIFT FUR KLINISCHE PSYCHOLOGIE PSYCHIATRIE UND PSYCHOTHERAPIE LA German DT Article DE stress; support; coping; marriage; Down syndrome; externalizing behavior ID FAMILY RESILIENCE; ADJUSTMENT; FATHERS; MOTHERS; AUTISM AB Background: Coping in parents with a higher stress level has been a neglected research topic so far. Method. Multivariate analyses of variance are computed to compare stress and coping between three groups of parents (N = 150) of a 6- to 14-year-old child (43 couples of a normally developed child, 53 parents of a child with Down syndrome and 54 parents of a child with externalizing behavior problems). Results: Parents of a child with Down syndrome reported more family related stress and stress with regard to social isolation, but reported also the highest scores of dyadic coping. Parents of a child with externalizing behavior problems perceived more parenting stress, psychological distress and a lack of dyadic coping. Conclusion: Dyadic coping reveals to be an important issue in parent's coping with daily hassles. C1 Univ Fribourg, Inst Familienforsch & Beratung, CH-1700 Fribourg, Switzerland. RP Gabriel, B (reprint author), Univ Fribourg, Inst Familienforsch & Beratung, Ave Gare 1, CH-1700 Fribourg, Switzerland. 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PY 2005 VL 53 IS 4 BP 315 EP 327 PG 13 WC Psychology, Clinical SC Psychology GA 990NN UT WOS:000233750600003 ER PT J AU Tiganov, AS Bashina, VM AF Tiganov, AS Bashina, VM TI Current approaches to understanding of autism in childhood SO ZHURNAL NEVROLOGII I PSIKHIATRII IMENI S S KORSAKOVA LA Russian DT Article DE autism in childhood; spectrum of autistic disorders; clinical manifestations; etiology; pathogenesis; classification ID EARLY INFANTILE-AUTISM; NERVE GROWTH-FACTOR; RETT-SYNDROME; HEAD CIRCUMFERENCE; ASPERGER-SYNDROME; FOLLOW-UP; CHILDREN; AUTOANTIBODIES; SCHIZOPHRENIA; PSYCHOSIS AB The authors analyse the trends in the study of childhood autism in the XX century and state of the art in view of nosology, systematics, clinical phenomenology, etiology and pathogenesis of autistic disorders. Mental Health Research Center of Russian Academy of Medical Sciences proposes a new classification of autism in children basing on the study of 500 cases. Each form of autistic disorders is characterized in clinicopsychopathological and pathogenetic aspects. The phenomenon of autism in childhood psychopathology is universal, dependent on peculiarities of ontogenesis of the nervous system, individual development of a child, genetic and environmental factors. C1 Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. RP Tiganov, AS (reprint author), Russian Acad Med Sci, Mental Hlth Res Ctr, Moscow 109801, Russia. 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Nevrol. Psikhiatrii Im S S Korsakova PY 2005 VL 105 IS 8 BP 4 EP 13 PG 10 WC Clinical Neurology; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 963OZ UT WOS:000231814900001 PM 16180492 ER PT J AU Morrice, P AF Morrice, P TI Animals in translation - Using the mysteries of autism to decode animal behavior SO NEW YORK TIMES BOOK REVIEW LA English DT Book Review CR GRANDIN T, ANIMALS TRANSLATION NR 1 TC 0 Z9 0 PU NEW YORK TIMES PI NEW YORK PA 229 W 43RD ST, NEW YORK, NY 10036-3959 USA SN 0028-7806 J9 NY TIMES BK REV JI N. Y. Times Book Rev. PD DEC 26 PY 2004 BP 16 EP 16 PG 1 WC Humanities, Multidisciplinary SC Arts & Humanities - Other Topics GA 881CP UT WOS:000225841300015 ER PT J AU Sivendran, S Patterson, D Spiegel, E McGown, I Cowley, D Colman, RF AF Sivendran, S Patterson, D Spiegel, E McGown, I Cowley, D Colman, RF TI Two novel mutant human adenylosuccinate Lyases (ASLs) associated with autism and characterization of the equivalent mutant Bacillus subtilis ASL SO JOURNAL OF BIOLOGICAL CHEMISTRY LA English DT Article ID INBORN ERROR; ACTIVE-SITE; DEFICIENCY; ENZYME; IDENTIFICATION; PURIFICATION; CATALYSIS; MUTATION; HIS(141); DISEASE AB An Australian patient with autism was found to be heterozygous for two mutations in the gene encoding adenylosuccinate lyase (ASL), resulting in the protein mutations E80D and D87E. The patient's mother carried only the E80D mutation. The equivalent positions are 62 and 69 in Bacillus subtilis ASL. Although both human and B. subtilis enzymes normally have Asp at position 87 (or 69), the B. subtilis ASL has Ile and Asp at 62 and 65, respectively, whereas human ASL has Glu and Arg at the equivalent positions. We have constructed, expressed, and purified the double mutant I62E/D65R as a "humanized" normal B. subtilis enzyme to compare with enzymes with a single mutation at position 62 (I62D/D65R), at position 69 (I62E/D65R/D69E), or at both positions (I62D/D65R/D69E). V-max for conversion of adenylosuccinate to AMP and fumarate is 0.57 mumol/min/mg for I62E/D65R, 0.064 mumol/min/mg for I62D/D65R, 0.27 mumol/min/mg for I62E/D65R/D69E, and 0.069 mumol/min/mg for I62D/D65R/D69E. The K-m for adenylosuccinate is elevated in the X62D mutants, and I62D/D65R is the least stable of these ASLs at 37 degreesC. The CD spectra of mutant and wild type enzymes are similar; thus, there are no appreciable structural changes. Clearly the Asp(62) causes the most drastic effect on ASL function, whereas the Glu(69) mutation produces only modest change. These results emphasize the importance of expanding tests for ASL deficiency to individuals with developmental delay of any severity, including individuals with autistic spectrum disorder. This study further demonstrates the usefulness of the B. subtilis ASL as a model to mimic the defective enzyme in ASL deficiency. C1 Univ Delaware, Dept Chem & Biochem, Newark, DE 19716 USA. Univ Denver, Eleanor Roosevelt Inst, Denver, CO 80206 USA. Mater Misericordiae Hosp, Brisbane, Australia. RP Colman, RF (reprint author), Univ Delaware, Dept Chem & Biochem, Newark, DE 19716 USA. 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Biol. Chem. PD DEC 17 PY 2004 VL 279 IS 51 BP 53789 EP 53797 DI 10.1074/jbc.M409974200 PG 9 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 878XL UT WOS:000225680600117 PM 15471876 ER PT J AU Castro-Rebolledo, R Giraldo-Prieto, M Hincapie-Henao, L Lopera, F Pineda, DA AF Castro-Rebolledo, R Giraldo-Prieto, M Hincapie-Henao, L Lopera, F Pineda, DA TI Specific developmental language disorder: A theoretical approach to its diagnosis, aetiology and clinical symptoms SO REVISTA DE NEUROLOGIA LA Spanish DT Review DE children; development; genetics; language; specific impairment ID FAMILIAL AGGREGATION; IMPAIRED CHILDREN; SEVERE SPEECH; PROFILES; MARKING; AUTISM; TENSE; GENE; SLI AB Aim. This article presents an updated review about the definition, diagnostic criteria, classifications, etiology and the evolution of the specific language impairment (SLI). Development. The specific language impairment is characterized by a developmental language delay and an impaired language, that persist over time and it is not explained by sensorial, motor and mental disabilities, neither by psycopathological disorders, socio-emotional deprivation, nor brain injury. The diagnosis is based on exclusional criteria. Some researchers propose different classifications considering the children performance in language comprehension and language production. Genetical linkage to the FOXP2 gen in the SPCH1 region of the chromosome 7 and to the chromosomes 13, 16 y 19 has been reported. The neuroimage studies have shown alterations in the volume and perfusion of some brain structures related to language. The manifestations of SLI may change during the development of the children and may disturb the self-steem, the academic performance and the social abilities. Conclusions. 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Neurologia PD DEC 16 PY 2004 VL 39 IS 12 BP 1173 EP 1181 PG 9 WC Clinical Neurology SC Neurosciences & Neurology GA 883KB UT WOS:000226008900015 PM 15625638 ER PT J AU Koves, K Kausz, M Reser, D Illyes, G Takacs, J Heinzlmann, A Gyenge, E Horvath, K AF Koves, K Kausz, M Reser, D Illyes, G Takacs, J Heinzlmann, A Gyenge, E Horvath, K TI Secretin and autism: a basic morphological study about the distribution of secretin in the nervous system SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT 6th International Symposium on VIP/PACAP CY SEP 01-04, 2003 CL Hakone, JAPAN DE immunohistochemistry; cat; rat; human ID PERVASIVE DEVELOPMENTAL DISORDER; RAT-BRAIN; CHILDREN; IMMUNOREACTIVITY; LOCALIZATION; CEREBELLUM; BINDING; MOUSE AB For the first time, the relationship between secretin and autism has been demonstrated by one of us. Intravenous administration of secretin in autistic children caused a fivefold higher pancreaticobiliary fluid secretion than in healthy ones and, at least in some of the patients, better mental functions were reported after the secretin test. Because the precise localization of secretin in the brain is still not completely known, the abovementioned observation led us to map secretin immunoreactivity in the nervous system of several mammalian species. In the present work, the distribution of secretin immunoreactivity in cat and human nervous systems was compared with that of rats using an immunohistochemical approach. Secretin inummoreactivity was observed in the following brain structures of both humans and in colchicine-treated rats: (1) Purkinje cells in the cerebellar cortex; (2) central cerebellar nuclei; (3) pyramidal cells in the motor cortex; and (4) primary sensory neurons. Additionally, secretin immunoreactive cells were observed in the human hippocampus and amygdala and in third-order sensory neurons of the rat auditory system. In cats, secretin was only observed in the spinal ganglia. Our findings support the view that secretin is not only a gastrointestinal peptide but that it is also a neuropeptide. Its presence or the lack of its presence may have a role in the development of behavioral disorders. (C) 2004 Elsevier B.V. All rights reserved. C1 Semmelweis Univ, Fac Med, Dept Human Morphol & Dev Biol, H-1094 Budapest, Hungary. Semmelweis Univ, Fac Med, Dept Pathol 2, Budapest, Hungary. Hungarian Acad Sci, Div Neurobiol, Budapest, Hungary. Univ Pecs, Coll Hlth Care, Dept Clin Hlth Care, Pecs, Hungary. Univ Maryland, Sch Med, Div Pediat Gastroenterol & Nutr, Baltimore, MD USA. RP Koves, K (reprint author), Semmelweis Univ, Fac Med, Dept Human Morphol & Dev Biol, Tuzolto U 58, H-1094 Budapest, Hungary. 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PD DEC 15 PY 2004 VL 123 IS 1-3 BP 209 EP 216 DI 10.1016/j.regpep.2004.04.026 PG 8 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA 871ST UT WOS:000225154400030 PM 15518914 ER PT J AU Masuo, Y Morita, M Oka, S Ishido, M AF Masuo, Y Morita, M Oka, S Ishido, M TI Motor hyperactivity caused by a deficit in dopaminergic neurons and the effects of endocrine disruptors: a study inspired by the physiological roles of PACAP in the brain SO REGULATORY PEPTIDES LA English DT Article; Proceedings Paper CT 6th International Symposium on VIP/PACAP CY SEP 01-04, 2003 CL Hakone, JAPAN DE 6-hydroxydopamine; attention-deficit hyperactivity disorder (ADHD); autism; DNA array; dopamine; endocrine disruptor ID ACTIVATING POLYPEPTIDE PACAP; CENTRAL-NERVOUS-SYSTEM; NEONATAL 6-HYDROXYDOPAMINE; GENE-EXPRESSION; ATTENTION-DEFICIT; BINDING-SITES; RAT-BRAIN; POLYCHLORINATED-BIPHENYLS; CAUDATE-PUTAMEN; D-4 RECEPTORS AB Recent studies have revealed that the pituitary adenylate cyclase-activating polypeptide (PACAP) might act as a psychostimulant. Here we investigated the mechanisms underlying motor hyperactivity in patients with pervasive developmental disorders, such as autism, and attention-deficit hyperactivity disorder (ADHD). We studied the effects of intracisternal administration of 6-hydroxydopamine (6-OHDA) or endocrine disruptors (EDs) on spontaneous motor activity (SMA) and multiple gene expression in neonatal rats. Treatment with 6-OHDA caused significant hyperactivity during the dark phase in rats aged 4-5 weeks. Motor hyperactivities also were observed after treatment with endocrine disruptors, such as bisphenol A, nonylphenol, diethylhexyl phthalate and dibutyl phthalate, during both dark and light phases. Gene-expression profiles produced using cDNA macroarrays of 8-week-old rats with 6-OHDA lesions revealed the altered expression of several classes of gene, including the N-methyl-D-aspartate (NMDA) receptor 1, glutamate/aspartate transporter, gamma-aminobutyric-acid transporter, dopamine transporter 1, D4 receptor, and peptidergic elements such as the galanin receptor, arginine vasopressin receptor, neuropeptide Y and tachykinin 2. The changes in gene expression caused by treatment with endocrine disruptors differed from those induced by 6-OHDA. These results suggest that the mechanisms underlying the induction of motor hyperactivity and/or compensatory changes in young adult rats might differ between 6-OHDA and endocrine disr-uptors. (C) 2004 Elsevier B.V. All rights reserved. C1 Natl Inst AIST, Human Stress Signal Res Ctr, Tsukuba, Ibaraki 3058566, Japan. Natl Inst Environm Studies, Endocrine Disruptors & Dioxin Res Projects, Tsukuba, Ibaraki 3058506, Japan. 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Pept. PD DEC 15 PY 2004 VL 123 IS 1-3 BP 225 EP 234 DI 10.1016/j.regpep.2004.05.010 PG 10 WC Endocrinology & Metabolism; Physiology SC Endocrinology & Metabolism; Physiology GA 871ST UT WOS:000225154400032 PM 15518916 ER PT J AU Minshew, NJ Sung, KB Jones, BL Furman, JM AF Minshew, NJ Sung, KB Jones, BL Furman, JM TI Underdevelopment of the postural control system in autism SO NEUROLOGY LA English DT Article ID HIGH-FUNCTIONING AUTISM; ASPERGER-SYNDROME; DEVELOPMENTAL DISORDERS; DIAGNOSTIC INTERVIEW; PARKINSONS-DISEASE; CHILDHOOD AUTISM; CHILDREN; POSTUROGRAPHY; CLUMSINESS; STABILITY AB Objective: To determine if abnormalities exist in postural control in autism and if they are related to age. Methods: Dynamic posturography was performed in 79 autistic individuals without mental retardation and 61 healthy volunteers between ages 5 and 52 years. Both the sensory organization and the movement coordination portions of the test were performed. Results: The autistic subjects had reduced postural stability ( p = 0.002). Examination of age effects revealed that the development of postural stability was delayed in the autistic subjects ( p < 0.001) and failed to achieve adult levels ( p = 0.004). Postural stability was reduced under all conditions but was clinically significant only when somatosensory input was disrupted alone or in combination with other sensory challenges ( mean reduction in stability of 2.6 +/- 1.0 for the first three conditions without somatosensory disruption vs 6.7 +/- 2.7 for the last three conditions with somatosensory disruption), indicating problems with multimodality sensory integration. Conclusions: The evidence from this and studies of the motor system suggests more general involvement of neural circuitry beyond the neural systems for social behavior, communication, and reasoning, all of which share a high demand on neural integration of information. C1 Univ Pittsburgh, Sch Med, Dept Psychiat, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Neurol, Pittsburgh, PA 15213 USA. Univ Pittsburgh, Sch Med, Dept Otolaryngol, Pittsburgh, PA 15213 USA. Carnegie Mellon Univ, H John Heinz III Sch Publ Policy & Management, Pittsburgh, PA 15213 USA. Soonchunhyang Univ Hosp, Dept Neurol, Bucheon, South Korea. RP Minshew, NJ (reprint author), Univ Pittsburgh, Sch Med, Dept Psychiat, 3811 OHara St,Webster Hall,Suite 300, Pittsburgh, PA 15213 USA. 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Genomic screens, including our own, have shown suggestive evidence for linkage over a 20-30 cM region on chromosome 2q31-q33. Two subsequent reports showed that the linkage evidence increased in the subset of families with phrase speech delay (PSD), defined as onset of phrase speech later than 3 years of age. To further investigate the linkage in the presumptive candidate region, microsatellite markers in a 2 cM grid covering the interval from 164 to 203 cM were analyzed in 110 multiplex (2 or more sampled autism patients) families. A maximum heterogeneity LOD (HLOD) score of 1.54 was detected at D2S1776 (173 cM) in the overall dataset (dominant model), increasing to 1.71 in the PSD subset. While not conclusive, these data continue to provide suggestive evidence for linkage, particularly considering replication by multiple independent groups. Positive LOD scores extended over the entire region, continuing to define a broad candidate interval. Association studies were performed on several functional candidates mapping within the region. These included GAD1, encoding GAD67, whose levels are reduced in autopsy brain material from autistic subjects, and STK17B, AB12, CTLA4, CD28, NEUROD1, PDE1A, HOXD1 and DLX2. We found no evidence for significant allelic association between autism and any of these candidates, suggesting that they do not play a major role in the genetics of autism or that substantial allelic heterogeneity at any one of these loci dilutes potential disease-allele association. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Duke Univ, Med Ctr, Ctr Human Genet, Dept Med,Div Pediat, Durham, NC 27710 USA. Vanderbilt Univ, Med Ctr, Ctr Human Genet Res, Dept Physiol & Mol Biophys, Nashville, TN 37232 USA. Univ S Carolina, WS Hall Psychiat Inst, Columbia, SC 29208 USA. RP Pericak-Vance, MA (reprint author), Duke Univ, Med Ctr, Ctr Human Genet, Dept Med,Div Pediat, 595 LaSalle St,Box 3445, Durham, NC 27710 USA. 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PD DEC 6 PY 2004 VL 372 IS 3 BP 209 EP 214 DI 10.1016/j.neulet.2004.09.037 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 876BG UT WOS:000225469900007 PM 15542242 ER PT J AU James, SJ Cutler, P Melnyk, S Jernigan, S Janak, L Gaylor, DW Neubrander, JA AF James, SJ Cutler, P Melnyk, S Jernigan, S Janak, L Gaylor, DW Neubrander, JA TI Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism SO AMERICAN JOURNAL OF CLINICAL NUTRITION LA English DT Article DE autistic disorder; biomarkers; oxidative stress; methylation; methionine; S-adenosylmethionine; S-adenosylhomocysteine; adenosine; cysteine; glutathione ID S-ADENOSYLHOMOCYSTEINE HYDROLASE; COULOMETRIC ELECTROCHEMICAL DETECTION; MAMMALIAN METHIONINE SYNTHASE; HOMOCYSTEINE METABOLISM; PLASMA HOMOCYSTEINE; GLUTATHIONE SYNTHESIS; SPECTRUM DISORDERS; MENTAL-RETARDATION; RAT HEPATOCYTES; DOWN-SYNDROME AB Background: Autism is a complex neurodevelopmental disorder that usually presents in early childhood and that is thought to be influenced by genetic and environmental factors. Although abnormal metabolism of methionine and homocysteine has been associated with other neurologic diseases, these pathways have not been evaluated in persons with autism. Objective: The purpose of this study was to evaluate plasma concentrations of metabolites in the methionine transmethylation and transsulfuration pathways in children diagnosed with autism. Design: Plasma concentrations of methionine, S-adenosylmethionine (SAM). S-adenosylhomocysteine (SAH), adenosine, homocysteine, cystathionine, cysteine, and oxidized and reduced glutathione were measured in 20 children with autism and in 33 control children. On the basis of the abnormal metabolic profile, a targeted nutritional intervention trial with folinic acid, betaine, and methylcobalamin was initiated in a subset of the autistic children. Results: Relative to the control children, the children with autism had significantly lower baseline plasma concentrations of methionine, SAM, homocysteine, cystathionine, cysteine, and total glutathione and significantly higher concentrations of SAH, adenosine, and oxidized glutathione. This metabolic profile is consistent with impaired capacity for methylation (significantly lower ratio of SAM to SAH) and increased oxidative stress (significantly lower redox ratio of reduced glutathione to oxidized glutathione) in children with autism. The intervention trial was effective in normalizing the metabolic imbalance in the autistic children. Conclusions: An increased vulnerability to oxidative stress and a decreased capacity for methylation may contribute to the development and clinical manifestation of autism. C1 Arkansas Childrens Hosp, Res Inst, Little Rock, AR 72202 USA. Univ Arkansas Med Sci, Dept Pediat, Little Rock, AR 72202 USA. Gaylor & Assoc LLC, Eureka Springs, AR USA. RP James, SJ (reprint author), Arkansas Childrens Hosp, Res Inst, Slot 512-40B,1120 Marshall St, Little Rock, AR 72202 USA. 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PD DEC PY 2004 VL 56 IS 6 BP 755 EP 756 DI 10.1002/ana.20344 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 876NV UT WOS:000225504700001 PM 15562433 ER PT J AU De Fosse, L Hodge, SM Makris, N Kennedy, DN Caviness, VS McGrath, L Steele, S Ziegler, DA Herbert, MR Frazier, JA Tager-Flusberg, H Harris, GJ AF De Fosse, L Hodge, SM Makris, N Kennedy, DN Caviness, VS McGrath, L Steele, S Ziegler, DA Herbert, MR Frazier, JA Tager-Flusberg, H Harris, GJ TI Language-association cortex asymmetry in autism and specific language impairment SO ANNALS OF NEUROLOGY LA English DT Article ID AUTOMATED IMAGE REGISTRATION; PLANUM TEMPORALE ASYMMETRY; BRAIN ABNORMALITIES; PARS TRIANGULARIS; MRI ASYMMETRIES; STROKE PATIENTS; CHROMOSOME 7Q; IN-VIVO; SPEECH; DISORDER AB fLanguage deficits are among the core impairments of autism. We previously reported asymmetry reversal of frontal language cortex in boys with autism. Specific language impairment (SLI) and autism share similar language deficits and may share genetic links. This study evaluated asymmetry of frontal language cortex in a new, independent sample of right-handed boys, including a new sample of boys with autism and a group of boys with SLI. The boys with autism were divided into those with language impairment (ALI) and those with normal language ability (ALN). Subjects (right-handed, aged 6.2-13.4 years) included 22 boys with autism (16 ALI and 6 ALN), 9 boys with a history of or present SLI, and 11 normal controls. MRI brain scans were segmented into grey and white matter; then the cerebral cortex was parcellated into 48 gyral-based divisions per hemisphere. Group differences in volumetric asymmetry were predicted a priori in language-related regions in inferior lateral frontal (Broca's area) and posterior superior temporal cortex. Language impaired boys with autism and SLI both had significant reversal of asymmetry in frontal language-related cortex; larger on the right side in both groups of language impaired boys and larger on the left in both unimpaired language groups, strengthening a phenotypic link between ALI and SLI. Thus, we replicated the observation of reversed asymmetry in frontal language cortex reported previously in an independent autism sample, and observed similar reversal in boys with SLI, further strengthening a phenotypic link between SLI and a subgroup of autism. Linguistically unimpaired boys with autism had similar asymmetry compared with the control group, suggesting that Broca's area asymmetry reversal is related more to language impairment than specifically to autism diagnosis. C1 Massachusetts Gen Hosp, Ctr Morphomet Anal, Boston, MA 02114 USA. Massachusetts Gen Hosp, Radiol Comp Aided Diagnost Lab, Boston, MA 02114 USA. Boston Univ, Sch Med, Boston, MA 02215 USA. Harvard Univ, Sch Med, Dept Psychiat, Boston, MA 02115 USA. McLean Hosp, Child Psychiat Outpatient Clin, Belmont, MA 02178 USA. RP Harris, GJ (reprint author), Zero Emerson Pl 3A, Boston, MA 02114 USA. 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Neurol. PD DEC PY 2004 VL 56 IS 6 BP 757 EP 766 DI 10.1002/ana.20275 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 876NV UT WOS:000225504700002 PM 15478219 ER PT J AU Shea, V AF Shea, V TI A perspective on the research literature related to early intensive behavioral intervention (Lovaas) for young children with autism SO AUTISM LA English DT Article DE autism early; intervention; EIBI; Lovaas young children ID PERVASIVE DEVELOPMENTAL DISORDER; PRESCHOOL-CHILDREN; PROJECT; PROGRAMS; ADULTS; AREAS AB Various aspects of the research literature on early intensive behavioral intervention (EIBI) have been poorly understood within the psychological, educational, and advocacy communities. Examination of the studies that are frequently cited by proponents of EIBI suggests that the expectation that 47 percent of youngsters who receive EIBI will reach normal developmental status is questionable. RP Shea, V (reprint author), 1506 E Franklin St,Suite 202, Chapel Hill, NC 27514 USA. 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Increasingly, education for children with autism is provided within mainstream settings, but given their particular difficulties, the adequate provision of educational services in such settings is challenging. This study presents observational data of the play behaviour and social interaction patterns of 10 children with autism in mainstream kindergartens and primary school playgrounds. The target children differed significantly in terms of their play and social interactions from typically developing children in the same settings. The adequacy of the provision of services for children with autism in mainstream provision is discussed. C1 Univ Auckland, Res Ctr Intervent Teaching & Learning, Auckland, New Zealand. RP Anderson, A (reprint author), Univ Auckland, Res Ctr Intervent Teaching & Learning, Private Bag 92019, Auckland, New Zealand. EM an.anderson@auckland.ac.nz CR ASHBAKER BY, 2000, GROWING ROLES TEACHE BALLARD K, 1998, UNDERSTANDING CHILDR Ballard K.D., 1981, ED PSYCHOL, V1, P185, DOI 10.1080/0144341810010207 BARONCOHEN S, 1989, J AUTISM DEV DISORD, V19, P579, DOI 10.1007/BF02212859 BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 BARONCOHEN S, 1986, BRIT J DEV PSYCHOL, V4, P113 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bayley N, 1993, BAYLEY SCALES INFANT Boomer LW, 1994, FOCUS AUTISTIC BEHAV, V9, P1 BROWN D, 2000, AUSTRALASIAN J SPECI, V24, P16 Campi A, 1996, INT J NEURORADIOL, V2, P134 Dancey C. P., 2002, STAT MATHS PSYCHOL U Dunn L. M., 1997, PEABODY PICTURE VOCA, V3rd EBER L, 1996, SPECIAL SERVICES SCH, V11, P135, DOI 10.1300/J008v11n01_03 El-Ghoroury NH, 1999, J AUTISM DEV DISORD, V29, P249, DOI 10.1023/A:1023036223397 FACTOR DC, 1980, CAN J BEHAV SCI, V12, P272, DOI 10.1037/h0081069 FEDERLEIN A C, 1982, Early Child Development and Care, V9, P245, DOI 10.1080/0300443820090304 FRESCHI DF, 1999, TEACHING EXCEPTIONAL, V31, P42 Giangreco MF, 1997, EXCEPT CHILDREN, V64, P7 GODFREY R, 2002, EVALUATION SOME PROG Green G, 1996, BEHAV INTERVENTION Y, P29 Hocutt AM, 1996, FUTURE CHILD, V6, P77, DOI 10.2307/1602495 JONES KH, 1993, REM SPEC EDUC, V14, P7 Koegel RL, 2001, J CLIN CHILD PSYCHOL, V30, P19, DOI 10.1207/S15374424JCCP3001_4 Kohler FW, 2001, TOP EARLY CHILD SPEC, V21, P93, DOI 10.1177/027112140102100203 LESLIE AM, 1988, BRIT J DEV PSYCHOL, V6, P315 Lovaas O. I., 1997, PREVENTION TREATMENT, P61 LOVAAS OI, 1989, J BEHAV THER EXP PSY, V20, P17 MIRON G, 1991, SCANDINAVIAN J ED RE, V35, P163, DOI 10.1080/0031383910350301 Newsom C., 1998, TREATMENT CHILDHOOD, P416 ODOM SL, 2001, INCLUSION PRESCHOOL REYNOLDS MC, 1989, REM SPEC EDUC, V10, P7 Roeyers H., 1995, BRIT J SPECIAL ED, V22, P161, DOI 10.1111/j.1467-8578.1995.tb00927.x RUBIN KH, 1978, CHILD DEV, V49, P534, DOI 10.1111/j.1467-8624.1978.tb02350.x RUSSELL J, 1991, BRIT J DEV PSYCHOL, V9, P331 STAINBACK S, 1994, EXCEPT CHILDREN, V60, P486 Stainback W., 1990, SUPPORT NETWORKS INC, P3 TAGERFLUSBERG H, 1992, CHILD DEV, V63, P161, DOI 10.1111/j.1467-8624.1992.tb03604.x Thomson C., 1999, CAUGHT STORIES SPECI Wechsler D., 1989, WECHSLER PRESCHOOL P Wechsler D., 1992, WECHSLER INTELLIGENC YANG L, 1995, ACTA PSYCHOL SINICA, V27 Ysseldyke J, 1996, SCHOOL PSYCHOL REV, V25, P418 NR 43 TC 20 Z9 22 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2004 VL 8 IS 4 BP 369 EP 385 DI 10.1177/1362361304045216 PG 17 WC Psychology, Developmental SC Psychology GA 878NV UT WOS:000225654400003 PM 15556957 ER PT J AU Bromley, J Hare, DJ Davison, K Emerson, E AF Bromley, J Hare, DJ Davison, K Emerson, E TI Mothers supporting children with autistic spectrum disorders - Social support, mental health status and satisfaction with services SO AUTISM LA English DT Article DE autism; families; mental health; respite stress ID FAMILY STRESS; BEHAVIOR PROBLEMS; ADOLESCENTS; PARENTS; IMPACT; DIFFICULTIES; ADJUSTMENT; DISABILITY AB Parents of children with autistic spectrum disorders (ASDs) are more likely to experience serious psychological distress than parents of children with other developmental disabilities. To examine the impact of a range of factors on psychological wellbeing, interviews were undertaken with 68 mothers of children with ASDs to explore aspects of social support, mental health status and satisfaction with services. Findings indicated that over half of mothers screened positive for significant psychological distress and that this was associated with low levels of family support and with bringing up a child with higher levels of challenging behaviour. Mothers were more likely to report lower levels of support if they were a lone parent, were living in poor housing, or were the mother of a boy with ASD. The study also investigated areas of useful support and areas of unmet need, the latter including care breaks and advice needs. C1 Univ Manchester, Wythenshawe Hosp, Div Clin Psychol, Manchester M23 9LT, Lancs, England. Univ Lancaster, Inst Hlth Res, Lancaster, England. RP Hare, DJ (reprint author), Univ Manchester, Wythenshawe Hosp, Div Clin Psychol, Educ & Res Bldg,Southmoor Rd, Manchester M23 9LT, Lancs, England. EM dougal.hare@man.ac.uk CR BEECHMAN J, 1995, EC EVALUATION MENTAL BOUMA R, 1990, J CLIN PSYCHOL, V46, P722, DOI 10.1002/1097-4679(199011)46:6<722::AID-JCLP2270460605>3.0.CO;2-6 Chamba R., 1999, EDGE MINORITY ETHNIC DONENBERG G, 1993, J ABNORM CHILD PSYCH, V21, P179, DOI 10.1007/BF00911315 DONOVAN AM, 1988, AM J MENT RETARD, V92, P502 Dumas J. E., 1991, EXCEPTIONALITY, V2, P97, DOI [10.1080/09362839109524770, DOI 10.1080/09362839109524770] Dunn ME, 2001, COMMUNITY MENT HLT J, V37, P39, DOI 10.1023/A:1026592305436 Dunst C., 1988, ENABLING EMPOWERING, P153 Einfeld S. 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P., 1988, USERS GUIDE GEN HLTH Gray David E., 1992, Australia and New Zealand Journal of Developmental Disabilities, V18, P83 Hastings RP, 2002, J INTELLECT DEV DIS, V27, P149, DOI 10.1080/1366825021000008657 Hastings RP, 2002, AM J MENT RETARD, V107, P222, DOI 10.1352/0895-8017(2002)107<0222:BPOCWA>2.0.CO;2 Hatton C., 2002, SUPPORTING S ASIAN F Hatton C, 1998, BRIT J SOC WORK, V28, P821 HENDERSON D, 1992, PSYCHOL REP, V71, P167, DOI 10.2466/PR0.71.5.167-171 Howlin P, 1998, J CHILD PSYCHOL PSYC, V39, P307, DOI 10.1017/S0021963097002138 KONSTANTAREAS MM, 1989, J CHILD PSYCHOL PSYC, V30, P459, DOI 10.1111/j.1469-7610.1989.tb00259.x Lambert N, 1993, AAMR ADAPTIVE BEHAV Meltzer H, 2000, MENTAL HLTH CHILDREN MOES D, 1992, PSYCHOL REP, V71, P1272, DOI 10.2466/PR0.71.8.1272-1274 Pisula E., 1998, POLISH PSYCHOL B, V29, P305 Sanders JL, 1997, CHILD FAM BEHAV THER, V19, P15, DOI 10.1300/J019v19n04_02 SELTZER MM, IN PRESS HDB METHODS WOLF R, 1915, FORSCHUNGEN THURINGI, V7, P6 NR 30 TC 106 Z9 108 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2004 VL 8 IS 4 BP 409 EP 423 DI 10.1177/1362361304047224 PG 15 WC Psychology, Developmental SC Psychology GA 878NV UT WOS:000225654400005 PM 15556959 ER PT J AU Hare, DJ Pratt, C Burton, M Bromley, J Emerson, E AF Hare, DJ Pratt, C Burton, M Bromley, J Emerson, E TI The health and social care needs of family carers supporting adults with autistic spectrum disorders SO AUTISM LA English DT Article DE autism; families; mental health; respite stress ID MENTAL-HEALTH; CHILDREN; STRESS; PARENTS; ADJUSTMENT; MOTHERS AB The families of 26 adults with autistic spectrum disorders (ASDs) who either lived at home or maintained close contact with their families were interviewed about their social and psychological needs related to caring for the person with ASD. In contrast to previous studies of familial carers of children with ASDs, a strong association between parental emotional distress and unmet need was found. Parents also reported a need for more autism-specific intervention and support for adults with ASDs. The study illustrates the continuing and under-reported role of families in supporting adults with ASDs. C1 Univ Manchester, Acad Div Clin Psychol, Wythenshawe Hosp, Manchester M23 9LT, Lancs, England. Manchester Learning Disabil Partnership, Manchester, Lancs, England. Inst Hlth Res, Lancaster, England. RP Hare, DJ (reprint author), Univ Manchester, Acad Div Clin Psychol, Wythenshawe Hosp, Educ & Res Bldg,Southmoor Rd, Manchester M23 9LT, Lancs, England. EM dougal.hare@man.ac.uk CR ABELL F, 2004, UNPUB EXPT INVESTIGA Beecham J., 1995, EC EVALUATION MENTAL Bromley J, 2004, AUTISM, V8, P409, DOI 10.1177/1362361304047224 CHAMBA E, 1999, EDGE MINORITY ETHNIC Department of Work and Pensions, 2003, HOUS BEL AV INC 2001 Dunn ME, 2001, COMMUNITY MENT HLT J, V37, P39, DOI 10.1023/A:1026592305436 Dunst C., 1988, ENABLING EMPOWERING, P153 FACTOR DC, 1990, J AUTISM DEV DISORD, V20, P139, DOI 10.1007/BF02206863 Fombonne E, 2001, J AM ACAD CHILD PSY, V40, P820, DOI 10.1097/00004583-200107000-00017 GILL MJ, 1991, J AUTISM DEV DISORD, V21, P407, DOI 10.1007/BF02206867 Goldberg DP, 1998, USERS GUIDE GEN HLTH HARE DJ, 2003, J LEARNING DISABILIT, V7, P267, DOI 10.1177/14690047030073006 Hastings RP, 2002, AM J MENT RETARD, V107, P222, DOI 10.1352/0895-8017(2002)107<0222:BPOCWA>2.0.CO;2 Hatton C., 2002, SUPPORTING S ASIAN F Hatton C, 1998, BRIT J SOC WORK, V28, P821 HENDERSON D, 1992, PSYCHOL REP, V71, P167, DOI 10.2466/PR0.71.5.167-171 KAGAN C, 1998, COMBINING WORK CARE KONSTANTAREAS MM, 1989, J CHILD PSYCHOL PSYC, V30, P459, DOI 10.1111/j.1469-7610.1989.tb00259.x MESIBOV G, 1996, MODEL PRACTICES SERV MOES D, 1992, PSYCHOL REP, V71, P1272, DOI 10.2466/PR0.71.8.1272-1274 Pendaries C, 1997, BRIT J LEARN DISABIL, V25, P122 Pisula E., 1998, POLISH PSYCHOL B, V29, P305 POPE A, 1998, DEV MANAGING HIGH QU Sanders JL, 1997, CHILD FAM BEHAV THER, V19, P15, DOI 10.1300/J019v19n04_02 WOLF LC, 1989, J AUTISM DEV DISORD, V19, P157, DOI 10.1007/BF02212727 NR 25 TC 28 Z9 28 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2004 VL 8 IS 4 BP 425 EP 444 DI 10.1177/1362361304047225 PG 20 WC Psychology, Developmental SC Psychology GA 878NV UT WOS:000225654400006 PM 15556960 ER PT J AU Cohen, BI AF Cohen, BI TI Rationale for further investigation of chromosome 16p 13.3, a region implicated for autism SO AUTISM LA English DT Letter ID GABA-TRANSAMINASE; INFANTILE-AUTISM; LIVER C1 Cohen Inst Adv GABA Studies, Nanuet, NY USA. RP Cohen, BI (reprint author), Cohen Inst Adv GABA Studies, Nanuet, NY USA. CR Cohen BI, 2002, MED HYPOTHESES, V59, P757, DOI 10.1016/S0306-9877(02)00325-0 Cohen BI, 2001, MED HYPOTHESES, V57, P673, DOI 10.1054/mehy.2001.1350 COHEN BI, 1999, AUTISM, V3, P437, DOI 10.1177/1362361399003004010 Cohen BI, 2002, MED HYPOTHESES, V59, P115, DOI 10.1016/S0306-9877(02)00157-3 *NCBI UN DAT, UN CLUST HS 1588 HOM Shao YJ, 2003, AM J HUM GENET, V72, P539, DOI 10.1086/367846 NR 6 TC 3 Z9 3 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD DEC PY 2004 VL 8 IS 4 BP 445 EP 447 DI 10.1177/1362361304047226 PG 3 WC Psychology, Developmental SC Psychology GA 878NV UT WOS:000225654400007 PM 15556961 ER PT J AU Bezzubova, E Globus, G AF Bezzubova, E Globus, G TI Underconstraint and overconstraint in psychiatry SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material AB Hallucination lies at an intriguina border between psychiatry, and philosophy Although Behrendt & Young (B&Y) tie their proposal to Kantian transcendental idealism, other philosophical positions are equally consistent. Cognition is underconstrained by reality not only in hallucination but also in autism and dreaming. Sensory underconstraint is insufficient to encompass schizophrenia. There is also a breakdown in integrative capacity on the cognitive side. From a wider clinical perspective than schizophrenia, there can be underconstraint or overconstraint in sensory and cognitive functionalities. C1 Univ Calif Irvine, Coll Med, Dept Med, Irvine, CA 92697 USA. Univ Calif Irvine, Coll Med, Dept Psychiat & Human Behav, Irvine, CA 92697 USA. RP Bezzubova, E (reprint author), Univ Calif Irvine, Coll Med, Dept Med, Irvine, CA 92697 USA. EM ebezzubo@uci.edu; ggglobus@uci.edu CR Bleuler E., 1911, DEMENTIA PRAECOX GRO GLOBUS G, 2001, DIMENSIONS CONSCIOUS Globus G., 2003, QUANTUM CLOSURES DIS Globus GG, 1987, DREAM LIFE WAKE LIFE Jaspers K, 1962, GEN PSYCHOPATHOLOGY NAKAGOMI T, 2004, BRAIN BEING Neisser U., 1976, COGNITION REALITY NR 7 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0140-525X J9 BEHAV BRAIN SCI JI Behav. Brain Sci. PD DEC PY 2004 VL 27 IS 6 BP 788 EP + PG 14 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 930UJ UT WOS:000229442300030 ER PT J AU Torrey, EF Dhavale, D Lawlor, JP Yolken, RH AF Torrey, EF Dhavale, D Lawlor, JP Yolken, RH TI Autism and head circumference in the first year of life SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; body length; body weight; head circumference; neurodevelopmental; prenatal bleeding ID POSTNATAL FACTORS; EARLY-CHILDHOOD; DISORDER; CHILDREN; INFANCY; GROWTH; MRI AB Background: It has been reported that children with autism and pervasive developmental disorder have a significantly smaller bead circumference at birth and that their bead circumference then increases disproportionately rapidly in the first year of life. Methods: We attempted to replicate these findings using 15 narrowly defined autistic children from the National Collaborative Perinatal Project and approximately 40, 000 nonautistic control subjects. Results. The autistic group bad a slightly but not signficantly larger bead circumference at birth. At 4 months, the bead circumference in the autistic group was not significantly larger than that of control subjects, but body weight and length were significantly larger in the autistic group. Conclusions: We believe this is the first report of significant general body growth in autistic children in infancy; the larger bead circumference may be pail of this excessive general growth. C1 Stanley Med Res Inst, Bethesda, MD USA. Johns Hopkins Univ, Sch Publ Hlth, Baltimore, MD USA. Stanley Lab Dev Neurovirol, Baltimore, MD USA. Johns Hopkins Univ, Med Ctr, Baltimore, MD 21218 USA. RP Torrey, EF (reprint author), 5430 Grosvenor Lane,Suite 200, Bethesda, MD 20814 USA. EM torreyf@stanleyresearch.org CR BAILEY A, 1995, PSYCHOL MED, V25, P63 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Carper RA, 2002, NEUROIMAGE, V16, P1038, DOI 10.1006/nimg.2002.1099 Courchesne E, 2001, NEUROLOGY, V57, P245 Courchesne E, 2003, JAMA-J AM MED ASSOC, V290, P337, DOI 10.1001/jama.290.3.337 Davidovitch M, 1996, J CHILD NEUROL, V11, P389 FILIPEK PA, 1992, ANN NEUROL, V32, P47519 Fombonne E, 1999, J AUTISM DEV DISORD, V29, P113, DOI 10.1023/A:1023036509476 Fombonne E, 2000, J AUTISM DEV DISORD, V30, P365, DOI 10.1023/A:1005591719811 GILBERG C, 2002, DEV MED CHILD NEUROL, V44, P296 Lainhart JE, 1997, J AM ACAD CHILD PSY, V36, P282, DOI 10.1097/00004583-199702000-00019 Lainhart JE, 2003, JAMA-J AM MED ASSOC, V290, P393, DOI 10.1001/jama.290.3.393 LEMONS JA, 1981, HUM BIOL, V53, P351 MASONBROTHERS A, 1990, PEDIATRICS, V86, P514 MASONBROTHERS A, 1987, J AM ACAD CHILD PSY, V26, P39, DOI 10.1097/00004583-198701000-00008 Niswander K., 1972, WOMEN THEIR PREGNANC Piven J, 1996, J AM ACAD CHILD PSY, V35, P530, DOI 10.1097/00004583-199604000-00020 PIVEN J, 1995, AM J PSYCHIAT, V152, P1145 Sparks BF, 2002, NEUROLOGY, V59, P184 Stevenson RE, 1997, LANCET, V349, P1744, DOI 10.1016/S0140-6736(05)62956-X TORREY EF, 1975, J AUTISM CHILD SCHIZ, V5, P287, DOI 10.1007/BF01540676 Volkmar FR, 2003, LANCET, V362, P1133, DOI 10.1016/S0140-6736(03)14471-6 WING JK, 1967, BRIT MED J, V3, P389 NR 23 TC 44 Z9 44 PU ELSEVIER SCIENCE INC PI NEW YORK PA 360 PARK AVE SOUTH, NEW YORK, NY 10010-1710 USA SN 0006-3223 J9 BIOL PSYCHIAT JI Biol. Psychiatry PD DEC 1 PY 2004 VL 56 IS 11 BP 892 EP 894 DI 10.1016/j.biopsych.2004.09.014 PG 3 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 878BR UT WOS:000225622000011 PM 15576067 ER PT J AU Palmen, SJMC van Engeland, H Hof, PR Schmitz, C AF Palmen, SJMC van Engeland, H Hof, PR Schmitz, C TI Neuropathological findings in autism SO BRAIN LA English DT Review DE autism; neuropathology; cerebral cortex; cerebellum; limbic system ID PERVASIVE DEVELOPMENTAL DISORDERS; EARLY INFANTILE-AUTISM; HEAD CIRCUMFERENCE; CEREBRAL-CORTEX; POSTERIOR-FOSSA; CORTICAL DEVELOPMENT; MENTAL-RETARDATION; NEUROANATOMICAL ABNORMALITIES; CEREBELLAR CORTICES; POSTMORTEM BRAIN AB Autism is currently viewed as a largely genetically determined neurodevelopmental disorder, although its underlying biological causes remain to be established. In this review, we examine the available neuropathological literature on autism and discuss the findings that have emerged. Classic neuropathological observations are rather consistent with respect to the limbic system (nine of 14 studied cases showed increased cell packing density and smaller neuronal size), the cerebellum (21 of 29 studied cases showed a decreased number of Purkinje cells, and in all of five cases that were examined for age-related morphological alterations, these changes were found in cerebellar nuclei and inferior olive) and the cerebral cortex (>50% of the studied cases showed features of cortical dysgenesis). However, all reported studies had to contend with the problem of small sample sizes, the use of quantification techniques not free of bias and assumptions, and high percentages of autistic subjects with comorbid mental retardation (at least 70%) or epilepsy (at least 40%). Furthermore, data from the limbic system and on age-related changes lack replication by independent groups. It is anticipated that future neuropathological studies hold great promise, especially as new techniques such as design-based stereology and gene expression are increasingly implemented and combined, larger samples are analysed, and younger subjects free of comorbidities are investigated. C1 Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, Rudolf Magnus Inst Neurosci, NL-3584 CX Utrecht, Netherlands. Univ Maastricht, European Grad Sch Neurosci, Maastricht, Netherlands. Univ Maastricht, Dept Psychiat & Neuropsychol, Div Cellular Neurosci, Maastricht, Netherlands. RWTH Aachen Univ, Dept Anat & Cell Biol, Aachen, Germany. CUNY Mt Sinai Sch Med, Dept Neurosci, New York, NY 10029 USA. CUNY Mt Sinai Sch Med, Dept Geriatr & Adult Dev, New York, NY 10029 USA. RP Palmen, SJMC (reprint author), Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, Rudolf Magnus Inst Neurosci, HP A01-468,Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. 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MONKEY; CHILDREN; LESIONS AB Oculomotor studies provide a novel strategy for evaluating the functional integrity of multiple brain systems and cognitive processes in autism. The current study compared pursuit eye movements of 60 high-functioning individuals with autism and 94 intelligence quotient, age and gender matched healthy individuals using ramp and oscillating target tasks. Individuals with autism had normal pursuit latency, but reduced closed-loop pursuit gain when tracking both oscillating and ramp targets. This closed-loop deficit was similar for leftward and rightward pursuit, but the difference between individuals with autism and their age-matched peers was more apparent after mid-adolescence, suggesting reduced maturational achievement of the pursuit system in autism. Individuals with autism also had lower open-loop pursuit gain (initial 100 ms of pursuit) and less accurate initial catch-up saccades during a foveofugal step-ramp task, but these deficits were only seen when targets moved into the right visual field. Pursuit performance in both open- and closed-loop phases was correlated with manual praxis in individuals with autism. Bilateral disturbances in the ability to use internally generated extraretinal signals for closed-loop pursuit implicate frontostriatal or cerebellar circuitry. The hemifield specific deficit in open-loop pursuit demonstrates a lateralized disturbance in the left extrastriate areas that extract visual motion information, or in the transfer of visual motion information to the sensorimotor areas that transform visual information into appropriate oculomotor commands. C1 Univ Illinois, Dept Psychiat MC 913, Ctr Cognit Med, Chicago, IL 60612 USA. Univ Pittsburgh, Pittsburgh, PA USA. RP Sweeney, JA (reprint author), Univ Illinois, Dept Psychiat MC 913, Ctr Cognit Med, 912 S Wood St,Suite 235, Chicago, IL 60612 USA. 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An alternative and potentially stronger test of FFA function in autism is one that attempts to affect levels of FFA activity using factors believed to modulate function in this brain region, such as face familiarity and the perception of face identity. The current study presented personally meaningful faces, such as mother and co-worker, as well as stranger faces in a rapid event-related FMRI design. Seven autistic and nine normal control adults participated and pressed a button in response to all female faces. A deconvolution analysis revealed significant FFA activity in response to familiar and stranger faces in both autism and normal control groups. Individuals with autism also showed greater fusiform activity in response to familiar faces than stranger faces, as well as the prototypical right hemisphere dominance in response to both types of faces. Normal subjects showed additional activation to familiar faces in the posterior cingulate, amygdala and medial frontal lobes, including the anterior cingulate. Subjects with autism showed a similar, but more limited, network in response to familiar faces. This network included the amygdala and implies that this structure, involved in multiple socio-emotional functions, can be responsive in autism in the presence of stimuli that represent high reward value, such as mother's face. Furthermore, the presence of a distinct network to process familiar faces in autism, one that included limbic structures and was not found in response to the faces of strangers, suggests socio-emotional processing in autism. A potentially noteworthy trend, however, was evidence for a reduction in medial frontal lobe function in the autism group. The main finding of FFA activity in autism stands in contrast to most past FMRI studies of face processing in this disorder. This positive result may reflect the use of personally significant faces that enhanced attention and motivation in the autistic participants. Furthermore, given the proposed role of the FFA in establishing person identity, the use of almost a dozen different personally familiar faces for each participant (totalling 32 non-repeating faces) may have additionally maximized FFA involvement. Therefore, dysfunction in the FFA found in other studies of autism may reflect defects in systems that modulate the FFA, rather than the FFA itself. C1 Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Dept Psychiat, La Jolla, CA 92093 USA. Childrens Hosp, Ctr Autism Res, San Diego, CA USA. RP Pierce, K (reprint author), 8110 La Jolla Shores Dr, La Jolla, CA 92037 USA. 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autism, a high degree of noncompliance with commands and symptoms of autonomic dysfunction by monitoring the brainstem autonomic tone during an attempt to perform isometric exercise. An index of cardiac vagal tone (CVT), cardiac sensitivity to baroreflex (CSB), heart rate (HR) and mean arterial blood pressure (MAP) were measured simultaneously. Physical non-compliance with our commands meant there was no force applied by the patient during the attempted exercise, but CVT and CSB were both reduced and sustained at very low levels throughout the attempt, while MAP and HR were increased concurrently to higher levels in the same period. This vagal withdrawal to allow concurrent increases in HR and MAP is an arousal response appropriate for isometric exercise, which is a sign of a positive mental effort to comply with our commands. These results demonstrate discordant mental and physical efforts in our patient. In this particular case, the physical inabilities in some instances could have been mislabelled as mental non-compliance due to autism. It would be worthwhile to investigate the prevalence of discordant mental and physical efforts in autism. (C) 2004 Elsevier B.V. All rights reserved. C1 UMDNJ New Jersey Med Sch, Dept Neurosci, Newark, NJ 07103 USA. Cent Middlesex Hosp, Dept Neurol, Peripheral Nerve & Automat Unit, London, England. UMDNJ Robert Wood Johnson Med Sch, Dept Pediat, Camden, NJ USA. S Glasgow Univ Hosp, NHS Trust, Dept Neurophysiol, Glasgow, Lanark, Scotland. S Glasgow Univ Hosp, NHS Trust, Dept Med Phys, Glasgow, Lanark, Scotland. RP Ming, X (reprint author), UMDNJ New Jersey Med Sch, Dept Neurosci, MSB-H506 185 S Orange Ave, Newark, NJ 07103 USA. 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We report the results of a comprehensive survey on musical behaviors and background administered to the largest sample of individuals with WS to date (n = 118, mean age = 20.4), and compare the results to those obtained from a control group of typically developing normal individuals (n = 118, mean age = 20.9) and two groups of individuals with other neurodevelopmental genetic disorders, Autism (n = 30, mean age = 18.2) and Down Syndrome (n = 40, mean age = 17.2). Individuals with WS were found to be rated higher in musical accomplishment, engagement, and interest than either of the comparison groups, and equivalent on most measures to the control group. Compared to all other groups including the controls, the WS individuals displayed greater emotional responses to music, manifested interest in music at an earlier age, and spent more hours per week listening to music. In addition, the effects of music listening (whether positive or negative) tended to last longer in the WS group. 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This study examined the prevalence of autism in AS in 19 children representing three known molecular classes of AS. Children were studied over the course of 1 year. Forty-two percent of this population, eight of 19 children, met criteria for autism according to the Autism Diagnostic Observation Schedule (ADOS). Parents of children who were diagnosed with autism according to Diagnostic and Statistical Manual of Mental Disorders (DSM)-IV criteria as well as the ADOS - Generic, Module 1 (ADOS-G) were administered the Autism Diagnostic Interview - Revised (ADI-R). Data from the ADI-R were convergent with data from the ADOS-G in all cases. Children with comorbid autism and AS scored lower on measures of language, adaptive behavior, and cognition, and demonstrated a slower rate of improvement over the course of the study. Furthermore, they demonstrated deficits in communication and socialization that mirror those observed in children with idiopathic autism. 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Neuropsychol. PD DEC PY 2004 VL 18 IS 4 BP 559 EP 572 DI 10.1080/13854040490888530 PG 14 WC Psychology, Clinical; Clinical Neurology; Psychology SC Psychology; Neurosciences & Neurology GA 895BH UT WOS:000226835400006 PM 15841957 ER PT J AU Trajkovski, V Ajdinski, L Spiroski, M AF Trajkovski, V Ajdinski, L Spiroski, M TI Plasma concentration of immunoglobulin classes and subclasses in children with autism in the Republic of Macedonia: Retrospective study SO CROATIAN MEDICAL JOURNAL LA English DT Article DE autistic disorder; immunoglobulin isotypes; Macedonia (Republic) ID IMMUNOLOGICAL TREATMENTS; AUTOANTIBODIES; ANTIBODIES; PROTEINS; AUTOIMMUNITY; ASSOCIATION; DISORDERS; GLOBULIN; BRAIN AB Aim. To examine plasma concentration of IgA, IgM, IgG classes, and IgG1, IgG2, IgG3, and IgG4 subclasses in children with autism. Methods. Infantile autism was diagnosed by the Diagnostic and Statistical Manual for Mental Disorders (DSM)-IV and the International Classification of Diseases (ICD)-10 criteria. Plasma samples were collected from 35 autistic subjects, and their 21 siblings (biological brothers and sisters) who served as healthy controls. Plasma samples were separated by centrifugation and stored at -20degreesC until the determination. Plasma immunoglobulin classes (IgM, IgA, IgG) and subclasses (IgG1, IgG2, IgG3, IgG4) were determined using a nephelometer. Results. Plasma concentrations (mean standard deviation) of IgM and IgG in autistic children (1.36+/-0.31 g/L and 13.14+/-1.27 g/L, respectively) were significantly higher (p=0.031 and p=0.023, respectively) in comparison with their healthy brothers or sisters (1.20+/-0.15 g/L and 12.39+/-0.96 g/L, respectively). Children with autism had significantly higher plasma concentrations of IgG4 (p<0.001) compared to their siblings (healthy brothers or sisters). Plasma concentration of IgA, IgG1, IgG2, and IgG3 were similar in autistic children and their healthy brothers or sisters. Increased plasma concentration of IgG1 was found (p=0.027) in autistic males (8.06+/-2.40), as compared with their healthy brothers (5.24+/-4.13 g/L). Plasma concentrations of IgG (14.28+/-3.66 g/L), and IgG1 (9.41+/-2.20 g/L) in autistic females were increased (p=0.012 and p=0.021, respectively) in comparison with IgG (11.07+/-2.07) and IgG1 (6.37+/-3.38 g/L) in their healthy sisters. Conclusion. Children with autism have increased plasma concentration of immunoglobulines. Increased immunoglobulines in children with autism could be a result of impaired development of the immune system, and/or genetic factors connected with defense mechanism in these children. C1 Fac Philosophy, Inst Special Educ & Rehabil, Skopje, Macedonia. Med Fac, Inst Immunobiol & Human Genet, Skopje, Macedonia. RP Spiroski, M (reprint author), Fac Philosophy, Inst Special Educ & Rehabil, Skopje, Macedonia. 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Aging modifies brain asymmetry, and an imbalance in specific asymmetries characterizes some brain disorders such as schizophrenia, depression, infantile autism or Alzheimer's disease. However, it is not clear whether these changes are a cause or a consequence of these disorders. Although this phenomenon has been extensively studied, its functional significance is not yet clear, and the neurochemical basis underlying anatomical or functional asymmetries in the brain is still poorly understood. In recent decades intensive research on the behaviour of neuropeptides has revealed asymmetries in their distribution in the brain, and there is evidence that the lateralized patterns of distribution are involved in the regulatory control of some neuropeptidase activities. Therefore, if these enzymatic activities are distributed asymmetrically, their endogenous substrates would presumably be affected in an asymmetrical way, as would the functions they are involved in. Here we review the most significant literature regarding human and animal brain asymmetry involving neuropeptides such as corticotropin-releasing hormone, cholecystokinin, luteinizing hormone-releasing hormone, thyrotropin-releasing hormone and angiotensin II, as well as their neuropeptidases. C1 Univ Jaen, Unit Physiol, Jaen 23071, Spain. Univ Granada, Federico Oloriz Inst Neurosci, E-18071 Granada, Spain. MG Consulting, CH-2842 Rossemaison, Switzerland. RP Ramirez, M (reprint author), Univ Jaen, Unit Physiol, Bldg B3,Room 213, Jaen 23071, Spain. 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The present study examined the degree to which individual differences in theory of mind and executive functions could explain variations in the severity of autism symptoms. Participants included 31 verbal, school-aged children with autism who were administered a battery of tests assessing the understanding of mental states (knowledge and false belief) and executive control skills (working memory, combined working memory and inhibitory control, and planning) and who were behaviorally evaluated for autism severity in the three core symptom domains. Whereas theory of mind and executive control abilities explained the significant variance beyond that accounted for by language level in communication symptoms, neither explained the significant variance in reciprocal social interaction or repetitive behaviors symptoms. These findings are discussed in terms of a proposed distinction between higher level, cognitive-linguistic aspects of theory of mind and related executive control skills, and more fundamental social-perceptual processes involved in the apprehension of mental state information conveyed through eyes, faces, and voices, which may be more closely linked to autistic deficits in social reciprocity. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Boston, MA 02118 USA. RP Joseph, RM (reprint author), Boston Univ, Sch Med, Dept Anat & Neurobiol, 715 Albany St L-814, Boston, MA 02118 USA. 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PD WIN PY 2004 VL 16 IS 1 BP 137 EP 155 DI 10.1017/S095457940404444X PG 19 WC Psychology, Developmental SC Psychology GA 805GY UT WOS:000220356000007 PM 15115068 ER PT J AU Bauminger, N AF Bauminger, N TI The expression and understanding of jealousy in children with autism SO DEVELOPMENT AND PSYCHOPATHOLOGY LA English DT Article ID HIGH-FUNCTIONING CHILDREN; SOCIAL-COMPARISON JEALOUSY; SELF-RECOGNITION; FRIENDSHIP; COMPLEX; CONTEXT; EMOTION; PRIDE; ENVY; AGE AB We investigated the expression and understanding of jealousy in 16 high-functioning children with autism and 17 typically developing children matched for IQ, chronological age, gender, and maternal education. We examined the expression of jealousy via children's behaviors, verbalizations, and affects demonstrated during two jealousy-provoking triadic scenarios (drawing and playing) enacted among the child in the experimental group (autism or typical), that child's main caregiver (mostly mothers), and a familiar peer or sibling. The two scenarios corresponded with the two types of jealousy described in past studies: social-comparison jealousy (drawing scenario) and social-relational jealousy (playing scenario). To tap children's understanding, we asked them to identify jealousy from a picture, to provide examples of times they felt jealous, and to offer suggestions for coping with jealousy. The main results revealed that children with autism expressed jealousy in situations similar to their typical age mates but manifested it in different behaviors. Moreover, children with autism revealed a less coherent understanding of the feeling. We discuss the meaning of the gap between demonstrating and understanding jealousy in light of the two central theoretical views conceptualizing the core emotional deficit in children with autism. C1 Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. RP Bauminger, N (reprint author), Bar Ilan Univ, Sch Educ, IL-52900 Ramat Gan, Israel. 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PD WIN PY 2004 VL 16 IS 1 BP 157 EP 177 DI 10.1017/S0954579404044451 PG 21 WC Psychology, Developmental SC Psychology GA 805GY UT WOS:000220356000008 PM 15115069 ER PT J AU [Anonymous] AF [Anonymous] TI Abstracts: International Society for Developmental Psychobiology, 37(th) Annual Meeting SO DEVELOPMENTAL PSYCHOBIOLOGY LA English DT Article AB This meeting, which contains 100 abstracts in English, focuses on developmental psychobiology. Topics include but are not limited to autism, animal models of schizophrenia, adult avoidance learning, visual recognition memory, prolonged maternal separation, EEGs of infants of depressed mothers, potential deleterious effects of maternal stress on the developing fetus, behavioral effects ofiron deficiency, postpartum depression, expression of acquired fear and social development of selective breeding for aggressive behavior, influence of gender on behavioral and neurodevelopmental effects, benefits of breastfeeding a premature infant, ontogeny of fear reactions, neophobia and agoraphobia and behavioral and neural systems regulating early social interactions. NR 0 TC 0 Z9 0 PU WILEY-BLACKWELL PI HOBOKEN PA 111 RIVER ST, HOBOKEN 07030-5774, NJ USA SN 0012-1630 EI 1098-2302 J9 DEV PSYCHOBIOL JI Dev. Psychobiol. PD DEC PY 2004 VL 45 IS 4 BP 259 EP 284 PG 26 WC Developmental Biology; Psychology SC Developmental Biology; Psychology GA 877OI UT WOS:000225579500008 ER PT J AU Myles, BS Hagiwara, T Dunn, W Rinner, L Reese, M Huggins, A Becker, S AF Myles, BS Hagiwara, T Dunn, W Rinner, L Reese, M Huggins, A Becker, S TI Sensory issues in children with Asperger syndrome and autism SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID HIGH-FUNCTIONING AUTISM; DISORDERS; PROFILE AB The purpose of this study was to examine whether children with Asperger Syndrome and children with autism exhibit difference sensory profiles. The Sensory Profile (Dunn, 1999), completed on 86 individuals with Asperger Syndrome and 86 persons with autism matched for age, revealed differences in three of 23 areas evaluated: (a) Emotional/Social Responses, (b) Emotional Reactivity, and (c) Inattention/Distractibility. Implications regarding these similarities and differences in profile are discussed. C1 Univ Kansas, Med Ctr, Lawrence, KS 66045 USA. RP Myles, BS (reprint author), Univ Kansas, Med Ctr, 1122 W Campus Rd,Room 521, Lawrence, KS 66045 USA. CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Attwood T., 1998, ASPERGERS SYNDROME G AYRES AJ, 1980, AM J OCCUP THER, V34, P375 Bagnato SJ, 1999, INFANT YOUNG CHILD, V12, P98 Bryson S. 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J., 1999, AUTISM, V3, P117, DOI DOI 10.1177/1362361399003002003 WILLEY LH, 1999, PRETENDING NORMAL LI NR 30 TC 15 Z9 15 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 2004 VL 39 IS 4 BP 283 EP 290 PG 8 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 879PE UT WOS:000225728900001 ER PT J AU Devlin, SD Harber, MM AF Devlin, SD Harber, MM TI Collaboration among parents and professionals with discrete trial training in the treatment for autism SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID CHILDREN; BEHAVIOR AB This study evaluates impact of collaborative efforts of parents and school professionals in the treatment of autism in a five year-old boy. Method of treatment was discrete trial training across settings (e.g., home and school) and change agents were the child's parents, siblings, special education, teacher, resource teacher, and speech pathologist. C1 Mississippi State Univ, Mississippi State, MS 39762 USA. RP Devlin, SD (reprint author), Mississippi State Univ, Box 9727, Mississippi State, MS 39762 USA. CR Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P353 Bimbrauer J. S., 1993, BEHAV CHANGE, V10, P63 BORDEN MC, 1994, J AUTISM DEV DISORD, V24, P23, DOI 10.1007/BF02172210 CARR EG, 1977, PSYCHOL BULL, V84, P800, DOI 10.1037//0033-2909.84.4.800 FENSKE EC, 1985, ANAL INTERVEN DEVEL, V5, P49, DOI 10.1016/S0270-4684(85)80005-7 LOVAAS O, 1987, J CONSULT CLIN PSYCH, V5, P3 Lovaas O. 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PD DEC PY 2004 VL 39 IS 4 BP 291 EP 300 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 879PE UT WOS:000225728900002 ER PT J AU Akmanoglu, N Batu, S AF Akmanoglu, N Batu, S TI Teaching pointing to numerals to individuals with autism using simultaneous prompting SO EDUCATION AND TRAINING IN DEVELOPMENTAL DISABILITIES LA English DT Article ID HIERARCHY STRATEGIES; SEVERE HANDICAPS; TIME-DELAY; STUDENTS; ACQUISITION; SKILLS AB The purpose of this study was to examine effectiveness of simultaneous prompting in teaching pointing to numerals to individuals with autism. Three individuals with autism were taught pointing to numerals, which were orally named by the teacher using simultaneous prompting. A multiple probe design was used across three behaviors and replicated across three subjects. Results revealed that simultaneous prompting was effective in teaching pointing to numerals, which were named by the teacher. Subjects managed to learn the numerals and generalize this skill to 'pointing to the numerals on a calendar page'. C1 Anadolu Univ, TR-26470 Eskisehir, Turkey. RP Batu, S (reprint author), Anadolu Univ, TR-26470 Eskisehir, Turkey. EM esbatu@anadolu.edu.tr CR Dogan OS, 2002, RES DEV DISABIL, V23, P237, DOI 10.1016/S0891-4222(02)00122-1 FARMER JA, 1991, EDUC TRAIN MENT RET, V26, P190 MCDONNELL J, 1989, J APPL BEHAV ANAL, V22, P85, DOI 10.1901/jaba.1989.22-85 Fetko KS, 1999, EDUC TRAIN MENT RET, V34, P318 Fickel K. M., 1998, J BEHAV ED, V8, P219, DOI 10.1023/A:1022887624824 GIBSON AN, 1992, TOP EARLY CHILD SPEC, V12, P247 Griffen AK, 1998, EDUC TRAIN MENT RET, V33, P42 Kircaali-Iftar G., 1997, TEK DENEKLI ARASTIRM KOEGEL RL, 1999, TEACHING CHILDREN AU MACFARLANDSMITH J, 1993, J EARLY INTERVENTION, V17, P50 McCurdy B. L., 1990, ED TREATMENT CHILDRE, V13, P226 MCDONNELL J, 1987, J ASSOC PERS SEVERE, V12, P227 Parrot K. A., 2000, J BEHAV ED, V10, P3, DOI 10.1023/A:1016639721684 SCHOEN SF, 1988, J DIVISION EARLY CHI, V12, P349 Schuster J. W., 1993, J BEHAV ED, V3, P299, DOI 10.1007/BF00961557 Schuster J. W., 1992, J BEHAVIORAL ED, V2, P305, DOI 10.1007/BF00948820 Singleton DK, 1999, EDUC TRAIN MENT RET, V34, P182 SINGLETON KC, 1995, EDUC TRAIN MENT RET, V30, P218 Snell M., 2000, INSTRUCTION STUDENTS SWELL TJ, 1998, J EARLY INTERVENTION, V2, P132 Tawney W. J., 1984, SINGLE SUBJECT RES S Tekin E., 2001, OZEL EGITIMDE YANLIS Wolery M., 1993, EARLY EDUC DEV, V4, P20, DOI 10.1207/s15566935eed0401_2 Wolery M., 1991, J BEHAVIORAL ED, V1, P79, DOI 10.1007/BF00956755 NR 24 TC 27 Z9 27 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 2004 VL 39 IS 4 BP 326 EP 336 PG 11 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 879PE UT WOS:000225728900006 ER PT J AU Skovgaard, AM Houmann, T Landorph, SL Christiansen, E AF Skovgaard, AM Houmann, T Landorph, SL Christiansen, E TI Assessment and classification of psychopathology in epidemiological research of children 0-3 years of age - A review of the literature SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Review DE infant; toddler psychopathology; assessment; epidemiology ID INFANT MENTAL-HEALTH; 3-YEAR-OLD CHILDREN; AUTISM; ATTACHMENT; VALIDITY; QUESTIONNAIRE; DISORDERS; DIAGNOSES; PATTERNS; BEHAVIOR AB The research of psychopathology in children 0-3 years of age is dominated by clinical case studies and theoretical reflections, and epidemiological studies are few. This paper reviews methods to assess and classify psychopathology in children 0-3 years old in an epidemiological context. Diagnostic assessments of children 0-3 years of age are based on information from different sources and investigation of several domains of mental functioning, and the rapid developmental changes and the relationship context are taken into account. The reviewed literature shows a range of methods to assess and classify psychopathology in children 0-3 years of age: screening instruments with established psychometric properties, such as the Child Behaviour Checklist (CBCL) and the Checklist for Autism in Toddlers (CHAT), and methods of in-depth assessment known from both clinical practice and research: developmental tests, such as the Bayley Scales, and relationship assessments, such as the Early Relational Assessment (ERA). The classification of psychopathology in young children can be approved by the Diagnostic Classification 0-3. The reliability and validity of DC 0-3 have not yet been established, but preliminary results seem promising. The demands made on diagnostic assessment procedures in epidemiological research of children 0-3 years of age can be met by a combination of well-established research instruments, such as the CBCL, with in-depth clinical assessment procedures, such as the Bayley Scales and the ERA, and diagnostic classification by DC 0-3. C1 Univ Copenhagen, Glostrup Hosp, Child & Adolescent Psychiat Ctr, DK-2600 Glostrup, Denmark. Univ Copenhagen, Bispebjerg Hosp, Dept Child & Adolescent Psychiat, DK-2400 Copenhagen, Denmark. RP Skovgaard, AM (reprint author), Univ Copenhagen, Glostrup Hosp, Child & Adolescent Psychiat Ctr, DK-2600 Glostrup, Denmark. CR Achenbach T, 2000, MANUAL ASEBA PRESCHO Achenbach T. M., 1995, EPIDEMIOLOGY CHILD A, P22 ACHENBACH TM, 1987, J ABNORM CHILD PSYCH, V15, P629, DOI 10.1007/BF00917246 Ainsworth M. 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N., 1993, HDB INFANT MENTAL HL Emde RN, 2003, INF MENTAL HLTH J, V24, P437, DOI 10.1002/imhj.10067 Esser G., 1989, MANNHEIMER ELTERNINT Fenson L, 1993, MACARTHUR COMMUNICAT Fombonne B, 2002, CHILD ADOL PSYCH CL, P52 Gilliam W, 2000, HDB INFANT MENTAL HL, P236 Greenspan S, 1993, HDB INFANT MENTAL HL, P280 GRIFFITH R, 1979, ABILITIES YOUNG CHIL JOHNSON JH, 1990, DEV ASSESSMENT CLIN Keren M, 2001, J AM ACAD CHILD PSY, V40, P27, DOI 10.1097/00004583-200101000-00013 Laucht M, 1997, J CHILD PSYCHOL PSYC, V38, P843, DOI 10.1111/j.1469-7610.1997.tb01602.x LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Lyons-Ruth K., 1993, HDB INFANT MENTAL HL, P14 *NAT CTR INF TODDL, 1994, ZERO 3 DIAGN CLASS 0 NORDBERG L, 1994, 1 4 YEARS CHILDRENS O'Connor T. G, 2002, CHILD ADOL PSYCH CL, P776 RICHMAN N, 1975, J CHILD PSYCHOL PSYC, V16, P277, DOI 10.1111/j.1469-7610.1975.tb00362.x Roid G. H., 1995, LEITER INT PERFORMAN Rothbart M. K., 1981, ADV DEV PSYCHOL, V1 RUTTER M, 1989, J AM ACAD CHILD PSY, V28, P633, DOI 10.1097/00004583-198909000-00001 RUTTER M, 1995, J CHILD PSYCHOL PSYC, V36, P549, DOI 10.1111/j.1469-7610.1995.tb02314.x SKOVGAARD AM, 2003, MENTAL HLTH DISTURBA Taylor E, 2002, CHILD ADOL PSYCH CL, P3 Thomas A., 1963, BEHAV INDIVIDUALITY Thomas JM, 1998, INF MENTAL HLTH J, V19, P229, DOI 10.1002/(SICI)1097-0355(199822)19:2<229::AID-IMHJ10>3.0.CO;2-# TRONICK E, 1978, J AM ACAD CHILD PSY, V17, P1, DOI 10.1016/S0002-7138(09)62273-1 WEINBERG MK, 1994, CHILD DEV, V65, P1503, DOI 10.2307/1131514 VAN IJZENDOORN MH, 1988, CHILD DEV, V59, P147, DOI 10.2307/1130396 VERHULST FC, 2002, CHILD ADOL PSYCH CL, P70 VERHULST FC, 1992, DEV CLIN PSYCHOL PSY, V23, P111 Verhust F., 1995, EPIDEMIOLOGY CHILD A, P1 World Health Organisation, 1992, ICD 10 ICD 10 CLASS, V10th Zeanah CH, 1997, J CHILD PSYCHOL PSYC, V38, P81, DOI 10.1111/j.1469-7610.1997.tb01506.x Zeanah CH, 1994, DEV ISSUES PSYCHIAT, V1, P1 Zeanah CH, 2000, HDB INFANT MENTAL HL, P267 Zeanah CH, 1997, INF MENTAL HLTH J, V18, P182, DOI 10.1002/(SICI)1097-0355(199722)18:2<182::AID-IMHJ7>3.0.CO;2-R ZIMMERMANN IL, 1992, PRESCHOOL LANGUAGE S NR 66 TC 24 Z9 24 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD DEC PY 2004 VL 13 IS 6 BP 337 EP 346 DI 10.1007/s00787-004-0393-z PG 10 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 890MV UT WOS:000226516400001 PM 15619045 ER PT J AU Simic, M Turk, J AF Simic, M Turk, J TI Autistic spectrum disorder associated with partial duplication of chromosome 15; three case reports SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autistic spectrum disorder; partial duplication chromosome 15; behavioural phenotype ID PRADER-WILLI-SYNDROME; TUBEROUS SCLEROSIS; MOLECULAR ANALYSIS; PREVALENCE; FEATURES; ORIGIN; 15Q AB Duplication of part or the entirety of chromosome 15 that involves the Prader-Willi/Angelman syndrome critical region (PWACR) is a genetic disorder which is associated with variable degrees of intellectual impairment, motor co-ordination problems and social and communication disorders. Published case reports indicate that phenotypic expression is dependent on parental origin of the duplication and implicate maternally derived duplications in the pathogenesis of autistic features. This article describes three individuals, two males and one female, aged between 5 and 8 years, all with partial duplication of chromosome 15. Autism (or autistic spectrum disorder) was present in all three instances with varying degrees of cognitive impairment. The aim of this paper is to describe the phenotypic characteristics of this genetic sequence and the possible associations between social and behavioural patterns on the one hand, and degree and nature of genetic impairment on the other. C1 Maudsley Hosp & Inst Psychiat, Michael Rutter Ctr Children & Young People, London SE5 8AZ, England. St George Hosp, Sch Med, Dept Clin Dev Sci, London SW17 0RE, England. RP Simic, M (reprint author), Maudsley Hosp & Inst Psychiat, Michael Rutter Ctr Children & Young People, London SE5 8AZ, England. EM mima.simic@slam.nhs.uk CR Baker P, 1998, J AUTISM DEV DISORD, V28, P279, DOI 10.1023/A:1026004501631 Bass MP, 2000, NEUROGENETICS, V2, P219, DOI 10.1007/s100480050067 BLENNOW E, 1994, PRENATAL DIAG, V14, P1019, DOI 10.1002/pd.1970141103 Borgatti R, 2001, PEDIATR NEUROL, V24, P111, DOI 10.1016/S0887-8994(00)00244-7 Clayton-Smith J, 2001, DEV MED CHILD NEUROL, V43, P476, DOI 10.1017/S0012162201000871 Cook EH, 1997, AM J HUM GENET, V60, P928 Descheemaeker MJ, 2002, J INTELL DISABIL RES, V46, P41, DOI 10.1046/j.1365-2788.2002.00354.x ELABD S, 1995, J CHILD PSYCHOL PSYC, V36, P1109 Flejter WL, 1996, AM J MED GENET, V61, P182, DOI 10.1002/(SICI)1096-8628(19960111)61:2<182::AID-AJMG17>3.0.CO;2-Q Gillberg C, 1998, J AUTISM DEV DISORD, V28, P415, DOI 10.1023/A:1026004505764 HACKNEY IM, 1968, J PEDIATR-US, V72, P646, DOI 10.1016/S0022-3476(68)80007-1 HUNT A, 1987, DEV MED CHILD NEUROL, V29, P190 Mao R, 2000, GENET MED, V2, P131, DOI 10.1097/00125817-200003000-00003 Martinsson T, 1996, EUR CHILD ADOLES PSY, V5, P185 MCGUFFIN P, 1997, J CHILD PSYCHOL PSYC, V28, P215 Mignon C, 1996, EUR J HUM GENET, V4, P88 OBRIEN G, 2002, BEHAV PHENOTYPES CLI Robinson Wendy P., 1993, European Journal of Human Genetics, V1, P37 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 TURK J, 2002, BEHAV PHEONTYPES CLI, P152 Turk J., 1997, AUTISM, V1, P175, DOI 10.1177/1362361397012005 TURK J, 1996, CHILD PSYCHOL PSYCHI, V1, P4, DOI 10.1111/j.1475-3588.1996.tb00002.x Turk J, 1998, J APPL RES INTELLECT, V11, P175 Veltman MWM, 2004, EUR CHILD ADOLES PSY, V13, P42, DOI 10.1007/s00787-004-0354-6 NR 24 TC 9 Z9 9 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD DEC PY 2004 VL 13 IS 6 BP 389 EP 393 DI 10.1007/s00787-004-0414-y PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 890MV UT WOS:000226516400008 PM 15619052 ER PT J AU Simpson, RL AF Simpson, RL TI Finding effective intervention and personnel preparation practices for students with autism spectrum disorders SO EXCEPTIONAL CHILDREN LA English DT Article ID FACILITATED COMMUNICATION; CHILDREN; YOUTH; PERSPECTIVE; SETTINGS; BEHAVIOR; SEARCH; ISSUES AB The CEC Research Award recognizes researchers for the significant contributions they have made to special education. We believe that the members of this distinguished group have much to share with our readers. We have invited each of them to contribute an article, addressing their perspectives on special education research and practices. Richard Simpson was awarded the Research Award in 2002. This article by Simpson presents his motivations for entering the field and what he has learned from his work with children and youth with autism spectrum disorders, selected representative references are also provided. C1 Univ Kansas, Lawrence, KS 66045 USA. RP Simpson, RL (reprint author), Univ Kansas, JR Pearson Hall,1122 W Campus Rd, Lawrence, KS 66045 USA. EM richsimp@ku.edu CR Bettelheim B., 1967, EMPTY FORTRESS Bijou S. W., 1961, CHILD DEV SYSTEMATIC Dettmer S., 2000, FOCUS AUTISM OTHER D, V15, P163, DOI DOI 10.1177/108835760001500307 Feinberg E., 2000, FOCUS AUTISM OTHER D, V15, P130, DOI [10.1177/108835760001500301, DOI 10.1177/108835760001500301] FINE MJ, 2000, COLLABORATION PARENT Griswold D. E., 2002, FOCUS AUTISM OTHER D, V17, P94, DOI 10.1177/10883576020170020401 Heflin L. J., 1998, FOCUS AUTISM OTHER D, V13, P212 Heflin L.J., 1998, FOCUS AUTISM OTHER D, V13, P194, DOI DOI 10.1177/108835769801300401 Kanner L, 1943, NERV CHILD, V2, P217 KANNER L, 1949, AM J ORTHOPSYCHIAT, V19, P416 Keeling K., 2003, FOCUS AUTISM OTHER D, V18, P105, DOI 10.1177/108835760301800204 LORIMER M, 2002, J POSIT BEHAV INTERV, V4, P53 LOVAAS I, 1969, BEHAV MODIFICATION T Myles B., 1996, FOCUS AUTISM OTHER D, V11, p[163, 190] MYLES B, 2002, EDUC HORIZONS, V81, P38 Myles B. S., 1997, AUTISM, V1, P77, DOI 10.1177/1362361397011008 Myles B. S., 2002, FOCUS AUTISM OTHER D, V17, P132, DOI 10.1177/10883576020170030201 Myles B. S., 1999, FOCUS AUTISM OTHER D, V14, P212, DOI 10.1177/108835769901400403 Myles B. S., 1996, FOCUS AUTISM OTHER D, V11, P37 MYLES BS, 2003, STUDENTS ASPERGER SY Myles BS, 2001, EDUC TRAIN MENT RET, V36, P304 Myles BS, 2001, FOCUS EXCEPT CHILD, V34, P1 MYLES BS, 1996, FOCUS AUTISM OTHER D, V11, P190 NEWMAN R, 1977, AAESPH REV, V2, P157 SASSO GM, 1985, ANAL INTERVEN DEVEL, V5, P233, DOI 10.1016/0270-4684(85)90013-8 SIMPSOIN R, 1994, PREVENTING SCH FAILU, V38, P40 SIMPSON R, 1999, FOCUS AUTISM OTHER D, V14, P230 SIMPSON R, 1978, AAESPH REV, V3, P145 SIMPSON R, 2000, REACHING TODAYS YOUT, V5, P12 SIMPSON R, 1998, SOCIAL SKILLS STUDEN SIMPSON R, 1998, ED CHILDREN YOUTH AU Simpson R. L., 1996, WORKING PARENTS FAMI Simpson R. L., 2002, COUNSEL HUM DEV, V34, P1 Simpson R. L., 1988, BEHAV DISORDERS, V13, P159 Simpson R. L, 1980, BEHAV DISORDERS, V5, P79 SIMPSON RL, 1995, FOCUS EXCEPT CHILD, V27, P1 Simpson R. L., 1992, FOCUS AUTISTIC BEHAV, V7, P1 Simpson R. L., 1998, PREVENTING SCH FAILU, V42, P149, DOI DOI 10.1080/10459889809603730 SIMPSON RL, 2000, AUTISM INFORMATION R Simpson RL, 2001, FOCUS AUTISM OTHER D, V16, P68, DOI 10.1177/108835760101600202 SIMPSON RL, 1993, REM SPEC EDUC, V14, P7 SIMPSON RL, 1995, J SPEC EDUC, V28, P424 Simpson RL, 1998, INTERV SCH CLIN, V33, P219 SIMPSON RL, 1993, FOCUS AUTISTIC BEHAV, V7, P1 SIMPSON RL, 1977, J AUTISM CHILD SCHIZ, V7, P349, DOI 10.1007/BF01540393 Simpson RL, 2003, TOP LANG DISORD, V23, P116 SIMPSON RL, 1988, BEHAV DISORDERS, V14, P40 Simpson RL, 1995, BEHAV DISORDERS, V21, P7 SIMPSON RL, 1986, MANAGEMENT AUTISTIC Simpson RL, 1999, J ASSOC PERS SEVERE, V24, P218, DOI 10.2511/rpsd.24.3.218 Smith Myles B., 2002, FOCUS AUTISM OTHER D, V17, P44 Spears R, 2001, BEHAV DISORDERS, V26, P227 Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 Whelan RJ, 1996, BEHAV DISORDERS, V22, P49 Young B., 1997, FOCUS AUTISM OTHER D, V12, P31 NR 55 TC 13 Z9 13 PU COUNCIL EXCEPTIONAL CHILDREN, DIVISION EARLY CHILHOOD PI ARLINGTON PA 1110 N GLEBE RD, ARLINGTON, VA 22201-5704 USA SN 0014-4029 J9 EXCEPT CHILDREN JI Except. Child. PD WIN PY 2004 VL 70 IS 2 BP 135 EP 144 PG 10 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 764KM UT WOS:000188206100001 ER PT J AU Skotko, BG Koppenhaver, DA Erickson, KA AF Skotko, BG Koppenhaver, DA Erickson, KA TI Parent reading behaviors and communication outcomes in girls with Rett syndrome SO EXCEPTIONAL CHILDREN LA English DT Article ID CHILDREN; AUTISM; MECP2; MUTATION; SPEECH AB We describe evidence and intervention strategies for parents, educators, and researchers who seek to enhance communication and literacy in children with Rett syndrome (RS). Four girls with RS and their mothers videotaped their storybook interactions at home for 4 months. Parent-child storybook interactions were coded for child behaviors (e.g., use of augmentative communication devices, attention to book, or vocalizations) and parent behaviors (e.g., pointing in the book or asking predictive questions). Correlation and multiple regression analyses of these variables revealed that girls with RS can learn to communicate in meaningful ways through storybooks; however, mothers may need to engage in different strategies to facilitate better use of augmentative strategies. Successful strategies are discussed for the mother-daughter dyads. C1 Harvard Univ, Sch Med, Cambridge, MA 02138 USA. Univ N Carolina, Chapel Hill, NC USA. RP Skotko, BG (reprint author), 12 Greenway Ct,Suite 5, Brookline, MA 02446 USA. EM Brian_Skotko@student.hms.harvard.edu RI Skotko, Brian/D-1375-2013 OI Skotko, Brian/0000-0002-5232-9882 CR American Association on Mental Retardation, 2002, MENT RET DEF CLASS S American Psychiatric Association, 2000, QUICK REF DIAGN CRIT Amir RE, 1999, NAT GENET, V23, P185 BARLOW DH, 1984, SINGLE CASE EXPT DES Bayley N, 1993, BAYLEY SCALES INFANT BEDROSIAN J, 1995, M AM SPEECH LANG HEA BELL KL, 2000, J BONE MINER RES, V15, P52 Carle E., 1990, VERY QUIET CRICKET Charlop-Christy MH, 2002, J APPL BEHAV ANAL, V35, P213, DOI 10.1901/jaba.2002.35-213 COLEMAN M, 1988, J MENT DEFIC RES, V32, P117 COLEMAN P, 1991, THESIS U N CAROLINA Crowe L. K., 2000, COMMUNICATION DISORD, V21, P131, DOI 10.1177/152574010002100302 Dexter M.E., 1998, THESIS J HOPKINS U B Grant S., 1995, J CHILDHOOD COMMUNIC, V16, P31 HAGBERG B, 1983, ANN NEUROL, V14, P471, DOI 10.1002/ana.410140412 Hetzroni O, 2002, J INTELLECT DEV DIS, V27, P57, DOI 10.1080/13668250120109204 HILL E, 1980, WHERES SPOT Koppenhaver D. 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Child. PD WIN PY 2004 VL 70 IS 2 BP 145 EP 166 PG 22 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 764KM UT WOS:000188206100002 ER PT J AU Kliewer, C Fitzgerald, LM Meyer-Mork, J Hartman, P AF Kliewer, C Fitzgerald, LM Meyer-Mork, J Hartman, P TI Citizenship for all in the literate community: An ethnography of young children with significant disabilities in inclusive early childhood settings SO HARVARD EDUCATIONAL REVIEW LA English DT Article ID AUTISM AB In this study, Christopher Kliewer, Linda Fitzgerald, Jodi Meyer-Mork, Patresa Hartman, Pat English-Sand, and Donna Raschke use ethnographic methods to explore literacy development in young children considered to have significant disabilities. The study settings included nine preschool and kindergarten Classrooms across five programs, all of which involved children with and without disabilities learning side-by-side. Over the course of two school years, the authors observed teachers emphasizing children's narratives, and in so doing effectively fostering the Citizenship of all children in the literate communities of the classrooms under study. The authors describe several themes that appeared in their data related to fostering effective literacy development in children historically segregated from rich curricular opportunities. In this effort, defining literacy as making meaning and interpreting children with disabilities as competent meaning makers was foremost. C1 Univ No Iowa, Cedar Falls, IA 50614 USA. Syracuse Univ, Syracuse, NY 13244 USA. RP Kliewer, C (reprint author), Univ No Iowa, Cedar Falls, IA 50614 USA. CR Adams M. J., 1990, BEGINNING READ THINK Adams M. 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A., 1992, INTERPRETING DISABIL, P197 Grandin T., 1986, EMERGENCE LABELED AU HUNT N, 1966, WORLD N HUNT DIARY M Kliewer C, 2001, J ASSOC PERS SEVERE, V26, P1, DOI 10.2511/rpsd.26.1.1 Kliewer C, 1998, DISABIL SOC, V13, P95 Kliewer C, 1998, SCH CHILDREN DOWN SY Kliewer C., 2002, DISABILITY CULTURE E, V1, P41 Kliewer C, 1998, EXCEPT CHILDREN, V64, P167 Kliewer C, 1999, EXCEPT CHILDREN, V66, P85 KLIEWER C, 2001, TASH CONNECTIONS, V27, P8 Kliewer C, 2001, TEACH COLL REC, V103, P450, DOI 10.1111/0161-4681.00122 KLUTH P, 2003, ACCESS ACAD STUDENTS Koppenhaver DA, 2003, TOP LANG DISORD, V23, P283 Maurice C., 1993, LET ME HEAR YOUR VOI McEwan H., 1995, NARRATIVE TEACHING L McGuiness D., 1997, WHY OUR CHILDREN CAN Mirenda P, 2003, TOP LANG DISORD, V23, P271 Paley V. G., 1988, BAD GUYS DONT HAVE B Paley V. G., 1992, YOU CANT SAY YOU CAN RESNICK DP, 1977, HARVARD EDUC REV, V47, P370 Richgels D. 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PD WIN PY 2004 VL 74 IS 4 BP 373 EP 403 PG 31 WC Education & Educational Research SC Education & Educational Research GA 967BC UT WOS:000232065500001 ER PT J AU Khalfa, S Bruneau, N Roge, B Georgieff, N Veuillet, E Adrien, JL Barthelemy, C Collet, L AF Khalfa, S Bruneau, N Roge, B Georgieff, N Veuillet, E Adrien, JL Barthelemy, C Collet, L TI Increased perception of loudness in autism SO HEARING RESEARCH LA English DT Article DE autism; auditory dynamic range; loudness; hyperacusis ID CHILDHOOD AUTISM; FOLLOW-UP; DYSFUNCTION; CHILDREN AB Clinical reports on autism describe abnormal responses to auditory stimuli such as intolerance to sounds. The present study assessed subjective perception of loudness in subjects with autism compared to healthy controls, using two psychoacoustic tests. First, the auditory dynamic range was evaluated at six different tone frequencies. Secondly, loudness growth as a function of the intensity level of a 1 kHz tone was estimated. Verbal responses from a group of 11 children and adolescents with autism were compared to responses of 11 age- and gender- matched healthy controls. Smaller auditory dynamic ranges were found in the autistic group than in the control group, as well as increased perception of loudness, indicating hyperacusis in subjects with autism. (C) 2004 Elsevier B.V. All rights reserved. C1 Univ Mediterranee, INSERM, EMI U 9926, Fac Med Timone,Lab Neurophysiol & Neuropsychol, F-13385 Marseille 5, France. CHU Bretonneau, INSERM, U619, Serv Neurophysiol Pedopsychiat,IFR 135, F-37044 Tours, France. Univ Toulouse Le Mirail, UFR Psychol, F-31058 Toulouse 1, France. ITTAC, F-69616 Villeurbanne, France. Hop Edouard Herriot, CNRS, UMR 5020, F-69003 Lyon, France. Univ Paris 05, Lab Psychol Clin Psychopathol, F-75270 Paris 06, France. RP Khalfa, S (reprint author), Univ Mediterranee, INSERM, EMI U 9926, Fac Med Timone,Lab Neurophysiol & Neuropsychol, 27 Bd Jean Moulin, F-13385 Marseille 5, France. 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Res. PD DEC PY 2004 VL 198 IS 1-2 BP 87 EP 92 DI 10.1016/j.heares.2004.07.006 PG 6 WC Audiology & Speech-Language Pathology; Neurosciences; Otorhinolaryngology SC Audiology & Speech-Language Pathology; Neurosciences & Neurology; Otorhinolaryngology GA 878IK UT WOS:000225640000010 PM 15617227 ER PT J AU Wersinger, SR Kelliher, KR Zufall, F Lolait, SJ O'Carroll, AM Young, WS AF Wersinger, SR Kelliher, KR Zufall, F Lolait, SJ O'Carroll, AM Young, WS TI Social motivation is reduced in vasopressin 1b receptor null mice despite normal performance in an olfactory discrimination task SO HORMONES AND BEHAVIOR LA English DT Article DE vasopressin V3 receptor; behavior; chemosensory; aggression ID HAMSTERS MESOCRICETUS-AURATUS; PAIR-BOND FORMATION; AGGRESSIVE-BEHAVIOR; MONOGAMOUS VOLE; GOLDEN-HAMSTERS; SEXUAL-BEHAVIOR; GENE-TRANSFER; BULB REMOVAL; AUTISM; HYPOTHALAMUS AB In this study, we characterized more thoroughly the social behavior of vasopressin 1b receptor null (V1bR-/-) mice. We confirmed that V1bR-/- males exhibit less social aggression than their wild-type (V1bR+/+) littermates. We tested social preference by giving male subjects a choice between pairs of soiled or clean bedding. In general, V1bR+/+ mice spent significantly more time engaged in chemoinvestigation of these social stimuli than V1bR-/- mice. Male V1bR+/+ mice preferred female-soiled bedding over male-soiled bedding, male-soiled bedding over clean bedding, and female-soiled bedding over clean bedding. In contrast, V1bR-/- males failed to exhibit a preference for any bedding. This difference in behavior is not explained by an anosmic condition as there were no differences between V1bR-/- and V1bR+/+ mice in their abilities to detect a cookie buried in clean bedding, or in their ability to perform in an operant conditioning task using a fully automated liquid dilution olfactometer. In the latter task, male V1bR-/- mice were fully capable of discriminating between male and female mouse urine. The latencies to learn this task did not differ between the two genotypes. Thus, a V1bR-/- male's ability to differentiate between male and female chemosensory cues appears no different than that of a V1bR+/+ male's. We propose that the V1bR plays an important role in social motivation, perhaps by coupling the processing, integration, and/or interpretation of chemosensory cues with the appropriate behavioral response. (C) 2004 Elsevier Inc. All rights reserved. C1 NIMH, Sect Neural Gene Express, DHHS, Bethesda, MD 20892 USA. Univ Maryland, Sch Med, Dept Anat & Neurobiol, Baltimore, MD 21201 USA. Univ Bristol, Henry Wellcome Labs Integrat Neurosci & Endocrino, LINE, Bristol, Avon, England. RP Young, WS (reprint author), NIMH, Sect Neural Gene Express, DHHS, 9000 Rockville Pike 36,Room 2A11, Bethesda, MD 20892 USA. 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Behav. PD DEC PY 2004 VL 46 IS 5 BP 638 EP 645 DI 10.1016/j.yhbeh.2004.07.004 PG 8 WC Behavioral Sciences; Endocrinology & Metabolism SC Behavioral Sciences; Endocrinology & Metabolism GA 876TO UT WOS:000225520800016 PM 15555506 ER PT J AU Adams, JB Holloway, C AF Adams, JB Holloway, C TI Pilot study of a moderate dose multivitamin/mineral supplement for children with autistic spectrum disorder SO JOURNAL OF ALTERNATIVE AND COMPLEMENTARY MEDICINE LA English DT Article ID DOUBLE-BLIND CROSSOVER; VITAMIN-B6; MAGNESIUM; ACID; PYRIDOXINE AB Objective: Determine the effect of a moderate dose multivitamin/mineral supplement on children with autistic spectrum disorder. Design: Randomized, double-blind, placebo-controlled 3-month study. Subjects: Twenty (20) children with autistic spectrum disorder, ages 3-8 years. Results: A Global Impressions parental questionnaire found that the supplement group reported statistically significant improvements in sleep and gastrointestinal problems compared to the placebo group. An evaluation of vitamin B-6 levels prior to the study found that the autistic children had substantially elevated levels of B6 compared to a control group of typical children (75% higher, p < 0.0000001). Vitamin C levels were measured at the end of the study, and the placebo group had levels that were significantly below average for typical children, whereas the supplement group had near-average levels. Discussion: The finding of high vitamin B-6 levels is consistent with recent reports of low levels of pyridoxal-5 -phosphate and low activity of pyridoxal kinase (i.e., pyridoxal is only poorly converted to pyridoxal-5-phosphate, the enzymatically active form). This may explain the functional need for high-dose vitamin B-6 supplementation in many children and adults with autism. C1 Arizona State Univ, Tempe, AZ 85287 USA. RP Adams, JB (reprint author), Arizona State Univ, POB 876006, Tempe, AZ 85287 USA. 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Altern. Complement Med. PD DEC PY 2004 VL 10 IS 6 BP 1033 EP 1039 PG 7 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 892TS UT WOS:000226673500021 PM 15673999 ER PT J AU Rapp, JT Vollmer, TR St Peter, C Dozier, CL Cotnoir, NM AF Rapp, JT Vollmer, TR St Peter, C Dozier, CL Cotnoir, NM TI Analysis of response allocation in individuals with multiple forms of stereotyped behavior SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE environmental enrichment; response restriction; stereotypy ID RESTRICTION ANALYSIS; ACTIVITY PREFERENCES; COLLATERAL BEHAVIOR; RETARDED PERSONS; REINFORCEMENT; DEPRIVATION; OVERCORRECTION; SUBSTITUTION; CHILDREN AB Three experiments were conducted to evaluate response allocation of stereotypy during free-operant and restricted-operant conditions. Five children with autism or related developmental disabilities participated in at least one and up to three of the experiments. In Experiment 1, the stereotypic response that emerged as most probable during a free-operant phase was restricted, and response allocation was again evaluated. The results for 3 participants showed that restricting the high-probability response was correlated with covarying reductions in a nontargeted stereotypy. In Experiment 2, the effect of environmental enrichment on response allocation was evaluated. One participant reallocated behavior to appropriate object manipulation, 1 participant showed no change in behavior, and a 3rd participant reallocated behavior to object manipulation only when the putative stimulus products of the object manipulation matched those of stereotypy. In Experiment 3, additional interventions were implemented to promote response reallocation. Results showed that both response restriction and reinforcement for object manipulation decreased stereotypy and increased object manipulation. 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PD WIN PY 2004 VL 37 IS 4 BP 481 EP 501 DI 10.1901/jaba.2004.37-481 PG 21 WC Psychology, Clinical SC Psychology GA 881WP UT WOS:000225900400005 PM 15669407 ER PT J AU Clark, KM Green, G AF Clark, KM Green, G TI Comparison of two procedures for teaching dictated-word/symbol relations to learners with autism SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article; Proceedings Paper CT 24th Annual Convention of the Association-for-Behavior-Analysis CY MAY, 1998 CL ORLANDO, FL SP Assoc Behav Anal DE autism; delayed cue; exclusion AB The efficacy of exclusion and delayed-cue procedures for establishing novel dictated-word/symbol relations with 2 boys with autism was compared using computerized match-to-sample procedures. Acquisition of the relations under the two training conditions was compared via an alternating treatments design. The delayed-cue procedure was more efficacious than the exclusion procedure in four of five comparisons across participants. C1 New England Ctr Children, Southborough, MA 01772 USA. Univ Massachusetts, Sch Med, Shriver Ctr, Amherst, MA 01003 USA. RP Clark, KM (reprint author), New England Ctr Children, 33 Turnpike Rd, Southborough, MA 01772 USA. EM kclark@necc.org CR Dube W. V., 1991, EXPT ANAL HUMAN BEHA, V9, P28 OPPENHEIMER M, 1993, RES DEV DISABIL, V14, P425, DOI 10.1016/0891-4222(93)90036-J Wilkinson K.M., 1998, AUGMENTATIVE ALTERNA, V14, P162, DOI 10.1080/07434619812331278336 NR 3 TC 19 Z9 19 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2004 VL 37 IS 4 BP 503 EP 507 DI 10.1901/jaba.2004.37-503 PG 5 WC Psychology, Clinical SC Psychology GA 881WP UT WOS:000225900400006 PM 15669408 ER PT J AU Sarokoff, RA Sturmey, P AF Sarokoff, RA Sturmey, P TI The effects of behavioral skills training on staff implementation of discrete-trial teaching SO JOURNAL OF APPLIED BEHAVIOR ANALYSIS LA English DT Article DE autism; behavioral skills training; discrete-trial teaching; staff training AB A behavioral skills training package was used to train 3 teachers to correctly implement discrete-trial teaching. The mean baseline proportion of possible correct teaching responses for Teachers 1, 2, and 3 increased from 43%, 49%, and 43%, respectively, during baseline to 97%, 98%, and 99%, respectively, following training. These data indicate that the training package consisting of instructions, feedback, rehearsal, and modeling produced rapid and large improvements in the teachers' implementation of discrete-trial teaching. 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. EM psturmey@aol.com CR Green G, 1996, BEHAV INTERVENTION Y, P29 Iwata BA, 2000, J APPL BEHAV ANAL, V33, P181, DOI 10.1901/jaba.2000.33-181 KOEGEL RL, 1977, J APPL BEHAV ANAL, V10, P197, DOI 10.1901/jaba.1977.10-197 Lavie T, 2002, J APPL BEHAV ANAL, V35, P209, DOI 10.1901/jaba.2002.35-209 MCCLANNAHAN LE, 1993, J APPL BEHAV ANAL, V26, P589, DOI 10.1901/jaba.1993.26-589 Reid D. H., 1995, MOTIVATING HUMAN SER SMITH T, 2001, DOCUS AUTISM OTHER D, V16, P86 NR 7 TC 49 Z9 49 PU JOURNAL APPL BEHAV ANAL PI LAWRENCE PA DEPT HUMAN DEVELOPMENT, UNIV KANSAS, LAWRENCE, KS 66045 USA SN 0021-8855 J9 J APPL BEHAV ANAL JI J. Appl. Behav. Anal. PD WIN PY 2004 VL 37 IS 4 BP 535 EP 538 DI 10.1901/jaba.2004.37-535 PG 4 WC Psychology, Clinical SC Psychology GA 881WP UT WOS:000225900400014 PM 15669415 ER PT J AU Palmen, SJMC Pol, HEH Kemner, C Schnack, HG Janssen, J Kahn, RS van Engeland, H AF Palmen, SJMC Pol, HEH Kemner, C Schnack, HG Janssen, J Kahn, RS van Engeland, H TI Larger brains in medication naive high-functioning subjects with pervasive developmental disorder SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article; Proceedings Paper CT 2nd International Meeting for Autism Research CY NOV 01-02, 2002 CL Orlando, FL DE brain MRI; autism; gray matter; white matter; cortical lobes ID CAUDATE-NUCLEUS VOLUME; HEAD CIRCUMFERENCE; STRUCTURAL ABNORMALITIES; SCHIZOPHRENIC-PATIENTS; AUTISTIC DISORDER; INFANTILE-AUTISM; WHITE-MATTER; MRI VOLUMES; CHILDREN; INTELLIGENCE AB Background: Are brain volumes of individuals with Pervasive Developmental Disorder (PDD) still enlarged in adolescence and adulthood, and if so, is this enlargement confined to the gray and/or the white matter and is it global or more prominent in specific brain regions. Methods: Brain MRI scans were made of 21 adolescents with PDD and 21 closely matched controls. Results: All brain volumes, except the white matter, were significantly larger in patients. After correction for brain volume, ventricular volumes remained significantly larger in patients. Conclusions: Patients showed a proportional, global increase in gray matter and cerebellum volume, and a disproportional increase in ventricular volumes. Thus, at least in high-functioning patients with PDD, brain enlargement may still be present in adult life. C1 Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, Rudolf Magnus Inst Neurosci, NL-3584 CX Utrecht, Netherlands. Univ Med Ctr Utrecht, Dept Psychiat, Rudolf Magnus Inst Neurosci, NL-3584 CX Utrecht, Netherlands. RP Palmen, SJMC (reprint author), Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, Rudolf Magnus Inst Neurosci, HP A01-468,Heidelberglaan 100, NL-3584 CX Utrecht, Netherlands. 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Autism Dev. Disord. PD DEC PY 2004 VL 34 IS 6 BP 603 EP 613 DI 10.1007/s10803-004-5282-2 PG 11 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900003 PM 15679181 ER PT J AU Filipek, PA Juranek, J Nguyen, MT Cummings, C Gargus, JJ AF Filipek, PA Juranek, J Nguyen, MT Cummings, C Gargus, JJ TI Relative carnitine deficiency in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE lactic acidosis; mitochondrial disease; autism; hyperammonemia ID FATTY-ACID OXIDATION; VALPROIC ACID; METABOLISM; DISORDERS; CHILDREN; ACYLCARNITINES; ABNORMALITIES; INSUFFICIENCY; INHIBITION; DIAGNOSIS AB A random retrospective chart review was conducted to document serum carnitine levels on 100 children with autism. Concurrently drawn serum pyruvate, lactate, ammonia, and alanine levels were also available in many of these children. Values of free and total carnitine (p < 0.001), and pyruvate (p = 0.006) were signi. cantly reduced while ammonia and alanine levels were considerably elevated ( p < 0.001) in our autistic subjects. The relative carnitine deficiency in these patients, accompanied by slight elevations in lactate and signi. cant elevations in alanine and ammonia levels, is suggestive of mild mitochondrial dysfunction. It is hypothesized that a mitochondrial defect may be the origin of the carnitine deficiency in these autistic children. C1 Univ Calif Irvine, Coll Med, Dept Pediat, Irvine, CA 92717 USA. Univ Calif Irvine, Coll Med, Div Child Neurol, Irvine, CA 92717 USA. Univ Calif Irvine, Coll Med, Div Human Genet, Irvine, CA 92717 USA. Univ Calif Irvine, Coll Med, Dept Physiol & Biophys, Irvine, CA 92717 USA. RP Filipek, PA (reprint author), UCI Med Ctr, Route 81-4482,101 City Dr S, Orange, CA 92868 USA. 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PD DEC PY 2004 VL 34 IS 6 BP 615 EP 623 DI 10.1007/s10803-004-5283-1 PG 9 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900004 PM 15679182 ER PT J AU Downs, A Smith, T AF Downs, A Smith, T TI Emotional understanding, cooperation, and social behavior in high-functioning children with autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; ADHD; social skills; cooperation; emotion ID ASPERGER-SYNDROME; RECOGNITION; FACES; INFORMATION; PEOPLE; MIND; INDIVIDUALS; COMPETENCE; PATTERNS; DISORDER AB In contrast to typically developing children, children with autism rarely exhibit cooperative social behavior. To examine whether this problem reflects global developmental delays or autism-specific deficits, the present study compared cooperation, emotional understanding, personality characteristics, and social behavior of 10 children with autism who had average IQ to those of 16 children with Attention-Deficit/Hyperactivity Disorder (ADHD) and Oppositional De. ant Disorder ( ODD) and 10 typically developing children. In cooperative behavior, level of emotional understanding, and aloof behavior, the autism group outperformed the ADHD/ODD group and did not differ significantly from typically developing children. However, the autism group showed worse emotion recognition and more active-but-odd behavior than the other groups. The results indicate that high-functioning children with autism can develop cooperative social behavior and advanced theory of mind abilities, but continue to show deficits in identifying emotions and displaying socially appropriate behavior. 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H., 1992, HDB SOCIAL DEV LIFES, P283 RUTTER MR, 1994, AUTISM DIAGNOSTIC IN Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 Smith JR, 1999, IEEE ROBOT AUTOM MAG, V6, P49, DOI 10.1109/100.755814 SPARREVOHN R, 1995, J CHILD PSYCHOL PSYC, V36, P249, DOI 10.1111/j.1469-7610.1995.tb01823.x STRAIN PS, 1984, ANAL INTERVEN DEVEL, V4, P15, DOI 10.1016/0270-4684(84)90015-6 TANTAM D, 1989, J CHILD PSYCHOL PSYC, V30, P623, DOI 10.1111/j.1469-7610.1989.tb00274.x Wechsler D., 1989, WECHSLER PRESCHOOL P Wechsler D., 1991, MANUAL WECHSLER INTE NR 43 TC 58 Z9 58 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 2004 VL 34 IS 6 BP 625 EP 635 DI 10.1007/s10803-004-5284-0 PG 11 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900005 PM 15679183 ER PT J AU Kerr, S Durkin, K AF Kerr, S Durkin, K TI Understanding of thought bubbles as mental representations in children with autism: Implications for theory of mind SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE children with autism; theory of mind; false belief task; thought bubbles; mental states; mindreading ID VERBAL-ABILITY; FALSE BELIEF; INDIVIDUALS; PERFORMANCE; KNOWLEDGE; LINKS AB Standard false belief tasks indicate that normally developing children do not fully develop a theory of mind until the age of 4 years and that children with autism have an impaired theory of mind. Recent evidence, however, suggests that children as young as 3 years of age understand that thought bubbles depict mental representations and that these can be false. Twelve normally developing children and 11 children with autism were tested on a standard false belief task and a number of tasks that employed thought bubbles to represent mental states. While the majority of normally developing children and children with autism failed the standard false belief task, they understood that (i) thought bubbles represent thought, (ii) thought bubbles can be used to infer an unknown reality, (iii) thoughts can be different, and (iv) thoughts can be false. These results indicate that autistic children with a relatively low verbal mental age may be capable of understanding mental representations. C1 Univ Western Australia, Nedlands, WA 6009, Australia. RP Durkin, K (reprint author), Univ Strathclyde, Dept Psychol, 40 George St, Glasgow G1 1QE, Lanark, Scotland. EM kevin.durkin@strath.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baron- Cohen S., 1989, DEV PSYCHOPATHOL, V1, P185, DOI 10.1017/ S0954579400000377 BARONCOHEN S, 1987, BRIT J DEV PSYCHOL, V5, P139 Baron-Cohen Simon, 1996, British Journal of Psychiatry, V168, P158, DOI 10.1192/bjp.168.2.158 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 Simon, 1995, MINDBLINDNESS ESSAY Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x Charman T, 1998, J AUTISM DEV DISORD, V28, P33, DOI 10.1023/A:1026058802381 DAVIS HL, 1995, AUST J PSYCHOL, V47, P25, DOI 10.1080/00049539508258765 Dunn J., 1999, DEV PSYCHOL ACHIEVEM, P55 Dunn L M., 1982, BRIT PICTURE VOCABUL Dunn L. 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Autism Dev. Disord. PD DEC PY 2004 VL 34 IS 6 BP 637 EP 648 DI 10.1007/s10803-004-5285-z PG 12 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900006 PM 15679184 ER PT J AU Solomon, M Goodlin-Jones, BL Anders, TF AF Solomon, M Goodlin-Jones, BL Anders, TF TI A social adjustment enhancement intervention for high functioning autism, Asperger's syndrome, and pervasive developmental disorder NOS SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE high functioning autism; Asperger's syndrome; PDDNOS; social skills; intervention; training groups ID EXECUTIVE FUNCTIONS; SPECTRUM DISORDERS; CHILDS APPRAISAL; REVISED VERSION; NORMAL ADULTS; SKILLS GROUP; MIND; INDIVIDUALS; RECOGNITION; EMOTION AB This paper reports the findings of a 20-week social adjustment enhancement curriculum for boys aged 8-12. The curriculum was designed to address three areas hypothesized to be deficient in persons with HFA, AS, and PDDNOS: emotion recognition and understanding; theory of mind; and executive functions/real life type problem solving. Parents attended a semi-structured concurrent psychoeducational training meeting during children's sessions. Statistically significant improvements in facial expression recognition, and problem solving were reported for intervention group children compared to waiting list control group children. For the intervention group ( the only group for whom data were available), older and less cognitively able boy's scores on a depression inventory decreased significantly more than younger children's. Mother's depression scores tended to decrease and there were significant reductions in child problem behaviors reported. 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Autism Dev. Disord. PD DEC PY 2004 VL 34 IS 6 BP 649 EP 668 DI 10.1007/s10803-004-5286-y PG 20 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900007 PM 15679185 ER PT J AU Channon, S Sinclair, E Waller, D Healey, L Robertson, MM AF Channon, S Sinclair, E Waller, D Healey, L Robertson, MM TI Social cognition in Tourette's syndrome: Iintact theory of mind and impaired inhibitory functioning SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE theory of mind; mentalising; inhibition; social cognition; Tourette's syndrome ID EXECUTIVE FUNCTIONS; ORBITOFRONTAL CORTEX; STORY COMPREHENSION; FRONTAL LOBES; CHILDREN; LESIONS; BRAIN; ANTERIOR; EMPATHY; AUTISM AB Although associations between social cognition involving theory of mind and non-social executive skills have frequently been reported, dissociations in performance have also been found. The present study was designed to examine social and non-social cognition in uncomplicated Tourette Syndrome (TS). Adult TS participants without comorbid diagnoses were compared to matched healthy control participants on social cognition measures involving theory of mind and empathy, and on non-social executive tasks. Participants with TS were found to make more errors than a matched control group on an inhibitory task, but did not differ on other executive measures or on the social cognition measures. The implications of the findings for our understanding of TS and of the relationship between social cognition and executive skills are discussed. C1 UCL, Dept Psychol, London WC1E 6BT, England. UCL, Sch Med, Dept Psychiat & Behav Sci, London WC1E 6BT, England. RP Channon, S (reprint author), UCL, Dept Psychol, Gower St, London WC1E 6BT, England. EM s.channon@ucl.ac.uk RI Channon, Shelley/C-1754-2008 CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT Bach L. 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Autism Dev. Disord. PD DEC PY 2004 VL 34 IS 6 BP 669 EP 677 DI 10.1007/s10803-004-5287-x PG 9 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900008 PM 15679186 ER PT J AU Gagnon, L Mottron, L Bherer, L Joanette, Y AF Gagnon, L Mottron, L Bherer, L Joanette, Y TI Quantification judgement in high functioning autism: Superior or different? SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE high functioning autism; special abilities; subitizing; counting; hierarchical perception ID SAVANT CALENDRICAL CALCULATORS; NUMERICAL ABILITY; CENTRAL COHERENCE; WORKING-MEMORY; VISUAL-SEARCH; CHILDREN; NUMBERS; DEFICIT; APPREHENSION; ATTENTION AB This study examined the hypothesis of superior quanti. cation abilities of persons with high functioning autism (HFA). Fourteen HFA individuals ( mean age: 15 years) individually matched with 14 typically developing ( TD) participants ( gender, chronological age, full-scale IQ) were asked to quantify as accurately and quickly as possible numerosities, represented by the number of squares ( 2-9) presented in random configurations. In addition, the visual angles of stimuli presentation were manipulated in order to induce a local ( large visual angle) and a global ( small visual angle) bias on participants' quanti. cation performance ( accuracy and naming time). Findings revealed no effect of local and global bias of stimuli presentation in the two groups' performance, and no superior quanti. cation abilities in HFA participants. However, analyses of the naming time slopes for identification by HFA participants of small consecutive numerosities ( 2-5), suggested their use of counting processes instead of subitizing ( or immediate apprehension of numerosities) as in TD participants. Possible explanations for these results are discussed with reference to models of locally-oriented information processing in autism. C1 Hop Riviere Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada. Inst Univ Geriatrie Montreal, Ctr Rech, Montreal, PQ, Canada. Univ Montreal, Dept Psychiat, Montreal, PQ H3C 3J7, Canada. Univ Montreal, Fac Med, Dept Audiol Orthophonie, Montreal, PQ H3C 3J7, Canada. RP Mottron, L (reprint author), Hop Riviere Prairies, Clin Specialisee Troubles Envahissants Dev, 7070 Blvd Perras, Montreal, PQ H1E 1A4, Canada. 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PD DEC PY 2004 VL 34 IS 6 BP 679 EP 689 DI 10.1007/s10803-004-5288-9 PG 11 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900009 PM 15679187 ER PT J AU Stone, WL Coonrod, EE Turner, LM Pozdol, SL AF Stone, WL Coonrod, EE Turner, LM Pozdol, SL TI Psychometric properties of the STAT for early autism screening SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE AUTISM; screening; early identification; young children ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; SPECTRUM DISORDERS; FOLLOW-UP; DIAGNOSIS; COMMUNICATION; SURVEILLANCE; CHECKLIST; TODDLERS; DELAYS AB The STAT is an interactive screening measure for autism that assesses behaviors in the areas of play, communication, and imitation skills. In Study 1, signal detection procedures were employed to identify a cutoff score for the STAT using developmentally matched groups of 2-year-old children with autism and with nonspectrum disorders. The resulting cutoff yielded high sensitivity, specificity, and predictive values for the development sample as well as for an independent validation sample. Study 2 examined psychometric properties of the STAT and revealed acceptable levels of interrater agreement, test-retest reliability, and agreement between STAT risk category and ADOS-G classification. The STAT demonstrates strong psychometric properties and shows promising utility as a Level 2 screening measure for autism. C1 Vanderbilt Childrens Hosp, Nashville, TN USA. Vanderbilt Univ, Nashville, TN USA. RP Stone, WL (reprint author), Vanderbilt Child Dev Ctr, 426 Med Ctr S,2100 Pierce Ave, Nashville, TN 37232 USA. EM wendy.stone@vanderbilt.edu CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Baird G, 2001, ARCH DIS CHILD, V84, P468, DOI 10.1136/adc.84.6.468 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 Bayley N, 1993, BAYLEY SCALES INFANT Sandler AD, 2001, PEDIATRICS, V107, P1221 Committee on Educational Interventions for Children with Autism, 2001, ED CHILDR AUT Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 FEWELL RR, 1991, UNPUB PLAY ASSESSMEN Filipek PA, 2000, NEUROLOGY, V55, P468 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Glascoe FP, 2000, CHILD CARE HLTH DEV, V26, P137, DOI 10.1046/j.1365-2214.2000.00173.x HAPPE FGE, 1994, J CHILD PSYCHOL PSYC, V35, P215, DOI 10.1111/j.1469-7610.1994.tb01159.x HARRIS SL, 1991, J AUTISM DEV DISORD, V21, P281, DOI 10.1007/BF02207325 HEDRICK HL, 1984, SEQUENCED INVENTORY Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 Lord C, 2000, J AUTISM DEV DISORD, V30, P205, DOI 10.1023/A:1005592401947 Lord C, 1995, J CHILD PSYCHOL PSYC, V36, P1365, DOI 10.1111/j.1469-7610.1995.tb01669.x LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 MEISELS SJ, 1994, DEV SCREENING EARLY Mullen E, 1995, MULLEN SCALES EARLY Mundy P, 1997, J AUTISM DEV DISORD, V27, P653, DOI 10.1023/A:1025802832021 Newborg J., 1984, BATTELLE DEV INVENTO Robins DL, 2001, J AUTISM DEV DISORD, V31, P131, DOI 10.1023/A:1010738829569 ROGERS SJ, 1989, J AM ACAD CHILD PSY, V28, P207, DOI 10.1097/00004583-198903000-00010 Scambler D, 2001, J AM ACAD CHILD PSY, V40, P1457, DOI 10.1097/00004583-200112000-00017 Schopler E., 1988, CHILDHOOD AUTISM RAT SIEGEL B, 1998, NIH STAT SCI AUT SCR SIEGEL B, 1996, UNPUB PERVASIVE DEV SIEGEL B, 1988, J DEV BEHAV PEDIATR, V9, P199 SIEGEL B, 1999, BIENN M SOC RES CHIL Stone WL, 1999, J CHILD PSYCHOL PSYC, V40, P219, DOI 10.1017/S0021963098003370 Stone WL, 1997, J ABNORM CHILD PSYCH, V25, P475, DOI 10.1023/A:1022685731726 Stone WL, 1997, J AUTISM DEV DISORD, V27, P677, DOI 10.1023/A:1025854816091 Stone WL, 2000, J AUTISM DEV DISORD, V30, P607, DOI 10.1023/A:1005647629002 STONE WL, 1997, UNPUB STAT MANUAL SC STONE WL, 1994, ARCH PEDIAT ADOL MED, V148, P174 STRAIN PS, 1985, J DIVISION EARLY SPR, P105 TURNER LM, 2002, INT M AUT RES ORL FL NR 41 TC 65 Z9 66 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 2004 VL 34 IS 6 BP 691 EP 701 DI 10.1007/s10803-004-5289-8 PG 11 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900010 PM 15679188 ER PT J AU Rellini, E Tortolani, D Trillo, S Carbone, S Montecchi, F AF Rellini, E Tortolani, D Trillo, S Carbone, S Montecchi, F TI Childhood Autism Rating Scale (CARS) and Autism Behavior Checklist (ABC) correspondence and conflicts with DSM-IV criteria in diagnosis of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; diagnosis; childhood autism rating scale; autism behavior checklist; DSM-IV ID CLASSIFICATION; DISORDERS; VALIDITY AB Childhood Autism Rating Scale ( CARS) and Autism Behavior Checklist (ABC) are tests widely used for screening and diagnosis of autism. This study verified their correspondence and conflict with a diagnosis made with DSM-IV criteria. The sample consisted of 65 children, aged 18 months to 11 years. 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PD DEC PY 2004 VL 34 IS 6 BP 703 EP 708 DI 10.1007/s10803-004-5290-2 PG 6 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900011 PM 15679189 ER PT J AU Lecavalier, L Aman, MG Hammer, D Stoica, W Mathews, GL AF Lecavalier, L Aman, MG Hammer, D Stoica, W Mathews, GL TI Factor analysis of the Nisonger Child Behavior Rating Form in children with autism spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; behavior problem; children; construct validity; factor analysis; rating scale ID MENTAL-RETARDATION; SCREENING QUESTIONNAIRE; PSYCHOMETRIC PROPERTIES; REPETITIVE BEHAVIOR; SOCIAL COMPETENCE; ASPERGER-SYNDROME; PRESCHOOL CHILD; CHECKLIST; SCALE; PSYCHOPATHOLOGY AB The Nisonger Child Behavior Rating Form ( NCBRF) is a behavior rating scale designed for children and adolescents with mental retardation. The purpose of this study was to explore the psychometric properties of the NCBRF in a sample of 330 children and adolescents with autism spectrum disorders ( ASDs). Parent and teacher ratings were independently submitted to both exploratory and confirmatory factor analysis. As reported with the original validation study, parent and teacher versions shared similar but somewhat different factor structures. Social competence items showed more similarity with the original solutions than did problem behavior items. Problem behavior items were distributed into a somewhat simpler five-factor solution for both rating forms. Self-injurious and stereotypic items loaded on two distinct subscales for the teacher form, but not on the parent form. Factor loadings and internal consistencies were generally lower than those reported for the original versions but still within the acceptable range. 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PD DEC PY 2004 VL 34 IS 6 BP 709 EP 721 DI 10.1007/s10803-004-5291-1 PG 13 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900012 PM 15679190 ER PT J AU Steiner, CE Guerreiro, MM Marques-de-Faria, AP AF Steiner, CE Guerreiro, MM Marques-de-Faria, AP TI Brief report: Acrocallosal syndrome and autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; acrocallosal syndrome; corpus callosum; dysmorphology; neuroimaging ID GENOMEWIDE SCREEN; INFANTILE-AUTISM; MR AB The authors describe a boy presenting with acrocallosal syndrome and autism. Clinical features included craniofacial dysmorphisms, polydactyly, and mental retardation, besides behavioral symptoms compatible with autism. Neuroimaging revealed hypoplasia of the corpus callosum and cerebellar abnormalities. The role of this entity and other associated conditions in autism may be coincidental or reveal new clues to the understanding of autism as a behavioral syndrome. 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Autism Dev. Disord. PD DEC PY 2004 VL 34 IS 6 BP 727 EP 730 DI 10.1007/s10803-004-5293-z PG 4 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900014 PM 15679192 ER PT J AU Siperstein, R Volkmar, F AF Siperstein, R Volkmar, F TI Brief report: Parental reporting of regression in children with pervasive developmental disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; regression; childhood disintegrative disorder ID CHILDHOOD PSYCHOSES; AUTISM; RECOGNITION; AGE; PHENOMENOLOGY AB Information on age and nature of the onset of autism and other developmental disorders was obtained through review of parent completed developmental history; in addition information on the child's early development, diagnostic information, and information on parent characteristics was also obtained. In this relatively large series of cases the parents of children with autism were more likely than parents of children with other developmental disorders to report possible loss of developmental skills. However, the question of actual skill loss was complicated since in some cases parents also had reported even earlier developmental delays or a pattern more of developmental stagnation than clear loss of abilities. Only a few children exhibited a clear and unequivocal loss of developmental skills. C1 Yale Univ, New Haven, CT 06520 USA. RP Volkmar, F (reprint author), POB 207900, New Haven, CT 06520 USA. EM fred.volkmar@yale.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BROWN J, 1995, J AUTISM DEV DISORD, V25, P305, DOI 10.1007/BF02179291 Davidovitch M, 2000, J AUTISM DEV DISORD, V30, P113, DOI 10.1023/A:1005403421141 De Giacomo A, 1998, EUR CHILD ADOLES PSY, V7, P131 Kanner L, 1943, NERV CHILD, V2, P217 Kobayashi R, 1998, ACTA PSYCHIAT SCAND, V98, P296, DOI 10.1111/j.1600-0447.1998.tb10087.x KOLVIN I, 1971, BRIT J PSYCHIAT, V118, P385, DOI 10.1192/bjp.118.545.385 Krug DA, 1993, AUTISM SCREENING INS KURITA H, 1985, J AM ACAD CHILD PSY, V24, P191, DOI 10.1016/S0002-7138(09)60447-7 Lord C., 1997, HDB AUTISM PERVASIVE, P460 Lotter V., 1966, SOC PSYCHIAT, P124, DOI DOI 10.1007/BF00584048 OSTERLING J, 1994, J AUTISM DEV DISORD, V24, P247, DOI 10.1007/BF02172225 SHORT AB, 1988, J AUTISM DEV DISORD, V18, P207, DOI 10.1007/BF02211947 Sparrow S, 1984, VINELAND ADAPTIVE BE Volkmar F. 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SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID PERVASIVE DEVELOPMENTAL DISORDERS C1 Univ Missouri, Kansas City Sch Med, Childrens Mercy Hosp & Clin, Sect Med Genet & Mol Med, Kansas City, MO 64108 USA. Univ Missouri, Sch Med, Div Med Genet, Columbia, MO 65212 USA. Stanford Univ, Med Ctr, Dept Neurol, Stanford, CA 94305 USA. RP Talebizadeh, Z (reprint author), Univ Missouri, Kansas City Sch Med, Childrens Mercy Hosp & Clin, Sect Med Genet & Mol Med, Kansas City, MO 64108 USA. EM mgbutler@cmh.edu CR Jamain S, 2003, NAT GENET, V34, P27, DOI 10.1038/ng1136 Laumonnier F, 2004, AM J HUM GENET, V74, P552, DOI 10.1086/382137 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Talebizadeh Z, 2002, J Med Genet, V39, pe70, DOI 10.1136/jmg.39.11.e70 VOLKMAR FR, 1993, J AUTISM DEV DISORD, V23, P579, DOI 10.1007/BF01046103 NR 5 TC 27 Z9 28 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 2004 VL 34 IS 6 BP 735 EP 736 DI 10.1007/s10803-004-5295-x PG 2 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900016 PM 15679194 ER PT J AU Minshew, NJ AF Minshew, NJ TI Untitled SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Letter ID AUTISM CR Casanova MF, 2002, NEUROLOGY, V58, P428 Herbert MR, 2004, ANN NEUROL, V55, P530, DOI 10.1002/ana.20032 JUST MA, 2004, UNPUB FUNCTIONAL ANA JUST MA, 2004, BRAIN, V127, P1 Palmen SJMC, 2004, J NEURAL TRANSM, V111, P903, DOI 10.1007/s00702-003-0068-9 NR 5 TC 1 Z9 1 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 2004 VL 34 IS 6 BP 737 EP 738 PG 2 WC Psychology, Developmental SC Psychology GA 878AW UT WOS:000225619900017 PM 15679195 ER PT J AU Goodlin-Jones, BL Tassone, F Gane, LW AF Goodlin-Jones, BL Tassone, F Gane, LW TI Autistic spectrum disorder and the fragile X premutation SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Article DE autism; premutation; fragile X syndrome ID FMR1 MESSENGER-RNA; PERVASIVE DEVELOPMENTAL DISORDERS; RAPID ANTIBODY-TEST; NEUROBEHAVIORAL PHENOTYPE; TREMOR/ATAXIA SYNDROME; BEHAVIORAL-PHENOTYPE; FEMALE CARRIERS; ELEVATED LEVELS; FULL MUTATION; MALES AB Fragile X syndrome (FXS) is the most common inherited cause of mental retardation. It is also one of the most common identifiable causes of Autism Spectrum Disorder (ASD). Carriers of FXS are often considered to be cognitively and behaviorally unaffected. However, we report here on six individuals in the premutation range who also have ASD. A comparison is made with five subjects in the premutation range who did not receive a diagnosis of ASD. The six individuals with ASD had a range of cognitive ability levels from no impairment to moderate retardation. Discussion includes the impact of molecular variables including lowered FMR1 protein and elevated FMR1 mRNA in addition to environmental factors leading to the complex neurodevelopmental disorder of ASD. C1 Univ Calif Davis, Med Ctr, UCDHS, Dept Psychiat & Behav Sci,MIND Inst, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Biol Chem, Davis, CA 95616 USA. UCDHS, Dept Pediat, MIND Inst, Sacramento, CA USA. RP Goodlin-Jones, BL (reprint author), Univ Calif Davis, Med Ctr, UCDHS, Dept Psychiat & Behav Sci,MIND Inst, 2825 50th St, Sacramento, CA 95817 USA. 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Dev. Behav. Pediatr. PD DEC PY 2004 VL 25 IS 6 BP 392 EP 398 DI 10.1097/00004703-200412000-00002 PG 7 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 885HJ UT WOS:000226147400002 PM 15613987 ER PT J AU Goldson, E AF Goldson, E TI Educating children with autism SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Book Review C1 Univ Colorado, Denver, CO 80202 USA. RP Goldson, E (reprint author), Univ Colorado, Denver, CO 80202 USA. CR HEALY JM, 1999, ENDANGERED MINDS CHI NR 1 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD DEC PY 2004 VL 25 IS 6 BP 435 EP 435 DI 10.1097/00004703-200412000-00009 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 885HJ UT WOS:000226147400008 ER PT J AU Foxx, RM Schreck, KA Garito, J Smith, A Weisenberger, S AF Foxx, RM Schreck, KA Garito, J Smith, A Weisenberger, S TI Replacing the echolalia of children with autism with functional use of verbal labeling SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE echolalia; autism; language training; cues-pause-point; generalization ID SPEECH; REPERTOIRES; QUESTIONS; RESPONSES; LANGUAGE AB We evaluated the direct and generalized effects of cues-pause-point language training procedures on immediate echolalia and correct responding in two children with autism. The overall goal was to teach the children to remain quiet before, during, and briefly after the presentation of questions and then to verbalize on the basis of the cues (pictures) whose labels represented the correct responses. A multiple baseline design across question/response pairs demonstrated that echolalia was rapidly replaced by correct responding on the trained stimuli and there were clear improvements in one childs responding to untrained stimuli. These results replicate and extend previous research with adults with mental retardation and autism which demonstrated that cues-pause-point procedures can be effective in teaching individuals displaying echolalia to use their verbal labeling repertoires functionally. C1 Penn State Harrisburg, Psychol Program, Middletown, PA 17057 USA. RP Foxx, RM (reprint author), Penn State Harrisburg, Psychol Program, 777 W Harrisburg Pike, Middletown, PA 17057 USA. EM rmf4@psu.edu CR CARR EG, 1975, J ABNORM CHILD PSYCH, V3, P331 Foxx R. 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PD DEC PY 2004 VL 16 IS 4 BP 307 EP 320 DI 10.1007/s10882-004-0688-5 PG 14 WC Rehabilitation SC Rehabilitation GA 891CK UT WOS:000226558700001 ER PT J AU Kurita, H Osada, H Shimizu, K Tachimori, H AF Kurita, H Osada, H Shimizu, K Tachimori, H TI Bipolar disorders in mentally retarded persons with pervasive developmental disorders SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE bipolar disorders; manic episode; pervasive developmental disorders (PDD) ID AUTISM RATING-SCALE; ASPERGERS SYNDROME; CHILDHOOD AUTISM; RETARDATION; DEPRESSION; CHILDREN; INDIVIDUALS; SYMPTOMS; MANIA; LIFE AB To examine clinical features of mentally retarded patients with pervasive developmental disorders (PDD) with a comorbid bipolar disorder, 23 PDD patients (mean age = 23.5 years, SD = 4.2) with an episode satisfying modified DSM-IV criteria for manic/hypomanic episode (PDD-B), and 23 age, sex, diagnosis, and retardation matched control PDD patients without a mood episode (PDD-C) were compared on 26 variables (e.g., family history, development, autistic symptoms, epilepsy). Although many of the variables did not show a significant difference, autistic symptoms tended to be more severe in the PDD-B than PDD-C patients, and epilepsy tended to occur earlier in 14 PDD-C than 13 PDD-B patients. Twenty two of the 23 PDD-B patients had taken mood stabilizers clinically judged effective. Bipolar disorders are not rare and are diagnosable in mentally retarded PDD patients with modified DSM-IV criteria consisting of items observable by others, and their treatment by mood stabilizers seems worthy for further research. C1 Univ Tokyo, Fac Med, Dept Mental Hlth, Bunkyo Ku, Tokyo 1130033, Japan. Natl Ctr Neurol & Psychiat, NIMH, Dept Mental Hlth Adm, Ichikawa, Japan. Univ Tokyo, Fac Med, Dept Mental Hlth, Tokyo 113, Japan. RP Kurita, H (reprint author), Univ Tokyo, Fac Med, Dept Mental Hlth, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. 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Dev. Phys. Disabil. PD DEC PY 2004 VL 16 IS 4 BP 377 EP 389 DI 10.1007/s10882-004-0693-8 PG 13 WC Rehabilitation SC Rehabilitation GA 891CK UT WOS:000226558700005 ER PT J AU Kemner, C van der Geest, JN Verbaten, MN van Engeland, H AF Kemner, C van der Geest, JN Verbaten, MN van Engeland, H TI In search of neurophysiological markers of pervasive developmental disorders: smooth pursuit eye movements? SO JOURNAL OF NEURAL TRANSMISSION LA English DT Article DE autism; smooth pursuit ID BRAIN ANATOMY; AUTISM; SCHIZOPHRENIA; CHILDREN; DYSFUNCTION; DEFICITS; REELIN; TWIN AB Genetic studies of autism would benefit from the identification of (neurophysiological) markers of the disease. Reports that subjects with autism suffer from abnormalities of visual motor processing, indicate that abnormalities in smooth pursuit eye movements (SPEM) may be a marker of the disorder. Sixteen high-functioning school-aged children with pervasive developmental disorder (PDD) were compared with a matched group of eighteen normally developing controls on performance of a SPEM task and a task which tested the integrity of visually guided saccadic eye movements. Both groups of children had normal eye movements during performance of these tasks. Thus abnormalities in SPEM would appear not to be a marker of PDD. The earlier reported abnormalities in visual motion processing might need to be reinterpreted. C1 Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, NL-3514 CX Utrecht, Netherlands. Erasmus MC, Dept Neurosci, Rotterdam, Netherlands. Univ Utrecht, Dept Psychopharmacol, NL-3508 TC Utrecht, Netherlands. RP Kemner, C (reprint author), Univ Med Ctr Utrecht, Dept Child & Adolescent Psychiat, B01-324,Heidelberglaan 100, NL-3514 CX Utrecht, Netherlands. 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Neural Transm. PD DEC PY 2004 VL 111 IS 12 BP 1617 EP 1626 DI 10.1007/s00702-004-0164-5 PG 10 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 873VY UT WOS:000225310700011 PM 15565496 ER PT J AU Kendrick, KM AF Kendrick, KM TI The neurobiology of social bonds SO JOURNAL OF NEUROENDOCRINOLOGY LA English DT Article AB When released in the brain through giving birth or mating, the neuropeptides oxytocin and vasopressin are involved in promoting parent-offspring and monogamous bonds in animals such as sheep and voles. Bonds are only formed in species where receptors for these neuropeptides are highly expressed in dopamine-producing reward centres. In humans, dysfunctions in these same systems can be associated with autism and, when we see people we love, these systems become activated. C1 Babraham Inst, Cambridge CB2 4AT, England. RP Kendrick, KM (reprint author), Babraham Inst, Babraham Res Campus, Cambridge CB2 4AT, England. NR 0 TC 28 Z9 28 PU BLACKWELL PUBLISHING LTD PI OXFORD PA 9600 GARSINGTON RD, OXFORD OX4 2DG, OXON, ENGLAND SN 0953-8194 J9 J NEUROENDOCRINOL JI J. Neuroendocrinol. PD DEC PY 2004 VL 16 IS 12 BP 1007 EP 1008 DI 10.1111/j.1365-2826.2004.01262.x PG 2 WC Endocrinology & Metabolism; Neurosciences SC Endocrinology & Metabolism; Neurosciences & Neurology GA 893WF UT WOS:000226750500008 PM 15667456 ER PT J AU Manoach, DS Lindgren, KA Barton, JJS AF Manoach, DS Lindgren, KA Barton, JJS TI Deficient saccadic inhibition in Asperger's disorder and the social-emotional processing disorder SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID POSITRON-EMISSION-TOMOGRAPHY; NONVERBAL LEARNING-DISABILITIES; HIGH-FUNCTIONING AUTISM; SPATIAL WORKING-MEMORY; RIGHT-HEMISPHERE; EYE-MOVEMENTS; LOBE LESIONS; FRONTAL-LOBE; ANTISACCADES; DYSFUNCTION AB Background: Both Asperger's disorder and the social-emotional processing disorder (SEPD), a form of non-verbal learning disability, are associated with executive function deficits. SEPD has been shown to be associated with deficient saccadic inhibition. Objective: To study two executive functions in Asperger's disorder and SEPD, inhibition and task switching, using a single saccadic paradigm. Methods: 22 control subjects and 27 subjects with developmental social processing disorders-SEPD, Asperger's disorder, or both syndromes-performed random sequences of prosaccades and anti-saccades. This design resulted in four trial types, prosaccades and antisaccades, that were either repeated or switched. The design allowed the performance costs of inhibition and task switching to be isolated. Results: Subjects with both Asperger's disorder and SEPD showed deficient inhibition, as indicated by increased antisaccade errors and a disproportionate increase in latency for antisaccades relative to prosaccades. In contrast, task switching error and latency costs were normal and unrelated to the costs of inhibition. Conclusions: This study replicates the finding of deficient saccadic inhibition in SEPD, extends it to Asperger's disorder, and implicates prefrontal cortex dysfunction in these syndromes. The finding of intact task switching shows that executive function deficits in Asperger's disorder and SEPD are selective and suggests that inhibition and task switching are mediated by distinct neural networks. C1 Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02129 USA. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Athinoula A Martinos Ctr Biomed Imaging, Boston, MA 02129 USA. Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA. RP Manoach, DS (reprint author), Harvard Univ, Sch Med, Massachusetts Gen Hosp, Dept Psychiat, Charlestown Navy Yard,36 1st Ave,Room 420, Boston, MA 02129 USA. 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Neurol. Neurosurg. Psychiatry PD DEC PY 2004 VL 75 IS 12 BP 1719 EP 1726 DI 10.1136/jnnp.2003.025981 PG 8 WC Clinical Neurology; Psychiatry; Surgery SC Neurosciences & Neurology; Psychiatry; Surgery GA 871UZ UT WOS:000225162400018 PM 15548490 ER PT J AU Tchofo, PJ De Tiege, X Goldman, S Van Bogaert, P David, PH Pruvo, JP Ares, GS AF Tchofo, PJ De Tiege, X Goldman, S Van Bogaert, P David, PH Pruvo, JP Ares, GS TI Supratentorial functional disturbances in two children with cerebellar cortical dysplasia SO JOURNAL OF NEURORADIOLOGY LA English DT Article DE MR imaging; PET; cortical dysplasia; cerebellum ID DEVELOPMENTAL DELAY/MENTAL RETARDATION; MENTAL-RETARDATION; PERINATAL ASPHYXIA; CEREBRAL-PALSY; BRAIN SPECT; AUTISM; MRI; DYSFUNCTION; TOMOGRAPHY; DELAY AB When evaluating children with mental retardation, subtle cerebral and cerebellar morphologic anomalies are often noted at Magnetic Resonance Imaging (MRI). Some, such as cerebellar cortical dysplasia (CCD), have been considered as subtle markers of cerebral dysgenesis. Their functional significance and their effect on brain function, remain unknown. To study supratentorial functional disturbances related to CCD we performed Positron-Emission-Tomography (PET) studies in two children with isolated CCD, in order to investigate the degree of involvement of supratentorial structures. One had developmental delay, motor disturbances and ataxia, and the other one only had mental retardation. PET studies revealed hypoperfusion and hypometabolism within the vermis, thalamus and the right striatum in one case, and hypometabolism in the basal ganglia and cerebellar deep grey nuclei in the other case. Our results could lead to a hypothesis explaining motor disturbances as well as cognitive impairment, and could suggest a pathological functional significance of CCD. Nevertheless, the relationship between these findings and mental retardation needs further investigation. C1 Hop Erasme, Clin Neuroradiol, Brussels, Belgium. Ctr Hosp Reg & Univ Lille, Hop Salengro, Serv Neuroradiol, F-59037 Lille, France. Hop Erasme, Unite TEP Cyclotron Biomed, Brussels, Belgium. Hop Erasme, Serv Neuropediat, Brussels, Belgium. RP Tchofo, PJ (reprint author), Hop Erasme, Clin Neuroradiol, Brussels, Belgium. EM jissendi@netscape.net CR Andreasen NC, 1998, SCHIZOPHRENIA BULL, V24, P203 Battaglia A, 2003, AM J MED GENET C, V117C, P3, DOI 10.1002/ajmg.c.10015 Battaglia A, 2003, AM J MED GENET C, V117C, P25, DOI 10.1002/ajmg.c.10017 Cunningham RD, 1996, J PEDIATR-US, V128, P302 Curry CJ, 1997, AM J MED GENET, V72, P468, DOI 10.1002/(SICI)1096-8628(19971112)72:4<468::AID-AJMG18>3.0.CO;2-P Demaerel P, 1998, AM J NEURORADIOL, V19, P984 Filippi CG, 2002, AM J NEURORADIOL, V23, P882 Gokcora N, 1999, BRAIN DEV-JPN, V21, P107, DOI 10.1016/S0387-7604(98)00081-3 HOUK JC, 1997, PROGR BRAIN RES, P144 KAO CH, 1994, CLIN NUCL MED, V19, P309, DOI 10.1097/00003072-199404000-00007 Lee JD, 1998, J NUCL MED, V39, P619 MAINEMER A, 1995, J PEDIATR, V127, P193 Mehler MF, 2000, BRAIN RES REV, V32, P277, DOI 10.1016/S0165-0173(99)00090-9 Middleton FA, 2001, J NEUROSCI, V21, P700 Middleton FA, 2000, BRAIN COGNITION, V42, P183, DOI 10.1006/brcg.1999.1099 Parsons LM, 2000, P NATL ACAD SCI USA, V97, P2332, DOI 10.1073/pnas.040555497 Riikonen R, 1999, DEV MED CHILD NEUROL, V41, P652, DOI 10.1017/S0012162299001358 Ryu YH, 1999, EUR J NUCL MED, V26, P253, DOI 10.1007/s002590050385 Sasaki M, 2001, NEURORADIOLOGY, V43, P151 SCHAEFER GB, 1994, NEUROL CLIN, V12, P773 SCHAEFER GB, 1992, PEDIATR CLIN N AM, V39, P929 SCHAEFER GB, 1991, ARCH NEUROL-CHICAGO, V48, P139 Soto-Ares G, 2000, AM J NEURORADIOL, V21, P1511 Townsend J, 2001, COGNITIVE BRAIN RES, V11, P127, DOI 10.1016/S0926-6410(00)00072-0 Yoon CS, 2000, NEURORADIOLOGY, V42, P908 Zilbovicius M, 2000, AM J PSYCHIAT, V157, P1988, DOI 10.1176/appi.ajp.157.12.1988 NR 26 TC 1 Z9 1 PU MASSON EDITEUR PI MOULINEAUX CEDEX 9 PA 21 STREET CAMILLE DESMOULINS, ISSY, 92789 MOULINEAUX CEDEX 9, FRANCE SN 0150-9861 J9 J NEURORADIOLOGY JI J. Neuroradiol. PD DEC PY 2004 VL 31 IS 5 BP 399 EP 405 PG 7 WC Clinical Neurology; Neuroimaging; Radiology, Nuclear Medicine & Medical Imaging SC Neurosciences & Neurology; Radiology, Nuclear Medicine & Medical Imaging GA 881RX UT WOS:000225888200011 ER PT J AU Icasiano, F Hewson, P Machet, P Cooper, C Marshall, A AF Icasiano, F Hewson, P Machet, P Cooper, C Marshall, A TI Childhood autism spectrum disorder in the Barwon region: A community based study SO JOURNAL OF PAEDIATRICS AND CHILD HEALTH LA English DT Article DE associations; autism spectrum disorder; prevalence; subgroups ID FAMILY HISTORY; CHILDREN; PREVALENCE; STRESS; PHENOTYPE; SUBTYPES; PARENTS; PROFILE AB Objective: To establish a community database for children with autism spectrum disorder (ASD) to determine prevalence and identify subgroups based on key intellectual, clinical and family parameters. Methods: Data were collected for children previously diagnosed with an ASD in the Barwon region using parental interview and review of the child's paediatric and psychological records. Preschool diagnoses were typically made by specialist psychologists and school-age diagnoses made by a multidisciplinary team. Results: One hundred and seventy-seven children in the Barwon region were identified as having ASD (82% response rate). The prevalence of ASD was one per 255 children aged two to 17 years. The prevalence increased 10 fold over a 16-year period and this increase was relatively even across all levels of child intellectual functioning. Forty-two percent of children were intellectually disabled (IQ < 70) and performance IQ was significantly higher than verbal IQ but typical block design-comprehension subtest patterns were not common. Nine sibling pair families were identified, 24% were labelled as having attention deficit hyperactivity disorder (ADHD), 6% had epilepsy, and 18.3% were macrocephalic where data were available. Family difficulty was associated with the degree of obsessions/rituals, frequency and intensity of anger/aggression, and ADHD but overall was not associated with the child's intellectual status. Conclusions: The relatively rapid increase in prevalence is consistent with overseas studies and suggests significant changes in diagnostic criteria, increasing community awareness and the need for support at all levels of intellectual functioning. Increased occurrence in siblings and relatives gives further evidence for a genetic cause. C1 Barwon Hlth, Dept Paediat, Barwon Child Hlth Unit, Geelong, Vic 3220, Australia. RP Hewson, P (reprint author), Barwon Hlth, Dept Paediat, Barwon Child Hlth Unit, 106 McKilop St, Geelong, Vic 3220, Australia. 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EM james.bale@hsc.utah.edu CR Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 Jiang YH, 2004, ANNU REV GENOM HUM G, V5, P479, DOI 10.1146/annurev.genom.5.061903.180014 Smeeth L, 2004, LANCET, V364, P963, DOI 10.1016/S0140-6736(04)17020-7 Veenstra-VanderWeele J, 2004, ANNU REV GENOM HUM G, V5, P379, DOI 10.1146/annurev.genom5.061903.180050 Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 NR 5 TC 0 Z9 0 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 1474-4422 J9 LANCET NEUROL JI Lancet Neurol. PD DEC PY 2004 VL 3 IS 12 BP 706 EP 707 DI 10.1016/S1474-4422(04)00931-7 PG 2 WC Clinical Neurology SC Neurosciences & Neurology GA 873MD UT WOS:000225283500015 PM 15556801 ER PT J AU Hutchinson, A AF Hutchinson, A TI Animals in translation: Using the mysteries of autism to decode animal behavior. SO LIBRARY JOURNAL LA English DT Book Review C1 Smithsonian Inst, Lib, Washington, DC 20560 USA. RP Hutchinson, A (reprint author), Smithsonian Inst, Lib, Washington, DC 20560 USA. CR Grandin Temple, 2005, ANIMALS TRANSLATION 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 DEC PY 2004 VL 129 IS 20 BP 154 EP + PG 2 WC Information Science & Library Science SC Information Science & Library Science GA 878TN UT WOS:000225669900331 ER PT J AU Seeman, C AF Seeman, C TI The autism encyclopedia: 500+entries for parents and professionals. SO LIBRARY JOURNAL LA English DT Book Review C1 Univ Toledo Libs, Toledo, OH USA. RP Seeman, C (reprint author), Univ Toledo Libs, Toledo, OH USA. CR NEISWORTH JT, 2004, AUTISM ENCY 500 PLUS 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 DEC PY 2004 VL 129 IS 20 BP 168 EP 168 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 878TN UT WOS:000225669900365 ER PT J AU Kumar, S Alexander, M Gnanamuthu, C AF Kumar, S Alexander, M Gnanamuthu, C TI Recent experience with Rett syndrome at a tertiary care center SO NEUROLOGY INDIA LA English DT Article DE Rett syndrome; mental retardation; clinical diagnosis AB Rett syndrome (RS), a neurological developmental disorder, is one of the commonest causes of cognitive impairment in girls and women. These patients are often initially misdiagnosed as idiopathic mental retardation, cerebral palsy, or autism. Despite several reports from the West, there are very few reports from the Indian population. We present four female children with RS and emphasize the importance of early diagnosis. C1 Christian Med Coll & Hosp, Dept Neurol Sci, Vellore 632004, Tamil Nadu, India. RP Kumar, S (reprint author), Christian Med Coll & Hosp, Dept Neurol Sci, Vellore 632004, Tamil Nadu, India. EM drsudhirkumar@yahoo.com CR Amir RE, 1999, NAT GENET, V23, P185 Banapurmath C. 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India PD DEC PY 2004 VL 52 IS 4 BP 494 EP 495 PG 2 WC Neurosciences SC Neurosciences & Neurology GA 887RV UT WOS:000226324100019 PM 15626843 ER PT J AU Mukaetova-Ladinska, EB Arnold, H Jaros, E Perry, R Perry, E AF Mukaetova-Ladinska, EB Arnold, H Jaros, E Perry, R Perry, E TI Depletion of MAP2 expression and laminar cytoarchitectonic changes in dorsolateral prefrontal cortex in adult autistic individuals SO NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY LA English DT Article DE autism; dendrites; dorsolateral prefrontal cortex; glia; MAP2; neurone ID INFANTILE-AUTISM; WHITE-MATTER; CEREBRAL-CORTEX; MORPHOMETRIC-ANALYSIS; NEURONAL DENSITY; CHILDHOOD AUTISM; RETT-SYNDROME; BRAIN-STEM; ABNORMALITIES; PROTEIN AB The neuropathological substrates underlying the characteristic clinical phenotype of autism are unknown. Neuroimaging studies have identified a decrease in task-related activation in the dorsolateral prefrontal cortex in autism. In the current study, we have analysed the dorsolateral prefrontal cortex in two adult individuals with a clinical diagnosis of autism, using Nissl staining and MAP2 immunohistochemistry. There was unchanged density of both neuronal and glial cell pools, although the autistic individuals had ill-defined neocortical cellular layers, substantially depleted MAP2 neuronal expression, and reduced dendrite numbers. Further studies on a larger number of individuals with autism are needed to establish the clinical relevance of the described changes, especially to determine whether the loss of dendritic markers is age associated or disease specific. C1 Univ Newcastle Upon Tyne, Res Neuropathol Lab, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. Univ Newcastle Upon Tyne, Dept Old Age Psychiat, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. Univ Newcastle Upon Tyne, Dept Neuropathol, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. Univ Newcastle Upon Tyne, Inst Ageing & Hlth, Newcastle Upon Tyne NE1 7RU, Tyne & Wear, England. RP Mukaetova-Ladinska, EB (reprint author), Newcastle Gen Hosp, Dept Old Age Psychiat, Wolfson Res Ctr, Newcastle Upon Tyne NE4 6BE, Tyne & Wear, England. 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Appl. Neurobiol. PD DEC PY 2004 VL 30 IS 6 BP 615 EP 623 DI 10.1111/j.1365-2990.2004.00574.x PG 9 WC Clinical Neurology; Neurosciences; Pathology SC Neurosciences & Neurology; Pathology GA 870RJ UT WOS:000225075200006 PM 15541002 ER PT J AU Kies, SD Devine, DP AF Kies, SD Devine, DP TI Self-injurious behaviour: a comparison of caffeine and pemoline models in rats SO PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR LA English DT Article DE caffeine; pemoline; self-injury; self-injurious behaviour; Lesch Nyhan syndrome; autism; animal model; toxicity ID LESCH-NYHAN-SYNDROME; PRADER-WILLI-SYNDROME; RHESUS-MONKEYS; CLINICAL FEATURES; CALCIUM-CHANNELS; PREPUBERTAL RATS; PURINE SYNTHESIS; BRAIN; MUTILATION; MICE AB Self-injurious behaviour (SIB) is a debilitating behaviour disorder that can have life-threatening consequences. It is often exhibited in intellectually handicapped and autistic populations, and it has been modeled with pharmacological manipulations in animals. We have characterized the induction of SIB using high doses of caffeine and pemoline in rats. Caffeine only produced very mild SIB in a small proportion of the rats, when administered repeatedly at very high doses (140-185 mg/kg/day). All the caffeine-treated rats showed profound signs of caffeine-toxicity at these doses, and lower doses did not induce any self-injury. On the other hand, pemoline was effective across a range of doses (100-300 mg/kg/day), including doses that did not produce overt signs of toxicity (100-200 mg/kg/day). The topography of the tissue injury sites (tail vs. paws and ventrum) differed between caffeine and pemoline treatments, and across doses of pemoline. The speed of onset, the incidence, and the severity of SIB occurred in a dose-orderly manner across the pemoline doses, and there was substantial individual variability in the induction of SIB when a moderately high dose (200 mg/kg/day) was used. These individual differences in vulnerability to self-injure are reminiscent of the fact that some humans with specific neurobiological disorders express SIB and some individuals with those same disorders do not. Accordingly, the pemoline model of SIB may be useful to investigate the neurobiological basis of factors that contribute to etiology of SIB. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Florida, Dept Psychol, Behav Neurosci Program, Gainesville, FL 32611 USA. RP Devine, DP (reprint author), Univ Florida, Dept Psychol, Behav Neurosci Program, POB 112250, Gainesville, FL 32611 USA. 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PD DEC PY 2004 VL 95 IS 3 BP 1050 EP 1054 PN 1 PG 5 WC Psychology, Multidisciplinary SC Psychology GA 881VG UT WOS:000225896900057 PM 15666954 ER PT J AU Jones, CD Schwartz, IS AF Jones, CD Schwartz, IS TI Siblings, peers, and adults: Differential effects of models for children with autism SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID DEVELOPMENTAL-DISABILITIES; HANDICAPPED-CHILDREN; ACQUISITION; BEHAVIOR AB Employing typically developing children and adults as models of appropriate behavior for children with autism and other developmental disabilities has been a common practice for more than four decades, and peer modeling serves as one of the theoretical cornerstones of inclusion and related innovations. In addition to examining adult and peer modeling, this study extends previous modeling research by including a subset of peers-siblings. 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Early Child. Spec. Educ. PD WIN PY 2004 VL 24 IS 4 BP 187 EP 198 DI 10.1177/02711214040240040101 PG 12 WC Education, Special SC Education & Educational Research GA 895FS UT WOS:000226846900001 ER PT J AU Segal, NL AF Segal, NL TI Twin paternity; twin study summaries; Why twins fascinate SO TWIN RESEARCH LA English DT Article AB An unusual case of uncertain twin paternity is presented. New research on inbred strains of mice may hold important clues for paternity testing of twins in the future. Next, four recent twin studies examining selected topics in autism, color perception, language development and high-order pregnancy risk are reviewed. Finally, several unusual twin-related situations are variously considered with respect to their research significance and practical applications. C1 Calif State Univ Fullerton, Dept Psychol, Fullerton, CA 92834 USA. RP Segal, NL (reprint author), Calif State Univ Fullerton, Dept Psychol, Fullerton, CA 92834 USA. EM nsegal@fullerton.edu CR Annett M, 2003, NEUROPSYCHOLOGIA, V41, P469, DOI 10.1016/S0028-3932(02)00137-9 BRYAN EM, 1983, NATUE NURTURE TWINS Gottesman II, 1991, SCHIZOPHRENIA GENESI Kates WR, 2004, AM J PSYCHIAT, V161, P539, DOI 10.1176/appi.ajp.161.3.539 *OMG, 1997, ON LIN MED DICT Paramei Galina V, 2004, Clin Exp Optom, V87, P305 RAYKAN VK, 2002, TRENDS GENET, V18, P348 Segal N. L., 2000, ENTWINED LIVES TWINS Segal NL, 2000, J EDUC PSYCHOL, V92, P442, DOI 10.1037//0022-0663.92.3.442 SILBER SJ, 1978, FERTIL STERIL, V30, P181 Thorpe K, 2001, INT J LANG COMM DIS, V36, P43, DOI 10.1080/13682820150217563 Wen SW, 2004, AM J OBSTET GYNECOL, V191, P254, DOI 10.1016/j.ajog.2003.12.003 WENIG G, 2004, JEWISH J, P20 2004, BIRTH TWO SETS IDENT 2004, ECONOMIST 0814, P70 NR 15 TC 1 Z9 1 PU AUSTRALIAN ACAD PRESS PI BOWEN HILLS PA 32 JEAYS ST, BOWEN HILLS, QLD 4006, AUSTRALIA SN 1369-0523 J9 TWIN RES JI Twin Res. PD DEC PY 2004 VL 7 IS 6 BP 675 EP 679 PG 5 WC Genetics & Heredity; Obstetrics & Gynecology; Reproductive Biology SC Genetics & Heredity; Obstetrics & Gynecology; Reproductive Biology GA 878BY UT WOS:000225622700018 PM 15607019 ER PT J AU Spence, SA Hunter, MD Farrow, TFD Green, RD Leung, DH Hughes, CJ Ganesan, V AF Spence, SA Hunter, MD Farrow, TFD Green, RD Leung, DH Hughes, CJ Ganesan, V TI A cognitive neurobiological account of deception: evidence from functional neuroimaging SO PHILOSOPHICAL TRANSACTIONS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES LA English DT Article DE lying; deception; executive function; prefrontal cortex; functional magnetic resonance imaging ID PREFRONTAL CORTEX; BRAIN; LESIONS; TRUTH; LIES; TIME; WILL; MIND AB An organism may use misinformation, knowingly (through deception) or unknowingly (as in the case of camouflage), to gain advantage in a competitive environment. From an evolutionary perspective, greater tactical deception occurs among primates closer to humans, with larger neocortices. In humans, the onset of deceptive behaviours in childhood exhibits a developmental trajectory, which may be regarded as 'normal' in the majority and deficient among a minority with certain neurodevelopmental disorders (e.g. autism). In the human adult, deception and lying exhibit features consistent with their use of 'higher' or 'executive' brain systems. Accurate detection of deception in humans may be of particular importance in forensic practice, while an understanding of its cognitive neurobiology may have implications for models of 'theory of mind' and social cognition, and societal notions of responsibility, guilt and mitigation. In recent years, functional neuroimaging techniques (especially functional magnetic resonance imaging) have been used to study deception. Though few in number, and using very different experimental protocols, studies published in the peer-reviewed literature exhibit certain consistencies. Attempted deception is associated with activation of executive brain regions (particularly prefrontal and anterior cingulate cortices), while truthful responding has not been shown to be associated with any areas of increased activation (relative to deception). Hence, truthful responding may comprise a relative 'baseline' in human cognition and communication. The subject who lies may necessarily engage 'higher' brain centres, consistent with a purpose or intention (to deceive). While the principle of executive control during deception remains plausible, its precise anatomy awaits elucidation. C1 Univ Sheffield, Dept Acad Clin Psychiat, Div Gen Med, Sheffield S5 7JT, S Yorkshire, England. RP Spence, SA (reprint author), Univ Sheffield, Dept Acad Clin Psychiat, Div Gen Med, Longley Ctr,Norwood Grange Dr, Sheffield S5 7JT, S Yorkshire, England. EM s.a.spence@sheffield.ac.uk RI Spence, Sean/A-6218-2008; Farrow, Tom/B-5003-2009; Kaylor-Hughes, Catherine/B-7970-2009 CR ABED RT, 1995, IRISH J PSYCHOL MED, V12, P24 Adenzato M, 1999, PROCEEDINGS OF THE TWENTY FIRST ANNUAL CONFERENCE OF THE COGNITIVE SCIENCE SOCIETY, P7 BADDELEY AD, 1966, Q J EXP PSYCHOL, V18, P119, DOI 10.1080/14640746608400019 Badgaiyan RD, 2000, HUM BRAIN MAPP, V9, P38, DOI 10.1002/(SICI)1097-0193(2000)9:1<38::AID-HBM4>3.0.CO;2-T Brooks Peter, 2000, TROUBLING CONFESSION BUTTERS N, 1973, EXP NEUROL, V39, P204, DOI 10.1016/0014-4886(73)90223-9 Byrne R. W., 2003, SOCIAL BRAIN EVOLUTI, P43, DOI 10.1002/0470867221.ch3 CHAMBERS, 1991, CHAMBERS CONCISE DIC CHINWEIZU, 2001, TIMES LIT S, P6 Dunbar R. I. 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Trans. R. Soc. B-Biol. Sci. PD NOV 29 PY 2004 VL 359 IS 1451 BP 1755 EP 1762 DI 10.1098/rstb.2004.1555 PG 8 WC Biology SC Life Sciences & Biomedicine - Other Topics GA 878KM UT WOS:000225645700011 PM 15590616 ER PT J AU Sankar, R AF Sankar, R TI Initial treatment of epilepsy with antiepileptic drugs - Pediatric issues SO NEUROLOGY LA English DT Review ID LENNOX-GASTAUT-SYNDROME; JUVENILE MYOCLONIC EPILEPSY; IDIOPATHIC GENERALIZED EPILEPSY; ACID HEPATIC FATALITIES; PSYCHIATRIC ADVERSE EVENTS; AUTISM SPECTRUM DISORDERS; BENIGN CHILDHOOD EPILEPSY; MAJOR DEPRESSIVE DISORDER; HYPOXIA-INDUCED SEIZURES; TEMPORAL-LOBE EPILEPSY AB The selection of an antiepileptic drug (AED) for initial treatment of epilepsy in infancy, childhood, and adolescence should ideally be made after a clear syndromic diagnosis of the patient's seizure disorder. A common cause of failure of the first AED is erroneous diagnosis. The availability of new-generation AEDs has expanded the choice of available agents with comparable efficacy for most syndromes. Efficacy data based on class I or II evidence are not available for many syndromes of childhood, and selection must therefore be based on the best data available. It is also important to assess the relative toxicity and tolerability of AEDs in making the selection. It is especially important to appreciate age-specific organ toxicities. Moreover, the use of AEDs in childhood requires an understanding of their neurobehavioral effects. Important neuropsychiatric co-morbidities in children with epilepsy include attention deficit/hyperactivity disorder, autistic spectrum disorders, depression and anxiety, and thought disorders. These problems can be exacerbated or ameliorated by specific AEDs. The effect of AEDs on body weight, insulin sensitivity, lipid profile, and bone health is becoming better appreciated. Newer AEDs may offer significant advantages in this regard. Co-morbid migraine in children with epilepsy may benefit from some AEDs. There remains a continuing need for the development of newer AEDs that are targeted for the developing brain to improve the efficacy and tolerability of treatment in childhood seizure disorders. C1 Univ Calif Los Angeles, Med Ctr, David Geffen Sch Med, Los Angeles, CA 90095 USA. Univ Calif Los Angeles, Med Ctr, Mattel Childrens Hosp, Los Angeles, CA 90095 USA. RP Sankar, R (reprint author), Univ Calif Los Angeles, Med Ctr, David Geffen Sch Med, Room 22-474 MDCC, Los Angeles, CA 90095 USA. 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SO NEW SCIENTIST LA English DT News Item NR 0 TC 0 Z9 0 PU REED BUSINESS INFORMATION LTD PI SUTTON PA QUADRANT HOUSE THE QUADRANT, SUTTON SM2 5AS, SURREY, ENGLAND SN 0262-4079 J9 NEW SCI JI New Sci. PD NOV 20 PY 2004 VL 184 IS 2474 BP 12 EP 12 PG 1 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 873CK UT WOS:000225256300012 ER PT J AU Shouse, MN Scordato, JC Farber, PR AF Shouse, MN Scordato, JC Farber, PR TI Ontogeny of feline temporal lobe epilepsy in amygdala-kindled kittens: an update SO BRAIN RESEARCH LA English DT Article DE brain development; seizure; animal model; behavior disorder; neural plasticity ID DAILY ELECTRICAL-STIMULATION; PARTIAL STATUS EPILEPTICUS; KLUVER-BUCY-SYNDROME; DEVELOPING RATS; SEIZURE SUSCEPTIBILITY; INFANT RATS; CATS; ADULTHOOD; DISORDER; AUTISM AB This report describes amygdala-kindled seizure development and the post-kindling course in 58 cats (29 males and 29 females), including 40 preadolescents between 2.5 and 6.5 months of age and 18 adults >1 year of age at the beginning of kindling. The results extend previous findings, as follows: (1) Youngest animals (<5.0 months, n=30) are far more likely than older kittens and adults to exhibit spontaneous epilepsy, indexed by seizures that occur >1 h after stimulus-evoked seizures. (2) The youngest animals also exhibit accelerated kindling rates and rapid post-kindling onset of multifocal spontaneous epilepsy with a catastrophic clinical course. The profile includes a variety of EEG and/or clinical seizure manifestations and a progressive increase in the number and density of convulsive seizure clusters. Behavioral sequelae accompany seizure clusters and can range from sensory or motor deficits (visual agnosia, sensory hypersensitivity, atonic episodes, restricted mobility) to social isolation and placidity. (3) Onset of spontaneous epilepsy with developmental deterioration is substantially enhanced by recurrent evoked seizures early in the post-kindling course. The post-kindling progression can be stopped or minimized by suspension of evoked seizure trials and/or by management of frequent spontaneous convulsions (>1 per hour) with anticonvulsants. (4) In older cats, many more evoked seizures are required to generate fewer spontaneous seizures with relatively innocuous behavioral disorders. The findings suggest a 'critical period' in kindled kittens for onset of spontaneous temporal lobe epilepsy with severe behavioral consequences and a favorable prognosis for the young following early detection and intervention. Published by Elsevier B.V. C1 Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90064 USA. RP Shouse, MN (reprint author), Univ Calif Los Angeles, Sch Med, 2242 S Bentley Ave 4, Los Angeles, CA 90064 USA. 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CR FITZPATRICK M, 2004, MMR AUTISM PARENTS N 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 18 PY 2004 VL 432 IS 7015 BP 275 EP 276 DI 10.1038/432275a PG 2 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 871UX UT WOS:000225161400020 ER PT J AU Jiang, YH Sahoo, T Michaelis, RC Bercovich, D Bressler, J Kashork, CD Liu, Q Shaffer, LG Schroer, RJ Stockton, DW Spielman, RS Stevenson, RE Beaudet, AL AF Jiang, YH Sahoo, T Michaelis, RC Bercovich, D Bressler, J Kashork, CD Liu, Q Shaffer, LG Schroer, RJ Stockton, DW Spielman, RS Stevenson, RE Beaudet, AL TI A mixed epigenetic/genetic model for oligogenic inheritance of autism with a limited role for UBE3A SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE Angelman syndrome; autism; complex disease traits; DNA methylation; epigenetics; ubiquitin ligase ID ANGELMAN-SYNDROME GENE; INTRACYTOPLASMIC SPERM INJECTION; CHROMOSOME 15Q11-Q13; INTERSTITIAL DUPLICATIONS; ANTISENSE RNA; PROXIMAL 15Q; PRADER-WILLI; DISORDERS; EPILEPSY; CHILDREN AB The genetic contribution to autism is often attributed to the combined effects of many loci (ten or more). This conclusion is based in part on the much lower concordance for dizygotic (DZ) than for monozygotic (MZ) twins, and is consistent with the failure to find strong evidence for linkage in genome-wide studies. We propose that the twin data are compatible with oligogenic inheritance combined with a major, genetic or epigenetic, de novo component to the etiology. Based on evidence that maternal but not paternal duplications of chromosome 15q cause autism, we attempted to test the hypothesis that autism involves oligogenic inheritance (two or more loci) and that the Angelman gene (UBE3A), which encodes the E6-AP ubiquitin ligase, is one of the contributing genes. A search for epigenetic abnormalities led to the discovery of a tissue-specific differentially methylated region (DMR) downstream of the UBE3A coding exons, but the region was not abnormal in autism lymphoblasts or brain samples. Based on evidence for allele sharing in 15q among sib-pairs, abnormal DNA methylation at the 5'-CpG island of UBE3A in one of 17 autism brains, and decreased E6-AP protein in some autism brains, we propose a mixed epigenetic and genetic model for autism with both de novo and inherited contributions. The role of UBE3A may be quantitatively modest, but interacting proteins such as those ubiquitinated by UBE3A may be candidates for a larger role in an oligogenic model. A mixed epigenetic and genetic and mixed de novo and inherited (MEGDI) model could be relevant to other 64 complex disease traits". (C) 2004 Wiley-Liss, Inc. C1 Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA. Baylor Coll Med, Dept Pediat, Houston, TX 77030 USA. Greenwood Genet Ctr, JC Self Res Inst Human Genet, Greenwood, SC 29646 USA. Univ Penn, Sch Med, Dept Genet, Philadelphia, PA 19104 USA. RP Beaudet, AL (reprint author), Baylor Coll Med, Dept Mol & Human Genet, 1 Baylor Pl,Room T619, Houston, TX 77030 USA. 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Several studies have indicated strong involvement of multigenic components in the etiology of autism. Linkage analyses and candidate gene search approaches so far have not identified any reliable susceptibility genes. We are using a proteomic approach to identify protein abnormalities due to aberrant gene expression in autopsied autism brains. In four of eight autism brains, we have found an increase in polarity (more acidic) of glyoxalase I (Glo1) by two-dimensional gel electrophoresis. To identify the molecular change resulting in the shift of Glo1 polarity, we undertook sequencing of GLO1 gene. Direct sequencing of GLO1 gene/mRNA in these brains, has identified a single nucleotide polymorphism (SNP), C419A. The SNP causes an Ala111Glu change in the protein sequence. Population genetics of GLO1 C419A SNP studied in autism (71 samples) and normal and neurological controls (49 samples) showed significantly higher frequency for the A419 (allele frequency 0.6 in autism and 0.4 in controls, one-tailed Fisher's test P < 0.0079). Biochemical measurements have revealed a 38% decrease in Glo1 enzyme activity in autism brains (one-tailed t-test P < 0.026). Western blot analysis has also shown accumulation of advanced glycation end products (AGE's) in autism brains. These data suggest that homozygosity for A419 GLO1 resulting in Glu111 is a predisposing factor in the etiology of autism. (C) 2004 Wiley-Liss, Inc. C1 New York State Inst Basic Res Dev Disabil, Dept Dev Biochem, Staten Isl, NY 10314 USA. New York State Inst Basic Res Dev Disabil, Dept Human Genet, Staten Isl, NY 10314 USA. RP Junaid, MA (reprint author), New York State Inst Basic Res Dev Disabil, Dept Dev Biochem, 1050 Forest Hill Rd, Staten Isl, NY 10314 USA. 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J. Med. Genet. A PD NOV 15 PY 2004 VL 131A IS 1 BP 11 EP 17 DI 10.1002/ajmg.a.30349 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 868FN UT WOS:000224899600002 PM 15386471 ER PT J AU Marui, T Hashimoto, O Nanba, E Kato, C Tochigi, M Umekage, T Ishijima, M Kohda, K Kato, N Sasaki, T AF Marui, T Hashimoto, O Nanba, E Kato, C Tochigi, M Umekage, T Ishijima, M Kohda, K Kato, N Sasaki, T TI Association between the neurofibromatosis-1 (NF1) locus and autism in the Japanese population SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; genetic association study; neurofibromatosis-1; Alu; tetranucleotide repeat ID LINKAGE DISEQUILIBRIUM; GENE; REPEAT; TWIN; POLYMORPHISM; DISORDER AB Autistic patients have a 100 to 190-fold increased risk of neurofibromatosis compared to the general population. This suggests that the two diseases may share a common etiological background. Recently, a new allele (or the six-repeat allele) of the (AAAT)(n) repeat polymorphism in an Alu sequence in the neurofibromatosis-1 (NF1) gene was observed exclusively in severe autistic patients, not in controls, in Caucasians of French ancestry. This suggests a role of the NF1 gene in the development of autism. We investigated three microsatellite polymorphisms within the intron-27b and intron-38 of the NF1 region, including the (AAAT)(n) and two (CA)n repeat polymorphisms, in Japanese subjects with autism (n=74) and controls (n=122). The six-repeat allele of the (AAAT)(n) polymorphism was not found either in patients or controls, possibly indicating an ethnic difference in the polymorphism. However, significant differences were observed in the allele distributions of the (AAAT)(n) and a (CA)(n), which were located at intron-27b, between patients and controls, although an association was not significant between autism and another polymorphism at intron-38. This may suggest an involvement of the NF1 locus in susceptibility to autism, although further investigations are recommended. (C) 2004 Wiley-Liss, Inc. C1 Univ Tokyo, Hlth Serv Ctr, Dept Psychiat, Bunkyo Ku, Tokyo 113, Japan. Univ Tokyo, Grad Sch Med, Dept Psychiat, Tokyo, Japan. Tsurugaoka Hosp, Tokyo, Japan. Tokyo Univ Hosp, Dept Psychiat, Outpatient Clin Dev Disorders, Tokyo 113, Japan. Tottori Univ, Ctr Gene Res, Yonago, Tottori, Japan. Nagoya Univ, Grad Sch Med, Dept Psychiat, Aichi, Japan. RP Sasaki, T (reprint author), Univ Tokyo, Hlth Serv Ctr, Dept Psychiat, Bunkyo Ku, 7-3-1 Hongo, Tokyo 113, Japan. 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Recently, Jamain et al. [Mol Psychiatry 7:302-310] reported that the glutamate receptor 6 (GluR6 or GRIK2) is in linkage disequilibrium. with autism. In the present study, the transmission disequilibrium test (TDT) and the haplotype transmission were performed to analyze the four SNPs (SNP1: rs995640; SNP2: rs2227281; SNP3: rs2227283; SNP4: rs2235076) of GluR6 in 174 Chinese Han parent-offspring trios. The TDT demonstrated that the two SNPs (SNP2 and SNP3) showed preferential transmission (TDT P=0.032). The global chi(2) test for haplotype transmission also revealed an association between GluR6 and autism (chi(2)=10.78, df=3, P=0.013). Our results suggested that GluR6 is in linkage disequilibrium with autism. (C) 2004 Wiley-Liss, Inc. C1 Peking Univ, Inst Mental Hlth, Beijing 100083, Peoples R China. RP Yang, XL (reprint author), Peking Univ, Inst Mental Hlth, Beijing 100083, Peoples R China. 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Chromosome 15q11.2-q13 is a candidate region for autism susceptibility based on observations of chromosomal duplications in a small percentage of affected individuals and findings of linkage and association. We performed linkage disequilibrium (LD) mapping across a 1-Mb interval containing a cluster of GABA(A) receptor subunit genes (GABRB3, GABRA5, and GABRG3) which are good positional and functional candidates. Intermarker LD was measured for 59 single nucleotide polymorphism (SNP) markers spanning this region, corresponding to an average marker spacing of 17.7 kb(-1). We identified haplotype blocks, and characterized these blocks for common (>5%) haplotypes present in the study population. At this marker resolution, haplotype blocks comprise <50% of the DNA in this region, consistent with a high local recombination rate. Identification of haplotype tag SNPs reduces the overall number of markers necessary to detect all common alleles by only 12%. Individual SNPs and multi-SNP haplotypes were examined for evidence of allelic association to autism, using a dataset of 123 multiplex autism families. Six markers individually, across GABRB3 and GABRA5, and several haplotypes inclusive of those markers, demonstrated nominally significant association. These results are positively correlated with the position of observed linkage. These studies support the existence of one or more autism risk alleles in the GABA(A) receptor subunit cluster on 15q12 and have implications for analysis of LD and association in regions with high local recombination. This article contains supplementary material, which may be viewed at the American Journal of Medical Genetics website at http://www.interscience.wiley.com/jpages/0148-7299:1/suppmat/index.html. (C) 2004 Wiley-Liss, Inc. C1 Vanderbilt Univ, Ctr Human Genet Res, Dept Mol Physiol & Biophys, Nashville, TN 37232 USA. Vanderbilt Univ, Ctr Mol Neurosci, Nashville, TN 37232 USA. 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PD NOV 4 PY 2004 VL 26 IS 21-22 BP 1330 EP 1334 DI 10.1080/09638280412331280361 PG 5 WC Rehabilitation SC Rehabilitation GA 863UG UT WOS:000224588300014 PM 15513733 ER PT J AU von Tetzchner, S Ovreeide, KD Jorgensen, KK Ormhaug, BM Oxholm, B Warme, R AF von Tetzchner, S Ovreeide, KD Jorgensen, KK Ormhaug, BM Oxholm, B Warme, R TI Acquisition of graphic communication by a young girl without comprehension of spoken language SO DISABILITY AND REHABILITATION LA English DT Article ID CHILDREN; SIGN; SYMBOL AB Purpose: To describe a graphic-mode communication intervention involving a girl with intellectual impairment and autism who did not develop comprehension of spoken language. The aim was to teach graphic-mode vocabulary that reflected her interests, preferences, and the activities and routines of her daily life, by providing sufficient cues to the meanings of the graphic representations so that she would not need to comprehend spoken instructions. Method: An individual case study design was selected, including the use of written records, participant observation, and registration of the girl's graphic vocabulary and use of graphic signs and other communicative expressions. Results: While the girl's comprehension (and hence use) of spoken language remained lacking over a 3-year period, she acquired an active use of over 80 photographs and pictograms. Conclusions: The girl was able to cope better with the cognitive and attentional requirements of graphic communication than those of spoken language and manual signs, which had been focused in earlier interventions. Her achievements demonstrate that it is possible for communication-impaired children to learn to use an augmentative and alternative communication system without speech comprehension, provided the intervention utilizes functional strategies and non-anguage cues to the meaning of the graphic representations that are taught. C1 Univ Oslo, Dept Psychol, NO-0317 Oslo, Norway. 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Ther. Health Med. PD NOV-DEC PY 2004 VL 10 IS 6 BP 70 EP 75 PG 6 WC Integrative & Complementary Medicine SC Integrative & Complementary Medicine GA 874BL UT WOS:000225325800012 PM 15645598 ER PT J AU Klin, A Chawarska, K Paul, R Rubin, E Morgan, T Wiesner, L Volkmar, F AF Klin, A Chawarska, K Paul, R Rubin, E Morgan, T Wiesner, L Volkmar, F TI Autism in a 15-month-old child SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; EARLY RECOGNITION; YOUNG-CHILDREN; 2-YEAR-OLD CHILDREN; MENTAL-RETARDATION; SPECTRUM DISORDERS; BRAIN-DEVELOPMENT; HOME VIDEOTAPES; JOINT ATTENTION; FOLLOW-UP C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. Yale Univ, Sch Med, Dept Genet, New Haven, CT 06510 USA. So Connecticut State Univ, Dept Commun Disorders, New Haven, CT 06515 USA. Commun Crossroads, Carmel, CA USA. RP Klin, A (reprint author), Yale Univ, Ctr Child Study, POB 207900, New Haven, CT 06520 USA. 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J. Psychiat. PD NOV PY 2004 VL 161 IS 11 BP 1981 EP 1988 DI 10.1176/appi.ajp.161.11.1981 PG 8 WC Psychiatry SC Psychiatry GA 866IY UT WOS:000224768400007 PM 15514396 ER PT J AU Rojas, DC Smith, JA Benkers, TL Camou, SL Reite, ML Rogers, SJ AF Rojas, DC Smith, JA Benkers, TL Camou, SL Reite, ML Rogers, SJ TI Hippocampus and amygdala volumes in parents of children with autistic disorder SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article; Proceedings Paper CT 58th Annual Convention of the Society-of-Biological-Psychiatry CY MAY 15-17, 2003 CL SAN FRANCISCO, CA SP Soc Biol Psychiat ID FRAGILE-X-SYNDROME; INFANTILE-AUTISM; CHILDHOOD AUTISM; TEMPORAL-LOBE; BRAIN; MRI; SCHIZOPHRENIA; ABNORMALITIES; SPECTRUM; DEFICITS AB Objective: Structural and functional abnormalities in the medial temporal lobe, particularly the hippocampus and amygdala, have been described in people with autism. The authors hypothesized that parents of children with a diagnosis of autistic disorder would show similar changes in these structures. Method: Magnetic resonance imaging scans were performed in 17 biological parents of children with a diagnosis of DSM-IV autistic disorder. The scans were compared with scans from 15 adults with autistic disorder and 17 age-matched comparison subjects with no personal or familial history of autism. The volumes of the hippocampus, amygdala, and total brain were measured in all participants. Results: The volume of the left hippocampus was larger in both the parents of children with autistic disorder and the adults with autistic disorder, relative to the comparison subjects. The hippocampus was significantly larger in the adults with autistic disorder than in the parents of children with autistic disorder. The left amygdala was smaller in the adults with autistic disorder, relative to the other two groups. No differences in total brain volume were observed between the three groups. Conclusions: The finding of larger hippocampal volume in autism is suggestive of abnormal early neurodevelopmental processes but is partly consistent with only one prior study and contradicts the findings of several others. The finding of larger hippocampal volume for the parental group suggests a potential genetic basis for hippocampal abnormalities in autism. C1 Univ Colorado, Hlth Sci Ctr, Dept Psychiat, Denver, CO 80262 USA. RP Rojas, DC (reprint author), Box C268-68 CPH,4200 E 9th Ave, Denver, CO 80262 USA. EM Don.Rojas@uchsc.edu RI Rojas, Don/F-4296-2012 CR Abell F, 1999, NEUROREPORT, V10, P1647, DOI 10.1097/00001756-199906030-00005 Aylward EH, 1999, NEUROLOGY, V53, P2145 Aylward EH, 2002, NEUROLOGY, V59, P175 BAILEY A, 1995, PSYCHOL MED, V25, P63 Bauman K. 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J. Psychiat. PD NOV PY 2004 VL 161 IS 11 BP 2038 EP 2044 DI 10.1176/appi.ajp.161.11.2038 PG 7 WC Psychiatry SC Psychiatry GA 866IY UT WOS:000224768400015 PM 15514404 ER PT J AU Posey, DJ Kem, DL Swiezy, NB Sweeten, TL Wiegand, RE McDougle, CJ AF Posey, DJ Kem, DL Swiezy, NB Sweeten, TL Wiegand, RE McDougle, CJ TI A pilot study of D-cyloserine in subjects with autistic disorder SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article AB Objective: The authors assessed the effects Of D-cycloserine on the core symptom of social impairment in subjects with autism. Method: Following a 2-week, single-blind placebo lead-in phase, drug-free subjects with autistic disorder were administered three different doses Of D-cycloserine during each of three 2-week periods. Measures used for subject ratings included the Clinical Global Impression (CGI) scale and Aberrant Behavior Checklist. Results: Significant improvement was found on the CGI and social withdrawal subscale of the Aberrant Behavior Checklist. D-Cycloserine was well tolerated at most of the doses used in this study. Conclusions: In this pilot study, D-Cycloserine treatment resulted in significant improvement in social withdrawal. Further controlled studies Of D-cycloserine in autism appear warranted. C1 James Whitcomb Riley Hosp Children, Christian Sarkine Autism Treatment Ctr, Indianapolis, IN 46220 USA. Indiana Univ, Sch Med, Dept Psychiat, Bloomington, IN 47405 USA. RP Posey, DJ (reprint author), James Whitcomb Riley Hosp Children, Christian Sarkine Autism Treatment Ctr, Room 4300,702 Barnhill Dr, Indianapolis, IN 46220 USA. CR Carlsson ML, 1998, J NEURAL TRANSM, V105, P525, DOI 10.1007/s007020050076 Danysz W, 1998, PHARMACOL REV, V50, P597 Goff DC, 1999, ARCH GEN PSYCHIAT, V56, P21, DOI 10.1001/archpsyc.56.1.21 Krystal JH, 1999, HARVARD REV PSYCHIAT, V7, P125, DOI 10.1093/hrp/7.3.125 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 NR 5 TC 76 Z9 77 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD NOV PY 2004 VL 161 IS 11 BP 2115 EP 2117 DI 10.1176/appi.ajp.161.11.2115 PG 3 WC Psychiatry SC Psychiatry GA 866IY UT WOS:000224768400025 PM 15514414 ER PT J AU Boddaert, N Chabane, N Belin, P Bourgeois, M Royer, V Barthelemy, C Mouren-Simeoni, MC Philippe, A Brunelle, F Samson, Y Zilbovicius, M AF Boddaert, N Chabane, N Belin, P Bourgeois, M Royer, V Barthelemy, C Mouren-Simeoni, MC Philippe, A Brunelle, F Samson, Y Zilbovicius, M TI Perception of complex sounds in autism: Abnormal auditory cortical processing in children SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Article ID CHILDHOOD AUTISM; ACTIVATION AB Objective: The authors have previously described less activation of left speech-related temporal areas in adults with autism when listening to speech-like sounds than in normal adults. Here, they investigated whether this abnormal cortical processing was also present in children with primary autism. Method: Regional cerebral blood flow was measured with positron emission tomography after premedication in 11 autistic children and six nonautistic mentally retarded children during rest and while they were listening to speech-like sounds. Results: As with autistic adults, direct comparison between the two groups revealed significantly less activation in the autistic group localized in left speech-related areas. Conclusions: For the first time to their knowledge, an activation study was performed in children with autism and has confirmed previous results obtained in adults. The abnormal cortical auditory processing observed in both children and adults with autism could be involved in inadequate behavioral responses to sounds and in language impairments characteristic of autism. C1 CEA, Serv Hosp Frederic Joliot, INSERM,Equipe Rech Methodol 0205, DSV,DRM, F-91406 Orsay, France. Assistance Publ Hop Paris, Serv Radiol Pediat, Serv Neurochirurg Pediat, Paris, France. Assistance Publ Hop Paris, Dept Med Genet, Paris, France. Assistance Publ Hop Paris, Hop Robert Debre, Serv Pedopsychiat, Paris, France. Univ Montreal, Dept Psychol, Montreal, PQ H3C 3J7, Canada. CHU Bretonneau, INSERM U316, F-37044 Tours, France. Assistance Publ Hop Paris, Hop La Pitie Salpetriere, Serv Urgences Cerebrovasc, Paris, France. RP Zilbovicius, M (reprint author), CEA, Serv Hosp Frederic Joliot, INSERM,Equipe Rech Methodol 0205, DSV,DRM, 4 Pl Gen Leclerc, F-91406 Orsay, France. EM zilbo@shfj.cea.fr RI Belin, Pascal/C-6247-2009 OI Belin, Pascal/0000-0002-7578-6365 CR Altman NR, 2001, RADIOLOGY, V221, P56, DOI 10.1148/radiol.2211010074 Boddaert N, 2003, AM J PSYCHIAT, V160, P2057, DOI 10.1176/appi.ajp.160.11.2057 BRUNET O, 1976, ECHELLE DEV PSYCHOMO FOX PT, 1984, J CEREBR BLOOD F MET, V4, P329 Friston KJ, 1994, HUMAN BRAIN MAPPING, V2, P189, DOI DOI 10.1002/HBM.460020402 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Ohnishi T, 2000, BRAIN, V123, P1838, DOI 10.1093/brain/123.9.1838 Price CJ, 1996, BRAIN, V119, P919, DOI 10.1093/brain/119.3.919 Rapin I, 1998, ANN NEUROL, V43, P7, DOI 10.1002/ana.410430106 Samson Y, 2001, REV NEUROL-FRANCE, V157, P837 Thivard L, 2000, NEUROREPORT, V11, P2969, DOI 10.1097/00001756-200009110-00028 Wise RJS, 2001, BRAIN, V124, P83, DOI 10.1093/brain/124.1.83 Zilbovicius M, 2000, AM J PSYCHIAT, V157, P1988, DOI 10.1176/appi.ajp.157.12.1988 NR 13 TC 86 Z9 90 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD NOV PY 2004 VL 161 IS 11 BP 2117 EP 2120 DI 10.1176/appi.ajp.161.11.2117 PG 4 WC Psychiatry SC Psychiatry GA 866IY UT WOS:000224768400026 PM 15514415 ER PT J AU Folb, PI Bernatowska, E Chen, R Clemens, J Dodoo, ANO Ellenberg, SS Farrington, P John, TJ Lambert, PH MacDonald, NE Miller, E Salisbury, D Schmitt, HJ Siegrist, CA Wimalaratne, O AF Folb, PI Bernatowska, E Chen, R Clemens, J Dodoo, ANO Ellenberg, SS Farrington, P John, TJ Lambert, PH MacDonald, NE Miller, E Salisbury, D Schmitt, HJ Siegrist, CA Wimalaratne, O TI A global perspective on vaccine safety and public health: The global advisory committee on vaccine safety SO AMERICAN JOURNAL OF PUBLIC HEALTH LA English DT Article ID INFLAMMATORY-BOWEL-DISEASE; SERIOUS ADVERSE EVENTS; RUBELLA VACCINE; CAUSAL ASSOCIATION; ASEPTIC-MENINGITIS; MASS VACCINATION; MEASLES-VIRUS; MUMPS VACCINE; NO EVIDENCE; FOLLOW-UP AB Established in 1999, the Global Advisory Committee on Vaccine Safety advises the World Health Organization (WHO) on vaccine-related safety issues and enables WHO to respond promptly, efficiently, and with scientific rigor to issues of vaccine safety with potential global importance. The committee also assesses the implications of vaccine safety for practice worldwide and for WHO policies. We describe the principles on which the committee was established-its modus operandi, and the scope of the work undertaken, both present and future. We highlight its recent recommendations on major issues, including the purported link between the measles-mumps-rubella vaccine and autism and the safety of the mumps, influenza, yellow fever, BCG, and smallpox vaccines as well as that of thiomersal-containing vaccines. C1 MRC, ZA-7505 Cape Town, South Africa. Childrens Mem Hlth Inst, Dept Immunol, Warsaw, Poland. Ctr Dis Control & Prevent, Immunizat Safety Branch, Atlanta, GA USA. Int Vaccine Inst, Seoul, South Korea. Univ Ghana, Sch Med, Ctr Trop Clin Pharmacol & Therapeut, Accra, Ghana. US FDA, Off Biostat & Epidemiol, Rockville, MD 20857 USA. Open Univ, Dept Stat, Milton Keynes MK7 6AA, Bucks, England. Kerala State Inst Virol & Infect Dis, Vellore, Tamil Nadu, India. Ctr Med Univ Geneva, Collaborating Ctr Neonatal Vaccinol, WHO, CH-1211 Geneva, Switzerland. Dalhousie Univ, Dept Paediat, Halifax, NS, Canada. Hlth Protect Agcy, Immunisat Dept, London, England. Dept Hlth, Communicable Dis & Immunisat Team, London SE1 6TE, England. Univ Mainz, Ctr Prevent Pediat, D-6500 Mainz, Germany. Med Res Inst, Dept Rabies & Vaccines, Colombo, Sri Lanka. RP Folb, PI (reprint author), MRC, POB 19070, ZA-7505 Cape Town, South Africa. EM pfolb@mrc.ac.za CR Aaby P, 2003, LANCET, V361, P2183, DOI 10.1016/S0140-6736(03)13771-3 [Anonymous], 2001, WKLY EPIDEMIOL REC, V76, P85 Biellik R, 2002, LANCET, V359, P1564, DOI 10.1016/S0140-6736(02)08517-3 Chan RC, 2001, LANCET, V358, P121, DOI 10.1016/S0140-6736(01)05341-7 da Cunha SS, 2002, VACCINE, V20, P1106, DOI 10.1016/S0264-410X(01)00438-8 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 DeWilde S, 2001, BRIT J GEN PRACT, V51, P226 Dos Santos Boaventura Antônio, 2002, Rev Panam Salud Publica, V12, P240 Dourado I, 2000, AM J EPIDEMIOL, V151, P524 Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 Fine P, 2000, BRIT MED J, V321, P1439 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 Fullerton KE, 2002, INT J EPIDEMIOL, V31, P983, DOI 10.1093/ije/31.5.983 Galazka AM, 1999, B WORLD HEALTH ORGAN, V77, P3 GILLBERG G, 1991, BRIT J PSYCHIAT, V158, P403 *GLOB ADV COMM VAC, 2004, WKLY EPIDEMIOL REC, V79, P16 *GLOB ADV COMM VAC, 2003, WKLY EPIDEMIOL REC, V78, P282 ISAACS SL, 2001, AM PROPECT, V12, P26 Kawashima H, 2000, DIGEST DIS SCI, V45, P723, DOI 10.1023/A:1005443726670 Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Kristensen I, 2000, BRIT MED J, V321, P1435, DOI 10.1136/bmj.321.7274.1435 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Martin CM, 2002, MOL PSYCHIATR, V7, pS47, DOI 10.1038/sj.mp.4001179 Martin M, 2001, LANCET, V358, P98, DOI 10.1016/S0140-6736(01)05327-2 Patja A, 2000, PEDIATR INFECT DIS J, V19, P1127, DOI 10.1097/00006454-200012000-00002 Peltola H, 1998, LANCET, V351, P1327, DOI 10.1016/S0140-6736(98)24018-9 Singh VK, 2002, J BIOMED SCI, V9, P359, DOI 10.1159/000065007 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 *US DEP HLTH WELF, 1964, PHS PUBL, V1103 Vasconcelos PFC, 2001, LANCET, V358, P91, DOI 10.1016/S0140-6736(01)05326-0 *WHO, 2003, REP STRAT ADV GROUP World Health Organization UNICEF World Bank, 2002, STAT WORLDS VACC IMM 2003, MMWR MORB MORTAL WKL, V52, P819 2003, MMWR MORB MORTAL WKL, V52, P639 NR 35 TC 24 Z9 28 PU AMER PUBLIC HEALTH ASSOC INC PI WASHINGTON PA 1015 FIFTEENTH ST NW, WASHINGTON, DC 20005 USA SN 0090-0036 J9 AM J PUBLIC HEALTH JI Am. J. Public Health PD NOV PY 2004 VL 94 IS 11 BP 1926 EP 1931 DI 10.2105/AJPH.94.11.1926 PG 6 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 866NS UT WOS:000224780800022 PM 15514229 ER PT J AU Renaud, S Guile, JM AF Renaud, S Guile, JM TI A neurobiological approach to temperamental traits associated with personality disorders SO ANNALES MEDICO-PSYCHOLOGIQUES LA French DT Article DE endophenotype; environment; neurobiology; personality disorders; temperament ID BORDERLINE PERSONALITY; SCHIZOTYPAL PERSONALITY; ENVIRONMENT CORRELATIONS; SCHIZOPHRENIC-PATIENTS; SPECTRUM PERSONALITY; FACTORIAL STRUCTURE; SALIVARY CORTISOL; CONDUCT DISORDERS; EARLY ADOLESCENCE; GENETIC-STRUCTURE AB Recent publications in the field of neurobiology related to personality disorders allow some consideration on the bidirectional relationship between genetically determined temperamental traits and environment, interactions observed in the normal development of personality during childhood and adolescence or on the contrary in the building of a disordered personality revealed at adulthood. Based on the review of studies about development of personality disorders in children, adolescents and adults, this article puts forward the interactive quality of relations between genetic background and environmental factors and proposes hypotheses concerning the role of temperament in the development of personality. Correlations between genes and environment (rGE) and interactions gene-environment (GxE) are examined. Bidirectional feedback between temperament and environment where individual temperamental characteristics determine environment selection or adjustment and not the opposite is an example of an interaction of evocative type. However, actual research designs face difficulties in the establishment of a causal link due to the multitude and complexity of involved factors linking personality traits with temperamental genetic markers. This might explain the emergence of an endophenotype concept as it has been used with autism. An endophenotype consists in a mesurable cognitive, neurophysiological or neurochemical variable expressing the genetic defect present before the onset of the illness. Some studies put forward possible endophenotypes for borderline, antisocial and schizotypal personality disorders. Longitudinal research has shown the predictive quality of externalized conduct disorders of childhood leading to antisocial and to a lesser extent borderline personality disorders in adulthood. Impulsivity and affective lability might be based on minor neurocognitive abnormalities, subclinical attention deficits and/or marked neuropsychological dimensions such as strong extraversion. Suboptimal serotoninergic regulation has been established in destructive impulsivity and suicidability. Abnormalities in the dopaminergic and noradrenergic systems might also be implicated but it remains unclear to what extent repeated trauma and abuse during childhood might modify the hypothalamic-pituitary-corticotropic axis in response to chronic stress and transform permanently the modulation of physiological and psychological reactions of these children to their perturbed environment. Researches on conduct disorders have also demonstrated the evocative interaction of a particular temperament with the environment responding to marked novelty seeking behaviour, hyperactivity, impulsivity and lack of proper physiological reaction to extreme stimuli. Lack of behaviour inhibition found in antisocial individuals is. attributed to noradrenergic and serotoninergic abnormalities and neurocognitive deficits. The dimensional continuity of schizotypal personality to schizophrenia is well established and electrophysiological markers such as abnormal eye tracking movements, P300 evoked potentials, prolonged electrodermal reactions with cognitive disorganization and deficits in inhibition of attention to usual stimuli might be the future endophenotypical markers to schizophrenia susceptibility. Further studies on temperamental traits might lead to the identification of genetic markers as precursors to personality disorders. (C) 2004 Elsevier SAS. Tous droits reserves. C1 Univ Montreal, Hop St Luc, Ctr Sante Mentale Communautaire, Dept Psychiat,CHUM, Montreal, PQ H2X 1N4, Canada. Univ Montreal, CTA Hop Riviere Prairies, Dept Psychiat, Montreal, PQ H1E 1A4, Canada. RP Renaud, S (reprint author), Univ Montreal, Hop St Luc, Ctr Sante Mentale Communautaire, Dept Psychiat,CHUM, 190 Rene Levesque Est, Montreal, PQ H2X 1N4, Canada. 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Med.-Psychol. PD NOV PY 2004 VL 162 IS 9 BP 731 EP 738 DI 10.1016/j.amp.2004.03.015 PG 8 WC Pharmacology & Pharmacy; Psychiatry; Psychology; Psychology, Multidisciplinary SC Pharmacology & Pharmacy; Psychiatry; Psychology GA 874IO UT WOS:000225344300004 ER PT J AU Song, YL Liu, CX Finegold, SA AF Song, YL Liu, CX Finegold, SA TI Real-time PCR quantitation of clostridia in Feces of autistic children SO APPLIED AND ENVIRONMENTAL MICROBIOLOGY LA English DT Article ID 16S RIBOSOMAL-RNA; GRADIENT GEL-ELECTROPHORESIS; IN-SITU HYBRIDIZATION; TARGETED OLIGONUCLEOTIDE PROBES; SPECIES-SPECIFIC PRIMERS; FECAL SAMPLES; GASTROINTESTINAL MICROFLORA; BACTERIAL-POPULATIONS; MOLECULAR BEACONS; RAPID DETECTION AB Based on the hypothesis that intestinal clostridia play a role in late-onset autism, we have been characterizing clostridia from stools of autistic and control children. We applied the TaqMan real-time PCR procedure to detect and quantitate three Clostridium clusters and one Clostridium species, C. bolteae, in stool specimens. Group- and species-specific primers targeting the 16S rRNA genes were designed, and specificity of the primers was confirmed with DNA from related bacterial strains. In this procedure, a linear relationship exists between the threshold cycle (C-T) fluorescence value and the number of bacterial cells (CFU). The assay showed high sensitivity: as few as 2 cells of members of cluster 1, 6 cells of cluster XI, 4 cells of cluster XIVab, and 0.6 cell of C. bolteae could be detected per PCR. Analysis of the real-time PCR data indicated that the cell count differences between autistic and control children for C. bolteae and the following Clostridium groups were statistically significant: mean counts of C. bolteae and clusters I and XI in autistic children were 46-fold (P = 0.01), 9.0-fold (P = 0.014), and 3.5-fold (P = 0.004) greater than those in control children, respectively, but not for cluster XIVab (2.6 X 10(8) CFU/g in autistic children and 4.8 X 10(8) CFU/g in controls; respectively). More subjects need to be studied. The assay is a rapid and reliable method, and it should have great potential for quantitation of other bacteria in the intestinal tract. C1 VA Med Ctr W Los Angeles, Res Serv, Los Angeles, CA 90073 USA. VA Med Ctr W Los Angeles, Infect Dis Sect, Los Angeles, CA 90073 USA. Univ Calif Los Angeles, Sch Med, Dept Med, Los Angeles, CA USA. Univ Calif Los Angeles, Sch Med, Dept Microbiol Immunol & Mol Genet, Los Angeles, CA USA. RP Song, YL (reprint author), VA Med Ctr W Los Angeles, Res Serv, 11301 Wilshire Blvd,Room E3-237,Bldg 304, Los Angeles, CA 90073 USA. 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SO AUTOIMMUNITY REVIEWS LA English DT Article DE autism; autoimmune; neurodevelopment ID PERVASIVE DEVELOPMENTAL DISORDERS; FAMILIAL AUTOIMMUNITY; INFANTILE-AUTISM; RISK-FACTORS; ANTIBODIES; CHILDREN; AUTOANTIBODIES; PREVALENCE; PROTEIN; SYSTEM AB Autism spectrum disorder (ASD) is a spectrum of behavioral anomalies characterized by impaired social interaction and communication, often accompanied by repetitive and stereotyped behavior. The condition manifests within the first 3 years of life and persists into adulthood. There are numerous hypotheses regarding the etiology and pathology of ASD, including a suggested role for immune dysfunction. However, to date, the evidence for involvement of the immune system in autism has been inconclusive. While immune system abnormalities have been reported in children with autistic disorder, there is little consensus regarding the nature of these differences which include both enhanced autoimmunity and reduced immune function. 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Rev. PD NOV PY 2004 VL 3 IS 7-8 BP 557 EP 562 DI 10.1016/j.autrev.2004.07.036 PG 6 WC Immunology SC Immunology GA 878SB UT WOS:000225666000013 PM 15546805 ER PT J AU Fisch, GS Simensen, RJ Schroer, RJ AF Fisch, GS Simensen, RJ Schroer, RJ TI Longitudinal assessment of cognitive-behavioral features of children and adolescents with either autism or the fragile X mutation SO BEHAVIOR GENETICS LA English DT Meeting Abstract CT 34th Annual Meeting of the Behavior-Genetics-Association CY JUN 27-30, 2004 CL Aix en Provence, FRANCE SP Behav Genet Assoc C1 N Shore LIJ Res Inst, Biostat Unit, Manhasset, NY 11030 USA. Greenwood Genet Ctr, Greenwood, SC 29646 USA. EM gfisch@nshs.edu NR 0 TC 1 Z9 1 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD NOV PY 2004 VL 34 IS 6 BP 638 EP 638 PG 1 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 866YB UT WOS:000224808200035 ER PT J AU Lamb, JA Bonora, E Barnby, G Sykes, N Maestrini, E Blasi, F Bacchelli, E Beyer, KS Klauck, SM Poustka, A Bailey, AJ Monaco, AP AF Lamb, JA Bonora, E Barnby, G Sykes, N Maestrini, E Blasi, F Bacchelli, E Beyer, KS Klauck, SM Poustka, A Bailey, AJ Monaco, AP TI International molecular genetic study of autism consortium (IMGSAC). Towards identification of autism susceptibility variants in the IMGSAC sample SO BEHAVIOR GENETICS LA English DT Meeting Abstract CT 34th Annual Meeting of the Behavior-Genetics-Association CY JUN 27-30, 2004 CL Aix en Provence, FRANCE SP Behav Genet Assoc C1 Univ Oxford, Wellcome Trust Ctr Human Genet, Oxford, England. Univ Bologna, Dept Biol, I-40126 Bologna, Italy. Deutsch Krebsforschungszentrum, Dept Mol Genome Anal, D-6900 Heidelberg, Germany. Pk Hosp Children, Sect Child & Adolescent Psychiat, Oxford, England. RI Bailey, Anthony/J-2860-2014 OI Bailey, Anthony/0000-0003-4257-972X NR 0 TC 0 Z9 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD NOV PY 2004 VL 34 IS 6 BP 647 EP 647 PG 1 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 866YB UT WOS:000224808200068 ER PT J AU Tordjman, S AF Tordjman, S TI Towards an integrated clinico-biological approach to autism SO BEHAVIOR GENETICS LA English DT Meeting Abstract CT 34th Annual Meeting of the Behavior-Genetics-Association CY JUN 27-30, 2004 CL Aix en Provence, FRANCE SP Behav Genet Assoc C1 Hop La Pitie Salpetriere, CNRS, UMR 7593, Lab Vulnerabil Adaptat & Psychopathol, F-75073 Paris, France. EM lubart@idf.ext.jussieu.fr NR 0 TC 0 Z9 0 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0001-8244 J9 BEHAV GENET JI Behav. Genet. PD NOV PY 2004 VL 34 IS 6 BP 662 EP 662 PG 1 WC Behavioral Sciences; Genetics & Heredity; Psychology, Multidisciplinary SC Behavioral Sciences; Genetics & Heredity; Psychology GA 866YB UT WOS:000224808200123 ER PT J AU Bidwell, MA Rehfeldt, RA AF Bidwell, MA Rehfeldt, RA TI Using video modeling to teach a domestic skill with an embedded social skill to adults with severe mental retardation SO BEHAVIORAL INTERVENTIONS LA English DT Article ID CHILDREN; AUTISM AB We assessed whether three adults with severe mental retardation would acquire a domestic skill (making coffee) with an embedded social skill (serving coffee to and sitting down beside a peer) via video modeling procedures. Training was conducted in a classroom in the participants' day treatment setting. The intervention consisted of (i) watching a video of an adult with a developmental disability making coffee and initiating a social interaction with a peer; and (ii) receiving verbal praise for each step of the task that was performed correctly. All three participants mastered the task and demonstrated generalization across settings, stimuli, and people. Two participants performed with 100% accuracy on maintenance probes conducted 1 month following mastery, and one participant did so following booster training. Copyright (C) 2004 John Wiley Sons, Ltd. C1 So Illinois Univ, Rehabil Inst, Rehab Serv Program, Carbondale, IL 62901 USA. RP Rehfeldt, RA (reprint author), So Illinois Univ, Rehabil Inst, Rehab Serv Program, Mail Code 4609, Carbondale, IL 62901 USA. EM rehfeldt@siu.edu CR Brady M. 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PD NOV PY 2004 VL 19 IS 4 BP 263 EP 274 DI 10.1002/bin.165 PG 12 WC Psychology, Clinical SC Psychology GA 871PI UT WOS:000225145300003 ER PT J AU Morgadinho, MT Ribeiro, CAF Macedo, TRA AF Morgadinho, MT Ribeiro, CAF Macedo, TRA TI Influence of the sample preparation method on the serotonin determination in plasma and platelets SO BIOMEDICAL CHROMATOGRAPHY LA English DT Article DE serotonin measurement; platelet serotonin; plasma serotonin ID ELECTROCHEMICAL DETECTION; WHOLE-BLOOD; HYPERSEROTONEMIA; VARIANTS; AUTISM; HPLC AB Plasma or platelet serotonin concentration is commonly used to provide information about the serotonergic activity in various psychiatric or neurological diseases. Some difficulties have been described in the measurement of serotonin (5-HT) levels in plasma or platelets. We describe an isocratic liquid-chromatographic assay with amperometric detection for determination of 5-HT in the platelet pellet and in platelet-rich and platelet-poor plasma (PRP and PPP) in sample sizes of 100 muL of plasma. The method uses an RP, column and an amperometric detector with a thin-layer type electrochemical flow cell, with glassy carbon electrode maintained at a potential of +0.600 V vs an Ag/AgCl reference electrode. Determinations were performed in the presence or in the absence of plasma, since the biological matrix may affect the results. Different validation parameters were analysed: selectivity. accuracy, precision, linearity and stability. Reference values for 5-HT concentration in healthy adults (n = 12) were 6.6 nmol/10(9) platelets, for the platelet pellet, and 5.5 nmol/10(9) platelets, for PRP. The 100muL sample volume used for the preparation of PPP did not make possible the determination of 5-HT levels with accuracy and precision. Copyright (C) 2004 John Wiley Sons, Ltd. C1 Univ Coimbra, Fac Med, Inst Pharmacol & Therapeut, P-3004054 Coimbra, Portugal. RP Macedo, TRA (reprint author), Univ Coimbra, Fac Med, Inst Farmacol & Terapeut Expt, P-3004054 Coimbra, Portugal. 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PD NOV PY 2004 VL 18 IS 9 BP 739 EP 744 DI 10.1002/bmc.387 PG 6 WC Biochemical Research Methods; Biochemistry & Molecular Biology; Chemistry, Analytical; Pharmacology & Pharmacy SC Biochemistry & Molecular Biology; Chemistry; Pharmacology & Pharmacy GA 875TY UT WOS:000225445900021 PM 15386580 ER PT J AU Berguno, G Bowler, D AF Berguno, G Bowler, D TI Understanding pretence and understanding action SO BRITISH JOURNAL OF DEVELOPMENTAL PSYCHOLOGY LA English DT Article ID INDIVIDUAL-DIFFERENCES; CHILDS THEORY; MIND; PLAY; BELIEF; REPRESENTATIONS; FEELINGS; FANTASY; AUTISM; STATE AB Two studies were carried out in an attempt to replicate an earlier but controversial set of findings that suggested that young children are able to understand pretence in a mentalistic sense (Hickling, Wellman, & Gottfried, 1997). 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PD NOV PY 2004 VL 49 IS 11 BP 784 EP 785 PG 2 WC Psychiatry SC Psychiatry GA V24CG UT WOS:000208387900017 PM 15633858 ER PT J AU Song, BJ Katial, RK AF Song, BJ Katial, RK TI Update on side effects from common vaccines SO CURRENT ALLERGY AND ASTHMA REPORTS LA English DT Review ID THIMEROSAL-CONTAINING VACCINES; OCULO-RESPIRATORY SYNDROME; GUILLAIN-BARRE-SYNDROME; EVENT REPORTING SYSTEM; INFLUENZA VACCINATION; RUBELLA VACCINE; EPIDEMIOLOGIC EVIDENCE; ADVERSE EVENTS; AUTISM; CHILDREN AB Vaccines have had a tremendous impact on public health by reducing morbidity and mortality from a variety of virulent pathogens. However, unintended side effects continue to pose a potential risk that may outweigh the vaccine's protective attributes. In this review, we discuss recent articles and controversies pertaining to vaccine-associated adverse events. Included in the discussion are influenza, hepatitis B, measles-mumps-rubella, diphtheriatetanus-pertussis, polio, Hoemophilus influenzae type b, and rotavirus vaccines. The importance and contribution of vaccine constituents (such as thimerosal) to side effects is also reviewed. C1 Natl Jewish Med & Res Ctr, Div Adult Allergy & Immunol, Denver, CO 80206 USA. RP Song, BJ (reprint author), Natl Jewish Med & Res Ctr, Div Adult Allergy & Immunol, 1400 Jackson St, Denver, CO 80206 USA. 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High-resolution structural magnetic resonance images were acquired for nine males with high-functioning autism (HFA; mean age 14y [SD3y 4mo]), 11 with Asperger syndrome (ASP; mean age 13y 6mo [SD2y 5mo]), and 13 comparison (COM) participants (mean age 13y 7mo [SD3y 1mo]). Using statistical parametric mapping, we examined contrasts of gray matter differences between the groups. Males with HFA and ASP had a pattern of decreased gray matter density in the ventromedial regions of the temporal cortex in comparison with males from an age-matched comparison group. Examining contrasts revealed that the COM group had increased gray matter density compared with the ASP or combined HFA and ASP group in the right inferior temporal gyrus, entorhinal cortex, and rostral fusiform gyrus. The ASP group had less gray matter density in the body of the cingulate gyrus in comparison with either the COM or HFA group. 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PD NOV PY 2004 VL 40 IS 6 BP 1093 EP 1104 DI 10.1037/0012-1649.40.6.1093 PG 12 WC Psychology, Developmental SC Psychology GA 865SJ UT WOS:000224722800014 PM 15535759 ER PT J AU Manning, JT Stewart, A Bundred, PE Trivers, RL AF Manning, JT Stewart, A Bundred, PE Trivers, RL TI Sex and ethnic differences in 2nd to 4th digit ratio of children SO EARLY HUMAN DEVELOPMENT LA English DT Article DE 2D : 4D; children; sex and ethnic differences ID LENGTH; FINGER; DIMORPHISM; GENES; MICE AB Background: The ratio between the length of the 2nd or index finger and the 4th or ring finger (2D:4D) differs between the sexes, such that males have lower 2D:4D than females, and shows considerable ethnic differences, with low values found in Black populations. It has been suggested that the sex difference in 2D:4D arises early in development and that finger ratio is a correlate of prenatal testosterone and oestrogen. In children, 2D:4D has been reported to be associated with measures of-fetal growth, congenital adrenal hyperplasia, developmental psychopathology, autism and Asperger's syndrome. However, little is known of the patterns of sex and ethnic differences in the 2D:4D ratio of children. Aim: To investigate sex and ethnic differences in 2D:4D in Caucasian, Oriental and Black children. Study design: Population survey. Method: The 2D:4D ratio was measured from photocopies of the right hand of Berber children from Morocco, Uygur and Han children from the North-West province of China, and children from Jamaica. Results: There were 798 children in the total sample (90 Berbers, 438 Uygurs, 118 Han, and 152 Jamaicans). The 2D:AD ratio was lower in males than in females and this was significant for the overall sample and for the Uygur, Han and Jamaican samples. There were significant ethnic differences in 2D:4D. The Oriental Han had the highest mean 2D:4D, followed by the Caucasian Berbers and Uygurs, with the lowest mean ratios found in the Afro-CaribbeanJamaicans. The sex and ethnic differences were independent of one another with no significant interaction effect. In the overall sample there were no associations between 2D:4D and age and height. Conclusions: In common with adults, the 2D:4D ratio of children shows sex and ethnic differences with low values found in a Black group. There was no overall association between 2D:4D and age and height suggesting that the sex and ethnic differences in 2D:4D appear early and do not show appreciable change with growth. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Univ Cent Lancashire, Dept Psychol, Preston PR1 2HE, Lancs, England. Univ Liverpool, Dept Publ Hlth, Liverpool L69 3GX, Merseyside, England. Univ Liverpool, Dept Primary Care, Liverpool L69 3GX, Merseyside, England. Rutgers State Univ, Dept Anthropol, Rutgers, NJ 08903 USA. RP Manning, JT (reprint author), Univ Cent Lancashire, Dept Psychol, Preston PR1 2HE, Lancs, England. 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Dev. PD NOV PY 2004 VL 80 IS 2 BP 161 EP 168 DI 10.1016/j.earlhumdev.2004.06.004 PG 8 WC Obstetrics & Gynecology; Pediatrics SC Obstetrics & Gynecology; Pediatrics GA 870LA UT WOS:000225057400008 PM 15500996 ER PT J AU Tchanturia, K Happe, F Godley, J Treasure, J Bara-Carril, N Schmidt, U AF Tchanturia, K Happe, F Godley, J Treasure, J Bara-Carril, N Schmidt, U TI 'Theory of mind' in anorexia nervosa SO EUROPEAN EATING DISORDERS REVIEW LA English DT Article DE anorexia; theory of mind; adults ID LOW BODY-WEIGHT; PERSONALITY-DISORDERS; ASPERGERS-DISORDER; MALE-CHILDREN; ADOLESCENTS; ATTACHMENT; ONSET; BRAIN AB The ability to make inferences about others' mental states has been termed 'theory of mind' (ToM). It underlies the ability to engage in complex social interaction and is impaired in autism. A subgroup of anorexia nervosa (AN) sufferers has autism-spectrum disorders/empathy disorders. The aim of the study was to explore whether, even in the absence of clear-cut autistic features, impairments in their ability to mentalize could be found in AN patients. Twenty patients with AN and 20 female healthy control (HC) subjects were tested using: (1) a story comprehension task (ToM stories and control stories); and (2) a cartoon task (ToM cartoons and control cartoons). Individuals with AN performed worse than HC subjects on ToM and on control tasks. However, there was no evidence of any selective impairment of ToM in AN sufferers. These findings do not support a specific link between impaired ToM and AN. Copyright (C) 2004 John Wiley & Sons, Ltd and Eating Disorders Association. C1 Inst Psychiat, London SE5 8AF, England. Inst Psychiat, Social Genet & Dev Psychiat Res Ctr, London, England. Guys Kings & St Thomas Med Sch, London, England. Maudsley Hosp & Inst Psychiat, London SE5 8AZ, England. RP Schmidt, U (reprint author), Inst Psychiat, De Crespigny Pk, London SE5 8AF, England. 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Eat. Disord. Rev. PD NOV-DEC PY 2004 VL 12 IS 6 BP 361 EP 366 DI 10.1002/erv.608 PG 6 WC Psychology, Clinical SC Psychology GA 875VF UT WOS:000225449400004 ER PT J AU [Anonymous] AF [Anonymous] TI Evidence of association of autism with a region on chromosome 7q SO GENETIC EPIDEMIOLOGY LA English DT Meeting Abstract 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 0741-0395 J9 GENET EPIDEMIOL JI Genet. Epidemiol. PD NOV PY 2004 VL 27 IS 3 BP 295 EP 295 PG 1 WC Genetics & Heredity; Public, Environmental & Occupational Health SC Genetics & Heredity; Public, Environmental & Occupational Health GA 866ZZ UT WOS:000224813200132 ER PT J AU Geier, DA Geier, MR AF Geier, DA Geier, MR TI Neurodevelopmental disorders following thimerosal-containing childhood immunizations: A follow-up analysis SO INTERNATIONAL JOURNAL OF TOXICOLOGY LA English DT Article DE autistic spectrum disorders; ethylmercury; merthiolate; thiomersal; VAERS ID EVENT REPORTING SYSTEM; CONTAINING VACCINES; INVITRO; AUTISM; ASSOCIATION; ACTIVATION; MERCURY; SAFETY; VAERS AB The authors previously published the first epidemiological study from the United States associating thimerosal from childhood vaccines with neurodevelopmental disorders (NDs) based upon assessment of the Vaccine Adverse Event Reporting System (VAERS). A number of years have gone by since their previous analysis of the VAERS. The present study was undertaken to determine whether the previously observed effect between thimerosal-containing childhood vaccines and NDs are still apparent in the VAERS as children have had a chance to further mature and potentially be diagnosed with additional NDs. In the present study, a cohort of children receiving thimerosal-containing diphtheria-tetanus-acellular pertussis (DTaP) vaccines in comparison to a cohort of children receiving thimerosal-free DTaP vaccines administered from 1997 through 2000 based upon an assessment of adverse events reported to the VAERS were evaluated. It was determined that there were significantly increased odds ratios (ORs) for autism (OR = 1.8,p <.05), mental retardation (OR = 2.6, p <.002), speech disorder (OR = 2.1,p <.02), personality disorders (OR = 2.6,p <.01), and thinking abnormality (OR = 8.2, p <.01) adverse events reported to the VAERS following thimerosal-containing DTaP vaccines in comparison to thimerosal-free DTaP vaccines. Potential confounders and reporting biases were found to be minimal in this assessment of the VAERS. It was observed, even though the media has reported a potential association between autism and thimerosal exposure, that the other NDs analyzed in this assessment of the VAERS had significantly higher ORs than autism following thimerosal-containing DTaP vaccines in comparison to thimerosal-free DTaP vaccines. The present study provides additional epidemiological evidence supporting previous epidemiological, clinical and experimental evidence that administration of thimerosal-containing vaccines in the United States resulted in a significant number of children developing NDs. C1 MedCon Inc, Silver Spring, MD USA. Genet Ctr Amer, Silver Spring, MD USA. RP Geier, MR (reprint author), 14 Redgate Ctr, Silver Spring, MD 20905 USA. 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However, the familial transmission of these disorders cannot be explained by simple Mendelian models of inheritance, and non-genetic factors must also play a substantial role in their etiologies. Furthermore, the prevalence of any major psychiatric disorder is a great deal higher than that of Mendelian disorders. It has been suggested that evolutionary forces would rapidly eliminate large gene effects, which would suggest that mental disorders, which are highly prevalent, are associated with minor gene effects (Risch, 1994). The current paradigm is that genes with small interacting genetic effects, in conjunction with environmental factors, affect the risk for psychiatric disease. New laboratory and statistical methodology and database tools, and the availability of large clinical samples for the study of linkage and association sustain optimism that genes involved with these diseases will be characterized in the near future. 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Rev. Psych. PD NOV PY 2004 VL 16 IS 4 BP 284 EP 293 DI 10.1080/09540260400014393 PG 10 WC Psychiatry SC Psychiatry GA 882YR UT WOS:000225976800004 PM 16194761 ER PT J AU Balog, HL Roberts, FD AF Balog, HL Roberts, FD TI Perception of utterance relatedness during the first-word-period SO JOURNAL OF CHILD LANGUAGE LA English DT Article ID COMMUNICATIVE FUNCTIONS; INTONATION CONTOURS; MATERNAL SPEECH; INFANTS; LANGUAGE; ATTENTION; PROSODY; MOTHERS; AUTISM AB Interactions between six toddlers (aged 1;0 to 1;6) and adults were examined to ascertain adult perceptions of toddler utterance relatedness and to determine temporal and interactional features that underlie those perceptions. Five raters made judgments regarding relatedness of the child utterances to the previous adult utterances; 251 utterances were examined. Utterances judged by adults as related occurred within 4-25 seconds of the preceding adult utterance nearly 90% of the time. This study also points to the need for using interactional categories that go beyond describing utterance relatedness, and introduces terms (i.e. coparticipatory, initiation narrowed focus) for doing so. C1 Purdue Univ, W Lafayette, IN 47907 USA. RP Balog, HL (reprint author), Wayne State Univ, Dept Audiol & Speech Language Pathol, 581 Manoogian Hall,906 W Warren Ave, Detroit, MI 48201 USA. EM hbalog@wayne.edu CR BACRI N, 1984, P 10 INT C PHON SCI Baldwin D. 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M., 1996, PHONOLOGICAL DEV ORI WARREN SF, 1998, TRANSITIONS PRELINGU NR 43 TC 1 Z9 1 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0305-0009 J9 J CHILD LANG JI J. Child Lang. PD NOV PY 2004 VL 31 IS 4 BP 837 EP 854 DI 10.1017/S0305000904006579 PG 18 WC Psychology, Developmental; Linguistics; Psychology, Experimental SC Psychology; Linguistics GA 888TM UT WOS:000226397100006 PM 15658748 ER PT J AU Zaroff, CM Devinsky, O Miles, D Barr, WB AF Zaroff, CM Devinsky, O Miles, D Barr, WB TI Cognitive and behavioral correlates of tuberous sclerosis complex SO JOURNAL OF CHILD NEUROLOGY LA English DT Review ID LEARNING-DISABILITY; SLEEP DISORDERS; AUTISM; EPILEPSY; PREVALENCE; CHILDREN; SEVERITY; SCOTLAND; SEIZURES; DEFICITS AB Tuberous sclerosis complex is a multisystem disorder in which neurologic problems cause the greatest disability. High rates of mental retardation and autism spectrum disorders are associated with the diagnosis. Early-onset seizures and increased tuber burden are risk factors for cognitive impairment. Early-onset seizures, particularly infantile spasms, are risk factors for autism. Tubers within the temporal lobe and cerebellum are often mentioned as risk factors for autism, although the findings are inconsistent. Seizure control is important for developmental outcome and quality of life. Early behavioral assessment and therapeutic intervention, as well as seizure control, are the most effective means of promoting neurodevelopmental outcome. C1 NYU, Comprehens Epilepsy Ctr, New York, NY 10016 USA. RP Zaroff, CM (reprint author), NYU, Comprehens Epilepsy Ctr, 403 E 13th St,Rivergate Bldg,4th Floor, New York, NY 10016 USA. EM charles.zaroff@med.nyu.edu CR ASANO E, 2001, NEUROLOGY, V57, P1267 Baker P, 1998, J AUTISM DEV DISORD, V28, P279, DOI 10.1023/A:1026004501631 Barry JJ, 2002, EPILEPSY AND DEVELOPMENTAL DISABILITIES, P205 Bolton PF, 2002, BRAIN, V125, P1247, DOI 10.1093/brain/awf124 Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 BRUNI O, 1995, BRAIN DEV-JPN, V17, P52, DOI 10.1016/0387-7604(94)00118-H Buelow JM, 2002, EPILEPSY BEHAV, V3, P210, DOI 10.1016/S1525-5050(02)00024-0 Carlson B, 1999, TUBEROUS SCLEROSIS C, P85 CORNELL J, 1986, S AFR MED J, V63, P966 CURATOLO P, 1991, ANN NY ACAD SCI, V615, P8, DOI 10.1111/j.1749-6632.1991.tb37743.x Dabora SL, 2001, AM J HUM GENET, V68, P64, DOI 10.1086/316951 ETTINGER AB, 2002, PSYCHOTROPIC PROPERT, P219 NELLIST M, 1993, CELL, V75, P1305 Ferguson AP, 2002, DEV MED CHILD NEUROL, V44, P256, DOI 10.1017/S0012162201002031 GILLBERG IC, 1994, DEV MED CHILD NEUROL, V36, P50 Goodman M, 1997, J CHILD NEUROL, V12, P85 Harrison JE, 1999, AM J MED GENET, V88, P642, DOI 10.1002/(SICI)1096-8628(19991215)88:6<642::AID-AJMG12>3.0.CO;2-O HUNT A, 1993, J AUTISM DEV DISORD, V23, P323, DOI 10.1007/BF01046223 HUNT A, 1987, DEV MED CHILD NEUROL, V29, P190 HUNT A, 1983, DEV MED CHILD NEUROL, V25, P346 HUNT A, 1994, DEV MED CHILD NEUROL, V36, P108 HUNT A, 1984, J MED GENET, V21, P272, DOI 10.1136/jmg.21.4.272 Hunt A, 1998, J APPL RES INTELLECT, V11, P227 INOUE Y, 1988, NEURORADIOLOGY, V30, P379 JAMBAQUE I, 1991, DEV MED CHILD NEUROL, V33, P698 Jambaque I, 2000, EPILEPSY RES, V38, P151, DOI 10.1016/S0920-1211(99)00082-0 Joinson C, 2003, PSYCHOL MED, V33, P335, DOI 10.1017/S0033291702007092 Jozwiak S, 1998, ARCH NEUROL-CHICAGO, V55, P379, DOI 10.1001/archneur.55.3.379 KINGSLEY DPE, 1986, NEURORADIOLOGY, V28, P38 MAEDA M, 1995, J COMPUT ASSIST TOMO, V19, P660, DOI 10.1097/00004728-199507000-00033 Maki Y, 1979, Brain Dev, V1, P38 O'Callaghan FJK, 1999, DEV MED CHILD NEUROL, V41, P123, DOI 10.1017/S0012162299000237 Parker M, 1996, FAM COMMUNITY HEALTH, V19, P73 Ramesh V, 2003, BIOCHEM SOC T, V31, P579, DOI 10.1042/BST0310579 RIIKONEN R, 1981, DEV MED CHILD NEUROL, V23, P747 Roach ES, 1998, J CHILD NEUROL, V13, P624 Romanelli P, 2002, J CHILD NEUROL, V17, P689, DOI 10.1177/088307380201700907 Seri S, 1999, CLIN NEUROPHYSIOL, V110, P1825, DOI 10.1016/S1388-2457(99)00137-6 SHEPHERD CW, 1995, AM J NEURORADIOL, V16, P149 SHEPHERD CW, 1992, DEV MED CHILD NEUROL, V34, P766 Slegtenhorst MV., 1997, SCIENCE, V277, P805, DOI 10.1126/science.277.5327.805 SMALLEY SL, 1992, J AUTISM DEV DISORD, V22, P339, DOI 10.1007/BF01048239 UMAPATHY D, 1989, J MENT DEFIC RES, V33, P349 Vogt H, 1908, MON PSYCHIATR NEUROL, V24, P106 Walz NC, 2002, J CHILD NEUROL, V17, P830, DOI 10.1177/08830738020170111401 WEBB DW, 1991, ARCH DIS CHILD, V66, P1375 WEBB DW, 1991, J MED GENET, V28, P395, DOI 10.1136/jmg.28.6.395 Weber AM, 2000, J AUTISM DEV DISORD, V30, P511, DOI 10.1023/A:1005679108529 NR 48 TC 15 Z9 15 PU B C DECKER INC PI HAMILTON PA 20 HUGHSON ST SOUTH, PO BOX 620, L C D 1, HAMILTON, ONTARIO L8N 3K7, CANADA SN 0883-0738 J9 J CHILD NEUROL JI J. Child Neurol. PD NOV PY 2004 VL 19 IS 11 BP 847 EP 852 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 920PW UT WOS:000228703600001 PM 15658788 ER PT J AU Aldred, C Green, J Adams, C AF Aldred, C Green, J Adams, C TI A new social communication intervention for children with autism: pilot randomised controlled treatment study suggesting effectiveness SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; intervention; treatment; social communication; RCT ID CONTROLLED-TRIAL; YOUNG-CHILDREN; ASPERGER-SYNDROME; CONDUCT DISORDER; BEHAVIOR; DEFICITS; PROGRAM; ADOLESCENTS; CAREGIVERS; MOTHERS AB Background: Psychosocial treatments are the mainstay of management of autism in the UK but there is a notable lack of a systematic evidence base for their effectiveness. Randomised controlled trial (RCT) studies in this area have been rare but are essential because of the developmental heterogeneity of the disorder. We aimed to test a new theoretically based social communication intervention targeting parental communication in a randomised design against routine care alone. Methods: The intervention was given in addition to existing care and involved regular monthly therapist contact for 6 months with a further 6 months of 2-monthly consolidation sessions. It aimed to educate parents and train them in adapted communication tailored to their child's individual competencies. Twenty-eight children with autism were randomised between this treatment and routine care alone, stratified for age and baseline severity. Outcome was measured at 12 months from commencement of intervention, using standardised instruments. Results: All cases studied met full Autism Diagnostic Interview (ADI) criteria for classical autism. Treatment and controls had similar routine care during the study period and there were no study dropouts after treatment had started. The active treatment group showed significant improvement compared with controls on the primary outcome measure - Autism Diagnostic Observation Schedule (ADOS) total score, particularly in reciprocal social interaction - and on secondary measures of expressive language, communicative initiation and parent-child interaction. Suggestive but non-significant results were found in Vineland Adaptive Behaviour Scales (Communication Subdomain) and ADOS stereotyped and restricted behaviour domain. Conclusions: A Randomised Treatment Trial design of this kind in classical autism is feasible and acceptable to patients. This pilot study suggests significant additional treatment benefits following a targeted (but relatively non-intensive) dyadic social communication treatment, when compared with routine care. The study needs replication on larger and independent samples. It should encourage further RCT designs in this area. C1 Booth Hall Childrens Hosp, Acad Dept Child Psychiat, Manchester M9 7AA, Lancs, England. Univ Manchester, Human Commun & Deafness Grp, Manchester, Lancs, England. RP Green, J (reprint author), Booth Hall Childrens Hosp, Acad Dept Child Psychiat, Manchester M9 7AA, Lancs, England. EM jonathan.green@man.ac.uk CR Abidin R., 1995, PARENTAL STRESS INDE Adams C, 2002, J CHILD PSYCHOL PSYC, V43, P679, DOI 10.1111/1469-7610.00056 AGERFLUSBERG H, 1993, UNDERSTANDING OTHERS, P138 ALDRED CR, 2001, J ED CHILD PSYCHOL, V18, P76 Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Baker N. 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Child Psychol. Psychiatry PD NOV PY 2004 VL 45 IS 8 BP 1420 EP 1430 DI 10.1111/j1469-7610.2004.00338.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 865BS UT WOS:000224678100010 PM 15482502 ER PT J AU Bishop, DVM Maybery, M Maley, A Wong, D Hill, W Hallmayer, J AF Bishop, DVM Maybery, M Maley, A Wong, D Hill, W Hallmayer, J TI Using self-report to identify the broad phenotype in parents of children with autistic spectrum disorders: a study using the Autism-Spectrum Quotient SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; genetics; family; questionnaire; broad phenotype ID FAMILY-HISTORY; FUNCTIONING AUTISM; INDIVIDUALS; RELATIVES; PATTERNS AB Background: The concept of the 'broad phenotype' of autism refers to the finding that relatives of people with autism often have mild forms of autistic-like characteristics, such as social and communicative difficulties. This study used the Autism Spectrum Quotient (AQ), a questionnaire devised to assess features of the broad phenotype in adults, with parents of people with autism, to see whether they would be more likely to obtain extreme scores than a control group. Methods: The AQ was administered to parents of 69 people with an autism spectrum disorder and parents of 52 controls. Results: On two of the five subscales of the AQ, social skills and communication, parents of people with autism obtained higher scores than control parents. The other three scales, attention to detail, attention switching, and imagination, did not differentiate groups. The correlation between social skills and communication scales was .663. The scales can be combined to give an index of broad phenotype. Conclusions: The AQ appears to be sensitive to the broad phenotype, provided attention is restricted to the social skills and communication scales. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. Univ Western Australia, Nedlands, WA 6009, Australia. Stanford Univ, Stanford, CA 94305 USA. RP Bishop, DVM (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. EM dorothy.bishop@psy.ox.ac.uk RI Maybery, Murray/H-5390-2014 CR Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 BAILEY A, 1995, PSYCHOL MED, V25, P63 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Baron-Cohen S, 2003, PHILOS T ROY SOC B, V358, P361, DOI 10.1098/rstb.2002.1206 Berument SK, 1999, BRIT J PSYCHIAT, V175, P444, DOI 10.1192/bjp.175.5.444 BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x FOLSTEIN S, 1977, NATURE, V265, P726, DOI 10.1038/265726a0 Folstein SE, 1999, J CHILD PSYCHOL PSYC, V40, P1117, DOI 10.1017/S0021963099004461 Fombonne E, 1997, J CHILD PSYCHOL PSYC, V38, P667, DOI 10.1111/j.1469-7610.1997.tb01694.x LANDA R, 1992, PSYCHOL MED, V22, P245 LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 Piven J, 1997, AM J PSYCHIAT, V154, P185 Rutter M, 2000, J ABNORM CHILD PSYCH, V28, P3, DOI 10.1023/A:1005113900068 Szatmari P, 2000, J CHILD PSYCHOL PSYC, V41, P579, DOI 10.1017/S0021963099005831 Wechsler D., 1997, WECHSLER ADULT INTEL, VIII WOLFF S, 1988, J CHILD PSYCHOL PSYC, V29, P143, DOI 10.1111/j.1469-7610.1988.tb00699.x NR 17 TC 94 Z9 97 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 PD NOV PY 2004 VL 45 IS 8 BP 1431 EP 1436 DI 10.1111/j.1469-7610.2004.00325.x PG 6 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 865BS UT WOS:000224678100011 PM 15482503 ER PT J AU Geurts, HM Verte, S Osterlaan, J Roeyers, H Hartman, CA Mulder, EJ van Berckelaer-Onnes, IA Sergeant, JA AF Geurts, HM Verte, S Osterlaan, J Roeyers, H Hartman, CA Mulder, EJ van Berckelaer-Onnes, IA Sergeant, JA TI Can the Children's Communication Checklist differentiate between children with autism, children with ADHD, and normal controls? SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE pragmatics; CCC; ADHD; autism ID DEFICIT-HYPERACTIVITY DISORDER; ATTENTION-DEFICIT/HYPERACTIVITY DISORDER; PSYCHIATRICALLY DISTURBED-CHILDREN; DEVELOPMENTAL LANGUAGE DISORDERS; DIAGNOSTIC INTERVIEW; BEHAVIORAL-CHARACTERISTICS; EXECUTIVE FUNCTIONS; SPECTRUM DISORDERS; MIND; IMPAIRMENT AB Background: The Children's Communication Checklist (CCC; Bishop, 1998) is a questionnaire that was developed to measure pragmatic language use and may be completed by parents and teachers. Two studies are reported, which were designed to investigate: (1) whether children with Attention Deficit Hyperactivity Disorder (ADHD) encounter pragmatic language problems in comparison with normal controls (NC), (2) whether children with ADHD and children with High Functioning Autism (HFA) can be differentiated using the CCC, (3) the usefulness of the CCC for parents and teachers in a clinical and in a research setting, and (4) the role of age in pragmatic language use in ADHD and HFA. Method: In the first study (clinical sample) 50 children with ADHD, 50 children with HFA, and 50 NC were compared to each other using the CCC. In the second study (research sample) CCC data was gathered on 23 children with ADHD (without co-morbid disorders), 42 children with HFA, and 35 NC. Results: Compared to NC, children with HFA showed pragmatic deficits on all CCC scales. Children with ADHD demonstrated deficits compared to NC as well. Moreover, the ADHD and HFA groups differed from each other on most of the scales. Discriminant analyses showed that CCC scales were relevant for case identification in these samples. Furthermore, profiles of impairment seen in children with HFA and ADHD did not vary with age. Conclusion: Pragmatic difficulties do occur in both HFA and ADHD. The present studies indicate that the CCC is a useful instrument to obtain information concerning pragmatic language use in both a clinical and a research setting. Although the information of parents is more tightly linked to the diagnosis, combining the information of both parent and teacher slightly improves case identification. C1 Vrije Univ Amsterdam, Dept Clin Neuropsychol, Amsterdam, Netherlands. State Univ Ghent, Dept Psychol, B-9000 Ghent, Belgium. Univ Groningen, Dept Psychiat, Groningen, Netherlands. Leiden Univ, Dept Educ Sci, Leiden, Netherlands. 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Child Psychol. Psychiatry PD NOV PY 2004 VL 45 IS 8 BP 1437 EP 1453 DI 10.1111/j.1469-7610.2004.00326.x PG 17 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 865BS UT WOS:000224678100012 PM 15482504 ER PT J AU Ashwood, P Anthony, A Torrente, F Wakefield, AJ AF Ashwood, P Anthony, A Torrente, F Wakefield, AJ TI Spontaneous mucosal lymphocyte cytokine profiles in children with autism and gastrointestinal symptoms: Mucosal immune activation and reduced counter regulatory interleukin-10 SO JOURNAL OF CLINICAL IMMUNOLOGY LA English DT Article DE inflammation; mucosa; TNF alpha; IL-10 ID DEVELOPMENTAL REGRESSION; DISORDERS; RESPONSES; INNATE AB A lymphocytic enterocolitis has been reported in a cohort of children with autistic spectrum disorder (ASD) and gastrointestinal (GI) symptoms. This study tested the hypothesis that dysregulated intestinal mucosal immunity with enhanced proinflammatory cytokine production is present in these ASD children. Comparison was made with developmentally normal children with, and without, mucosal inflammation. Duodenal and colonic biopsies were obtained from 21 ASD children, and 65 developmentally normal paediatric controls, of which 38 had signs of histological inflammation. Detection of CD3(+) lymphocyte staining for spontaneous intracellular TNFalpha, IL-2, IL-4, IFNgamma, and IL-10, was performed by multicolor flow cytometry. Duodenal and colonic mucosal CD3(+) lymphocyte counts were elevated in ASD children compared with noninflamed controls (p<0.03). In the duodenum, the proportion of lamina propria ( LP) and epithelial CD3(+) TNF alpha(+) cells in ASD children was significantly greater compared with noninflamed controls (p<0.002) but not coeliac disease controls. In addition, LP and epithelial CD3(+) IL-2(+) and CD3(+) IFNgamma(+), and epithelial CD3(+) IL-4(+) cells were more numerous in ASD children than in noninflamed controls (p<0.04). In contrast, CD3(+)IL-10(+) cells were fewer in ASD children than in noninflamed controls (p<0.05). In the colon, LP CD3(+) TNFalpha(+) and CD3(+) IFNgamma(+) were more frequent in ASD children than in noninflamed controls (p<0.01). In contrast with Crohn's disease and non-Crohn's colitis, LP and epithelial CD3(+)IL-10(+) cells were fewer in ASD children than in nondisease controls (p<0.01). There was a significantly greater proportion of CD3(+) TNFalpha(+) cells in colonic mucosa in those ASD children who had no dietary exclusion compared with those on a gluten and/or casein free diet (p<0.05). There is a consistent profile of CD3(+) lymphocyte cytokines in the small and large intestinal mucosa of these ASD children, involving increased pro-inflammatory and decreased regulatory activities. The data provide further evidence of a diffuse mucosal immunopathology in some ASD children and the potential for benefit of dietary and immunomodulatory therapies. C1 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. Thoughtful House Ctr Children, Austin, TX USA. Int Child Dev Resource Ctr, Boca Raton, FL USA. RP Ashwood, P (reprint author), Univ Calif Davis, Genome & Biomed Sci Facil, Div Rheumatol Allergy & Clin Immunol, 451 E Hlth Sci Dr,Suite 6510, Davis, CA 95616 USA. 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Clin. Immunol. PD NOV PY 2004 VL 24 IS 6 BP 664 EP 673 DI 10.1007/s10875-004-6241-6 PG 10 WC Immunology SC Immunology GA 882UA UT WOS:000225962800010 PM 15622451 ER PT J AU Perry, R AF Perry, R TI Early diagnosis of Asperger's disorder: Lessons from a large clinical practice SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Article ID HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS C1 NYU, Sch Med, New York, NY USA. Bellevue Hosp Ctr, Pediat Consultat Liaison Unit, New York, NY USA. RP Perry, R (reprint author), 55 W 74th St, New York, NY 10023 USA. 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PD NOV 1 PY 2004 VL 129 IS 18 BP 109 EP 109 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 867FI UT WOS:000224827400179 ER PT J AU Guedeney, A Dumond, C Grasso, F Starakis, N AF Guedeney, A Dumond, C Grasso, F Starakis, N TI Social withdrawal behaviour in infant: clinical and research interest SO M S-MEDECINE SCIENCES LA French DT Article ID ALARM DISTRESS SCALE; DEPRESSION; CHILDREN; VALIDITY AB The social withdrawal behaviour concept is presented, along with its historical background and its links to infant depression. Sustained social withdrawal behaviour in infancy is observed either with attachment disorders, in autism, sensory Impairment, intense and chronic pain, or in interaction disorders and as effects of maternal depression on the infant. The alarm distress baby scale (ADBB) is a 8 item-assessment scale. It has been built to help screening early withdrawal behaviour, making use for example of the routine physical examination in a Well Baby clinic. Current clinical and research application and validations of the scale are presented. C1 Univ Paris 07, Serv Psychiat Infanto Juvenile, Intersecteur 18, Fac Med Xavier Bichat,Hop Bichat Claude Bernard,P, F-75018 Paris, France. DASES, Paris, France. Univ Sienne, Siena, Italy. RP Guedeney, A (reprint author), Univ Paris 07, Serv Psychiat Infanto Juvenile, Intersecteur 18, Fac Med Xavier Bichat,Hop Bichat Claude Bernard,P, 124 Blvd Ney, F-75018 Paris, France. 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PD NOV 1 PY 2004 VL 181 IS 9 BP 514 EP 515 PG 2 WC Medicine, General & Internal SC General & Internal Medicine GA 868XE UT WOS:000224945600018 PM 15516200 ER PT J AU [Anonymous] AF [Anonymous] TI Calcium tied to autism SO NATURE MEDICINE LA English DT News Item CR SPLAWSKI I, CELL, V119, P19 NR 1 TC 0 Z9 0 PU NATURE PUBLISHING GROUP PI NEW YORK PA 345 PARK AVE SOUTH, NEW YORK, NY 10010-1707 USA SN 1078-8956 J9 NAT MED JI Nat. Med. PD NOV PY 2004 VL 10 IS 11 BP 1172 EP 1172 PG 1 WC Biochemistry & Molecular Biology; Cell Biology; Medicine, Research & Experimental SC Biochemistry & Molecular Biology; Cell Biology; Research & Experimental Medicine GA 866PR UT WOS:000224785900029 ER PT J AU Takahashi, H Yahata, N Koeda, M Matsuda, T Asai, K Okubo, Y AF Takahashi, H Yahata, N Koeda, M Matsuda, T Asai, K Okubo, Y TI Brain activation associated with evaluative processes of guilt and embarrassment: an fMRI study SO NEUROIMAGE LA English DT Article DE guilt; embarrassment; social cognition; theory of mind; medial prefrontal cortex; superior temporal sulcus ID SOCIAL COGNITION; FRONTOTEMPORAL DEMENTIA; MIND; EMOTION; BEHAVIOR; AUTISM; SCHIZOPHRENIA; PERCEPTION; DAMAGE; PET AB We aimed to investigate the neural substrates associated with evaluative process of moral emotions. Using functional magnetic resonance imaging (fMRI), we examined the similarities and differences between evaluative process of guilt and that of embarrassment at the neural basis level. Study of the neural basis of judgments of moral emotions might contribute to a better understanding of the amoral behavior observed in neurological and psychiatric disorders. Nineteen healthy volunteers were studied. The participants read sentences carrying neutral, guilty, or embarrassing contents during the scans. Both guilt and embarrassment conditions commonly activated the medial prefrontal cortex (MPFC), left posterior superior temporal sulcus (STS), and visual cortex. Compared to guilt condition, embarrassment condition produced greater activation in the right temporal cortex (anterior), bilateral hippocampus, and visual cortex. Most of these regions have been implicated in the neural substrate of social cognition or Theory of Mind (ToM). Our results support the idea that both are self-conscious emotions, which are social emotions requiring the ability to represent the mental states of others. At the same time, our functional fMRI data are in favor of the notion that evaluative process of embarrassment might be a more complex process than that of guilt. (C) 2004 Elsevier Inc. All rights reserved. C1 Nippon Med Coll, Dept Neuropsychiat, Bunkyo Ku, Tokyo 1138603, Japan. Tokyo Med & Dent Univ, Grad Sch Med, Sect Psychiat & Behav Sci, Tokyo, Japan. Tokyo Med & Dent Univ, Med Res Inst, Dept Bioinformat, Tokyo, Japan. Tamagawa Univ, Inst Res, Brain Activ Imaging Ctr, Tokyo, Japan. RP Okubo, Y (reprint author), Nippon Med Coll, Dept Neuropsychiat, Bunkyo Ku, 1-1-5,Sendagi, Tokyo 1138603, Japan. 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SO PEDIATRICS LA English DT Editorial Material ID ENDOGENOUS OPIOIDS; MORPHINE; BIRTH; ANALGESIA; FENTANYL; CHILDREN; AUTISM; ABNORMALITIES; BEHAVIOR; EXPOSURE C1 George Washington Univ, Dept Neonatol, Washington, DC 20037 USA. Childrens Natl Med Ctr, Washington, DC 20037 USA. RP Aly, H (reprint author), 900 23rd St NW,Suite G-2092, Washington, DC 20037 USA. 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Yale Univ, Sch Med, Ctr Child Study, New Haven, CT 06510 USA. Tufts Univ, New England Med Ctr, Sch Med,Floating Hosp Children, Ctr Children Special Needs, Boston, MA 02111 USA. RP Stein, MT (reprint author), Univ Calif San Diego, La Jolla, CA 92093 USA. CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT JESSOP DJ, 1994, PEDIATRICS, V93, P602 Klin A., 1997, HDB AUTISM PERVASIVE, P94 KLIN A, 1995, J CHILD PSYCHOL PSYC, V36, P1127, DOI 10.1111/j.1469-7610.1995.tb01361.x Klin A, 2003, PHILOS T ROY SOC B, V358, P345, DOI 10.1098/rstb.2002.1202 KLIN A, 1997, HDB AUTISM PERVASIVE, P411 Lord C., 1999, ADOS G AUTISM DIAGNO LORD C, 1994, J AUTISM DEV DISORD, V24, P659, DOI 10.1007/BF02172145 National Research Council, 2001, ED CHILDR AUT Perrin J. M., 1993, HOME COMMUNITY CARE Rourke B. P, 1989, NONVERBAL LEARNING D Rourke BP, 2002, ANNU REV PSYCHOL, V53, P309, DOI 10.1146/annurev.psych.53.100901.135204 Stein MT, 2004, J DEV BEHAV PEDIATR, V25, P190, DOI 10.1097/00004703-200406000-00008 Stein MT, 2001, J DEV BEHAV PEDIATR, V22, P188 Volkmar F. R., 2000, ASPERGER SYNDROME, P340 Wolraich M, 1996, CLASSIFICATION CHILD NR 16 TC 1 Z9 1 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD NOV PY 2004 VL 114 IS 5 SU S BP 1458 EP 1463 DI 10.1542/peds.2004-1721L PG 6 WC Pediatrics SC Pediatrics GA 867LB UT WOS:000224843000013 ER PT J AU Shea, S Turgay, A Carroll, A Schulz, M Orlik, H Smith, I Dunbar, F AF Shea, S Turgay, A Carroll, A Schulz, M Orlik, H Smith, I Dunbar, F TI Risperidone in the treatment of disruptive behavioral symptoms in children with autistic and other pervasive developmental disorders SO PEDIATRICS LA English DT Article DE autistic disorder; pervasive developmental disorders; risperidone ID RATING-SCALE; PRESCHOOL-CHILDREN; YOUNG-CHILDREN; OPEN TRIAL; ADOLESCENTS; TOLERABILITY; MONOTHERAPY; TERM AB Objective. To investigate the efficacy and safety of risperidone for the treatment of disruptive behavioral symptoms in children with autism and other pervasive developmental disorders (PDD). Methods. In this 8-week, randomized, double-blind, placebo-controlled trial, risperidone/placebo solution (0.01-0.06 mg/kg/day) was administered to 79 children who were aged 5 to 12 years and had PDD. Behavioral symptoms were assessed using the Aberrant Behavior Checklist (ABC), Nisonger Child Behavior Rating Form, and Clinical Global Impression-Change. Safety assessments included vital signs, electrocardiogram, extrapyramidal symptoms, adverse events, and laboratory tests. Results. Subjects who were taking risperidone ( mean dosage: 0.04 mg/kg/day; 1.17 mg/day) experienced a significantly greater mean decrease on the irritability subscale of the ABC (primary endpoint) compared with those who were taking placebo. By study endpoint, risperidone-treated subjects exhibited a 64% improvement over baseline in the irritability score almost double that of placebo-treated subjects (31%). Risperidone-treated subjects also exhibited significantly greater decreases on the other 4 subscales of the ABC; on the conduct problem, insecure/anxious, hyperactive, and overly sensitive subscales of the Nisonger Child Behavior Rating Form ( parent version); and on the Visual Analog Scale of the most troublesome symptom. More risperidone-treated subjects (87%) showed global improvement in their condition compared with the placebo group (40%). Somnolence, the most frequently reported adverse event, was noted in 72.5% versus 7.7% of subjects (risperidone vs placebo) and seemed manageable with dose/dose-schedule modification. Risperidone-treated subjects experienced statistically significantly greater increases in weight (2.7 vs 1.0 kg), pulse rate, and systolic blood pressure. Extrapyramidal symptoms scores were comparable between groups. Conclusions. Risperidone was well tolerated and efficacious in treating behavioral symptoms associated with PDD in children. C1 IWK Hlth Ctr, Dev Clin, Halifax, NS B3J 3G9, Canada. Dalhousie Univ, Halifax, NS, Canada. Univ Toronto, Toronto, ON, Canada. Glenrose Rehabil Hosp, Edmonton, AB, Canada. SciAn Clin, Etobicoke, ON, Canada. Janssen Ortho Inc, Toronto, ON, Canada. RP Shea, S (reprint author), IWK Hlth Ctr, Dev Clin, 5850 Univ Ave,8th Fl, Halifax, NS B3J 3G9, Canada. EM sarah.shea@iwk.nshealth.ca CR Aman M., 1986, ABERRANT BEHAV CHECK AMAN MG, 1985, AM J MENT DEF, V89, P485 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th CAMPBELL M, 1995, COMPREHENSIVE TXB PS, V4, P2277 Casaer P, 1994, PEDIATR NEUROL, V11, P89, DOI 10.1016/0887-8994(94)90174-0 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 CHOUINARD G, 1980, CAN J NEUROL SCI, V7, P233 Findling RL, 1997, PSYCHOPHARMACOL BULL, V33, P155 Fisman S, 1996, J CHILD ADOL PSYCHOP, V6, P177, DOI 10.1089/cap.1996.6.177 *JANSS ORTH INC, RISP PROD MON JANSSEN PAJ, 1988, J PHARMACOL EXP THER, V244, P685 LEYSEN JE, 1988, J PHARMACOL EXP THER, V247, P661 Malone RP, 2002, J AM ACAD CHILD PSY, V41, P140, DOI 10.1097/00004583-200202000-00007 Masi G, 2001, J CHILD NEUROL, V16, P395, DOI 10.1177/088307380101600602 Masi G, 2001, J AM ACAD CHILD PSY, V40, P1206, DOI 10.1097/00004583-200110000-00015 McDougle CJ, 2000, CHILD ADOL PSYCH CL, V9, P201 McDougle CJ, 1997, J AM ACAD CHILD PSY, V36, P685, DOI 10.1097/00004583-199705000-00020 Nicolson R, 1998, J AM ACAD CHILD PSY, V37, P372, DOI 10.1097/00004583-199804000-00014 OWENS DGC, 1994, J CLIN PSYCHIAT, V55, P29 Perry R, 1997, J CHILD ADOL PSYCHOP, V7, P167, DOI 10.1089/cap.1997.7.167 Posey DJ, 2000, HARVARD REV PSYCHIAT, V8, P45, DOI 10.1093/hrp/8.2.45 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 Schopler E., 1986, CHILDHOOD AUTISM RAT SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P91, DOI 10.1007/BF02408436 Tasse MJ, 1996, RES DEV DISABIL, V17, P59, DOI 10.1016/0891-4222(95)00037-2 Turgay A., 2002, PEDIATRICS, V110 VOLKMAR FR, 1996, CHILD ADOL PSYCH CL, P489 Zuddas A, 2000, J CHILD ADOL PSYCHOP, V10, P79, DOI 10.1089/cap.2000.10.79 NR 28 TC 155 Z9 158 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD NOV PY 2004 VL 114 IS 5 BP E634 EP E641 DI 10.1542/peds.2003-0264-F PG 8 WC Pediatrics SC Pediatrics GA 867KY UT WOS:000224842700062 PM 15492353 ER PT J AU Kritskaya, VP Meleshko, TK AF Kritskaya, VP Meleshko, TK TI Pathopsychological syndrome in system research of mental activity pathology SO PSIKHOLOGICHESKII ZHURNAL LA Russian DT Article DE system approach; pathopsychological syndrome; autism; social direction; self-regulation; longitude; psychological correction. ID VOLUNTARY ACTIVITY; SELF-REGULATION AB The pathopsychological syndrome, specific for schizotypic and schizophrenic pathology is defined. The longitudinal data are-described,possessed to trace the dynamic of components of named syndrome. The ways of application of system approach from the position of pathopsychological syndrome to the developing the problems of differential diagnostic and psychological correction of patients with endogenious psychosis are pointed out. C1 SCMH RAMS, Dept Clin Psychol, Moscow, Russia. RP Kritskaya, VP (reprint author), SCMH RAMS, Dept Clin Psychol, Moscow, Russia. 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RP Geller, JL (reprint author), Univ Massachusetts, Sch Med, Worcester, MA USA. CR KARASIK P, 2003, RIDE TOGETHER BROTHE NR 1 TC 1 Z9 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD NOV PY 2004 VL 55 IS 11 BP 1320 EP 1322 DI 10.1176/appi.ps.55.11.1320 PG 3 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 866MW UT WOS:000224778600034 ER PT J AU Geller, JL AF Geller, JL TI The boy who loved windows: Opening the heart and mind of a child threatened with autism SO PSYCHIATRIC SERVICES LA English DT Book Review C1 Univ Massachusetts, Sch Med, Worcester, MA USA. RP Geller, JL (reprint author), Univ Massachusetts, Sch Med, Worcester, MA USA. CR Stacey Patricia, 2003, BOY WHO LOVED WINDOW NR 1 TC 1 Z9 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD NOV PY 2004 VL 55 IS 11 BP 1320 EP 1322 DI 10.1176/appi.ps.55.11.1320 PG 3 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 866MW UT WOS:000224778600033 ER PT J AU Geller, JL AF Geller, JL TI A different kind of boy: A father's memoir of raising a gifted child with autism SO PSYCHIATRIC SERVICES LA English DT Book Review C1 Univ Massachusetts, Sch Med, Worcester, MA USA. RP Geller, JL (reprint author), Univ Massachusetts, Sch Med, Worcester, MA USA. CR MONT D, 2001, DIFFERENT KIND BOY F NR 1 TC 1 Z9 1 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD NOV PY 2004 VL 55 IS 11 BP 1320 EP 1322 DI 10.1176/appi.ps.55.11.1320 PG 3 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 866MW UT WOS:000224778600032 ER PT J AU Park, CC AF Park, CC TI Autism: From research to individualized practice SO PSYCHIATRIC SERVICES LA English DT Book Review C1 Williams Coll, Williamstown, MA 01267 USA. RP Park, CC (reprint author), Williams Coll, Williamstown, MA 01267 USA. CR GABRIELS RL, 2000, AUTISM RES INDIVIDUA NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 EI 1557-9700 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD NOV PY 2004 VL 55 IS 11 BP 1323 EP 1324 PG 2 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 866MW UT WOS:000224778600036 ER PT J AU Haynes, K Geller, J AF Haynes, K Geller, J TI Songs of the gorilla nation: My journey through autism SO PSYCHIATRIC SERVICES LA English DT Book Review CR Prince-Hughes Dawn, 2004, SONGS GORILLA NATION NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD NOV PY 2004 VL 55 IS 11 BP 1324 EP 1326 DI 10.1176/appi.ps.55.11.1324 PG 3 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 866MW UT WOS:000224778600040 ER PT J AU Tantam, D AF Tantam, D TI A parents' guide to Asperger syndrome and high-functioning autism: How to meet the challenges and help your child thrive SO PSYCHIATRIC SERVICES LA English DT Book Review C1 Univ Sheffield, Sch Hlth & Related Res, Ctr Study Conflict Reconciliat, Sheffield S10 2TN, S Yorkshire, England. RP Tantam, D (reprint author), Univ Sheffield, Sch Hlth & Related Res, Ctr Study Conflict Reconciliat, Sheffield S10 2TN, S Yorkshire, England. CR OZONOFF S, 2002, PARTENS GUIDE ASPERG NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD NOV PY 2004 VL 55 IS 11 BP 1327 EP 1328 DI 10.1176/appi.ps.55.11.1327 PG 2 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 866MW UT WOS:000224778600044 ER PT J AU Isaacson, B AF Isaacson, B TI Helping children with autism learn: A guide to treatment approaches for parents and professionals SO PSYCHIATRIC SERVICES LA English DT Book Review CR Siegel B., 2003, HELPING CHILDREN AUT NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD NOV PY 2004 VL 55 IS 11 BP 1328 EP 1328 DI 10.1176/appi.ps.55.11.1328 PG 1 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 866MW UT WOS:000224778600045 ER PT J AU Volkmar, FR AF Volkmar, FR TI Autism spectrum disorders: A research review for practitioners SO PSYCHIATRIC SERVICES LA English DT Book Review C1 Yale Univ, Sch Med, Child Study Ctr, New Haven, CT 06520 USA. RP Volkmar, FR (reprint author), Yale Univ, Sch Med, Child Study Ctr, New Haven, CT 06520 USA. CR OZONOGG S, 2003, AUTISM SPECTRUM DISO NR 1 TC 0 Z9 0 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 1075-2730 J9 PSYCHIAT SERV JI Psychiatr. Serv. PD NOV PY 2004 VL 55 IS 11 BP 1328 EP 1329 DI 10.1176/appi.ps.55.11.1328-a PG 2 WC Health Policy & Services; Public, Environmental & Occupational Health; Psychiatry SC Health Care Sciences & Services; Public, Environmental & Occupational Health; Psychiatry GA 866MW UT WOS:000224778600046 ER PT J AU Schiffman, J Lam, CW Jiwatram, T Ekstrom, M Sorensen, H Mednick, S AF Schiffman, J Lam, CW Jiwatram, T Ekstrom, M Sorensen, H Mednick, S TI Perspective-taking deficits in people with schizophrenia spectrum disorders: a prospective investigation SO PSYCHOLOGICAL MEDICINE LA English DT Article ID MIND; CHILDREN; AUTISM; SKILLS AB Background. This study examined data from a Danish prospective longitudinal project in attempt to address the state/trait controversy regarding theory of mind deficits in schizophrenia. Deficits in nperspective-taking - a component of theory of mind - were investigated prospectively among children who developed schizophrenia spectrum disorders as adults in comparison to children who did not develop schizophrenia spectrum disorders. Method. A total of 265 high risk and control subjects were studied in 1972. At the time of initial assessment, the Role-Taking Task (RTT) was administered. Two hundred and forty-two of these children were evaluated in 1992 during follow-up examinations. Sixteen developed schizophrenia, 10 developed a schizophrenia spectrum disorder, 70 had outcomes of other psychopathology, and 146 did not develop a mental illness. Results. Children who later developed schizophrenia or a schizophrenia spectrum disorder had lower RTT scores, controlling for verbal IQ and age, compared to those who did not develop any mental illness. Although in the expected direction, RTT scores for those with schizophrenia spectrum disorders were not significantly different from those who developed a non-psychotic disorder. Conclusions. Deficits in perspective-taking among children who later developed schizophrenia spectrum disorders suggest that a facet of theory of mind is impaired prior to development of schizophrenia. Our findings lend support to the hypothesis that theory of mind deficits in schizophrenia are trait markers of the disorder. C1 Univ Hawaii Manoa, Dept Psychol, Honolulu, HI 96822 USA. Univ Copenhagen Hosp, Inst Prevent Med, DK-2100 Copenhagen, Denmark. Univ So Calif, Social Sci Res Inst, Los Angeles, CA 90089 USA. RP Schiffman, J (reprint author), Univ Hawaii Manoa, Dept Psychol, 2430 Campus Rd,Gartley Hall 110, Honolulu, HI 96822 USA. 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Med. PD NOV PY 2004 VL 34 IS 8 BP 1581 EP 1586 DI 10.1017/S0033291704002703 PG 6 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 878XM UT WOS:000225680700020 PM 15724888 ER PT J AU Blaxill, MF AF Blaxill, MF TI What's going on? The question of time trends in Autism SO PUBLIC HEALTH REPORTS LA English DT Editorial Material ID PERVASIVE DEVELOPMENTAL DISORDERS; ET-AL. 2002; INFANTILE-AUTISM; CHANGING PREVALENCE; SPECTRUM DISORDERS; CHILDHOOD AUTISM; EPIDEMIOLOGIC SURVEY; PRESCHOOL-CHILDREN; TOTAL POPULATION; RUBELLA VACCINE AB Increases in the reported prevalence of autism and autistic spectrum disorders in recent years have fueled concern over possible environmental causes. The author reviews the available survey literature and finds evidence of large increases in prevalence in both the United States and the United Kingdom that cannot be explained by changes in diagnostic criteria or improvements in case ascertainment. Incomplete ascertainment of autism cases in young child populations is the largest source of predictable bias in prevalence surveys; however, this bias has, if anything, worked against the detection of an upward trend in recent surveys. Comparison of autism rates by year of birth for specific geographies provides the strongest basis for trend assessment. Such comparisons show large recent increases in rates of autism and autistic spectrum disorders in both the U.S. and the U.K. Reported rates of autism in the United States increased from <3 per 10,000 children in the 1970s to >30 per 10,000 children in the 1990s, a 10-fold increase. In the United Kingdom, autism rates rose from <10 per 10,000 in the 1980s to roughly 30 per 10,000 in the 1990s. Reported rates for the full spectrum of autistic disorders rose from the 5 to 10 per 10,000 range to the 50 to 80 per 10,000 range in the two countries. 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PD NOV-DEC PY 2004 VL 119 IS 6 BP 536 EP 551 DI 10.1016/j.phr.2004.09.003 PG 16 WC Public, Environmental & Occupational Health SC Public, Environmental & Occupational Health GA 864XB UT WOS:000224665200004 PM 15504445 ER PT J AU Williams, JHG Massaro, DW Peel, NJ Bosseler, A Suddendorf, T AF Williams, JHG Massaro, DW Peel, NJ Bosseler, A Suddendorf, T TI Visual-auditory integration during speech imitation in autism SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE autistic disorder; speech perception; audio-visual integration; imitation; mirror neurons ID MIRROR NEURONS; CORTEX; PERCEPTION; INDIVIDUALS; CHILDREN; BRAIN AB Children with autistic spectrum disorder (ASD) may have poor audio-visual integration, possibly reflecting dysfunctional 'mirror neuron' systems which have been hypothesised to be at the core of the condition. In the present study, a computer program, utilizing speech synthesizer software and a 'virtual' head (Baldi), delivered speech stimuli for identification in auditory, visual or bimodal conditions. Children with ASD were poorer than controls at recognizing stimuli in the unimodal conditions, but once performance on this measure was controlled for, no group difference was found in the bimodal condition. A group of participants with ASD were also trained to develop their speech-reading ability. Training improved visual accuracy and this also improved the children's ability to utilize visual information in their processing of speech. Overall results were compared to predictions from mathematical models based on integration and non-integration, and were most consistent with the integration model. We conclude that, whilst they are less accurate in recognizing stimuli in the unimodal condition, children with ASD show normal integration of visual and auditory speech stimuli. 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Studies on the homologous Ca(v)1.2 channel revealed non-canonical CaM interactions, providing a framework for exploring Na+ channels. In contrast to previous reports, we found that Ca2+ does not bind directly to Na+ channel C termini. Rather, Ca2+ sensitivity appears to be mediated by CaM bound to the C termini in a manner that differs significantly from CaM regulation of Ca(v)1.2. In Na(v)1.2 or Na(v)1.5, CaM bound to a localized region containing the IQ motif and did not support the large Ca2+-dependent conformational change seen in the Ca(v)1.2 . CaM complex. Furthermore, CaM binding to Na(v)1 C termini lowered Ca2+ binding affinity and cooperativity among the CaM-binding sites compared with CaM alone. Nonetheless, we found suggestive evidence for Ca2+/CaM-dependent effects upon Na(v)1 channels. The R1902C autism mutation conferred a Ca2+-dependent conformational change in Na(v)1.2 C terminus . CaM complex that was absent in the wild-type complex. In Na(v)1.5, CaM modulates the C-terminal interaction with the III-IV linker, which has been suggested as necessary to stabilize the inactivation gate, to minimize sustained channel activity during depolarization, and to prevent cardiac arrhythmias that lead to sudden death. Together, these data offer new biochemical evidence for Ca2+/CaM modulation of Na+ channel function. C1 Columbia Univ Coll Phys & Surg, Dept Pharmacol, Div Cardiol, New York, NY 10032 USA. Columbia Univ Coll Phys & Surg, Dept Med, Div Cardiol, New York, NY 10032 USA. RP Pitt, GS (reprint author), Columbia Univ Coll Phys & Surg, Dept Pharmacol, Div Cardiol, 630 W 168th St,PH7W318, New York, NY 10032 USA. 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We compared lipid peroxidation status in the plasma of children with autism, and their developmentally normal non-autistic siblings by quantifying the levels of malonyldialdehyde, an end product of fatty acid oxidation. Lipid peroxidation was found to be elevated in autism indicating that oxidative stress is increased in this disease. Levels of major antioxidant proteins namely, transferrin (iron-binding protein) and ceruloplasmin (copper-binding protein) in the serum, were significantly reduced in autistic children as compared to their developmentally normal non-autistic siblings. A striking correlation was observed between reduced levels of these proteins and loss of previously acquired language skills in children with autism. These results indicate altered regulation of transferrin and ceruloplasmin in autistic children who lose acquired language skills. 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Given that the pituitary adenylate cyclase-activating polypeptide (PACAP) type 1 receptor (PAC1) is highly expressed in the olfactory bulb, we examined its role in regulating olfaction and social investigation. We found that olfactory detection of nonsocial stimuli was similar in PAC1-deficient mice and wild-type (WT) littermates. In contrast, PAC1-deficient mice displayed markedly abnormal social behaviors. PAC1-deficient mice exhibited a faster decrease in social investigation after repeated exposure to social cues or ovariectomized female urine compared with WT mice. Moreover, PAC1-deficient females exhibited delayed affiliative behavior when housed with novel males, and PAC1-deficient males displayed excessive sexual mounting toward both females and males as well as reduced aggression and increased licking and grooming toward intruder males. 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In recent years an increasing number of patients with microscopic as well as cryptic terminal deletion involving band 22q13 have been described and their phenotype shows clinical features overlapping with patients with ring chromosome 22. Loss of DNA in the 22q13.3 region may lead to a clinically recognizable syndrome named "22q13.3 deletion syndrome." We report a patient with a ring chromosome 22 who has hypotonia, profound mental retardation, language impairment, dysmorphic features, and behavioral disorders. To check if the critical region responsible for "22q13.3 deletion syndrome" was absent in this ring, a fluorescent in situ hybridization (FISH) analysis using a probe corresponding to the ARSA locus was performed. In our patient, only one ARSA signal could be detected, indicating that the deletion encompassed the critical 22q13.3 region. A more detailed analysis of the deletion extent then was performed using a panel of fluorescent probes located within 22q13. These experiments allowed the identification of the breakpoint between CTA-299D3 and RP5-925J7 probe, located in 22q13.32. Deletion extent could be estimated to be about 2.5 Mb, and this larger deletion may explain the severity of clinical features observed in our patient. (C) 2004 Wiley-Liss, Inc. C1 Stella Maris Clin Res Inst Child & Adolescent Neu, Pisa, Italy. Chiara Hosp S, Cytogenet & Mol Genet Lab, Pisa, Italy. Univ Pisa, Div Child Neurol & Psychiat, Pisa, Italy. RP Battini, R (reprint author), Clin Res Inst Child & Adolescent Neuropsychiat, Via Giacinti 2, I-56018 Pisa, Italy. 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Pediatr. PD OCT PY 2004 VL 11 IS 10 BP 1213 EP 1216 DI 10.1016/j.arcped.2004.03.121 PG 4 WC Pediatrics SC Pediatrics GA 866EY UT WOS:000224757800011 PM 15475279 ER PT J AU Kelley, E Janovicz, A Mayeux, L Paul, J Vear, D Naigles, L Fein, D AF Kelley, E Janovicz, A Mayeux, L Paul, J Vear, D Naigles, L Fein, D TI Continuing linguistic deficits in children with a history of autism SO BRAIN AND COGNITION LA English DT Meeting Abstract C1 Univ Connecticut, Dept Psychol, Unit 1020, Storrs, CT 06269 USA. EM elizabeth.kelley@uconn.edu NR 0 TC 0 Z9 0 PU ACADEMIC PRESS INC ELSEVIER SCIENCE PI SAN DIEGO PA 525 B ST, STE 1900, SAN DIEGO, CA 92101-4495 USA SN 0278-2626 J9 BRAIN COGNITION JI Brain Cogn. PD OCT PY 2004 VL 56 IS 1 BP 121 EP 121 PG 1 WC Neurosciences; Psychology, Experimental SC Neurosciences & Neurology; Psychology GA 860BU UT WOS:000224313600035 ER PT J AU Ito, M AF Ito, M TI 'Nurturing the brain' as an emerging research field involving child neurology SO BRAIN & DEVELOPMENT LA English DT Article DE nurturing; attention deficit/hyperactivity disorder; autism; asperger; critical period; sensitive period; theory of mind; internal model; cognitive control ID FRONTAL-LOBE; CRITICAL-PERIOD; VISUAL-CORTEX; AUTISM; CEREBELLUM; ADOLESCENCE; MATURATION; PLASTICITY; FMRI; MRI AB `Nurturing the brain' is an emerging research field integrating brain science, child care and education, which also involves child neurology. It has emerged from the recent remarkable progress in brain science and strong social demands for improvements in child care and education. This article reviews the current status of three major research themes in this field. First, developmental disorders represented by attention deficit/hyperactivity disorder, autism and Asperger syndrome often introduce difficulties in child care and education, which are to be addressed by appropriate assessment and treatment of affected children based on new knowledge of the pathogenesis of these disorders. Second, recent progress in research on the critical/sensitive periods of development of brain structures and functions promises useful advice for teachers and parents regarding optimal timing and ways of teaching various subjects. Third, the development of the brain throughout infancy, childhood and adolescence is paralleled by the growth and maturation of the mind. Neuronal mechanisms underlying the theory of mind, mirror neurons, internal model, cognitive control, and cognitive emotion regulation are important themes that bridge our understandings of the brain and the mind. (C) 2004 Elsevier B.V. All rights reserved. C1 RIKEN, Brain Sci Inst, Wako, Saitama 3510198, Japan. RP Ito, M (reprint author), RIKEN, Brain Sci Inst, 2-1 Hirosawa, Wako, Saitama 3510198, Japan. 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Its role in other tissues is unclear. Here we present Timothy syndrome, a novel disorder characterized by multiorgan dysfunction including lethal arrhythmias, webbing of fingers and toes, congenital heart disease, immune deficiency, intermittent hypoglycemia, cognitive abnormalities, and autism. In every case, Timothy syndrome results from the identical, de novo Ca(v)1.2 missense mutation G406R. Ca(v)1.2 is expressed in all affected tissues. Functional expression reveals that G406R produces maintained inward Ca2+ currents by causing nearly complete loss of voltage-dependent channel inactivation. This likely induces intracellular Ca2+ overload in multiple cell types. In the heart, prolonged Ca2+ current delays cardiomyocyte repolarization and increases risk of arrhythmia, the ultimate cause of death in this disorder. These discoveries establish the importance of Ca(v)1.2 in human physiology and development and implicate Ca2+ signaling in autism. 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PD OCT PY 2004 VL 13 IS 4 BP 923 EP + DI 10.1016/j.chc.2004.04.002 PG 19 WC Psychiatry SC Psychiatry GA 956KU UT WOS:000231299400009 PM 15380789 ER PT J AU Cederlund, M Gillberg, C AF Cederlund, M Gillberg, C TI One hundred males with Asperger syndrome: a clinical study of background and associated factors SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID LOW BODY-WEIGHT; AUTISM SPECTRUM DISORDERS; HIGH-FUNCTIONING AUTISM; HEAD CIRCUMFERENCE; TOTAL POPULATION; MALE-CHILDREN; ADOLESCENTS; COMPLICATIONS; EPIDEMIOLOGY; DIAGNOSIS AB The objective of this study was to investigate the background and associated factors in a representative group of young males with Asperger syndrome (AS) presenting at a specialized autism clinic. One hundred males aged 5 years 6 months to 24 years 6 months, with a mean age of 11 years 4 months (SD 3y 10mo), who had a clinical diagnosis of AS were included in the study. An in-depth review of their medical records and neuropsychological test data was performed. There was a high rate (51%) of non-verbal learning disability (defined as Verbal IQ more than 15 points higher than Performance IQ), but otherwise there was little or no support for the notion of right-hemisphere brain dysfunction being at the core of the syndrome. There was a very high rate of close relatives with autism spectrum problems, but also high rates of prenatal and perinatal problems, including prematurity and postmaturity. In comparison with general population data, those with AS very often had a combination of genetic and prenatal and perinatal risk factors. Non-verbal learning disability test results applied in about half the group. There was a subgroup of individuals with AS who had macrocephalus. However, there was no support for an association of AS with low body mass index. C1 Univ Gothenburg, Queen Silvias Hosp Children & Adolescents, Dept Child & Adolescent Psychiat, S-41118 Gothenburg, Sweden. Univ London, St Georges Hosp, Sch Med, Dept Child & Adolescent Psychiat, London, England. RP Cederlund, M (reprint author), Univ Gothenburg, Queen Silvias Hosp Children & Adolescents, Dept Child & Adolescent Psychiat, Otterhallegatan 12A, S-41118 Gothenburg, Sweden. EM mats.cederlund@vgregion.se CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 Berglund A, 2000, ACTA OBSTET GYN SCAN, V79, P854, DOI 10.1034/j.1600-0412.2000.079010854.x Bolte S, 2002, INT J EAT DISORDER, V31, P349, DOI 10.1002/eat.10015 Carruth BR, 2002, J AM COLL NUTR, V21, P88 Clark T, 1999, EUR CHILD ADOLES PSY, V8, P50 CLARKSON JE, 1984, AUST PAEDIATR J, V20, P303 Deutsch CK, 2003, J AUTISM DEV DISORD, V33, P209, DOI 10.1023/A:1022903913547 Eaton WW, 2001, J AUTISM DEV DISORD, V31, P279, DOI 10.1023/A:1010743203048 Ehlers S, 1999, J AUTISM DEV DISORD, V29, P129, DOI 10.1023/A:1023040610384 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x Fraser WI, 2002, J INTELL DISABIL RES, V46, P1, DOI 10.1046/j.1365-2788.2002.00009.x GILLBERG C, 1989, DEV MED CHILD NEUROL, V31, P520 Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 Gillberg C, 2002, GUIDE ASPERGER SYNDR GILLBERG C, 1992, DEV MED CHILD NEUROL, V34, P389 Gillberg C, 2002, DEV MED CHILD NEUROL, V44, P296 Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 Gillberg C., 1991, AUTISM ASPERGER SYND, P122, DOI 10.1017/CBO9780511526770.004 Gillberg C, 1999, DEV PSYCHOPATHOL, V11, P567, DOI 10.1017/S0954579499002217 GILLBERG IC, 1989, J CHILD PSYCHOL PSYC, V30, P631, DOI 10.1111/j.1469-7610.1989.tb00275.x Hebebrand J, 1997, ACTA PSYCHIAT SCAND, V96, P64, DOI 10.1111/j.1600-0447.1997.tb09906.x Howlin P, 1999, DEV MED CHILD NEUROL, V41, P834, DOI 10.1017/S0012162299001656 Kadesjo B, 1999, J AUTISM DEV DISORD, V29, P327, DOI 10.1023/A:1022115520317 Karlberg P, 1976, ACTA PAEDIATR SC S, V258, P7 KNUDTZON J, 1988, Tidsskrift for den Norske Laegeforening, V108, P2125 Kopp S, 2003, EUR CHILD ADOLES PSY, V12, P30, DOI 10.1007/s00787-003-0309-3 LeCouteur A, 1996, J CHILD PSYCHOL PSYC, V37, P785 MESIBOV GB, 1989, J AM ACAD CHILD PSY, V28, P538, DOI 10.1097/00004583-198907000-00012 MESIBOV GB, 1998, ASPERGER SYNDROME HI Miller JN, 1997, J CHILD PSYCHOL PSYC, V38, P247 Rosenhall U, 2003, EAR HEARING, V24, P206, DOI 10.1097/01.AUD.0000069326.11466.7E ROURKE BP, 1988, J CONSULT CLIN PSYCH, V56, P801, DOI 10.1037//0022-006X.56.6.801 Sobanski E, 1999, EUR CHILD ADOLES PSY, V8, P312 Stanitski DF, 2000, J PEDIATR ORTHOPED, V20, P686 *STAT SWED, 2004, DAT MAT AG 1971 1977 *SWED MED BIRTH RE, 2001, DAT DEL BIRTH STAT S *SWED MED BIRTH RE, 2004, DAT MAT AG 1978 1988 Klin A, 2003, CHILD ADOL PSYCH CL, V12, P1, DOI 10.1016/S1056-4993(02)00052-4 Wechsler D., 1992, WECHSLER INTELLIGENC Wechsler D., 1974, MANUAL WECHSLER INTE Wechsler D, 1981, WAIS R MANUAL WECHSL Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 WING L, 1980, HANDICAP BEHAV SKILL WING L, 1981, PSYCHOL MED, V11, P115 Woodhouse W, 1996, J CHILD PSYCHOL PSYC, V37, P665, DOI 10.1111/j.1469-7610.1996.tb01458.x World Health Organisation, 1993, INT CLASS DIS CLASS NR 48 TC 72 Z9 76 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD OCT PY 2004 VL 46 IS 10 BP 652 EP 660 PG 9 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 860KW UT WOS:000224343500002 PM 15473168 ER PT J AU Magerotte, G Roge, B AF Magerotte, G Roge, B TI Early intervention in autism: a challenge for practitioners SO EVOLUTION PSYCHIATRIQUE LA French DT Article DE autism; pervasive developmental disorders; early intervention ID BEHAVIORAL TREATMENT; SPECTRUM DISORDERS; YOUNG-CHILDREN; REPLICATION AB When the three main characteristics of autism (i.e. a qualitative alteration in reciprocal social relations; in verbal and non-verbal communication; resistance to change) are considered, it can be seen that the child with autism derives little satisfaction from the social and communicational interactions that form part of his everyday life. Moreover, he experiences a great deal of difficulty in adapting to the numerous changes of location, activity, and persons that he meets during the day - all of which he might possibly wish to remain unchanged, or uniform. Autism therefore presents a considerable challenge to therapists who are preoccupied with improving the quality of life in the very young child with autism, and with the early intervention strategies that could be implemented. On the basis of the most recent studies in the field of behavioral science, the characteristics of efficient early intervention include the following: early intervention and initiation of treatment; intensity of treatment; involvement of the child's parents in the ongoing collaborative project; the necessity of taking into account the various daily environments to which the child is exposed; the introduction of individualized intervention programs; and finally, taking into consideration the biomedical aspect together with an educational-developmental approach. The implementation of an early intervention approach including the above-mentioned characteristics poses a major challenge to practitioner both as regards the evaluation of these children with autism, and also the implementation of the treatment program. (C) 2003 Elsevier SAS. Tous droits reserves. C1 Univ Mons, SUSA, Dept Orthoped, B-7000 Mons, Belgium. Univ Toulouse Le Mirail, UFR Psychol, F-31058 Toulouse, France. CHU La Grave, Secteur Diagnost & Evaluat Autisme, Serv Med Psychol, F-31052 Toulouse, France. RP Magerotte, G (reprint author), Univ Mons, SUSA, Dept Orthoped, 18 Pl Parc, B-7000 Mons, Belgium. EM ghislain.magerotte@umh.ac.be CR Adrien J. L., 1996, AUTISME JEUNE ENFANT ADRIEN JL, 1998, PSYCHOL FRANCAISE, V43, P239 ADRIEN JL, 1999, REV QUEBECOISE PSYCH, V20, P109 Anderson SR, 1999, J ASSOC PERS SEVERE, V24, P162, DOI 10.2511/rpsd.24.3.162 BAER DM, 1993, AM J MENT RETARD, V97, P373 BARTHELEMY C, 1995, THERAPIE ECHANGE DEV *BUR SERV INT ENF, 2000, BUR SERV INT ENF ONT BURY F, 1995, INTEGRATION PERSONNE, P215 Capps L., 1997, CHILDREN AUTISM DEV Carr E. G., 1999, POSITIVE BEHAV SUPPO CAVALLARO C, 1983, TEACHING EXCEPTIONAL, V16, P65 Choutka CM, 1999, J ASSOC PERS SEVERE, V24, P213, DOI 10.2511/rpsd.24.3.213 Cohen D. J, 1997, HDB AUTISM PERVASIVE Dawson G., 1997, EFFECTIVENESS EARLY, P307 Donnellan AM, 1999, J ASSOC PERS SEVERE, V24, P230, DOI 10.2511/rpsd.24.3.230 Dunlap G, 1999, J ASSOC PERS SEVERE, V24, P222, DOI 10.2511/rpsd.24.3.222 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 FOXX RM, 1993, AM J MENT RETARD, V97, P375 Greenspan SI, 1999, J ASSOC PERS SEVERE, V24, P147, DOI 10.2511/rpsd.24.3.147 Guralnick MJ., 1997, EFFECTIVENESS EARLY HAELEWYCK MC, 1992, ETAT RECHERCHE DEFIC, P459 Handleman JS, 2000, PRESCHOOL ED PROGRAM Happe F., 1994, AUTISM INTRO PSYCHOL HART B, 1975, J APPL BEHAV ANAL, V8, P411, DOI 10.1901/jaba.1975.8-411 Howlin P., 1999, TEACHING CHILDREN AU KAZDIN AE, 1993, AM J MENT RETARD, V97, P377 Koegel LK, 1999, J ASSOC PERS SEVERE, V24, P186, DOI 10.2511/rpsd.24.3.186 Koegel LK, 1999, J ASSOC PERS SEVERE, V24, P174, DOI 10.2511/rpsd.24.3.174 Koegel R. L., 1995, TEACHING CHILDREN AU Koegel R. L., 1989, TEACH PIVOTAL BEHAV LELORD G, 1998, EXPLORATION AUTISME Lord C., 1999, AUTISM DIAGNOSTIC OB Lord C., 2000, AUTISM SPECTRUM DISO, P11 LORD C, 1993, PRESCHOOL ISSUES AUT, P199 LOVAAS OI, 1987, J CONSULT CLIN PSYCH, V55, P3, DOI 10.1037/0022-006X.55.1.3 Lovaas O. I., 1981, TEACHING DEV DISABLE LUISELLI J, 1999, ANTECEDENT CONTROL I MAGEROTTE G, 2002, ENFANCE, V54, P31 MCEACHIN JJ, 1993, AM J MENT RETARD, V97, P359 McGee GG, 1999, J ASSOC PERS SEVERE, V24, P133, DOI 10.2511/rpsd.24.3.133 MESIBOV GB, 1993, AM J MENT RETARD, V97, P379 MUNDY P, 1993, AM J MENT RETARD, V97, P381 Neel R. S., 1989, IMPACT FUNCTIONAL CU *NEW YORK STAT DEP, 1999, CLIN PRACT GUID GUID Ozonoff S, 1998, J AUTISM DEV DISORD, V28, P25, DOI 10.1023/A:1026006818310 Parisy D, 1999, J ASSOC PERS SEVERE, V24, P226, DOI 10.2511/rpsd.24.3.226 Prizant B., 2000, AUTISM SPECTRUM DISO, P193 Prizant BM, 1999, J ASSOC PERS SEVERE, V24, P199, DOI 10.2511/rpsd.24.3.199 ROGE B, 1998, PSYCHOL FRANCAISE, V43, P205 ROGE B, 1998, PSYCHOL FRANCAISE, V43, P257 ROGE B, 2001, REEDUCATION ORTHOPHO, V207, P101 Rogers SJ, 1996, J AUTISM DEV DISORD, V26, P243, DOI 10.1007/BF02172020 SCHOPLER E, 1993, PRESCHOOL ISSUES AUT SCHOPLER E, 1989, J CONSULT CLIN PSYCH, V57, P162 Schopler E., 1988, CHILDHOOD AUTISM RAT Schopler E., 1997, HDB AUTISM PERVASIVE, P767 SMITH T, 1993, AM J MENT RETARD, V97, P385 Smith T, 2000, AM J MENT RETARD, V105, P269, DOI 10.1352/0895-8017(2000)105<0269:RTOIEI>2.0.CO;2 Sparrow S, 1984, VINELAND ADAPTIVE BE Wetherby A. M., 2000, AUTISM SPECTRUM DISO NR 60 TC 2 Z9 2 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD OCT-DEC PY 2004 VL 69 IS 4 BP 579 EP 588 DI 10.1016/j.evopsy.2003.07.003 PG 10 WC Psychiatry SC Psychiatry GA 886SG UT WOS:000226248200002 ER PT J AU Allouch, E AF Allouch, E TI Autism and infantile psychosis: differential diagnosis SO EVOLUTION PSYCHIATRIQUE LA French DT Article DE autism; infantile psychosis; direct contact; figurative contact; primary identification; subjective AB Taking into account corporeity (one of the very first kinds of thought representability) even more than words-which mean little when they exist at all for subjects in serious states of infantile psychosis and autism-the author proposes a metapsychological differentiation of these two psychopathologies, which are too often assimilated. The autistic withdrawal marks a failure of the dynamics of desire fastened, as it is, to the assumption of direct contact, when infantile psychosis makes obvious the impossibility for the child to access the figurative or metaphorical contact, which is born and enforced by the prohibition of incest. These two conditions thus undermine that way, each in its own manner, the coming of the subject to the "superior unity of contact" that Freud has theorized. To day it is seen as the first symbolisation, the foundation of the subjective process. (C) 2004 Elsevier SAS. Tous droits reserves. C1 Univ Paris 13, F-75012 Paris, France. RP Allouch, E (reprint author), Univ Paris 13, 10 Rue Erard C371, F-75012 Paris, France. EM elianeallouch@hotmail.com CR ALLOUCH E, 2000, PSYCHOL CLIN, V10, P115 ALLOUCH E, 2000, PSYCHOSE FONCTIONNEM ALLOUCH E, 1992, PSYCHANALYSE U, V17, P3 ALLOUCH E, 1999, SEUIL FIGURABLE AUST Allouch E, 1998, EVOL PSYCHIATR, V63, P379 AULAGNIER P, 1991, INTERPRETE QUETE Bion W.R., 1962, SOURCES EXPERIENCE CASTORIADISAULA.P, 1975, VIOLENCE INTERPRETAT FERENCZI S, 1982, PSYCHANALYSE Freud S., 1988, OEUVRES COMPLETES, VXIII Freud S, 1981, ESSAIS PSYCHANALYSE Freud Sigmund, 1969, NAISSANCE PSYCHANALY Freud Sigmund, 1993, TOTEM TABOU FREUND S, 1969, SEXUELLE GRANDIN T, 1988, AUTISTE Lacan J., 1975, ENCORE Racamier P.C., 1995, INCESTE INCESTUEL Racamier PC, 1980, SCHIZOPHRENES SELLIN B, 1993, PRISONNIERE TUSTIN F, 1972, AUTISME PSYCHOSE INF TUSTIN F, 1981, ETATS AUTISTIQUES EN NR 21 TC 1 Z9 1 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD OCT-DEC PY 2004 VL 69 IS 4 BP 605 EP 615 DI 10.1016/j.evopsy.2004.02.005 PG 11 WC Psychiatry SC Psychiatry GA 886SG UT WOS:000226248200004 ER PT J AU Houzel, D Moussaoui, E Ferretti, A AF Houzel, D Moussaoui, E Ferretti, A TI Early diagnosis of infantile autistic disorders in practice SO EVOLUTION PSYCHIATRIQUE LA English DT Article DE assessment; early diagnosis; infant psychiatry; infantile autism; invasive developmental disorders ID RELIABILITY; VALIDITY AB The work of the Unit for screening and assessment of early developmental disorders of Caen University Hospital aims at detecting all the autistic children in an administrative area as early as possible. The ambition would be to diagnose autistic syndromes before the age of two and a half, so that early treatment may benefit autistic children. The Unit activity is built around young children and their families in collaboration with professionals. Using standard and internationally accepted means for screening, diagnosis and assessment brings a maximum objectivity and allows comparisons. In addition to its task of diagnosing and assessing developmental disorders, the Unit is permanently concerned with training and research. Supplying information and training concerned professionals is a fundamental in improving early screening. As for research, it is to be carried out without any aetiological a priori and with the aim of clarifying the risk factors of infantile autism. (C) 2004 Elsevier SAS. Tous droits reserves. C1 Hop Clemenceau, F-14033 Caen, France. RP Houzel, D (reprint author), 6 Rue Acad, F-14000 Caen, France. EM dhouzel@hotmail.com CR ADRIEN JL, 1992, J AUTISM DEV DISORD, V22, P375, DOI 10.1007/BF01048241 BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Guedeney A, 2001, INF MENTAL HLTH J, V22, P559, DOI 10.1002/imhj.1018 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 SCHOPLER E, 1980, J AUTISM DEV DISORD, V10, P79 NR 5 TC 1 Z9 1 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD OCT-DEC PY 2004 VL 69 IS 4 BP 627 EP 639 DI 10.1016/j.evopsy.2004.08.001 PG 13 WC Psychiatry SC Psychiatry GA 886SG UT WOS:000226248200006 ER PT J AU Delion, P AF Delion, P TI Early detection and care in childhood autistic disorders SO EVOLUTION PSYCHIATRIQUE LA French DT Article DE infantile autism; early detection; early signs; therapeutic strategy; institutional organization AB The author offers an overview of practical questions regarding early detection of autistic disorders concerning clinical signs that must be observed for diagnosis. Based on ten years experience in child and adolescent psychiatry, the author presents his theories regarding the logic of professional intervention. He insists on the importance of the parents' role, the intensity of therapeutic care and the necessity for an institutional policy and research. Some clinical examples illustrate the main aspects of the therapeutic strategy. 2004 Elsevier SAS. Tous droits reserves. C1 CHRU, Serv Pedopsychiat, F-59037 Lille, France. RP Delion, P (reprint author), CHRU, Serv Pedopsychiat, F-59037 Lille, France. EM p-delion@chru-lille.fr CR ABGRALL MC, 1978, MEMOIRE OBTENTION CE DELION P, 2003, PSYCHIAT ENFANT, V46, P579 Delion P., 2000, ENFANT AUTISTE BEBE DELION P, 2003, PACKING ENFANTS AUTI DELION P, 2004, DEV SENSORI MOTEUR E DELION P, 1997, SEMINARIE AUTISME PS Haag G, 1995, PSYCHIAT ENFANT, V38, P495 HAAG M, 2002, METHODE ESTHER BICK LAFFORGUE P, 1996, PETIT POUCET DEVIEND MAZERT P, 1993, PSYCHOPATHOLOGIE NOU Meltzer D, 1980, EXPLORATION MONDE AU PICCO M, 2002, PSYCHIAT ENFANT, V45, P171 Tustin F., 1989, TROU NOIR PSYCHE Winnicott D. W., 2000, CRAINTE EFFONDREMENT NR 14 TC 2 Z9 2 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD OCT-DEC PY 2004 VL 69 IS 4 BP 641 EP 650 DI 10.1016/j.evopsy.2004.06.003 PG 10 WC Psychiatry SC Psychiatry GA 886SG UT WOS:000226248200007 ER PT J AU Goeb, JL Botbol, M Golse, B AF Goeb, JL Botbol, M Golse, B TI Have delusions in schizophrenia following childhood psychosis specific clinical features? SO EVOLUTION PSYCHIATRIQUE LA French DT Article DE adolescence; autism; pervasive developmental disorder; schizophrenia; separation; cognition; vulnerability ID DISORDERS AB Children with Pervasive Developmental Disorders who become schizophrenic during their adolescence are usually patients whose IQ is normal or high and who have a linguistic level which enables them to express certain symptoms required by international classifications to establish the diagnosis of schizophrenia: i.e. delusions and hallucinations. Within the group of schizophrenic disorders, we try here to distinguish: 1/ Schizophrenic patients within whom a schizophrenic process has appeared spontaneously during adolescence without any psychotic episodes in childhood ("de novo" schizophrenia). 2/ Those patients within whom the adolescent process breaks down on a schizophrenic manner; what was formely compensated for gives way to a serious early developmental disorder (secondary schizophrenia). Starting from a more precise examination of the schizophrenic delusional demonstrations, we endeavor to show how common signs regarding the descriptive criteria adopted by international classifications for the diagnosis of schizophrenia hide in fact fundamental psychopathological differences. In these cases the change of the expression of the symptoms between infancy and adolescence are insufficiently clear to define pathological continuity between childhood psychoses and some forms of schizophrenia in adolescence. Within the final common path of typical schizophrenic features, are thus determined radically distinct dynamic organizations which must be taken into account for the multifocal treatments indicated in these pathologies. These considerations are likely to modify our point of view regarding the concept of vulnerability with a different value for each of the two psychopathological types we define. (C) 2004 Elsevier SAS. Touts droits reserves. C1 Psychiat Hop, Serv Pedopsychiat Angers Est, Ctr Sante Mentale Angevin, F-49137 Les Ponts De Ce, France. Fdn Sante Edudiants France, Clin Dupre, Hosp Psychiat, F-92333 Sceaux, France. CHU Necker, Serv Psychiat Enfant & Adolescent, F-75015 Paris, France. RP Goeb, JL (reprint author), Psychiat Hop, Serv Pedopsychiat Angers Est, Ctr Sante Mentale Angevin, F-49137 Les Ponts De Ce, France. EM jlgoeb@wanadoo.fr CR AULAGNIER P, 1979, ALIENATION AMOUR PAS AULAGNIER P, 1984, DISCOURS IDENTIFIANT Aulagnier P., 1975, VIOLENCE INTERPRETAT BOTBOL M, 2001, ENCY MED CHIR BOTBOL M, 2001, ACTUALITE ATTACHEMEN DELION P, 1997, RAMONVILLE Freud S., 1973, NEVROSE PSYCHOSE PER GOEB J, 2004, ANN MED-PSYCHOL, V162, P503, DOI DOI 10.1016/S0003-4487(04)00110-6 GOEB J, 2004, ANN MED-PSYCHOL, V162, P511, DOI DOI 10.1016/S0003-4487(04)00112-X GOEB JL, 2001, NERVURE, V14, P31 GOEB JL, 2003, PSYCHIAT ENFANT, V46, P257 Gutton Ph., 1991, PUBERTAIRE HAAG G, 1985, TOPIQUE, V35, P47 HOCHMANN J, 1997, SOIGNER ENFANT AUTIS HOUZEL D, 2002, CARNET PSY NOV, P23 HOUZEL D, 1991, REV INT PSYCHOPATHOL, V3, P97 JEAMMET P, 1984, ADOLESCENCE, V2, P31 KRISTEVA J, 1987, DEPRESSION MELANCOLI MARCELLI D, 1997, NERVURE, V8, P64 PETTY LK, 1984, ARCH GEN PSYCHIAT, V41, P129 Tordjman S, 1997, PSYCHIAT ENFANT, V40, P473 TUSTIN F, 1977, AUTISME PSYCHOSES Volkmar FR, 1996, J AM ACAD CHILD PSY, V35, P843, DOI 10.1097/00004583-199607000-00009 Wolfson L., 1970, SCHIZO LANGUES NR 24 TC 0 Z9 0 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0014-3855 J9 EVOL PSYCHIATR JI Evol. Psychiatr. PD OCT-DEC PY 2004 VL 69 IS 4 BP 651 EP 662 PG 12 WC Psychiatry SC Psychiatry GA 886SG UT WOS:000226248200008 ER PT J AU Moy, SS Nadler, JJ Perez, A Barbaro, RP Johns, JM Magnuson, TR Piven, J Crawley, JN AF Moy, SS Nadler, JJ Perez, A Barbaro, RP Johns, JM Magnuson, TR Piven, J Crawley, JN TI Sociability and preference for social novelty in five inbred strains: an approach to assess autistic-like behavior in mice SO GENES BRAIN AND BEHAVIOR LA English DT Article DE autism; exploration; inbred strains; locomotion; mice; olfaction; rotarod; sociability; social interaction; social preference ID FRAGILE-X-SYNDROME; EARLY INFANTILE-AUTISM; FMR1 KNOCKOUT MOUSE; GENOMIC SCREEN; MENTAL-RETARDATION; SPECTRUM DISORDERS; ASPERGER-SYNDROME; RECOGNITION; ANXIETY; MEMORY AB Deficits in social interaction are important early markers for autism and related neurodevelopmental disorders with strong genetic components. Standardized behavioral assays that measure the preference of mice for initiating social interactions with novel conspecifics would be of great value for mutant mouse models of autism. We developed a new procedure to assess sociability and the preference for social novelty in mice. To quantitate sociability, each mouse was scored on measures of exploration in a central habituated area, a side chamber containing an unfamiliar conspecific (stranger 1) in a wire cage, or an empty side chamber. In a secondary test, preference for social novelty was quantitated by presenting the test mouse with a choice between the first, now-familiar, conspecific (stranger 1) in one side chamber, and a second unfamiliar mouse (stranger 2) in the other side chamber. Parameters scored included time spent in each chamber and number of entries into the chambers. Five inbred strains of mice were tested, C57BL/6J, DBA/2J, FVB/NJ, A/J and B6129PF2/J hybrids. Four strains showed significant levels of sociability (spending more time in the chamber containing stranger 1 than in the empty chamber) and a preference for social novelty (spending more time in the chamber containing stranger 2 than in the chamber containing the now-familiar stranger 1). These social preferences were observed in both male and female mice, and in juveniles and adults. The exception was A/J, a strain that demonstrated a preference for the central chamber. Results are discussed in terms of potential applications of the new methods, and the proper controls for the interpretation of social behavior data, including assays for health, relevant sensory abilities and motor functions. This new standardized procedure to quantitate sociability and preference for social novelty in mice provides a method to assess tendencies for social avoidance in mouse models of autism. C1 Univ N Carolina, Neurdev Disorders Res Ctr, Sch Med, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychiat, Sch Med, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Genet, Sch Med, Chapel Hill, NC 27599 USA. Univ N Carolina, N Carolina STAART Ctr Autism Res, Sch Med, Chapel Hill, NC 27599 USA. NIMH, Lab Behav Neurosci, Intramural Res Program, Bethesda, MD 20892 USA. RP Moy, SS (reprint author), Univ N Carolina, Neurdev Disorders Res Ctr, Sch Med, CB 7146, Chapel Hill, NC 27599 USA. 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PD OCT PY 2004 VL 3 IS 5 BP 287 EP 302 DI 10.1111/j.1601-183X.2004.00076.x PG 16 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 855QK UT WOS:000223988600004 PM 15344922 ER PT J AU Nadler, JJ Moy, SS Dold, G Trang, D Simmons, N Perez, A Young, NB Barbaro, RP Piven, J Magnuson, TR Crawley, JN AF Nadler, JJ Moy, SS Dold, G Trang, D Simmons, N Perez, A Young, NB Barbaro, RP Piven, J Magnuson, TR Crawley, JN TI Automated apparatus for quantitation of social approach behaviors in mice SO GENES BRAIN AND BEHAVIOR LA English DT Article DE autism; automated equipment; C57BL/6J; DBA/2J; exploratory activity; FVB/ NJ; inbred strains; mice; scoring methods; sociability; social behavior; social preference ID INBRED MOUSE STRAINS; WILLIAMS-SYNDROME; SCHIZOPHRENIA; AUTISM; DEFICITS; PHOBIA; NEUROBIOLOGY; RECOGNITION; PREFERENCES; GENETICS AB Mouse models of social dysfunction, designed to investigate the complex genetics of social behaviors, require an objective methodology for scoring social interactions relevant to human disease symptoms. Here we describe an automated, three chambered apparatus designed to monitor social interaction in the mouse. Time spent in each chamber and the number of entries are scored automatically by a system detecting photocell beam breaks. When tested with the automated equipment, juvenile male C57BL/6J mice spent more time in a chamber containing a stranger mouse than in an empty chamber (sociability), similar to results obtained by the observer scored method. In addition, automated scoring detected a preference to spend more time with an unfamiliar stranger than a more familiar conspecific (preference for social novelty), similar to results obtained by the observer scored method. Sniffing directed at the wire cage containing the stranger mouse correlated significantly with time spent in that chamber, indicating that duration in a chamber represents true social approach behavior. Number of entries between chambers did not correlate with duration of time spent in the chambers; entries instead proved a useful control measure of general activity. The most significant social approach behavior took place in the first five minutes of both the sociability and preference for social novelty tests. Application of these methods to C57BL/6J, DBA/2J and FVB/NJ adult males revealed that all three strains displayed tendencies for sociability and preference for social novelty. To evaluate the importance of the strain of the stranger mouse on sociability and preference for social novelty, C57BL/6J subject mice were tested either with A/J strangers or with C57BL/6J strangers. Sociability and preference for social novelty were similar with both stranger strains. The automated equipment provides an accurate and objective approach to measuring social tendencies in mice. Its use may allow higher-throughput scoring of mouse social behaviors in mouse models of social dysfunction. C1 Univ N Carolina, Dept Genet, Sch Med, Chapel Hill, NC 27599 USA. Univ N Carolina, Neurodev Disorders Res Ctr, Sch Med, Chapel Hill, NC 27599 USA. Univ N Carolina, N Carolina STAART Ctr Autism Res, Sch Med, Chapel Hill, NC 27599 USA. Univ N Carolina, Dept Psychiat, Sch Med, Chapel Hill, NC 27599 USA. NIMH, Res Serv Branch, Bethesda, MD 20892 USA. NINDS, Bethesda, MD 20892 USA. NIMH, Lab Behav Neurosci, Intramural Res Program, Bethesda, MD 20892 USA. RP Nadler, JJ (reprint author), Univ N Carolina, Dept Genet, Sch Med, Chapel Hill, NC 27599 USA. 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PD OCT PY 2004 VL 3 IS 5 BP 303 EP 314 DI 10.1111/j.1601-183X.2004.00071.x PG 12 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 855QK UT WOS:000223988600005 PM 15344923 ER PT J AU Beals, K AF Beals, K TI Early intervention in deafness and autism - One family's experiences, reflections, and recommendations SO INFANTS AND YOUNG CHILDREN LA English DT Article DE applied bebavioral analysis; auditory-verbal; autism; cochlear implant; deafness; early intervention; floor time; sign language AB This article describes one family's experiences with the early intervention system in its treatment of their son, first diagnosed as deaf, later as autistic, Parents in both deafness and autism quickly find themselves mired in bitter disagreements, whether between sign language and speech advocates, or between believers in developmental versus behavioral approaches to autism. Experts in deafness, for all their squabbling, agree on early intervention's top priority: language. Specific methods and materials abound for teaching both sign and spoken language to deaf people. Autism intervention, dominated as it is by psychology/psychiatry gurus rather than educators, offers only the vaguest and the most schematic of intervention strategies. While often passed off as comprehensive curricula, these strategies fall far short of the specificity, practicability, and effectiveness of intervention materials for deaf children. Ultimately, parents realize that it is up to them to devise specific lessons for their children, and that it is up to an of us who work with autistic children directly-parents, teachers, and therapists-to compile, collectively, the truly comprehensive autism curriculum that we all so desperately need. C1 Autism Language Therapies, Philadelphia, PA 19104 USA. RP Beals, K (reprint author), Autism Language Therapies, 516 Woodland Terrace, Philadelphia, PA 19104 USA. EM beals@autism-language-therapies.com NR 0 TC 6 Z9 6 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0896-3746 J9 INFANT YOUNG CHILD JI Infants Young Child. PD OCT-DEC PY 2004 VL 17 IS 4 BP 284 EP 290 PG 7 WC Education, Special; Psychology, Developmental; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 861BS UT WOS:000224391700002 ER PT J AU Yaguchi, K Tojo, Y Senju, A Ceponiene, R Naatanen, R AF Yaguchi, K Tojo, Y Senju, A Ceponiene, R Naatanen, R TI Why vowel familiality does not facilitate the discrimination in autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Jikei Univ, Sch Med, Tokyo, Japan. Univ Tokyo, Tokyo, Japan. Univ Calif San Diego, La Jolla, CA 92093 USA. Univ Helsinki, FIN-00014 Helsinki, Finland. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 53 EP 53 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118000483 ER PT J AU Zhou, NL Fang, JM AF Zhou, NL Fang, JM TI Experiment research for pretending play in preschool children with autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 E China Normal Univ, Shanghai, Peoples R China. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 324 EP 324 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118002949 ER PT J AU Lawson, CA AF Lawson, CA TI Innovative and successful interventions for children with autism spectrum disorders SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 337 EP 337 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118003077 ER PT J AU Yi, CL AF Yi, CL TI Case report: Reestablishing attachment - the family therapy of an autism boy SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Peking Univ, Beijing, Peoples R China. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 396 EP 396 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118003594 ER PT J AU Fang, JM Zhou, NL AF Fang, JM Zhou, NL TI The educational intervention research for improving pretend play of preschool children with autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 E China Normal Univ, Shanghai, Peoples R China. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 397 EP 397 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118003608 ER PT J AU Kawakubo, Y Yonaha, C Maekawa, H AF Kawakubo, Y Yonaha, C Maekawa, H TI Visual search in children with high-functioning autism SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Tsukuba, Tsukuba, Ibaraki 305, Japan. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 397 EP 397 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118003606 ER PT J AU Kunihira, Y Senju, A Hasegawa, T Tojo, Y AF Kunihira, Y Senju, A Hasegawa, T Tojo, Y TI Is imitation in children with autism also goal-directed? SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Tokyo, Tokyo, Japan. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 400 EP 400 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118003632 ER PT J AU Kunihira, Y Senju, A Hasegawa, T Tojo, Y AF Kunihira, Y Senju, A Hasegawa, T Tojo, Y TI Is imitation in children with autism also goal-directed? SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Tokyo, Tokyo, Japan. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 401 EP 401 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118003644 ER PT J AU Mottron, L AF Mottron, L TI Questioning the link between 'genetic' autism and epilepsy SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Montreal, Montreal, PQ, Canada. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 475 EP 475 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118004302 ER PT J AU Probst, P AF Probst, P TI Outcomes of psychological group trainings in parents and teachers of children with autism and hyperactive disorder SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Hamburg, Dept Psychol, Hamburg, Germany. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 510 EP 510 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118004613 ER PT J AU Cheung, C Cheung, V Wong, T Lam, G Chitnis, X AF Cheung, C Cheung, V Wong, T Lam, G Chitnis, X TI Mapping the brain in autism, a voxel-based approach SO INTERNATIONAL JOURNAL OF PSYCHOLOGY LA English DT Meeting Abstract C1 Univ Hong Kong, Hong Kong, Hong Kong, Peoples R China. Hong Kong Inst Educ, SECE, Tai Po, Hong Kong, Peoples R China. Kings Coll London, London WC2R 2LS, England. NR 0 TC 0 Z9 0 PU PSYCHOLOGY PRESS PI HOVE PA 27 CHURCH RD, HOVE BN3 2FA, EAST SUSSEX, ENGLAND SN 0020-7594 J9 INT J PSYCHOL JI Int. J. Psychol. PD OCT-DEC PY 2004 VL 39 IS 5-6 SU S BP 580 EP 580 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 884WS UT WOS:000226118005225 ER PT J AU Gross, TF AF Gross, TF TI The perception of four basic emotions in human and nonhuman faces by children with autism and other developmental disabilities SO JOURNAL OF ABNORMAL CHILD PSYCHOLOGY LA English DT Article DE face perception; facial emotion; autism ID FACIAL EXPRESSIONS; MENTAL-RETARDATION; NEGATIVE EMOTIONS; RECOGNITION; COMPREHENSION; SPECIFICITY; SITUATIONS; DISORDER; SALIENCE; DEFICITS AB Children who experienced autism, mental retardation, and language disorders; and, children in a clinical control group were shown photographs of human female, orangutan, and canine ( boxer) faces expressing happiness, sadness, anger, surprise and a neutral expression. For each species of faces, children were asked to identify the happy, sad, angry, or surprised expressions. In Experiment 1, error patterns suggested that children who experienced autism were attending to features of the lower face when making judgements about emotional expressions. Experiment 2 supported this impression. When recognizing facial emotion, children without autism performed better when viewing the full face, compared to the upper and lower face alone. Children with autism performed no better when viewing the full face than they did when viewing partial faces; and, performed no better than chance when viewing the upper face alone. The results are discussed with respect to differences in the manner that children with and without autism process social information communicated by the face. C1 Univ Redlands, Dept Psychol, Redlands, CA 92373 USA. RP Gross, TF (reprint author), Univ Redlands, Dept Psychol, POB 3080,1200 Colton Ave, Redlands, CA 92373 USA. 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L., 1986, STANFORDBINET INTELL 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 WALDEN TA, 1982, CHILD DEV, V53, P1312, DOI 10.1111/j.1467-8624.1982.tb04170.x Wechsler D, 1991, WECHSLER INTELLIGENC, V3rd WEEKS SJ, 1987, J CHILD PSYCHOL PSYC, V28, P137, DOI 10.1111/j.1469-7610.1987.tb00658.x YIRMIYA N, 1992, CHILD DEV, V63, P150, DOI 10.1111/j.1467-8624.1992.tb03603.x NR 59 TC 59 Z9 60 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0091-0627 J9 J ABNORM CHILD PSYCH JI J. Abnorm. Child Psychol. PD OCT PY 2004 VL 32 IS 5 BP 469 EP 480 DI 10.1023/B:JACP.0000037777.17698.01 PG 12 WC Psychology, Clinical; Psychology, Developmental SC Psychology GA 845UI UT WOS:000223270400001 PM 15500027 ER PT J AU Wetherby, AM Woods, J Allen, L Cleary, J Dickinson, H Lord, C AF Wetherby, AM Woods, J Allen, L Cleary, J Dickinson, H Lord, C TI Early indicators of autism spectrum disorders in the second year of life SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; CSBS DP; developmental delay; early identification; screening ID PERVASIVE DEVELOPMENTAL DISORDERS; 6-YEAR FOLLOW-UP; YOUNG-CHILDREN; NONVERBAL-COMMUNICATION; LANGUAGE-DEVELOPMENT; HOME VIDEOTAPES; JOINT ATTENTION; AGE; RELIABILITY; VALIDITY AB Three groups of 18 children were selected for this study, one group with autism spectrum disorders (ASD), one group with developmental delays in which ASD was ruled out (DD), and one group with typical development (TD), from a pool of 3026 children who were screened with the Communication and Symbolic Behavior Scales Developmental Pro. le (CSBS DP, Wetherby & Prizant, 2002) Infant-Toddler Checklist under 24 months of age. The CSBS DP Behavior Sample was videotaped on selected children as a second-level evaluation during the second year of life. The Infant-Toddler Checklist had a sensitivity and specificity of 88.9% for this sample of children. Significant group differences were found on the Infant-Toddler Checklist and the Behavior Sample, however, these differences did not distinguish children with ASD and DD with high accuracy. The videotapes of the Behavior Sample were reanalyzed to identify red flags of ASD. Nine red flags differentiated children in the ASD group from both the DD and TD groups and four red flags differentiated children in the ASD Group from the TD group but not the DD group. These 13 red flags were found to discriminate the three groups with a correct classification rate of 94.4%. C1 Florida State Univ, Dept Commun Disorders, Tallahassee, FL 32306 USA. Univ Michigan, Ann Arbor, MI 48109 USA. RP Wetherby, AM (reprint author), Florida State Univ, Dept Commun Disorders, RRC 107, Tallahassee, FL 32306 USA. 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Autism Dev. Disord. PD OCT PY 2004 VL 34 IS 5 BP 473 EP 493 DI 10.1007/s10803-004-2544-y PG 21 WC Psychology, Developmental SC Psychology GA 871JB UT WOS:000225125900002 PM 15628603 ER PT J AU Bono, MA Daley, T Sigman, M AF Bono, MA Daley, T Sigman, M TI Relations among joint attention, amount of intervention and language gain in autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; attention; language development; intervention ID NONVERBAL-COMMUNICATION; VISUAL-ATTENTION; NORMAL-CHILDREN; BEHAVIOR; RELIABILITY; CAREGIVERS; IMPAIRMENT; PREDICTORS; DISORDERS; INFANTS AB The purpose of the present study was to investigate the unconditional and conditional relations between amount of intervention and language development in children with autism. Joint attention skills were proposed as child characteristics that might moderate this relation. 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PD OCT PY 2004 VL 34 IS 5 BP 495 EP 505 DI 10.1007/s10803-004-2545-x PG 11 WC Psychology, Developmental SC Psychology GA 871JB UT WOS:000225125900003 PM 15628604 ER PT J AU Naito, M Nagayama, K AF Naito, M Nagayama, K TI Autistic children's use of semantic common sense and theory of mind: A comparison with typical and mentally retarded children SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; sentence comprehension; semantic knowledge; theory of mind ID SENTENCE COMPREHENSION STRATEGIES; VERBAL-ABILITY; LANGUAGE AB To compare Japanese autistic children's use of semantic knowledge and theory of mind with mentally retarded and typically developing children's, they were tested on their comprehension of active and passive sentences and false belief understanding. Autistic children were sensitive to plausibility levels of semantic bias as were 4-year-olds with typical development when comprehending sentences, although impaired in belief understanding as compared with mentally retarded children and typically developing 5-year-olds. Children's sentence comprehension had no association with belief understanding. Results suggest that autistic children with certain verbal intelligence can utilize semantic common sense to comprehend sentences as can typically developing children and that the ability to comprehend sentences is relatively independent of theory of mind. C1 Joetsu Univ Educ, Dept Sch Educ, Joetsu, Niigata 9438512, Japan. RP Naito, M (reprint author), Joetsu Univ Educ, Dept Sch Educ, 1 Yamayashikimachi, Joetsu, Niigata 9438512, Japan. 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PD OCT PY 2004 VL 34 IS 5 BP 507 EP 519 DI 10.1007/s10803-004-2546-9 PG 13 WC Psychology, Developmental SC Psychology GA 871JB UT WOS:000225125900004 PM 15628605 ER PT J AU Lyons, V Fitzgerald, M AF Lyons, V Fitzgerald, M TI Humor in autism and Asperger syndrome SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE autism; Asperger syndrome; humor; psychological theory; neural substrates ID HIGH-FUNCTIONING AUTISM; BRAIN-DAMAGED PATIENTS; RIGHT FRONTAL-LOBE; RIGHT-HEMISPHERE; EPISODIC MEMORY; LEARNING-DISABILITIES; EXECUTIVE FUNCTION; COGNITIVE DEFICIT; INFANTILE-AUTISM; CHILDHOOD AUTISM AB Research has shown that individuals with autism and Asperger syndrome are impaired in humor appreciation, although anecdotal and parental reports provide some evidence to the contrary. This paper reviews the cognitive and affective processes involved in humor and recent neurological findings. It examines humor expression and understanding in autism and Asperger syndrome in the context of the main psychological theories (Theory of Mind, Executive Functions, Weak Central Coherence and Laterization models) and associated neural substrates. In the concluding sections, examples of humor displayed by individuals with autism/Asperger syndrome which appear to challenge the above theories are analyzed and areas for further research are suggested. C1 Univ Dublin Trinity Coll, Dept Child Psychiat, Dublin 2, Ireland. RP Lyons, V (reprint author), 129 Newtownpk Ave, Dublin, Ireland. EM viktorialyons@yahoo.co.uk CR ADOLPHS R, 1994, NATURE, V372, P669, DOI 10.1038/372669a0 AGGLETON J. 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Bennetto, Pennington and Rogers (Child Development, 67, 1816-1835) found increased earlier-list intrusions in a multi-list free-recall paradigm (support absent), yet Farrant, Blades and Boucher (Journal of Autism and Developmental Disorders, 28, 43 50) reported no impairment in identification of who had spoken a particular word at study (support present). We tested the effects on source memory of presence or absence of support for source in participants with Asperger's syndrome. The Asperger participants' overall deficit in source memory was largely eliminated when source was supported at test. C1 City Univ London, Dept Psychol, London EC1V 0HB, England. Univ Sussex, Brighton BN1 9RH, E Sussex, England. RP Bowler, DM (reprint author), City Univ London, Dept Psychol, London EC1V 0HB, England. 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PD OCT PY 2004 VL 34 IS 5 BP 533 EP 542 DI 10.1007/s10803-004-2548-7 PG 10 WC Psychology, Developmental SC Psychology GA 871JB UT WOS:000225125900006 PM 15628607 ER PT J AU Esch, BE Carr, JE AF Esch, BE Carr, JE TI Secretin as a treatment for autism: A review of the evidence SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Review DE secretin; autism; efficacy ID PLACEBO-CONTROLLED TRIAL; PERVASIVE DEVELOPMENTAL DISORDER; SYNTHETIC HUMAN SECRETIN; DOUBLE-BLIND; PORCINE SECRETIN; CHILDREN; POPULATION; BENEFIT; BRAIN AB Secretin is used in the United States for diagnosis of pancreatic gastrointestinal (GI) dysfunction and disease. Repeated therapeutic use has not been approved. Widespread interest in secretin as a treatment for autism followed media reports of behavioral improvements in an autistic child who received the hormone during a GI diagnostic procedure. International demand for secretin soared in the absence of experimental evidence of its efficacy for autism. This review presents a brief history of secretin's rise to popularity and summarizes research on secretin as a treatment for autism. Seventeen studies are reviewed comparing the effects of secretin forms, dosage levels, and dosing intervals on outcome measures with approximately 600 children. Twelve of 13 placebo-controlled studies failed to demonstrate the differential efficacy of secretin. Implications for advocating treatment in the absence of empirical evidence are discussed. C1 Western Michigan Univ, Dept Psychol, Kalamazoo, MI 49008 USA. RP Esch, BE (reprint author), Western Michigan Univ, Dept Psychol, 1903 W Michigan Ave, Kalamazoo, MI 49008 USA. 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Autism Dev. Disord. PD OCT PY 2004 VL 34 IS 5 BP 543 EP 556 DI 10.1007/s10803-004-2549-6 PG 14 WC Psychology, Developmental SC Psychology GA 871JB UT WOS:000225125900007 PM 15628608 ER PT J AU LeGoff, DB AF LeGoff, DB TI Use of LEGO (c) as a therapeutic medium for improving social competence SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE social skills; autism; group therapy; play ID AUTISM AB A repeated-measures, waiting list control design was used to assess efficacy of a social skills intervention for autistic spectrum children focused on individual and group LEGO(C) play. The intervention combined aspects of behavior therapy, peer modeling and naturalistic communication strategies. Close interaction and joint attention to task play an important role in both group and individual therapy activities. The goal of treatment was to improve social competence (SC) which was construed as reflecting three components: (1) motivation to initiate social contact with peers; (2) ability to sustain interaction with peers for a period of time; and (3) overcoming autistic symptoms of aloofness and rigidity. Measures for the first two variables were based on observation of subjects in unstructured situations with peers; and the third variable was assessed using a structured rating scale, the SI subscale of the GARS. Results revealed significant improvement on all three measures at both 12 and 24 weeks with no evidence of gains during the waiting list period. No gender differences were found on outcome, and age of clients was not correlated with outcome. 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PD OCT PY 2004 VL 34 IS 5 BP 557 EP 571 DI 10.1007/s10803-004-2550-0 PG 15 WC Psychology, Developmental SC Psychology GA 871JB UT WOS:000225125900008 PM 15628609 ER PT J AU Sweeten, TL Posey, DJ McDougle, CJ AF Sweeten, TL Posey, DJ McDougle, CJ TI Brief report: Autistic disorder in three children with cytomegalovirus infection SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; cytomegalovirus; congenital infection; autoimmune ID PERVASIVE DEVELOPMENTAL DISORDERS; CONGENITAL CYTOMEGALOVIRUS; INFANTILE AUTISM; SPECTRUM; DEFICITS; RUBELLA AB Previous research has identified a relationship between autistic disorder (autism) and specific congenital infections. Three cases of congenital or perinatal cytomegalovirus (CMV) infection occurring in association with autism are described. Hypothetical mechanisms relating congenital infection, such as CMV, to the development of autism are discussed. A better understanding of the immunologic response to certain congenital infections may provide important information pertaining to the pathophysiology and etiology of autism in vulnerable individuals. C1 Indiana Univ, Sch Med, Dept Psychiat, Indianapolis, IN 46202 USA. James Whitcomb Riley Hosp Children, 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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PD OCT PY 2004 VL 34 IS 5 BP 589 EP 591 DI 10.1007/s10803-004-2554-9 PG 3 WC Psychology, Developmental SC Psychology GA 871JB UT WOS:000225125900012 ER PT J AU Herbert, MR AF Herbert, MR TI Neurointaging in disorders of social and emotional functioning: What is the question? SO JOURNAL OF CHILD NEUROLOGY LA English DT Review ID POSITRON-EMISSION-TOMOGRAPHY; PERVASIVE DEVELOPMENTAL DISORDERS; AUTISM SPECTRUM DISORDER; CEREBRAL WHITE-MATTER; CORPUS-CALLOSUM SIZE; HUMAN NEURAL SYSTEMS; MAGNETIC-RESONANCE; CHILDHOOD AUTISM; INFANTILE-AUTISM; HEAD CIRCUMFERENCE AB Social and emotional processing uses neural systems involving structures ranging from the brain stem to the associational cortex. Neuroimaging research has attempted to identify abnormalities in components of these systems that would underlie the behavioral abnormalities seen in disorders of social and emotional processing, notably autism spectrum disorders, the focus of this review. However, the findings have been variable. The most replicated anatomic finding (a tendency toward large brains) is not modular, and metabolic imaging and functional imaging (although showing substantial atypicality in activation) are not consistent regarding specific anatomic sites. Moreover, autism spectrum disorder demonstrates substantial heterogeneity on multiple levels. Here evidence is marshaled from a review of neuroiniaging data to support the claim that abnormalities in social and emotional processing on the autism spectrum are a consequence of systems disruptions in which the behaviors are a final common pathway and the focal findings can be variable, downstream of other pathogenetic mechanisms, and downstream of more pervasive abnormalities. (J Child Neurol 2004; 19:772-784). C1 Harvard Univ, Massachusetts Gen Hosp East, Div Pediat Neurol,Dept Neurol, Ctr Morphometr Anal,Neurosci Ctr,Med Sch, Charlestown, MA 02129 USA. RP Herbert, MR (reprint author), Harvard Univ, Massachusetts Gen Hosp East, Div Pediat Neurol,Dept Neurol, Ctr Morphometr Anal,Neurosci Ctr,Med Sch, 149 13th St Room 6012, Charlestown, MA 02129 USA. 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PD OCT PY 2004 VL 19 IS 10 BP 772 EP 784 PG 13 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 920PT UT WOS:000228703300007 PM 15559893 ER PT J AU McPartland, J Dawson, G Webb, SJ Panagiotides, H Carver, LJ AF McPartland, J Dawson, G Webb, SJ Panagiotides, H Carver, LJ TI Event-related brain potentials reveal anomalies in temporal processing of faces in autism spectrum disorder SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE event-related potential; N170; autism; face processing ID HUMAN EXTRASTRIATE CORTEX; OBJECT RECOGNITION; HOME VIDEOTAPES; ANATOMIC BASIS; NEURAL BASIS; PERCEPTION; CHILDREN; PROSOPAGNOSIA; MEMORY; INDIVIDUALS AB Background: Individuals with autism exhibit impairments in face recognition, and neuroimaging studies have shown that individuals with autism exhibit abnormal patterns of brain activity during face processing. The current study examined the temporal characteristics of face processing in autism and their relation to behavior. Method: High-density event-related brain potentials (ERPs) were recorded to images of faces, inverted faces, and objects from 9 individuals with autism spectrum disorder (15-42 years old) and 14 typical individuals (16-37 years old). Results: With respect to a face-sensitive ERP component (N170), individuals with autism exhibited longer N170 latencies to faces than typical individuals but comparable latencies to objects. Typical individuals exhibited longer N170 latencies to inverted as compared to upright faces, whereas individuals with autism did not show differences in N170 latency to upright versus inverted faces. Neural speed of face processing, as reflected in N170 latency, correlated with performance on a face recognition task for individuals with autism. Conclusions: These data provide evidence for slowed neural speed of face processing in autism and highlight the role of speed of processing in face processing impairments in autism. C1 Univ Washington, UW Autism Ctr, Seattle, WA 98195 USA. Univ Calif San Diego, San Diego, CA 92103 USA. RP Dawson, G (reprint author), Univ Washington, UW Autism Ctr, CHDD,Box 357920, Seattle, WA 98195 USA. 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Child Psychol. Psychiatry PD OCT PY 2004 VL 45 IS 7 BP 1235 EP 1245 DI 10.1111/j.1469-7610.2004.00318.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 854YQ UT WOS:000223940300007 PM 15335344 ER PT J AU Rouse, H Donnelly, N Hadwin, JA Brown, T AF Rouse, H Donnelly, N Hadwin, JA Brown, T TI Do children with autism perceive second-order relational features? The case of the Thatcher illusion SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; central coherence; faces; buildings; Thatcher illusion ID HIGH-FUNCTIONING AUTISM; FUSIFORM FACE AREA; RECOGNITION; PERCEPTION; INVERSION; INDIVIDUALS; DISORDER; ADOLESCENTS AB Background: This study presents two experiments that investigated whether children with autism were susceptible to the Thatcher illusion. Perception of the Thatcher illusion requires being able to compute second-order configural relations for facial stimuli. Method: In both experiments children with autism were matched for non-verbal and verbal ability with a group of children with moderate (non-specific) mental retardation (MLD) and a group of typically developing children respectively. Participants were asked to detect the 'unusual' face in a two-alternative-forced-choice version of the Margaret Thatcher illusion with grey-scale (Experiment 1) and monochrome 'Mooney' face images (Experiment 2). In Experiment 1 participants also performed a control task where buildings had been doctored in the same way as the facial stimuli. Results: Children with autism were as susceptible to the Thatcher illusion as both control groups, in terms of accuracy and reaction time to make decisions about which face was unusual. Children with autism performed more accurately than children with MLD in the buildings task. Conclusion: Children with autism are able to compute second-order configural features in faces and exhibit no difference in face processing, relative to appropriate control groups. C1 Univ Southampton, Ctr Visual Cognit, Sch Psychol, Southampton SO17 1BJ, Hants, England. Univ Southampton, Ctr Behav Res Anal & Intervent Dev Disabil, Sch Psychol, Southampton SO17 1BJ, Hants, England. Univ Southampton, Dev Brain Behav Unit, Sch Psychol, Southampton SO17 1BJ, Hants, England. RP Donnelly, N (reprint author), Univ Southampton, Ctr Visual Cognit, Sch Psychol, Southampton SO17 1BJ, Hants, England. 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PD OCT PY 2004 VL 25 IS 5 BP 375 EP 375 DI 10.1097/00004703-200410000-00023 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 867JU UT WOS:000224839700023 ER PT J AU Nickels, K Barbaresi, W Katusic, S Colligan, R Weaver, A AF Nickels, K Barbaresi, W Katusic, S Colligan, R Weaver, A TI Psychostimulant treatment in a population based cohort of research-identified autism cases SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Meeting Abstract C1 Mayo Clin, Rochester, MD USA. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD OCT PY 2004 VL 25 IS 5 BP 375 EP 376 DI 10.1097/00004703-200410000-00024 PG 2 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 867JU UT WOS:000224839700024 ER PT J AU Solomon, R Necheles, JW Ferch, C Bruckman, D AF Solomon, R Necheles, JW Ferch, C Bruckman, D TI Evaluation of a training program for young children with autism: The PLAY project home consultation model SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Meeting Abstract C1 Univ Michigan, Ann Arbor, MI 48109 USA. NR 0 TC 1 Z9 1 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 OCT PY 2004 VL 25 IS 5 BP 375 EP 375 DI 10.1097/00004703-200410000-00022 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 867JU UT WOS:000224839700022 ER PT J AU Gallagher, S Lekagul, K Nopmaneejumruslers, UC Roberts, W AF Gallagher, S Lekagul, K Nopmaneejumruslers, UC Roberts, W TI Sertraline and citalopram treatment in children with autism spectrum disorder SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Meeting Abstract C1 Univ Toronto, Hosp Sick Children, Toronto, ON M5G 1X8, Canada. NR 0 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0196-206X J9 J DEV BEHAV PEDIATR JI J. Dev. Behav. Pediatr. PD OCT PY 2004 VL 25 IS 5 BP 380 EP 380 DI 10.1097/00004703-200410000-00035 PG 1 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 867JU UT WOS:000224839700035 ER PT J AU Hanson, E Kalish, LA Curtis, C Bunce, E Ware, J Petry, J AF Hanson, E Kalish, LA Curtis, C Bunce, E Ware, J Petry, J TI The use of complementary and alternative therapy for children on the autism spectrum SO JOURNAL OF DEVELOPMENTAL AND BEHAVIORAL PEDIATRICS LA English DT Meeting Abstract C1 Harvard Univ, Sch Med, Childrens Hosp, Dev Med Ctr, Boston, MA USA. NR 0 TC 1 Z9 1 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 OCT PY 2004 VL 25 IS 5 BP 380 EP 381 DI 10.1097/00004703-200410000-00036 PG 2 WC Behavioral Sciences; Psychology, Developmental; Pediatrics SC Behavioral Sciences; Psychology; Pediatrics GA 867JU UT WOS:000224839700036 ER PT J AU Dietz, DM Vogel, MW Rubin, SA Moran, TH Carbone, KM Pletnikov, MV AF Dietz, DM Vogel, MW Rubin, SA Moran, TH Carbone, KM Pletnikov, MV TI Developmental alterations in serotoninergic neurotransmission in Borna disease virus (BDV)-infected rats: A multidisciplinary analysis SO JOURNAL OF NEUROVIROLOGY LA English DT Article DE animal model; Borna; developmental behavioral disorders; serotonin ID NEURODEVELOPMENTAL DAMAGE; BDV INFECTION; CNS DISEASES; AUTISM; BRAIN; PERSISTENT; MECHANISMS; RESPONSES; ABNORMALITIES; ORGANIZATION AB Neonatal Borna disease virus (BDV) infection of the rat brain serves as a valuable model for studying the pathogenesis of neurodevelopmental abnormalities following early brain injury. Previous experiments have demonstrated significant alterations in regional tissue content of serotonin (5-HT) in neonatally BDV-infected Lewis rats. The present study sought to provide more insights into postnatal virus-associated alterations in 5-HT neurotransmission by evaluating the density of 5-HT1a receptors in the hippocampus and 5-HT2a receptors in the cortex, regional 5-HT tissue concentrations, behavioral responses to a 5-HT agonist, quipazine, and numbers of neurons in specific subfields of the hippocampus on days 7, 14, and 30 after neonatal BDV infection in Lewis rats. Neonatal BDV infection was found to be associated with a gradual increase in the density of 5-HT2a and 5-HT1a postsynaptic receptors followed by an elevation of 5-HT contents at both the levels of synaptic terminals (i.e., cortex and hippocampus) and cell bodies (i.e., raphe nuclei). In addition, there was an enhanced behavioral response to quipazine. Virus-associated neurochemical and behavioral changes were accompanied by a decline in the number of neurons in the dentate gyrus and in the CA1 field of the hippocampus. No change in the number of neurons in the CA3/2 field of the hippocampus was observed. The present pattern of BDV-associated alterations in 5-HT brain system along with available data from other laboratories suggest that BDV might compromise axonal transport and/or release of 5-HT, resulting in decreased 5-HT neurotransmission. C1 Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA. Univ Maryland, Maryland Psychiat Res Ctr, Baltimore, MD 21201 USA. CBER, US FDA, Bethesda, MD USA. RP Pletnikov, MV (reprint author), Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, 720 Rutland Ave,Ross 618, Baltimore, MD 21205 USA. 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Neurovirol. PD OCT PY 2004 VL 10 IS 5 BP 267 EP 277 DI 10.1080/13550280490499506 PG 11 WC Neurosciences; Virology SC Neurosciences & Neurology; Virology GA 854ET UT WOS:000223884600001 PM 15385249 ER PT J AU Norbury, CF AF Norbury, CF TI Factors supporting idiom comprehension in children with communication disorders SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE specific language impairment; autism; idioms; context ID HIGH-FUNCTIONING ADULTS; SCHOOL-AGE-CHILDREN; LANGUAGE IMPAIRMENT; WORKING-MEMORY; SENTENCE COMPREHENSION; CENTRAL COHERENCE; AUTISM; MIND; TRANSPARENCY; ADOLESCENTS AB The current investigation explored understanding of idioms in context in 93 children with communication disorders and 39 age-matched peers. The clinical group was subdivided by (a) the presence of autistic features and (b) the presence of language impairment. Idiom definitions were gathered in isolation and in context. Related skills such as semantics and theory of mind were also measured. All children benefited significantly from context. However, 2 groups with language impairments (1 with and 1 without autistic features) did not benefit from context as much as the controls or a group of children with autistic features without additional language difficulties. Regression analyses found that age, memory for story context, and language abilities were significant predictors of id idioms in context performance. These findings are discussed in relation to theories of idiom acquisition and contextual processing in autism. C1 Univ Oxford, Dept Expt Psychol, Oxford OX1 3UD, England. RP Norbury, CF (reprint author), Univ Oxford, Dept Expt Psychol, S Parks Rd, Oxford OX1 3UD, England. 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Acad. Child Adolesc. Psychiatr. PD OCT PY 2004 VL 43 IS 10 BP 1193 EP 1193 DI 10.1097/01.chi.0000135624.89971.d1 PG 1 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 856KP UT WOS:000224044400009 PM 15381885 ER PT J AU Koenig, K AF Koenig, K TI Autism spectrum disorders: A research review for practitioners. SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Book Review C1 Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. RP Koenig, K (reprint author), Yale Univ, Ctr Child Study, New Haven, CT 06520 USA. CR Ozonoff S, 2003, AUTISM SPECTRUM DISO 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 OCT PY 2004 VL 43 IS 10 BP 1304 EP 1305 DI 10.1097/01.chi.0000135647.75228a4 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 856KP UT WOS:000224044400023 ER PT J AU Cohen, ED AF Cohen, ED TI The stolen child: Aspects of autism and Asperger syndrome. SO JOURNAL OF THE AMERICAN ACADEMY OF CHILD AND ADOLESCENT PSYCHIATRY LA English DT Book Review C1 Hartford Hosp, Inst Living, Hartford, CT USA. RP Cohen, ED (reprint author), Hartford Hosp, Inst Living, Hartford, CT USA. CR HEWETSON A, 2002, STOLEN CHILD ASPECTS 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 OCT PY 2004 VL 43 IS 10 BP 1309 EP 1310 DI 10.1097/01.chi.0000135645.81066.24 PG 2 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 856KP UT WOS:000224044400027 ER PT J AU Frith, C AF Frith, C TI Is autism a disconnection disorder? SO LANCET NEUROLOGY LA English DT Editorial Material C1 UCL, Inst Neurol, Wellcome Dept Imaging Neurosci, London, England. RP Frith, C (reprint author), UCL, Inst Neurol, Wellcome Dept Imaging Neurosci, Mortimer St, London, England. 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PD OCT PY 2004 VL 3 IS 10 BP 577 EP 577 DI 10.1016/S1474-4422(04)00875-0 PG 1 WC Clinical Neurology SC Neurosciences & Neurology GA 857SC UT WOS:000224137600008 PM 15380151 ER PT J AU Wassink, TH Piven, J Vieland, VJ Pietila, J Goedken, RJ Folstein, SE Sheffield, VC AF Wassink, TH Piven, J Vieland, VJ Pietila, J Goedken, RJ Folstein, SE Sheffield, VC TI Examination of AVPR1a as an autism susceptibility gene SO MOLECULAR PSYCHIATRY LA English DT Article DE candidate gene; linkage; linkage disequilibrium; reciprocal social interaction; language ID VASOPRESSIN RECEPTOR; LINKAGE ANALYSIS; POLYMORPHISMS; EXPRESSION; BEHAVIOR AB Impaired reciprocal social interaction is one of the core features of autism. While its determinants are complex, one biomolecular pathway that clearly influences social behavior is the arginine - vasopressin (AVP) system. The behavioral effects of AVP are mediated through the AVP receptor 1a (AVPR1a), making the AVPR1a gene a reasonable candidate for autism susceptibility. We tested the gene's contribution to autism by screening its exons in 125 independent autistic probands and genotyping two promoter polymorphisms in 65 autism affected sibling pair ( ASP) families. While we found no nonconservative coding sequence changes, we did identify evidence of linkage and of linkage disequilibrium. These results were most pronounced in a subset of the ASP families with relatively less severe impairment of language. Thus, though we did not demonstrate a disease-causing variant in the coding sequence, numerous nontraditional disease-causing genetic abnormalities are known to exist that would escape detection by traditional gene screening methods. Given the emerging biological, animal model, and now genetic data, AVPR1a and genes in the AVP system remain strong candidates for involvement in autism susceptibility and deserve continued scrutiny. C1 Univ Iowa, Coll Med, Psychiat Res MEB, Dept Psychiat, Iowa City, IA 52242 USA. Univ N Carolina, Dept Psychiat, Chapel Hill, NC USA. Univ N Carolina, Neurodev Disorders Res Ctr, Chapel Hill, NC USA. Univ Iowa, Coll Publ Hlth, Dept Biostat, Div Stat Genet, Iowa City, IA USA. Univ Iowa, Coll Med, Dept Pediat, Iowa City, IA 52242 USA. Univ Iowa, Coll Med, Howard Hughes Med Inst, Iowa City, IA 52242 USA. Tufts Univ, Sch Med, Dept Psychiat, Boston, MA 02111 USA. RP Wassink, TH (reprint author), Univ Iowa, Coll Med, Psychiat Res MEB, Dept Psychiat, Iowa City, IA 52242 USA. 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PD OCT PY 2004 VL 9 IS 10 BP 968 EP 972 DI 10.1038/sj.mp.4001503 PG 5 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 857CB UT WOS:000224092100011 PM 15098001 ER PT J AU Heiser, P Friedel, S Dempfle, A Konrad, K Smidt, J Grabarkiewicz, J Herpertz-Dahlmann, B Remschmidt, H Hebebrand, J AF Heiser, P Friedel, S Dempfle, A Konrad, K Smidt, J Grabarkiewicz, J Herpertz-Dahlmann, B Remschmidt, H Hebebrand, J TI Molecular genetic aspects of attention-deficit/hyperactivity disorder SO NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS LA English DT Review DE attention-deficit/hyperactivity disorder (ADHD); hyperkinetic syndrome; hyperactivity; attention deficit; impulsivity; genome scan; candidate gene; polymorphism; endophenotype; knockout; quantitative trait loci (QTL); dopamine ID DEFICIT HYPERACTIVITY DISORDER; QUANTITATIVE-TRAIT LOCI; DOPAMINE TRANSPORTER GENE; RECOMBINANT INBRED MICE; GENOME-WIDE SCAN; SPONTANEOUSLY HYPERTENSIVE-RAT; III REPEAT POLYMORPHISM; HAPLOTYPE RELATIVE RISK; COMPLEX HUMAN-DISEASES; BETA-HYDROXYLASE GENE AB Two genome wide scans, one of which was subsequently extended, have led to the identification of different chromosomal regions assumed to harbour genes underlying attention-deficit/hyperactivity disorder (ADHD). Some of these regions were also identified in patients with autism and/or dyslexia. The only region for which both studies detected a LOD score >1 was on chr 5p 13 which is in the vicinity of the location of the candidate gene DAT1. The candidate gene approach has revealed the most robust and replicated findings for DRD4, DRD5, and DAT1 polymorphisms. Meanwhile interesting endophenotype studies have also been conducted suggesting a genetic basis for different diagnostic and therapeutic criteria. Animal studies for ADHD have investigated especially hyperactivity and have focused mainly on knockout and QTL designs. In knockout mice models the most promising results were obtained for genes of the dopaminergic pathway. QTL results in rodents suggest multiple loci underlying different forms of natural and induced hyperactivity. The molecular results mentioned above are presented and discussed in detail, thus providing both clinicians and geneticists with an overview of the current research status of this important child and adolescent psychiatric disorder. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Duisburg Gesamthsch, Dept Child & Adolescent Psychiat & Psychotherapy, D-45147 Essen, Germany. Univ Marburg, Dept Child & Adolescent Psyvhiat & Psychotherapy, Marburg, Germany. Univ Marburg, Dept Med Biometry & Epidemiol, Marburg, Germany. Univ Aachen, Dept Child & Adolescent Psychiat & Psychotherapy, D-5100 Aachen, Germany. RP Hebebrand, J (reprint author), Univ Duisburg Gesamthsch, Dept Child & Adolescent Psychiat & Psychotherapy, Virchowstr 174, D-45147 Essen, Germany. 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Biobehav. Rev. PD OCT PY 2004 VL 28 IS 6 BP 625 EP 641 DI 10.1016/j.neubiorev.2004.09.010 PG 17 WC Behavioral Sciences; Neurosciences SC Behavioral Sciences; Neurosciences & Neurology GA 873CL UT WOS:000225256600007 PM 15527867 ER PT J AU Salerno, C Crifo, C AF Salerno, C Crifo, C TI Urinary methylxanthine and autistic disorder: Absence of previously reported correlation SO NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS LA English DT Article; Proceedings Paper CT Joint 11th International and 9th European Symposium on Purines and Pyrimidines in Man CY JUN 09-13, 2003 CL Egmond Aan Zee, NETHERLANDS DE theobromine; methylxanthine; autism; HPLC chromatography AB We were unable to reveal significant difference in the levels of xanthine and methylxanthines in the urine samples from 59 patients diagnosed with autistic symptoms and 64 age- and sex-matched normal volunteers. Our data suggest that abnormalities in xanthine and methylxanthine excretion (US Patent 20020019406 A1, Feb. 12, 2002) represent distincly uncommon symptoms in autism. C1 Univ Roma La Sapienza, Dept Gynecol Perinatol & Child Hlth, I-00185 Rome, Italy. Univ Roma La Sapienza, Dept Biochem Sci, I-00185 Rome, Italy. RP Salerno, C (reprint author), Univ Roma La Sapienza, Dept Gynecol Perinatol & Child Hlth, I-00185 Rome, Italy. CR RUSCHE JR, Patent No. 20020019406 ZHANG J, 2000, WORLD C PED GASTR BO NR 2 TC 1 Z9 1 PU MARCEL DEKKER INC PI NEW YORK PA 270 MADISON AVE, NEW YORK, NY 10016 USA SN 1525-7770 J9 NUCLEOS NUCLEOT NUCL JI Nucleosides Nucleotides Nucleic Acids PD OCT PY 2004 VL 23 IS 8-9 BP 1249 EP 1251 DI 10.1081/NCN-200027511 PG 3 WC Biochemistry & Molecular Biology SC Biochemistry & Molecular Biology GA 871EY UT WOS:000225113700035 PM 15571239 ER PT J AU Curtin, C Bandini, L Perrin, E Must, A AF Curtin, C Bandini, L Perrin, E Must, A TI Prevalence of overweight in youth with attention deficit hyperactivity disorder (ADHD) and autism spectrum disorders (ASD): A chart review SO OBESITY RESEARCH LA English DT Meeting Abstract CT NAASO Annual Scientific Meeting CY NOV 14-18, 2004 CL Las Vegas, NV SP NAASO NR 0 TC 0 Z9 0 PU NORTH AMER ASSOC STUDY OBESITY PI SILVER SPRING PA 8630 FENTON ST, SUITE 918, SILVER SPRING, MD 20910 USA SN 1071-7323 J9 OBES RES JI Obes. Res. PD OCT PY 2004 VL 12 SU S BP A226 EP A227 PG 2 WC Endocrinology & Metabolism; Nutrition & Dietetics SC Endocrinology & Metabolism; Nutrition & Dietetics GA 865GW UT WOS:000224691701427 ER PT J AU Stringer, MD AF Stringer, MD TI Informed consent and choice in cholecystectomy SO PEDIATRIC SURGERY INTERNATIONAL LA English DT Article DE cholecystectomy; laparoscopy; bile duct injury ID BILE-DUCT INJURIES; LAPAROSCOPIC CHOLECYSTECTOMY; COST-ANALYSIS; SINGLE-BLIND; CHILDREN AB As patients and parents seek more information and the threat of litigation increases, the process of informed consent has assumed greater importance. Data from large adult experiences indicate that the risk of bile duct injury, although small, is greater with laparoscopic cholecystectomy (LC) than open cholecystectomy. This complication has not yet been documented in pediatric practice, where cholecystectomy is relatively uncommon. What method do parents and patients choose if consent is truly informed? Of 57 consecutive children undergoing cholecystectomy, an open procedure was specifically indicated in 20 (previous major gastrointestinal surgery in 11, concomitant major abdominal operation in four, and complex biliary tract disease in five) and LC in two (cystic fibrosis, severe autism). The remaining 35 patients were counseled in a standard manner about the relative merits of LC versus mini-cholecystectomy (MC) and allowed to choose. Specifically, they were informed that LC offers better cosmesis, less postoperative discomfort, and a shorter hospital stay, but in adults is associated with a slightly increased rate of bile duct injury (0.3-0.5% vs. 0.2%). All MCs were performed through a 4-cm incision. Parents chose LC in 23 cases and MC in 12. The median age of both groups was similar. No surgical complications occurred, and there were no conversions in the LC group. No patient had retained stones. LC patients were discharged home after a mean of 1.7 days and MC patients after 2.3 days (0.1>p>0.05). If an open or laparoscopic technique is not specifically indicated and if parents/patients are fully informed, a significant minority may opt for mini-cholecystectomy. C1 St Jamess Univ Hosp, Childrens Liver Unit, Leeds LS9 7TF, W Yorkshire, England. RP Stringer, MD (reprint author), St Jamess Univ Hosp, Childrens Liver Unit, Gledhow Wing, Leeds LS9 7TF, W Yorkshire, England. EM mdstringer@dial.pipex.com CR AlSalem AH, 1997, PEDIATR SURG INT, V12, P587 Esposito C, 2001, SURG ENDOSC-ULTRAS, V15, P890, DOI 10.1007/s004640000042 Flum DR, 2003, JAMA-J AM MED ASSOC, V290, P2168, DOI 10.1001/jama.290.16.2168 Holcomb GW, 1999, J PEDIATR SURG, V34, P1236, DOI 10.1016/S0022-3468(99)90159-8 HOLCOMB GW, 1994, J PEDIATR SURG, V29, P900, DOI 10.1016/0022-3468(94)90012-4 KIM PCW, 1995, J PEDIATR SURG, V30, P971, DOI 10.1016/0022-3468(95)90323-2 Majeed AW, 1996, LANCET, V347, P989, DOI 10.1016/S0140-6736(96)90143-9 Miltenburg DM, 2000, PEDIATRICS, V105, P1250, DOI 10.1542/peds.105.6.1250 Ros A, 2001, ANN SURG, V234, P741, DOI 10.1097/00000658-200112000-00005 Savassi-Rocha PR, 2003, SURG ENDOSC, V17, P1356, DOI 10.1007/s00464-002-8726-9 Smith R, 2004, BMJ, V328 Stringer MD, 2002, SURG LIVER BILE DUCT, P189 Terpstra OT, 1996, BRIT MED J, V312, P1375 Ure BM, 1999, EUR J PEDIATR SURG, V9, P8, DOI 10.1055/s-2008-1072204 Vecchio R, 1998, INT SURG, V83, P215 Waldhausen JHT, 1999, AM J SURG, V177, P364, DOI 10.1016/S0002-9610(99)00063-X Wales PW, 2001, J PEDIATR SURG, V36, P718, DOI 10.1053/jpsu.2001.22944 WARE RE, 1992, J PEDIATR-US, V120, P58, DOI 10.1016/S0022-3476(05)80598-0 Way LW, 2003, ANN SURG, V237, P460, DOI 10.1097/00000658-200304000-00004 NR 19 TC 4 Z9 4 PU SPRINGER PI NEW YORK PA 233 SPRING STREET, NEW YORK, NY 10013 USA SN 0179-0358 J9 PEDIATR SURG INT JI Pediatr. Surg. Int. PD OCT PY 2004 VL 20 IS 10 BP 741 EP 743 DI 10.1007/s00383-004-1289-1 PG 3 WC Pediatrics; Surgery SC Pediatrics; Surgery GA 870OO UT WOS:000225067500003 PM 15490193 ER PT J AU Meissner, HC Strebel, PM Orenstein, WA AF Meissner, HC Strebel, PM Orenstein, WA TI Measles vaccines and the potential for worldwide eradication of measles SO PEDIATRICS LA English DT Article DE bioterrorism; measles-mumps-rubella vaccine; vaccines; measles; autism ID RUBELLA VACCINATION; UNITED-STATES; AUTISM; MUMPS; IMMUNIZATION; CHILDREN; POPULATION; EPIDEMIC; SEROCONVERSION; EXEMPTIONS AB The annual number of reported measles cases in the United States has declined from between 3 million and 4 million in the prevaccine era to <100 cases in association with the highest recorded immunization rates in history. Because of continued importation of measles into the United States, young children who are not vaccinated appropriately may experience more than a 60-fold increase in risk of disease. Unsubstantiated claims suggesting an association between measles vaccine and neurologic disorders have led to reduced vaccine use and a resurgence of measles in countries where immunization rates have declined below the level needed to maintain herd immunity. To address the possibility of worldwide control of measles, efforts to ensure high immunization rates among people in both developed and developing countries must be sustained. C1 Tufts Univ, Sch Med, New England Med Ctr, Div Pediat Infect Dis, Boston, MA 02111 USA. Ctr Dis Control & Prevent, Natl Immunizat Program, Atlanta, GA USA. Emory Univ, Emory Vaccine Ctr, Atlanta, GA 30322 USA. RP Meissner, HC (reprint author), Tufts New England Med Ctr, Pediat Infect Dis Div, 750 Washington St, Boston, MA 02111 USA. 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Method: Analysis of parental reporting of height and weight measurements in boys (n = 50) diagnosed with PDD and comparison with age and sex-matched reference populations. Results: The majority of patients were above the 50th percentile for height (70%), weight (74%) and BMI (80%) with 21% exceeding cut-off points for overweight and 10% for clinical obesity. There were no significant differences (P < 0.05) found between PDD subgroups for any of the measures. Conclusion: Further studies are required to validate findings of skewed height, weight and BMI data in PDD. C1 Univ Sunderland, Sch Hlth Nat & Social Sci, Autism Res Unit, Sunderland SR1 3SD, England. Univ Sunderland, Sch Pharm, 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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Int. PD OCT PY 2004 VL 46 IS 5 BP 531 EP 533 DI 10.1111/j.1442-200x.2004.01946.x PG 3 WC Pediatrics SC Pediatrics GA 861QL UT WOS:000224433000005 PM 15491378 ER PT J AU Yilmaz, I Yanardag, M Birkan, B Bumin, G AF Yilmaz, I Yanardag, M Birkan, B Bumin, G TI Effects of swimming training on physical fitness and water orientation in autism SO PEDIATRICS INTERNATIONAL LA English DT Article DE autism; swimming; water orientation C1 Anadolu Univ, Sch Phys Educ & Sports, Eskisehir, Turkey. Eskilehir Adult Mentally Retarded Women Care & Re, Eskisehir, Turkey. Anadolu Univ, Res Inst Handicapped, Eskisehir, Turkey. Hacettepe Univ, Sch Phys Therapy & Rehabil, Ankara, Turkey. RP Yilmaz, I (reprint author), Anadolu Univ, Sch Phys Educ & Sports, Eskisehir, Turkey. EM ilkery@anadolu.edu.tr CR BEST JF, 1972, AUST OCCUP THER J, V21, P72 BUMIN G, 2002, J REHABIL MED, V34, P1 KILLIAN K, 1994, ADAPT PHYS ACT Q, V1, P287 LEVINSON LJ, 1993, ADAPT PHYS ACT Q, V10, P255 MARIN B, 1985, ADAPT PHYS ACT Q, V2, P43 Martin H., 1981, PHYSIOTHERAPY, V67, P288 MOSHER R, 1975, J LEISURABILITY, V2, P29 WING L, 1976, EARLY CHILDHOOD AUTI, P198 YILMAZ I, 2002, Q EXERC SPORT S, V73, P108 NR 9 TC 18 Z9 18 PU BLACKWELL PUBLISHING ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 1328-8067 J9 PEDIATR INT JI Pediatr. Int. PD OCT PY 2004 VL 46 IS 5 BP 624 EP 626 DI 10.1111/j.1442-200x.2004.01938.x PG 3 WC Pediatrics SC Pediatrics GA 861QL UT WOS:000224433000026 PM 15491399 ER PT J AU Bell, JG MacKinlay, EE Dick, JR MacDonald, DJ Boyle, RM Glen, ACA AF Bell, JG MacKinlay, EE Dick, JR MacDonald, DJ Boyle, RM Glen, ACA TI Essential fatty acids and phospholipase A(2) in autistic spectrum disorders SO PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS LA English DT Article; Proceedings Paper CT 1st Brain Phospholipids Conference CY AUG-SEP -, 2003 CL Aviemore, SCOTLAND ID NEURODEVELOPMENTAL DISORDERS AB A health questionnaire based on parental observations of clinical signs of fatty acid deficiency (FAD) showed that patients with autism and Asperger's syndrome (ASP) had significantly higher FAD scores (6.34+/-4.37 and 7.64+/-6.20, respectively) compared to controls (1.78+/-1.68). Patients with regressive autism had significantly higher percentages of 18:0,18:2n-6 and total saturates in their RBC membranes compared to controls, while 24:0, 22:5n-6, 24:1 and the 20:4n-6/20:5n-3 ratio were significantly higher in both regressive autism and ASP groups compared to controls. By comparison, the 18: 1 n-9 and 20:4n-6 values were significantly lower in patients with regressive autism compared to controls while 22:5n-3, total n-3 and total dimethyl acetals were significantly lower in both regressive autism and ASP groups compared to controls. Storage of RBC at -20degreesC for 6 weeks resulted in significant reductions in highly unsaturated fatty acid levels in polar lipids of patients with regressive autism, compared to patients with classical autism or ASP, or controls. Patients diagnosed with both autism and ASP showed significantly increased levels of EPA (similar to 200%) and DHA (similar to 40%), and significantly reduced levels of ARA (similar to 20%), 20:3n-6 and ARA/EPA ratio in their RBC polar lipids, when supplemented with EPA-rich fish oils, compared to controls and non-supplemented patients with autism. Patients with both regressive autism and classical autism/Asperger's syndrome had significantly higher concentrations of RBC type IV phospholipase A(2) compared to controls. However, patients with autism/ASP, who had taken EPA supplements, had significantly reduced PLA(2) concentrations compared to unsupplemented patients with classical autism or ASP. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Stirling, Inst Aquaculture, Lipid Nutr Grp, Stirling FK9 4LA, Scotland. S Glasgow Univ Hosp, NHS Trust, Victoria Infirm, Dept Biochem, Glasgow, Lanark, Scotland. RP Bell, JG (reprint author), Univ Stirling, Inst Aquaculture, Lipid Nutr Grp, Stirling FK9 4LA, Scotland. EM g.j.bell@stir.ac.uk CR Bell JG, 2000, PROSTAG LEUKOTR ESS, V63, P21, DOI 10.1054/plef.2000.0186 FAROOQUI AA, 2003, PHOSPHOLIPID SPECTRU, P49 Fenton WS, 2000, BIOL PSYCHIAT, V47, P8, DOI 10.1016/S0006-3223(99)00092-X GLEN ACA, 2003, PHOSPHOLIPID SPECTRU, P183 Horrobin D.F., 2003, PHOSPHOLIPID SPECTRU, P3 HORROBIN DF, 2003, PHOSPHOLIPID SPECTRU, P123 Jarbrink K, 2001, AUTISM, V5, P7, DOI 10.1177/1362361301005001002 MacDonnell LEF, 2000, PROSTAG LEUKOTR ESS, V63, P37, DOI 10.1054/plef.2000.0189 Maes M, 1999, PSYCHIAT RES, V85, P275, DOI 10.1016/S0165-1781(99)00014-1 *MED RES COUNC, 2001, MRC REV AUT RES EP C PEET M, PHOSPHOLIPID SPECTRU Richardson AJ, 2000, PROSTAG LEUKOTR ESS, V63, P69, DOI 10.1054/plef.2000.0194 Ross MA, 2000, PROSTAG LEUKOTR ESS, V63, P61, DOI 10.1054/plef.2000.0192 Stevens L, 2000, AM J CLIN NUTR, V71, P327 STEVENS LJ, 1995, AM J CLIN NUTR, V62, P761 Stoll AL, 1999, PROSTAG LEUKOTR ESS, V60, P329, DOI 10.1016/S0952-3278(99)80008-8 Vancassel S, 2001, PROSTAG LEUKOTR ESS, V65, P1, DOI 10.1054/plef.2001.0281 Yao J.K., 2003, PHOSPHOLIPID SPECTRU, P193 NR 18 TC 63 Z9 71 PU CHURCHILL LIVINGSTONE PI EDINBURGH PA JOURNAL PRODUCTION DEPT, ROBERT STEVENSON HOUSE, 1-3 BAXTERS PLACE, LEITH WALK, EDINBURGH EH1 3AF, MIDLOTHIAN, SCOTLAND SN 0952-3278 J9 PROSTAG LEUKOTR ESS JI Prostaglandins Leukot. Essent. Fatty Acids PD OCT PY 2004 VL 71 IS 4 BP 201 EP 204 DI 10.1016/j.plefa.2004.03.008 PG 4 WC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism SC Biochemistry & Molecular Biology; Cell Biology; Endocrinology & Metabolism GA 848QL UT WOS:000223482100001 PM 15301788 ER PT J AU Lauritsen, MB Pedersen, CB Mortensen, PB AF Lauritsen, MB Pedersen, CB Mortensen, PB TI The incidence and prevalence of pervasive developmental disorders: a Danish population-based study SO PSYCHOLOGICAL MEDICINE LA English DT Article ID AUTISTIC SPECTRUM DISORDERS; PRESCHOOL-CHILDREN; RUBELLA VACCINE; MEASLES; MUMPS; CALIFORNIA; TRENDS AB Background. Based on prevalence studies and the few incidence studies of pervasive developmental disorders (PDDs) the prevalence and incidence of these disorders have been claimed to be increasing. Method. The annual and age-specific prevalence and incidence rates of childhood autism, atypical autism, Asperger's disorder, and pervasive developmental disorder not otherwise specified (PDD-NOS) in Denmark during the period 1971-2000 in children younger than 10 years were estimated using data from the Danish Psychiatric Central Register. Results. A total of 2.4 million children younger than 10 years were followed and 2061 cases with the PDDs studied were identified. Generally, the prevalence and incidence rates of the PDDs studied were stable until the early 1990s after which an increase in the occurrence of all disorders was seen, until 2000. The annual incidence rate per 10000 children younger than 10 years was 2.0 for childhood autism, 0.7 for atypical autism, 1.4 for Asperger's disorder, and 3.0 for PDD-NOS in 2000. We calculated a 'corrected' prevalence of childhood autism at 11.8, atypical autism at 3.3, Asperger's disorder at 4.7, and PDD-NOS at 14.6 per 10000 children younger than 10 years on 1 January 2001. Conclusions. We found that the estimated prevalences of the PDDs studied were probably underestimated. Furthermore, the increasing prevalence and incidence rates during the 1990s may well be explained by changes in the registration procedures and more awareness of the disorders, although a true increase in the incidence cannot be ruled out. C1 Hosp Psychiat, Dept Psychiat Demog, DK-8240 Risskov, Denmark. Aarhus Univ, Natl Ctr Register Based Res, Aarhus, Denmark. RP Lauritsen, MB (reprint author), Hosp Psychiat, Dept Psychiat Demog, Skovagervej 2, DK-8240 Risskov, Denmark. 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Med. PD OCT PY 2004 VL 34 IS 7 BP 1339 EP 1346 DI 10.1017/S0033291704002387 PG 8 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 876PA UT WOS:000225508200020 PM 15697060 ER PT J AU Klein, SB German, TP Cosmides, L Gabriel, R AF Klein, SB German, TP Cosmides, L Gabriel, R TI A theory of autobiographical memory: Necessary components and disorders resulting from their loss SO SOCIAL COGNITION LA English DT Review ID FUNCTIONING AUTISTIC INDIVIDUALS; EPISODIC MEMORY; SELF-CONSCIOUSNESS; AUTONOETIC CONSCIOUSNESS; SCHIZOPHRENIC-PATIENTS; UTILIZATION BEHAVIOR; ANTEROGRADE AMNESIA; RETROGRADE-AMNESIA; PREFRONTAL CORTEX; FRONTAL LOBES AB In this paper we argue that autobiographical memory can be conceptualized as a mental state resulting from the interplay of a set of psychological capacities-self-reflection, self-agency, self-ownership and personal temporality-that transform a memorial representation into an autobiographical personal experience. We first review evidence from a variety of clinical domains-for example, amnesia, autism, frontal lobe pathology, schizophrenia-showing that breakdowns in any of the proposed components can produce impairments in autobiographical recollection, and conclude that the self-reflection, agency, ownership, and personal temporality are individually necessary and jointly sufficient for autobiographical memorial experience. We then suggest a taxonomy of amnesic disorders derived from consideration of the consequences of breakdown in each of the individual component processes that contribute to the experience of autobiographical recollection. C1 Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA. RP Klein, SB (reprint author), Univ Calif Santa Barbara, Dept Psychol, Santa Barbara, CA 93106 USA. 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The articles in this Special Issue subject 'Theory of Mind' to sustained critical scrutiny, and also present alternative accounts of how we make sense of-and make sense to-other people. They trace the historical sources of 'Theory of Mind', criticize its fundamental assumptions and favoured methods, and examine its applications to child development and the explanation of schizophrenia and autism. C1 Univ Manchester, Dept Psychol, Manchester M13 9PL, Lancs, England. Univ Portsmouth, Dept Psychol, Portsmouth PO1 2DY, Hants, England. Manchester Metropolitan Univ, Fac Humanities Law & Social Sci, Manchester M15 6LL, Lancs, England. RP Leudar, I (reprint author), Univ Manchester, Dept Psychol, Oxford Rd, Manchester M13 9PL, Lancs, England. EM I.leuder@manchester.ac.uk; alan.costall@port.ac.uk; D.Francis@mmu.ac.uk CR BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Bennett J. F., 1976, LINGUISTIC BEHAV Bretherton I., 1981, INFANT SOCIAL COGNIT, P333 Byrne R. 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W., 1991, COGNITIVISM Suddendorf T, 2001, PSYCHOL BULL, V127, P629, DOI 10.1037//0033-2909.127.5.629 Wellman H. M., 1990, CHILDS THEORY MIND WHITEN A, 1991, FUNDAMENTAL ISSUES M NR 26 TC 23 Z9 23 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0959-3543 J9 THEOR PSYCHOL JI Theory Psychol. PD OCT PY 2004 VL 14 IS 5 BP 571 EP 578 DI 10.1177/0959354304046173 PG 8 WC Psychology, Multidisciplinary SC Psychology GA 870CM UT WOS:000225031600001 ER PT J AU Shanker, S AF Shanker, S TI The roots of mindblindness SO THEORY & PSYCHOLOGY LA English DT Article DE affect; autism; emotional capacity; Theory of Mind ID YOUNG AUTISTIC-CHILDREN; JOINT ATTENTION; MIND; EXPRESSION; KNOWLEDGE; PERFORMANCE; ABILITY; EMOTION; BELIEF AB This paper challenges the hypothesis that the type of social impairment observed in children with autism is evidence of an underlying malfunction in their 'Theory of Mind', resulting in 'mindblindness'. To establish this point, the paper takes up two interesting ideas in the Theory of Mind literature, purged of their Cartesianism: first, that the study of autism does indeed provide us with critical insights into the development of social understanding and empathy; and, second, that no meaningful distinction can be drawn between a child's interpersonal and intrapersonal development. The paper seeks to show how the ability to understand someone else's thoughts and emotions is a product of endless co-regulated interactions in which the child's own emotions and sense of self develop. The reason why children with autism so frequently exhibit impaired social relatedness is because basic biological challenges-such as sensory over-and under-reactivity-inhibit their ability to engage in these co-regulated interactive experiences. C1 York Univ, Atkinson Coll, Dept Psychol, N York, ON M3J 1P3, Canada. RP Shanker, S (reprint author), York Univ, Atkinson Coll, Dept Psychol, N York, ON M3J 1P3, Canada. EM shanker@yorku.ca CR Allen Christopher, 1998, SOFT UNDERBELLY REAS, P79 Astington J. W., 1993, CHILDS DISCOVERY MIN Baron-Cohen S., 2000, NEW COGNITIVE NEUROS, P1167 BARONCOHEN S, 1989, J CHILD PSYCHOL PSYC, V30, P285, DOI 10.1111/j.1469-7610.1989.tb00241.x Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY BELL S, 1970, CHILD DEV, V41, P219 BIALYSTOK E, 2003, J DEV LEARNING DISOR, V7, P37 Bieberich AA, 1998, J AUTISM DEV DISORD, V28, P333, DOI 10.1023/A:1026016804357 Bono J. 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M., 1990, CHILDS THEORY MIND Welsford Enid, 1966, FOOL HIS SOCIAL LIT WIMMER H, 1983, COGNITION, V13, P103, DOI 10.1016/0010-0277(83)90004-5 Wright Thomas, 1971, PASSIONS MINDE GEN Yirmiya N, 1998, PSYCHOL BULL, V124, P283, DOI 10.1037/0033-2909.124.3.283 ZAHLAVI D, 2003, J CONSCIOUSNESS STUD, V10, P53 ZAHLAVI D, 2002, OURSELVES 2 PERSON I, P151 NR 79 TC 6 Z9 6 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0959-3543 J9 THEOR PSYCHOL JI Theory Psychol. PD OCT PY 2004 VL 14 IS 5 BP 685 EP 703 DI 10.1177/0959354304046179 PG 19 WC Psychology, Multidisciplinary SC Psychology GA 870CM UT WOS:000225031600007 ER PT J AU Williams, E AF Williams, E TI Who really needs a 'Theory' of Mind? SO THEORY & PSYCHOLOGY LA English DT Article DE Asperger's syndrome; autism; autobiographical accounts; theory-theory ID AUTISM; CONSCIOUSNESS; CHILDREN AB According to the theory-theory account of understanding other minds, children develop a succession of theories of mind that, just like scientific theories, postulate abstract coherent mental entities and laws, and provide predictions, interpretations and explanations. These, in turn, enable them to interact successfully with other people. Individuals with autism or Asperger's syndrome are said to be unable to theorize about other minds, resulting in difficulties in relating to the people around them. This paper explores the possibility that we can reconceptualize the assumed relationship from the other direction, proposing that it is misleading to construe the task of achieving social understanding as a logical, scientific one. Rather, it will be suggested that typical children do not have to theorize that there are minds as they can immediately experience other people's intentions and feelings within their affective, co-regulated interactions with them. High-functioning individuals with autism, on the other hand, do need to engage in theorizing about mind if they are to bridge the gap that exists between themselves and other people. In support of this argument, this paper presents findings from an interpretative phenomenological analysis (IPA) of ten published autobiographical accounts written by individuals diagnosed with either high-functioning autism or Asperger's syndrome. C1 Univ Surrey, Dept Psychol, Guildford GU2 5XH, Surrey, England. RP Williams, E (reprint author), Univ Surrey, Dept Psychol, Guildford GU2 5XH, Surrey, England. EM e.i.williams@surrey.ac.uk CR Adrien J L, 1992, Acta Paedopsychiatr, V55, P71 ADRIEN JL, 1991, J AUTISM DEV DISORD, V21, P43, DOI 10.1007/BF02206996 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 ASTINGTON JW, 1991, BRIT J DEV PSYCHOL, V9, P7 Baron- Cohen S., 2002, FOCUS AUTISM OTHER D, V17, P186, DOI 10.1177/10883576020170030801 Baron-Cohen S., 2000, UNDERSTANDING OTHER, P3 BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Baron-Cohen Simon, 1995, MINDBLINDNESS ESSAY Bernabei P., 1998, AUTISM, V2, P243, DOI 10.1177/1362361398023003 Dawson G, 1998, J AUTISM DEV DISORD, V28, P479, DOI 10.1023/A:1026043926488 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 DREYFUS HL, 1991, COGNITIVISM ALTERNAT, P17 Flowers P., 1997, MAT DISCOURSES HLTH, P68 Frith U, 1999, MIND LANG, V14, P1 GOPNIK A, 1999, MIT ENCY COGNITIVE S, P830 GOPNIK A, 2000, UNDERSTANDING OTHER, P21 Grandin T, 1996, THINKING PICTURES OT Happe F, 1999, PSYCHOLOGIST, V12, P540 Kanner L, 1943, NERV CHILD, V2, P217 Lawson W., 2001, LIFE GLASS PERSONAL LESLIE A, 2000, ENCY PSYCHOL, V8, P60 Leslie A. 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M., 1992, MIND LANG, V7, P145, DOI DOI 10.1111/J.1468-0017.1992.TB00202.X WILLEY LH, 1999, PRETENDING NORMAL LI WILLIAMS E, 2004, UNPUB WHAT IS IT REA WING L, 1981, J AUTISM DEV DISORD, V11, P31, DOI 10.1007/BF01531339 World Health Organization, 1993, INT CLASS DIS DIAGN NR 43 TC 10 Z9 10 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0959-3543 J9 THEOR PSYCHOL JI Theory Psychol. PD OCT PY 2004 VL 14 IS 5 BP 704 EP 724 DI 10.1177/0959354304046180 PG 21 WC Psychology, Multidisciplinary SC Psychology GA 870CM UT WOS:000225031600008 ER PT J AU Colombino, T AF Colombino, T TI Theory of mind and the practical management of autistic behavior in the classroom environment SO THEORY & PSYCHOLOGY LA English DT Article DE autism; ethnomethodology; situated interaction; Theory of Mind; Theory of Mind Mechanism AB Theory of Mind Theory has provided a description of the mind which has been used as the basis for theories on the nature of the cognitive impairment found in individuals with autism, as exemplified in the work of Simon Baron-Cohen. This paper draws on the personal experience of the author observing autistic children in a special needs school, and provides a critical perspective on the conceptual framework that Theory of Mind Theory uses to account for our perception of other people's mental states. This paper's argument is that in the case of autism, the Theory of Mind Mechanism (ToMM) fails to provide a disease model that is sustainable in situated interactions with autistic children such as the one observed here, and that ultimately this is due to the theory's poorly conceptualized account of mentalistic understanding. C1 Univ Lancaster, Dept Sociol, Lancaster LA1 4YL, England. RP Colombino, T (reprint author), Univ Lancaster, Dept Sociol, Lancaster LA1 4YL, England. EM t.colombino@lancaster.ac.uk CR BARONCOHENS, 1995, MINDBLINDNESS ESSAY Bennett M., 2003, PHILOS FDN NEUROSCIE Benson D., 1991, ETHNOMETHODOLOGY HUM, P109 Coulter J., 1973, APPROACHES INSANITY Coulter J, 1989, MIND ACTION Garfinkel Harold, 1984, STUDIES ETHNOMETHODO Goffman E., 1963, BEHAV PUBLIC PLACES Goffman E, 1967, INTERACTION RITUAL E GOODE D, 1994, WORDL WITHOUT WORDS Hacking Ian, 1999, SOCIAL CONSTRUCTION WIEDER DL, 1980, SOCIOL INQ, V50, P75, DOI 10.1111/j.1475-682X.1980.tb00017.x NR 11 TC 2 Z9 2 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 0959-3543 J9 THEOR PSYCHOL JI Theory Psychol. PD OCT PY 2004 VL 14 IS 5 BP 725 EP 737 DI 10.1177/0959354304046181 PG 13 WC Psychology, Multidisciplinary SC Psychology GA 870CM UT WOS:000225031600009 ER PT J AU Butler, KG AF Butler, KG TI Asperger syndrome and high-functioning autism: Addressing social communication and emotional regulation SO TOPICS IN LANGUAGE DISORDERS LA English DT Editorial Material C1 San Jose State Univ, Commun Disorders & Sci Program, San Jose, CA 95192 USA. RP Butler, KG (reprint author), San Jose State Univ, Commun Disorders & Sci Program, San Jose, CA 95192 USA. CR HUXLEY A, 1945, RANDOM HOUSE QUOTATI PARKERPOPE T, 2004, WALL STREET J 1012, pD1 NR 2 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0271-8294 J9 TOP LANG DISORD JI Top. Lang. Disord. PD OCT-DEC PY 2004 VL 24 IS 4 BP 245 EP 245 PG 1 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 872FU UT WOS:000225193900001 ER PT J AU Rubins, E AF Rubins, E TI Asperger syndrome and high-functioning autism: Addressing social communication and emotional regulation - Foreword SO TOPICS IN LANGUAGE DISORDERS LA English DT Editorial Material CR Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Kanner L, 1943, NERV CHILD, V2, P217 National Research Council, 2000, NEUR NEIGHB National Research Council, 2001, ED CHILDR AUT PRIZANT BM, IN PRESS SCERTS TM M, V1 TSATSANIS KD, 2003, CHILD ADOL PSYCH CL, V12, P45 Klin A, 2003, CHILD ADOL PSYCH CL, V12, P1, DOI 10.1016/S1056-4993(02)00052-4 NR 7 TC 0 Z9 0 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0271-8294 J9 TOP LANG DISORD JI Top. Lang. Disord. PD OCT-DEC PY 2004 VL 24 IS 4 BP 246 EP 248 PG 3 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 872FU UT WOS:000225193900002 ER PT J AU Tsatsanis, KD Foley, C Donehower, C AF Tsatsanis, KD Foley, C Donehower, C TI Contemporary outcome research and programming guidelines for Asperger syndrome and high-functioning autism SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE Asperger syndrome; high-functioning autism; outcome research; treatment guidelines ID SOCIAL-SKILLS GROUP; BEHAVIORAL TREATMENT; CHILDREN; INTERVENTION; INDIVIDUALS; ADOLESCENTS; DISORDERS; DIAGNOSIS AB In recent years, there has been an extraordinary surge of interest in achieving a greater understanding of the needs of children and adolescents with Asperger syndrome and high-functioning autism, and with this increase in attention, research has provided a range of directions with respect to treatment guidelines. However, there is also a need for empirically supported evidence that can guide parents and professionals in their choices for educational programming for this unique population. A summary of the principal conclusions that can be drawn from the current treatment efficacy research is provided along with practical issues related to navigating the intervention literature, and directions for future research in this field. C1 Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Charlestown, MA 02129 USA. Yale Univ, Sch Med, New Haven, CT USA. Harvard Univ, Sch Med, Boston, MA USA. RP Tsatsanis, KD (reprint author), Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, 149 13th St,Floor 10, Charlestown, MA 02129 USA. 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PD OCT-DEC PY 2004 VL 24 IS 4 BP 249 EP 259 PG 11 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 872FU UT WOS:000225193900003 ER PT J AU Tsatsanis, KD AF Tsatsanis, KD TI Heterogeneity in learning style in Asperger syndrome and high-functioning autism SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE Asperger syndrome; attention; cognitive profiles; executive function; high-functioning autism ID RECEPTIVE LANGUAGE DISORDER; EARLY ADULT LIFE; EXECUTIVE FUNCTION; WORKING-MEMORY; AMNESIC SYNDROME; FOLLOW-UP; CHILDREN; ATTENTION; COMMUNICATION; INDIVIDUALS AB Although children and adolescents with high-functioning autism and Asperger syndrome present with some similar clinical features and challenges, heterogeneity of learning style coupled with the predominance of specific "packages" of materials and methods tends to understate the need for individualization when designing an educational and/or a therapeutic program. Treatment approaches will be enhanced when the core areas of strength and vulnerability are identified and evaluated over the course of development for each individual. A review of those aspects of cognition that are critical to consider when designing an educational program is provided. In addition to profiles on cognitive testing, several areas of specific functioning will be addressed including attention, memory, and executive function. C1 Yale Univ, Sch Med, New Haven, CT USA. Harvard Univ, Sch Med, Boston, MA USA. RP Tsatsanis, KD (reprint author), Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, 149 13th St,Floor 10, Charlestown, MA 02129 USA. EM ktsatsanis@partners.org CR American Psychiatric Association, 2000, DIAGN STAT MAN MENT American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Barnhill G., 2000, FOCUS AUTISM OTHER D, V15, P146, DOI [10.1177/108835760001500303, DOI 10.1177/108835760001500303] Bennetto L, 1996, CHILD DEV, V67, P1816, DOI 10.1111/j.1467-8624.1996.tb01830.x BOUCHER J, 1976, BRIT J PSYCHOL, V67, P73 BOUCHER J, 1981, J AUTISM DEV DISORD, V11, P293, DOI 10.1007/BF01531512 BOUCHER J, 1989, J CHILD PSYCHOL PSYC, V30, P99, DOI 10.1111/j.1469-7610.1989.tb00771.x BOUCHER J, 1981, BRIT J PSYCHOL, V72, P211 BUCHSBAUM MS, 1992, J AUTISM DEV DISORD, V22, P115, DOI 10.1007/BF01046407 CASEY BJ, 1993, J CLIN EXP NEUROPSYC, V15, P933, DOI 10.1080/01688639308402609 CHARLOP MH, 1989, J APPL BEHAV ANAL, V22, P275, DOI 10.1901/jaba.1989.22-275 COURCHESNE E, 1994, BEHAV NEUROSCI, V108, P848, DOI 10.1037//0735-7044.108.5.848 DELONG GR, 1992, NEUROSCI BIOBEHAV R, V16, P63, DOI 10.1016/S0149-7634(05)80052-1 Ehlers S, 1997, J CHILD PSYCHOL PSYC, V38, P207, DOI 10.1111/j.1469-7610.1997.tb01855.x Eisenmajer R, 1996, J AM ACAD CHILD PSY, V35, P1523, DOI 10.1097/00004583-199611000-00022 GARRETSON HB, 1990, J AUTISM DEV DISORD, V20, P101, DOI 10.1007/BF02206860 Ghaziuddin M, 2004, J AUTISM DEV DISORD, V34, P279, DOI 10.1023/B:JADD.0000029550.19098.77 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P279 Gilchrist A, 2001, J CHILD PSYCHOL PSYC, V42, P227, DOI 10.1017/S0021963001006631 Gillberg C, 2001, AUTISM, V5, P57, DOI 10.1177/1362361301005001006 Gillberg C, 1998, BRIT J PSYCHIAT, V172, P200, DOI 10.1192/bjp.172.3.200 Goldstein G, 2001, J AUTISM DEV DISORD, V31, P433, DOI 10.1023/A:1010620820786 Grandin T., 1992, HIGH FUNCTIONING IND, P105 Grant D., 1948, WISCONSIN CARD SORTI Gray C., 1995, TEACHING CHILDREN AU, P219 Griswold D. 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Lang. Disord. PD OCT-DEC PY 2004 VL 24 IS 4 BP 260 EP 270 PG 11 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 872FU UT WOS:000225193900004 ER PT J AU Rubin, E Lennon, L AF Rubin, E Lennon, L TI Challenges in social communication in Asperger syndrome and high-functioning autism SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE Asperger syndrome; differential diagnosis; high-functioning autism; learning style; social communication ID LISTENING PREFERENCES; INFANTILE-AUTISM; JOINT ATTENTION; FOLLOW-UP; DSM-IV; CHILDREN; DISORDER; LANGUAGE; INDIVIDUALS; FACE AB Despite the inclusion of Asperger syndrome in the Diagnostic and Statistical Manual of Mental Disorders-Fourth Edition (DSM-IV American Psychiatric Association [APA], 1994) 10 years ago, there is ongoing debate regarding its validity as a diagnostic construct, particularly relative to the diagnosis of autistic disorder when it is not accompanied by significant language and cognitive delays. This latter condition, referred to as high-functioning autism, is, indeed, characterized by social communication challenges similar to those found in Asperger syndrome. Nevertheless, there are distinctions in both learning style and social communication that have critical implications for treatment and educational programming. Although this article will begin with a review of those social communication challenges that are common to both of these disorders, a discussion of challenges that are more specific to children and adolescents with either Asperger syndrome or high-functioning autism will follow. C1 CCC, SLP, Carmel, CA 93922 USA. Yale Univ, Sch Med, New Haven, CT USA. Univ Calif Irvine, Coll Med, Speech Pathol Associates, Irvine, CA USA. Univ Calif Irvine, Coll Med, OC Kids Clin, Irvine, CA USA. RP Rubin, E (reprint author), CCC, SLP, POB 222171, Carmel, CA 93922 USA. 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PD OCT-DEC PY 2004 VL 24 IS 4 BP 271 EP 285 PG 15 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 872FU UT WOS:000225193900005 ER PT J AU Laurent, AC Rubin, E AF Laurent, AC Rubin, E TI Challenges in emotional regulation in Asperger syndrome and high-functioning autism SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE Asperger syndrome; autism; emotional regulation; intervention; problem behavior ID CHILDREN; COMMUNICATION; CHILDHOOD; DISORDER AB As positive outcomes for children and adolescents with either Asperger syndrome or high-functioning autism are related to the development of social communicative competence, recognition of the developmental capacities that contribute to this achievement is essential. Although social communication skills play a central role, developmental milestones in emotional regulation should be considered of equal importance. This article will describe emotional regulatory challenges commonly faced by individuals with Asperger syndrome and individuals with high-functioning autism that hinder success in social interactions. The impact of challenges in social communication (e.g., difficulty sharing and interpreting intentions, recognition of emotional states, and using socially conventional forms of emotional expression) and differences in neurophysiology (e.g., sensory sensitivities and learning style) on emotional regulation win be reviewed. C1 Commun Crossroads, N Kingstown, RI USA. Yale Univ, Sch Med, New Haven, CT USA. Commun Crossroads, Carmel, CA USA. RP Laurent, AC (reprint author), OTR L, 100 Juniper Dr, N Kingstown, RI 02852 USA. EM Amy@CommXRoads.com CR Anzalone M. 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PD OCT-DEC PY 2004 VL 24 IS 4 BP 286 EP 297 PG 12 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 872FU UT WOS:000225193900006 ER PT J AU Rubin, E Laurent, AC AF Rubin, E Laurent, AC TI Implementing a curriculum-based assessment to prioritize learning objectives in Asperger syndrome and high-functioning autism SO TOPICS IN LANGUAGE DISORDERS LA English DT Article DE Asperger syndrome; autism; curriculum; emotional regulation; intervention; social communication ID SPECTRUM DISORDERS; COMMUNICATION; CHILDREN AB To develop a comprehensive educational program for children and adolescents with Asperger syndrome and children and adolescents with high-functioning autism, goals and objectives need to be identified in those areas of development that support social communicative competence. The role of a child's social partners, however, is often neglected by relying on curricula that focus solely on prioritizing these child-specific objectives. Thus, it is important to consider that how a partner interacts with a child and how an environment is adapted with learning supports has a significant and long-term impact on that child's development. This article provides a description of the SCERTS Model, a comprehensive educational approach that includes a curriculum-based assessment designed to prioritize developmental objectives for the child as well as that child's partners. In this approach, the role of a child's partners in fostering more sophisticated language forms, the social conventions for appropriate behavior in different social situations, greater sensitivity to others' perspectives and emotional states, and the ability to plan and prepare for experiences is emphasized. C1 CCC, SLP, Carmel, CA 93922 USA. Commun Crossroads, N Kingstown, RI USA. Yale Univ, Sch Med, New Haven, CT USA. RP Rubin, E (reprint author), CCC, SLP, POB 222171, Carmel, CA 93922 USA. EM Emily@CommXRoads.com CR Attwood T., 1998, ASPERGERS SYNDROME G Attwood T, 2003, CHILD ADOL PSYCH CL, V12, P65, DOI 10.1016/S1056-4993(02)00054-8 Cole P. M., 1994, MONOGRAPHS SOC RES C, V59 DeGangi GA., 2000, PEDIAT DISORDERS REG Garcia Winner M., 2002, THINKING YOU THINKIN Garfin D. 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PD OCT-DEC PY 2004 VL 24 IS 4 BP 298 EP 315 PG 18 WC Linguistics; Rehabilitation SC Linguistics; Rehabilitation GA 872FU UT WOS:000225193900007 ER PT J AU Bayliss, S AF Bayliss, S TI Showcasing 'neurodiversity' - Artists with autism, cerebral palsy, and other disabilities are attracting mainstream attention SO ARTNEWS LA English DT News Item CR PARK J, 2004, THE CHRYSLER BUILDIN NR 1 TC 0 Z9 0 PU ARTNEWS ASSOCIATES PI NEW YORK PA 48 WEST 38TH STREET, NEW YORK, NY 10018 USA SN 0004-3273 J9 ART NEWS JI Artnews PD OCT PY 2004 VL 103 IS 9 BP 78 EP 78 PG 1 WC Art SC Art GA 885XL UT WOS:000226190500012 ER PT J AU Andreae, MC Freed, GL Katz, SL AF Andreae, MC Freed, GL Katz, SL TI Safety concerns regarding combination vaccines: the experience in Japan SO VACCINE LA English DT Article DE vaccine; safety; MMR ID UNITED-STATES; IMMUNIZATION; MEASLES; VACCINATION; UNDERSTAND; POPULATION; AUTISM; MMWR AB This study explored the safety concerns associated with combination vaccines in Japan. The impact of Japan's decision in 1975 to withdraw the combined diptheria, tetanus, and pertussis (DTP) vaccine, and then in 1993, the combined measles, mumps, and rubella (MMR) vaccine and provide only the single antigen vaccines was analyzed. Interviews with both governmental and non-governmental agency officials in Japan demonstrated that withdrawal of the DTP and MMR vaccines had significant impact on the rates of immunization and disease despite the availability of monovalent vaccines. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Michigan, CHEAR Unit, Div Gen Pediat, Ann Arbor, MI 48109 USA. Duke Univ, Med Ctr, Dept Pediat, Durham, NC 27710 USA. RP Andreae, MC (reprint author), Univ Michigan, CHEAR Unit, Div Gen Pediat, 300 N Ingalls 6E12, Ann Arbor, MI 48109 USA. 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Natl. Acad. Sci. U. S. A. PD SEP 21 PY 2004 VL 101 IS 38 BP 13915 EP 13920 DI 10.1073/pnas.0405939101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 856UF UT WOS:000224069800040 PM 15358863 ER PT J AU Buxbaum, JD Ramoz, N Reichert, J Smith, CJ Silverman, J Bespalova, I Davis, KL AF Buxbaum, JD Ramoz, N Reichert, J Smith, CJ Silverman, J Bespalova, I Davis, KL TI Linkage and association of an aspartate/glutamate carrier with autism: Genetic variants are associated with a several-fold increased risk SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 CUNY Mt Sinai Sch Med, New York, NY 10029 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 21 EP 21 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600078 ER PT J AU Conroy, J Segurado, R Meally, E Stallings, R Green, A Fitzgerald, M Gill, M Ennis, S Gallagher, L AF Conroy, J Segurado, R Meally, E Stallings, R Green, A Fitzgerald, M Gill, M Ennis, S Gallagher, L TI Evidence of association for a susceptibility region for autism on chromosome 2q SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Univ Dublin Trinity Coll, Dept Genet, Dublin 2, Ireland. Univ Dublin Trinity Coll, Dept Psychiat, Dublin 2, Ireland. Natl Ctr Med Genet, Dublin, Ireland. RI Segurado, Ricardo/K-6116-2014 OI Segurado, Ricardo/0000-0002-3547-6733 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 21 EP 21 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600077 ER PT J AU Ma, DQ Whitehead, PL Menold, MM Martin, ER Ashley-Koch, AA DeLong, GR Abramson, RK Wright, HH Cuccaro, ML Hussman, JP Gilbert, JR Pericak-Vance, MA AF Ma, DQ Whitehead, PL Menold, MM Martin, ER Ashley-Koch, AA DeLong, GR Abramson, RK Wright, HH Cuccaro, ML Hussman, JP Gilbert, JR Pericak-Vance, MA TI Identification of significant autism association on GABA(A) receptor subunit genes in chromosome 4 and 5 SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Duke Ctr Human Genet, Durham, NC USA. Univ S Carolina, Columbia, SC 29208 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 21 EP 22 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600080 ER PT J AU Jamain, S Quach, H Betancur, C Goubran-Botros, H Durand, C Melke, J Delorme, R Rastam, M Colineaux, C Gillberg, IC Soderstrom, H Bonneau, D Firth, H Leboyer, M Gillberg, C Bourgeron, T AF Jamain, S Quach, H Betancur, C Goubran-Botros, H Durand, C Melke, J Delorme, R Rastam, M Colineaux, C Gillberg, IC Soderstrom, H Bonneau, D Firth, H Leboyer, M Gillberg, C Bourgeron, T TI Rare variations and stop mutations in the neuroligin genes in autism and Asperger syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Inst Pasteur, Paris, France. Hop Henri Mondor, INSERM, U513, F-94010 Creteil, France. Univ Gothenburg, Gothenburg, Sweden. Addenbrookes Hosp, Cambridge, England. CHU Angers, Angers, France. RI Anckarsater, Henrik/C-2244-2009 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 22 EP 22 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600081 ER PT J AU Ronald, A Happe, F Bolton, P Wheelwright, S Baron-Cohen, S Plomin, R AF Ronald, A Happe, F Bolton, P Wheelwright, S Baron-Cohen, S Plomin, R TI Genetic heterogeneity for social and non-social behaviours characteristic of autism spectrum disorders in the general population and at the extreme SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Inst Psychiat, SGDP Ctr, London, England. Univ Cambridge, Autism Res Ctr, Cambridge, England. RI Happe, Francesca/D-5544-2012 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 23 EP 23 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600086 ER PT J AU Castermans, D Schrander-Stumpel, CT Fryns, JP Van de Ven, WJM Steyaert, J Creemers, JW Devriendt, K AF Castermans, D Schrander-Stumpel, CT Fryns, JP Van de Ven, WJM Steyaert, J Creemers, JW Devriendt, K TI Positional cloning of three condidate genes for autism: A possible role for neuron vesicle trafficking in the pathogenesis of autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Catholic Univ Louvain, B-3000 Louvain, Belgium. RI Steyaert, Jean/B-5326-2015 OI Steyaert, Jean/0000-0003-2512-4694 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 25 EP 25 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600093 ER PT J AU Brooks, P Roschmann, E Rousseau, F Philippi, A Hager, J AF Brooks, P Roschmann, E Rousseau, F Philippi, A Hager, J TI Genome wide mapping of autism susceptibility loci by enzymatic selection of identity-by-descent regions in autistic sibling pairs SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 IntegraGen, Evry, France. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 29 EP 29 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600108 ER PT J AU Vorstman, JAS Morcus, MEJ Swaab-Barneveld, H Heineman-de Boer, JA Duijff, SN Jansen, P Beemer, FA van Engeland, H AF Vorstman, JAS Morcus, MEJ Swaab-Barneveld, H Heineman-de Boer, JA Duijff, SN Jansen, P Beemer, FA van Engeland, H TI Autism phenotype in children with 22Q11 deletion syndrome SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Univ Med Ctr, Utrecht, Netherlands. Wilhelmina Childrens Hosp, Utrecht, Netherlands. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 73 EP 73 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600281 ER PT J AU Vorstman, JAS Staal, WG van Daalen, E Hochstenbach, R van Engeland, H AF Vorstman, JAS Staal, WG van Daalen, E Hochstenbach, R van Engeland, H TI Identification of risk genes and biological pathways: What we can learn from cytogenetic abnormalities associated with the autism phenotype SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Univ Med Ctr, Utrecht, Netherlands. Wilhelmina Childrens Hosp, Utrecht, Netherlands. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 74 EP 74 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600283 ER PT J AU Iourov, IY Vorsanova, SG Ulas, VY Yurov, YB AF Iourov, IY Vorsanova, SG Ulas, VY Yurov, YB TI X chromosome inactivation patterns in mothers of males with autistic spectrum disorder: Implications for genetic studies of autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Natl Ctr Mental Hlth RAMS, Moscow, Russia. Russian Minist Hlth, Inst Pediat & Children Surg, Moscow, Russia. RI Iourov, Ivan/O-7684-2014 OI Iourov, Ivan/0000-0002-4134-8367 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 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 90 EP 90 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600348 ER PT J AU Yirmiya, N Shaked, M Gamliel, I AF Yirmiya, N Shaked, M Gamliel, I TI Theory of mind abilities in young siblings of children with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Hebrew Univ Jerusalem, Jerusalem, Israel. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 90 EP 91 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600349 ER PT J AU Curran, SR Kasahara, M Veltman, M Powell, J Bolton, P AF Curran, SR Kasahara, M Veltman, M Powell, J Bolton, P TI Examination of the role of GABRG3 in autism spectrum disorder using within family analyses SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Inst Psychiat, London, England. RI Powell, John/G-4412-2011; Bolton, Patrick/E-8501-2010 OI Powell, John/0000-0001-6124-439X; Bolton, Patrick/0000-0002-5270-6262 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 91 EP 91 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600351 ER PT J AU Felder, B Radlwimmer, B Klauck, SM Benner, A Mincheva, A Poustka, F Lichter, P Poustka, A AF Felder, B Radlwimmer, B Klauck, SM Benner, A Mincheva, A Poustka, F Lichter, P Poustka, A TI Detection of submicroscopic chromosomal deletions and duplications in autism patients by matrix comparative genomic hybridisation (matrix-CGH) SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 91 EP 92 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600353 ER PT J AU Klauck, SM Schuster, C Felder, B Beyer, KS Benner, A Gohlke, H Illig, T Poustka, F Poustka, A AF Klauck, SM Schuster, C Felder, B Beyer, KS Benner, A Gohlke, H Illig, T Poustka, F Poustka, A TI Autism - Search for susceptibility variants in the German patient sample SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Deutsch Krebsforschungszentrum, D-6900 Heidelberg, Germany. GSF Natl Res Ctr Environm & Hlth, Inst Epidemiol, Neuherberg, Germany. Univ Frankfurt, Dept Child & Adolescent Psychiat, D-6000 Frankfurt, Germany. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 91 EP 91 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600350 ER PT J AU Curran, SR Roberts, S Thomas, S Veltman, M Browne, J Medda, E Pickles, A Sham, P Bolton, P AF Curran, SR Roberts, S Thomas, S Veltman, M Browne, J Medda, E Pickles, A Sham, P Bolton, P TI An association analysis of microsatellite markers across the Prader Willi/Angelman critical region on chromosome 15 (q11-13) and autism spectrum disorder SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Inst Psychiat, MRC, Social Genet & Dev Psychiat Ctr, London, England. Inst Psychiat, Dept Psychol Med, London SE5 8AF, England. Wessex Reg Genet Lab, Salisbury, Wilts, England. Southampton Gen Hosp, Paediat Med Unit, Southampton SO9 4XY, Hants, England. Ist Super Sanita, Epidemiol & Biostat Lab, I-00161 Rome, Italy. Univ Manchester, Manchester, Lancs, England. Univ Cambridge, Sect Dev Psychiat, Cambridge, England. RI Pickles, Andrew/A-9625-2011 OI Pickles, Andrew/0000-0003-1283-0346 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 92 EP 92 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600355 ER PT J AU Gratacos, M Armengol, LL Cerrato, C Hervas, A Suarez, M Estivill, X AF Gratacos, M Armengol, LL Cerrato, C Hervas, A Suarez, M Estivill, X TI Analysis of duplications in samples of autism using MAPH SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Ctr Regulacio Genom, Barcelona, Spain. Hosp Mutua Terrassa, Terrassa, Spain. RI Estivill, Xavier/E-2957-2012; Estivill, Xavier/A-3125-2013 OI Estivill, Xavier/0000-0002-0723-2256 NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 95 EP 95 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600365 ER PT J AU Haddad, SA Fagerness, J Yamaki, LH Andresen, KA Santangelo, SL AF Haddad, SA Fagerness, J Yamaki, LH Andresen, KA Santangelo, SL TI A genetic investigation of autism using extremely discordant sib pairs SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Harvard Univ, Sch Publ Hlth, Sch Med, Massachusetts Gen Hosp, Boston, MA 02115 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 95 EP 95 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600367 ER PT J AU McCauley, JL Olson, LM Amin, T Delahanty, R Haines, JL Sutcliffe, JS AF McCauley, JL Olson, LM Amin, T Delahanty, R Haines, JL Sutcliffe, JS TI Evidence for linkage and association to chromosome 19P in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Vanderbilt Univ, Ctr Human Genet Res, Nashville, TN USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 97 EP 97 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600372 ER PT J AU Neves-Pereira, M Massie, D Williams, J Miedzybrodzka, Z St Clair, D AF Neves-Pereira, M Massie, D Williams, J Miedzybrodzka, Z St Clair, D TI Genetic study of a de novo translocation in autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Univ Aberdeen, Aberdeen, Scotland. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 98 EP 98 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600377 ER PT J AU Rabionet, R Ma, DQ Martin, ER Ashley-Koch, AA DeLong, GR Abramson, RK Wright, HH Cuccaro, ML Gilbert, JR Pericak-Vance, MA AF Rabionet, R Ma, DQ Martin, ER Ashley-Koch, AA DeLong, GR Abramson, RK Wright, HH Cuccaro, ML Gilbert, JR Pericak-Vance, MA TI Fine mapping and association analysis of chromosome 19 and autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat 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 WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 99 EP 100 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600382 ER PT J AU Skaar, DA Jaworski, JM Martin, ER Ashley-Koch, AA Benton, J McCauley, JL Haines, JL Sutcliffe, JS DeLong, GR Wright, HH Abramson, RK Cuccaro, ML Gilbert, JR Pericak-Vance, MA AF Skaar, DA Jaworski, JM Martin, ER Ashley-Koch, AA Benton, J McCauley, JL Haines, JL Sutcliffe, JS DeLong, GR Wright, HH Abramson, RK Cuccaro, ML Gilbert, JR Pericak-Vance, MA TI Identification of significant autism associations on chromosome 7Q SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Duke Univ, Med Ctr, Durham, NC USA. Vanderbilt Univ, Med Ctr, Nashville, TN USA. Univ S Carolina, Columbia, SC 29208 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 100 EP 100 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600383 ER PT J AU Cuccaro, ML Cope, H Donnelly, S Wolpert, C Gabriels, R Wright, HH Abramson, RK Koch, AA Gilbert, J Pericak-Vance, MA AF Cuccaro, ML Cope, H Donnelly, S Wolpert, C Gabriels, R Wright, HH Abramson, RK Koch, AA Gilbert, J Pericak-Vance, MA TI The repetitive behavior phenotype in autism: Age-related changes SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Duke Univ, Med Ctr, Durham, NC USA. Univ S Carolina, Columbia, SC 29208 USA. Univ Colorado, Hlth Sci Ctr, Denver, CO USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 101 EP 101 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600386 ER PT J AU Betancur, C Heron, D Verloes, A Philippe, A Munnich, A Depienne, C Brice, A Leboyer, M AF Betancur, C Heron, D Verloes, A Philippe, A Munnich, A Depienne, C Brice, A Leboyer, M TI Etiological heterogeneity in autism: Implications for linkage and association studies SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 INSERM, U513, Creteil, France. Hop La Pitie Salpetriere, Unite Genet Clin, Paris, France. Hop Robert Debre, Unite Genet Clin, F-75019 Paris, France. Hop Necker Enfants Malad, INSERM, U393, Paris, France. Hop Necker Enfants Malad, Dept Genet, Paris, France. Hop La Pitie Salpetriere, INSERM, U289, Paris, France. Hop La Pitie Salpetriere, Dept Genet, Paris, France. Hop Albert Chenevier & Henri Mondor, Dept Psychiat, Creteil, France. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 104 EP 105 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600399 ER PT J AU Harvey, C Alfred, SE Mnatzakanian, G Roberts, WS Schanen, NC Scherer, SW Minassian, BA Vincent, JB AF Harvey, C Alfred, SE Mnatzakanian, G Roberts, WS Schanen, NC Scherer, SW Minassian, BA Vincent, JB TI Screening for mutations in exon 1 of MECP2, among individuals with either Rett syndrome, autism or mental retardation SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Ctr Addict & Mental Hlth, Toronto, ON, Canada. Hosp Sick Children, Toronto, ON M5G 1X8, Canada. Univ Delaware, Wilmington, DE USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 104 EP 104 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600397 ER PT J AU Malhotra, T Srinath, S Girimaji, SC Seshadri, SP AF Malhotra, T Srinath, S Girimaji, SC Seshadri, SP TI Are minor physical anomalies an endophenotype of autism? SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Hinchingbrooke Hosp, Dept Psychiat, Huntingdon, England. Natl Inst Mental Hlth & Neurosci, Dept Psychiat, Bangalore 560029, Karnataka, India. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 104 EP 104 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600398 ER PT J AU Correia, C AF Correia, C TI Mitochondrial dysfunction and autism: Lack of association of the aspartate/glutamate carrier SLC25A12 gene with autism or hyperlactacidemia in Portuguese patients SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Gulbenkian Inst Sci, Oeiras, Portugal. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 105 EP 105 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600400 ER PT J AU Wolpert, CM Boisen, K Cope, H Donnelly, S Cuccaro, ML Pericak-Vance, MA AF Wolpert, CM Boisen, K Cope, H Donnelly, S Cuccaro, ML Pericak-Vance, MA TI Genetic testing for autism: Current state of clinical practice in the southeastern United States SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Duke Univ, Med Ctr, Durham, NC 27706 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 107 EP 108 PG 2 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600409 ER PT J AU Hranilovic, D Bordukalo-Niksic, T Cicin-Sain, L Jernej, B AF Hranilovic, D Bordukalo-Niksic, T Cicin-Sain, L Jernej, B TI Wistar-Zagreb 5HT rat: Possible animal model for autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 Rudjer Boskovic Inst, Zagreb, Croatia. 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 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 149 EP 149 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600573 ER PT J AU Yan, J Oliveira, G Coutinho, A Yang, C Feng, J Cook, E Vicente, A Sommer, S AF Yan, J Oliveira, G Coutinho, A Yang, C Feng, J Cook, E Vicente, A Sommer, S TI Structural variants of the neuroligin 4 gene in us and Portuguese patients with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Meeting Abstract CT 12th World Congress of Psychiatric Genetics CY OCT 09-13, 2004 CL Dublin, IRELAND SP Int Soc Psychiat Genet C1 City Hope Natl Med Ctr, Duarte, CA 91010 USA. Hosp Pediat Coimbra, Coimbra, Portugal. Gulbenkian Inst Sci, Oeiras, Portugal. Univ Chicago, Chicago, IL 60637 USA. NR 0 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD SEP 15 PY 2004 VL 130B IS 1 BP 156 EP 156 PG 1 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 852GE UT WOS:000223742600600 ER PT J AU Seeman, C AF Seeman, C TI Autism spectrum disorders 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 Sicile-Kira C., 2004, AUTISM SPECTRUM DISO 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 SEP 15 PY 2004 VL 129 IS 15 BP 71 EP 71 PG 1 WC Information Science & Library Science SC Information Science & Library Science GA 853SJ UT WOS:000223847700160 ER PT J AU Hardan, AY Jou, RJ Keshavan, MS Varma, R Minshew, NJ AF Hardan, AY Jou, RJ Keshavan, MS Varma, R Minshew, NJ TI Increased frontal cortical folding in autism: a preliminary MRI study SO PSYCHIATRY RESEARCH-NEUROIMAGING LA English DT Article DE gyrification index; magnetic resonance imaging; prefrontal cortex; cerebral convolution; autistic disorder ID GYRIFICATION; CORTEX AB The gyrification index (GI), the ratio of total to outer cortical contour, was applied to measure the cerebral folding patterns in autism. GI was examined on a frontal coronal slice obtained from MRI scans of 30 nonmentally retarded individuals with autism and 32 matched healthy controls. In the autistic group, left frontal GI was higher in children and adolescents but not in adults. Cortical folding was decreased bilaterally with age in the total autistic sample but not in controls. These preliminary finding; suggest that the gyrification patterns in autism may be abnormal, which could be related to the various cortical anomalies observed in this disorder. (C) 2001 Elsevier Ireland Ltd. All rights reserved. C1 Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, Pittsburgh, PA 15213 USA. RP Hardan, AY (reprint author), Univ Pittsburgh, Sch Med, Western Psychiat Inst & Clin, Dept Psychiat, 3811 O Hara St, Pittsburgh, PA 15213 USA. EM hardanay@upmc.edu CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARMSTRONG E, 1995, CEREB CORTEX, V5, P56, DOI 10.1093/cercor/5.1.56 Aylward EH, 1998, NEUROLOGY, V50, P252 Casanova MF, 2002, NEUROLOGY, V58, P428 Courchesne E, 2001, NEUROLOGY, V57, P245 Hardan AY, 2000, NEUROLOGY, V55, P1033 Kemper TL, 1998, J NEUROPATH EXP NEUR, V57, P645, DOI 10.1097/00005072-199807000-00001 Kulynych JJ, 1997, BIOL PSYCHIAT, V41, P995, DOI 10.1016/S0006-3223(96)00292-2 Levitt JG, 2003, CEREB CORTEX, V13, P728, DOI 10.1093/cercor/13.7.728 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 Magnotta VA, 2002, COMPUT MED IMAG GRAP, V26, P251, DOI 10.1016/S0895-6111(02)00011-3 PIVEN J, 1990, AM J PSYCHIAT, V147, P734 RAKIC P, 1988, SCIENCE, V241, P170, DOI 10.1126/science.3291116 ZILBOVICIUS M, 1995, AM J PSYCHIAT, V152, P248 ZILLES K, 1988, ANAT EMBRYOL, V179, P173, DOI 10.1007/BF00304699 NR 16 TC 69 Z9 69 PU ELSEVIER SCI IRELAND LTD PI CLARE PA CUSTOMER RELATIONS MANAGER, BAY 15, SHANNON INDUSTRIAL ESTATE CO, CLARE, IRELAND SN 0925-4927 J9 PSYCHIAT RES-NEUROIM JI Psychiatry Res. Neuroimaging PD SEP 15 PY 2004 VL 131 IS 3 BP 263 EP 268 DI 10.1016/j.pscychresns.2004.06.001 PG 6 WC Clinical Neurology; Neuroimaging; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 864BV UT WOS:000224608800008 PM 15465295 ER PT J AU Smeeth, L Cook, C Fombonne, E Heavey, L Rodrigues, LC Smith, PG Hall, AJ AF Smeeth, L Cook, C Fombonne, E Heavey, L Rodrigues, LC Smith, PG Hall, AJ TI MMR vaccination and pervasive developmental disorders: a case-control study SO LANCET LA English DT Article ID MUMPS-RUBELLA VACCINATION; PRACTICE RESEARCH DATABASE; EPIDEMIOLOGIC EVIDENCE; CAUSAL ASSOCIATION; NO EVIDENCE; MEASLES; AUTISM; CHILDREN; POPULATION; IMMUNIZATION AB Background Concern that measles-mumps-rubella (MMR) vaccination might cause autism has led to a fall in vaccine coverage. We investigated whether MMR vaccination is associated with an increased risk of autism or other pervasive developmental disorders. Methods We did a matched case-control study using the UK General Practice Research Database. Cases were people born in 1973 or later who had first recorded diagnosis of pervasive developmental disorder while registered with a contributing general practice between 1987 and 2001. Controls were matched on age, sex, and general practice. Findings 1294 cases and 4469 controls were included. 1010 cases (78.1%) had MMR vaccination recorded before diagnosis, compared with 3671 controls (82.1%) before the age at which their matched case was diagnosed. After adjustment for age at joining the database, the odds ratio for association between MMR and pervasive developmental disorder was 0 . 86 (95% CI 0 . 68-1.09). Findings were similar when restricted to children with a diagnosis of autism, to those vaccinated with MMR before the third birthday, or to the period before media coverage of the hypothesis linking MMR with autism. Interpretation Our findings suggest that MMR vaccination is not associated with an increased risk of pervasive developmental disorders. C1 Univ London London Sch Hyg & Trop Med, Dept Epidemiol & Populat Sci, London WC1E 7HT, England. Univ London London Sch Hyg & Trop Med, Dept Infect & Trop Dis, London WC1E 7HT, England. McGill Univ, Montreal Childrens Hosp, Dept Psychiat, Montreal, PQ H3A 2T5, Canada. Univ London Kings Coll, Inst Psychiat, London WC2R 2LS, England. RP Smeeth, L (reprint author), Univ London London Sch Hyg & Trop Med, Dept Epidemiol & Populat Sci, Keppel St, London WC1E 7HT, England. 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In a previous study based on a load-lifting task, we showed impairment of anticipation in children with autism as evidenced by kinematics and eletromyographic recordings [Neurosci. Lett. 348 (2003) 17]. In the present study, we assessed the cortical counterparts of the use of anticipatory postural adjustments in a group of control children and in a group of children with autism. The tasks required maintaining a stable forearm position despite imposed or voluntary lifting of an object placed either on the controlateral forearm or on a support. We investigated the differences between the two groups of children on the Event-Related Desynchronisation (ERD) which precedes movement onset in adults [Electroencephalogr. Clin. Neurophysiol. 46 (1979) 138]. Electroencephalogram (EEG) power evolution of a 6-8-Hz frequency band was averaged before and after imposed or voluntary movement onset. EEG reactivity of control and autistic children did not differ during the imposed unloading condition, but significant differences appeared in the voluntary unloading situations. Before lifting the object, control children showed an ERD above the left motor areas. An ERD also occurred above the right motor areas when the object was placed on their forearm. This indicates that the ERD can also translate the use of anticipatory postural adjustments. By contrast, children with autism did not show an ERD in the two voluntary situations. This suggests a central deficit of anticipation in both postural and motor control in children with autism. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 CHRU Bretonneau, INSERM, U 619, F-37044 Tours 1, France. CNRS, Inst Neurosci Physiol & Cognit, F-13402 Marseille, France. RP Martineau, J (reprint author), CHRU Bretonneau, INSERM, U 619, 2 Bd Tonnelle, F-37044 Tours 1, France. 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Lett. PD SEP 9 PY 2004 VL 367 IS 3 BP 298 EP 303 DI 10.1016/j.neulet.2004.06.018 PG 6 WC Neurosciences SC Neurosciences & Neurology GA 855IT UT WOS:000223967500007 PM 15337253 ER PT J AU Edwards, DS Henley, WE Ely, ER Wood, JLN AF Edwards, DS Henley, WE Ely, ER Wood, JLN TI Vaccination and ill-health in dogs: a lack of temporal association and evidence of equivalence SO VACCINE LA English DT Article DE vaccination; canine; temporal-association; safety; equivalence-test ID RUBELLA VACCINATION; CAUSAL ASSOCIATION; MEASLES; AUTISM; MUMPS; RISK; MMR AB Following concerns raised over the safety of canine vaccines, an epidemiological investigation was conducted to evaluate the evidence for a temporal association between vaccination and ill-health in dogs. The owners of a randomly selected population of dogs were sent 9055 postal questionnaires, 4040 of which were returned. No temporal association was found between vaccination and ill-health in dogs after adjusting for potential confounders, such as age. However, reliable inferences from non-significant test results are limited and so equivalence-testing methods were also used to make informative inferences. Results demonstrated that recent vaccination (<3 months) does not increase signs of ill-health by more than 0.5% and may actually decrease it by as much as 5%. This general approach should be used in all field studies of vaccine safety. (C) 2004 Elsevier Ltd. All rights reserved. C1 Anim Hlth Trust, Newmarket CB8 7UU, Suffolk, England. RP Edwards, DS (reprint author), Anim Hlth Trust, Lanwades Pk, Newmarket CB8 7UU, Suffolk, England. EM david.edward@aht.org.uk RI Wood, James/A-1626-2008; Ely, Elizabeth/C-7575-2011 OI Wood, James/0000-0002-0258-3188; CR Agresti A., 1990, CATEGORICAL DATA ANA ALTMAN DG, 1995, BRIT MED J, V311, P485 Bellaby P, 2003, BRIT MED J, V327, P725, DOI 10.1136/bmj.327.7417.725 Christley RM, 2003, J AM VET MED ASSOC, V222, P433, DOI 10.2460/javma.2003.222.433 Farrington CP, 2001, VACCINE, V19, P3632, DOI 10.1016/S0264-410X(01)00097-4 FREEMAN TR, 1993, CAN MED ASSOC J, V149, P1669 GILMOUR AR, 1985, BIOMETRIKA, V72, P593, DOI 10.1093/biomet/72.3.593 Hastie T. 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SO ACTA PAEDIATRICA LA English DT Article DE immunization; parents; MMR; children; vaccine safety ID AUTISM; IMMUNIZATION; ASSOCIATION; MMR AB Background: Thanks to a successful voluntary vaccination programme, measles, mumps and rubella are rare diseases in Sweden. Coverage among children 18 mo of age has been 99%, but the measles, mumps and rubella vaccination (MMR) has increasingly been questioned among parents. Aim: To study reasons why parents choose not to vaccinate their child against measles, mumps and rubella, and their opinions on vaccines and the diseases themselves. A secondary objective was to compare coverage at 18 mo of age based on parental report with the national statistics based on patient charts. Methods: The official statistics were compared with patient charts for two birth cohorts in the city of Goteborg, Sweden. Out of these children born in 1995 and 1996, 300 unvaccinated and vaccinated children were identified. Their parents received a postal questionnaire assessing the parent's views on vaccines and childhood diseases. Results: The documented vaccine coverage in this study was higher in 1995 and 1996 than official statistics indicated. The major reason, for both groups, for accepting respectively declining vaccination was strengthening the child's immune system. Parents with children unvaccinated against MMR were also more likely to have declined vaccination against diphtheria, polio, tetanus, Haemophilus influenzae and pertussis. One-third of the parents with a child unvaccinated against MMR had not yet made their final decision 3 y after the vaccine offer. Few parents, both with vaccinated and unvaccinated children, had acquired vaccine information from the Internet. Both groups believed that insufficient time was allocated for vaccine information and discussion at the Child Health Centre. Conclusion: Our study indicates that official statistics on MMR vaccination uptake underestimate the number of vaccinated children. Vaccine safety is a major concern for many parents and needs to be addressed by healthcare professionals at institutions offering paediatric vaccinations. C1 Univ Gothenburg, Inst Womens & Childrens Hlth, Dept Paediat, Gothenburg, Sweden. Univ Orebro, Dept Biostat, Orebro, Sweden. RP Borres, MP (reprint author), Falun Cent Hosp, Dept Paediat, SE-79182 Falun, Sweden. EM magnus.borres@pharmacia.com CR Alm JS, 1999, LANCET, V353, P1485, DOI 10.1016/S0140-6736(98)09344-1 Altman D, 1991, PRACTICAL STAT MED R Borres MP, 2000, J INFECTION, V40, P141 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 DeStefano F, 1999, LANCET, V353, P1987, DOI 10.1016/S0140-6736(99)00160-9 Gellin BG, 2000, PEDIATRICS, V106, P1097, DOI 10.1542/peds.106.5.1097 Gust D A, 2003, Semin Pediatr Infect Dis, V14, P207, DOI 10.1016/S1045-1870(03)00035-9 HALL R, IMMUNISATION MYTHS R Offit PA, 2003, PEDIATRICS, V111, P653, DOI 10.1542/peds.111.3.653 PRISLIN R, 1998, AM J PUBLIC HEALTH, V88, P12 Strobino D, 1996, PEDIATRICS, V98, P1076 Sundelin C, 2000, ACTA PAEDIATR, V89, P76 *SWED I INF DIS CO, 2000, ANN REP 2000 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Thomas DR, 1998, LANCET, V351, P1927, DOI 10.1016/S0140-6736(98)24026-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 WOOD DL, 2003, PEDIATRICS, V112, P978 NR 17 TC 32 Z9 32 PU TAYLOR & FRANCIS AS PI OSLO PA CORT ADELERSGT 17, PO BOX 2562, SOLLI, 0202 OSLO, NORWAY SN 0803-5253 J9 ACTA PAEDIATR JI Acta Paediatr. PD SEP PY 2004 VL 93 IS 9 BP 1232 EP 1237 DI 10.1080/08035250410033970 PG 6 WC Pediatrics SC Pediatrics GA 850OE UT WOS:000223621500020 PM 15384890 ER PT J AU Kaufmann, WE Cortell, R Kau, CSM Bukelis, I Tierney, E Gray, RM Cox, C Capone, GT Stanard, P AF Kaufmann, WE Cortell, R Kau, CSM Bukelis, I Tierney, E Gray, RM Cox, C Capone, GT Stanard, P TI Autism spectrum disorder in fragile X syndrome: Communication, social interaction, and specific behaviors SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE fragile X; autism; autism diagnostic interview (ADI); social withdrawal; socialization; communication ID PERVASIVE DEVELOPMENTAL DISORDERS; ADAPTIVE-BEHAVIOR; DIAGNOSTIC INTERVIEW; MENTAL-RETARDATION; YOUNG BOYS; MALES; PHENOTYPE; CHILDREN; EXPRESSION; MUTATION AB The present study extends our previous work on social behavior impairment in young males with fragile X syndrome (FraX). Specifically, we evaluated whether the autistic phenomenon in FraX is expressed as a range of behavioral impairments as in idiopathic autism (Aut). We also examined whether there are behaviors, identified as items of the Autism Diagnostic Interview-Revised (ADI-R), that in FraX predispose to or differentiate subjects with autism spectrum disorder (ASD) diagnosis. Finally, regression models were utilized to test the relative contribution of reduced communication and socialization skills to ADI-R scores and diagnoses. A cohort of 56 boys (3-8 years) with FraX was examined in terms of scores on measures of cognition (IQ was a co-variate in most analyses.), autistic behavior, problem/aberrant behavior, adaptive behavior, and language development. We found that, indeed, in terms of problem behavior and adaptive skills, there is a range of severity from FraX + Aut to FraX + PDD (Pervasive Developmental Disorder) to FraX + none. ADI-R items representing "Play" types of interaction appear to be "susceptibility" factors since they were abnormal across the FraX cohort. Integrated regression models demonstrated that items reflecting complex social interaction differentiated the FraX + ASD (Aut + PDD) subgroup from the rest of the FraX cohort, while abnormalities in basic verbal and non-verbal communication distinguished the most severely affected boys with FraX + Aut from the milder FraX + PDD cohort. Models incorporating language, adaptive communication, and adaptive socialization skills revealed that socialization was not only the main influence on scores but also a predictor of ASD diagnosis. Altogether, our findings demonstrate that the diagnosis of ASD in FraX reflects, to a large extent, an impairment in social interaction that is expressed with variable severity in young males with FraX. (C) 2004 Wiley-Liss, Inc. C1 Kennedy Krieger Inst, Baltimore, MD 21211 USA. 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J. Med. Genet. A PD SEP 1 PY 2004 VL 129A IS 3 BP 225 EP 234 DI 10.1002/ajmg.a.30229 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 850IY UT WOS:000223605800003 PM 15326621 ER PT J AU Tyson, C McGillivray, B Chijiwa, C Rajcan-Separovic, E AF Tyson, C McGillivray, B Chijiwa, C Rajcan-Separovic, E TI Elucidation of a cryptic interstitial 7q31.3 deletion in a patient with a language disorder and mild mental retardation by array-CGH SO AMERICAN JOURNAL OF MEDICAL GENETICS PART A LA English DT Article DE balanced chromosomal rearrangements; array-CGH; FISH; language disorder ID COMPARATIVE GENOMIC HYBRIDIZATION; CHROMOSOME REARRANGEMENTS; SUSCEPTIBILITY GENE; SEVERE SPEECH; LONG ARM; IMPAIRMENT; AUTISM; REGION; TRANSLOCATION; MICROARRAYS AB We report on a 14-year-old boy who presented with bilateral cleft lip and palate, hearing loss, a language processing disorder, and mild mental retardation (MR). G-banded chromosome analysis of the patient and his family revealed he carried an apparently balanced de novo complex translocation involving chromosomes 5, 6, and 7. Chromosomal comparative genomic hybridization (CGH) was performed to investigate the possibility of any genomic imbalance as a result of the complex rearrangement. No abnormality was detected at any of the translocation breakpoint regions (5p13.2, 6p24, 7q21.1, and 7q21.3), nor was there any other imbalance which fell inside our significance level of 0.8-1.2. Array-CGH analysis was initiated to perform a higher resolution search for gains and losses, and revealed a deletion of two adjacent clones, CTB-133K23 and RP11-112P4, mapping to 7q31.3, which are 4.4 Mb apart. Fluorescence in situ hybridization (FISH) using these two clones confirmed the deletion. 7q31 has frequently been implicated in the search for genes involved in speech and language disorders. The specific 7q31.3 region deleted in our patient has significant overlap with some such areas of the genome. These findings are, therefore, of value in identifying genes involved in the speech and language phenotypes. This study has shown the importance of array-CGH in investigating patients who have clinical features suggestive of a chromosome abnormality, but with apparently balanced chromosome rearrangements. It has demonstrated that the array-CGH technique provides a much greater insight into submicroscopic chromosome imbalances than conventional cytogenetic techniques. (C) 2004 Wiley-Liss, Inc. C1 Univ British Columbia, Dept Pathol, Vancouver, BC V6H 3V4, Canada. Univ British Columbia, Dept Med Genet, Vancouver, BC V6H 3V4, Canada. RP Rajcan-Separovic, E (reprint author), Univ British Columbia, Dept Pathol Cytogenet, 4480 Oak St, Vancouver, BC V6H 3V4, Canada. 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J. Med. Genet. A PD SEP 1 PY 2004 VL 129A IS 3 BP 254 EP 260 DI 10.1002/ajmg.a.30245 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 850IY UT WOS:000223605800006 PM 15326624 ER PT J AU DeGrace, BW AF DeGrace, BW TI The everyday occupation of families with children with autism SO AMERICAN JOURNAL OF OCCUPATIONAL THERAPY LA English DT Article; Proceedings Paper CT Annual Conference of the Canadian-Occupational-Therapy-Association CY MAY, 2002 CL St John, CANADA SP Canadian Occupat Therapy Assoc ID PROBLEM BEHAVIOR; PERSPECTIVES; DISABILITIES; ROUTINES; RITUALS AB The purpose of this qualitative research study was to understand a family's experiences negotiating family daily life and the meanings they ascribed to these experiences when they had a child with severe autism. In-depth, semistructured interviews were conducted with five family units. The interviews explored the meaning of the family's participation in daily life activities. The transcribed interviews were analyzed with a phenomenological method. The results emerging from this study indicate that families with children with severe autism may experience difficulty engaging in daily activities that hold positive meaning and rely on stringent patterns of routines that revolve around the child with autism to meet the demands of daily life. C1 Univ Oklahoma, Hlth Sci Ctr, Coll Allied Hlth, Dept Rehabil Sci, Oklahoma City, OK 73190 USA. RP DeGrace, BW (reprint author), Univ Oklahoma, Hlth Sci Ctr, Coll Allied Hlth, Dept Rehabil Sci, POB 26901, Oklahoma City, OK 73190 USA. EM beth-degrace@ouhsc.edu CR AGNETTI G, 1997, NEW TRENDS EXPT CLIN, V2, P133 Boss P.G., 1988, FAMILY STRESS MANAGE BOYCE WT, 1983, SOC SCI MED, V17, P193, DOI 10.1016/0277-9536(83)90116-8 CAMPBELL M, 1995, FAMILY CELEBRATION Case-Smith J, 1999, AM J OCCUP THER, V53, P506 Cattell-Gordon D, 1998, INFANT YOUNG CHILD, V10, P79 Cohen S., 1998, TARGETING AUTISM WHA COOK DG, 1996, DEV DISABILITIES SPE, V19, P1 COOK JS, 1990, NEWS PHYSIOL SCI, V5, P1 Creswell JW, 1998, QUALITATIVE INQUIRY DILLON KM, 1995, LIVING AUTISM DUKES D, 1984, J RELIG HLTH, V23, P197 Dunst C. 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E., 1991, INTERVIEWING QUALITA STANCLIFF BL, 1996, OT PRACTICE, V1, P18 Turnbull AP, 1996, MENT RETARD, V34, P280 WOLIN SJ, 1984, FAM PROCESS, V23, P401, DOI 10.1111/j.1545-5300.1984.00401.x ZISSERMANN L, 1992, AM J OCCUP THER, V46, P547 NR 35 TC 34 Z9 34 PU AMER OCCUPATIONAL THERAPY ASSOC, INC PI BETHESDA PA 4720 MONTGOMERY LANE, BETHESDA, MD 20814-3425 USA SN 0272-9490 J9 AM J OCCUP THER JI Am. J. Occup. Ther. PD SEP-OCT PY 2004 VL 58 IS 5 BP 543 EP 550 PG 8 WC Rehabilitation SC Rehabilitation GA 855YD UT WOS:000224009900007 PM 15481781 ER PT J AU Gepner, B AF Gepner, B TI Autism, movement, and facial processing SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Letter ID MOTION; CHILDREN CR Gepner B, 2001, J AUTISM DEV DISORD, V31, P37, DOI 10.1023/A:1005609629218 Gepner B, 2002, TRENDS COGN SCI, V6, P455, DOI 10.1016/S1364-6613(02)02004-1 Gepner B, 2002, J AUTISM DEV DISORD, V32, P231, DOI 10.1023/A:1015410015859 Kemner C, 2003, AM J PSYCHIAT, V160, P1358, DOI 10.1176/appi.ajp.160.7.1358-a Klin A, 2002, AM J PSYCHIAT, V159, P895, DOI 10.1176/appi.ajp.159.6.895 NR 5 TC 6 Z9 8 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD SEP PY 2004 VL 161 IS 9 BP 1719 EP 1719 DI 10.1176/appi.ajp.161.9.1719 PG 1 WC Psychiatry SC Psychiatry GA 853BH UT WOS:000223800600038 PM 15337675 ER PT J AU Klin, A Jones, W Schultz, R Volkmar, F AF Klin, A Jones, W Schultz, R Volkmar, F TI Autism, movement, and facial processing - Dr. Klin and colleagues reply SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Letter CR Klin A, 2003, AM J PSYCHIAT, V160, P1359, DOI 10.1176/appi.ajp.160.7.1359 Klin A, 2003, PHILOS T ROY SOC B, V358, P345, DOI 10.1098/rstb.2002.1202 Klin A, 2002, ARCH GEN PSYCHIAT, V59, P809, DOI 10.1001/archpsyc.59.9.809 VANDERGEEST J, 2002, J CHILD PSYCHOL PSYC, V443, P669 NR 4 TC 2 Z9 2 PU AMER PSYCHIATRIC PUBLISHING, INC PI ARLINGTON PA 1000 WILSON BOULEVARD, STE 1825, ARLINGTON, VA 22209-3901 USA SN 0002-953X J9 AM J PSYCHIAT JI Am. J. Psychiat. PD SEP PY 2004 VL 161 IS 9 BP 1719 EP 1720 DI 10.1176/appi.ajp.161.9.1719-a PG 2 WC Psychiatry SC Psychiatry GA 853BH UT WOS:000223800600039 ER PT J AU Casanova, MF AF Casanova, MF TI White matter volume increase and minicolumns in autism SO ANNALS OF NEUROLOGY LA English DT Letter ID PATHOLOGY; BRAINS C1 Univ Louisville, Dept Psychiat, Gottfried & Gisela Kolb Endowed Chair Psychiat, Louisville, KY 40292 USA. RP Casanova, MF (reprint author), Univ Louisville, Dept Psychiat, Gottfried & Gisela Kolb Endowed Chair Psychiat, Louisville, KY 40292 USA. CR Casanova MF, 2002, J CHILD NEUROL, V17, P515, DOI 10.1177/088307380201700708 Casanova MF, 2002, NEUROLOGY, V58, P428 Casanova MF, 2002, J CHILD NEUROL, V17, P692, DOI 10.1177/088307380201700908 Casanova MF, 2004, J CHILD NEUROL, V19, P275, DOI 10.1177/088307380401900407 Herbert MR, 2004, ANN NEUROL, V55, P530, DOI 10.1002/ana.20032 Hofman MA, 2001, EVOLUTIONARY ANATOMY OF THE PRIMATE CEREBRAL CORTEX, P113 NR 6 TC 41 Z9 42 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2004 VL 56 IS 3 BP 453 EP 453 DI 10.1002/ana.20196 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 851LU UT WOS:000223687400023 PM 15349878 ER PT J AU Herbert, MR Ziegler, DA AF Herbert, MR Ziegler, DA TI White matter volume increase and minicolumns in autism - Reply SO ANNALS OF NEUROLOGY LA English DT Letter ID DISORDER C1 Massachusetts Gen Hosp, Ctr Morphometr Anal, Charlestown, MA USA. Massachusetts Gen Hosp, Ctr Morphometr Anal, Boston, MA 02114 USA. RP Herbert, MR (reprint author), Massachusetts Gen Hosp, Ctr Morphometr Anal, Charlestown, MA USA. CR Aylward EH, 2002, NEUROLOGY, V59, P175 Casanova MF, 2002, NEUROLOGY, V58, P428 Courchesne E, 2001, NEUROLOGY, V57, P245 Herbert MR, 2004, ANN NEUROL, V55, P530, DOI 10.1002/ana.20032 NR 4 TC 0 Z9 0 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0364-5134 J9 ANN NEUROL JI Ann. Neurol. PD SEP PY 2004 VL 56 IS 3 BP 454 EP 454 DI 10.1002/ana.20195 PG 1 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 851LU UT WOS:000223687400024 ER PT J AU Moore, ML Eichner, SF Jones, JR AF Moore, ML Eichner, SF Jones, JR TI Treating functional impairment of autism with selective serotonin-reuptake inhibitors SO ANNALS OF PHARMACOTHERAPY LA English DT Article DE autistic disorder; pervasive developmental disorders; selective serotonin-reuptake inhibitor ID PERVASIVE DEVELOPMENTAL DISORDERS; FLUVOXAMINE TREATMENT; FLUOXETINE TREATMENT; MENTAL-RETARDATION; OPEN-LABEL; CHILDREN; ADULTS; SERTRALINE; ADOLESCENTS; DEPRESSION AB OBJECTIVE: To review literature describing use of selective serotonin-reuptake inhibitors (SSRIs) in the management of functional impairments associated with autistic disorder. DATA SOURCES: EMBASE (1980-3rd quarter of 2003), International Pharmaceutical Abstracts (1970-August 2003), and MEDLINE (1966-August 2003) were searched. Search terms included autism, autistic disorder, citalopram, fluoxetine, fluvoxamine, paroxetine, selective serotonin-reuptake inhibitors, and sertraline. DATA SYNTHESIS: Studies and case reports evaluating treatment outcomes associated with the use of SSRIs in managing impairments of autism were reviewed. Multiple SSRI dosing ranges were evaluated in autistic patients of different ages with various functional impairments. No specific SSRI or dose range has been shown to improve a specific autistic symptom although some patients have demonstrated improvements. CONCLUSIONS: Benefits with SSRIs in treating functional impairments in autism have been observed. Response to therapy and adverse effects are individualized. Current evidence does not support selection of one SSRI over another for any impairment associated with autism. C1 Univ Tennessee, Ctr Hlth Sci, Drug Informat Ctr, Memphis, TN 38163 USA. Univ Tennessee, Coll Pharm, Memphis, TN 38163 USA. Methodist Healthcare Univ Hosp, Memphis, TN USA. RP Moore, ML (reprint author), Univ Tennessee, Ctr Hlth Sci, Drug Informat Ctr, 875 Monroe Ave,Ste 109, Memphis, TN 38163 USA. EM mmoore31@utmem.edu CR Buitelaar JK, 2000, EUR CHILD ADOLES PSY, V9, P185 CHUGANI DC, 2002, MOL PSYCHIAT S2, V7, P516 Cook Edwin H. 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Pharmacother. PD SEP PY 2004 VL 38 IS 9 BP 1515 EP 1519 DI 10.1345/aph.1D543 PG 5 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 848BO UT WOS:000223442300025 PM 15292500 ER PT J AU Indredavik, MS Vik, T Heyerdahl, S Kulseng, S Fayers, P Brubakk, AM AF Indredavik, MS Vik, T Heyerdahl, S Kulseng, S Fayers, P Brubakk, AM TI Psychiatric symptoms and disorders in adolescents with low birth weight SO ARCHIVES OF DISEASE IN CHILDHOOD LA English DT Article ID FOR-GESTATIONAL-AGE; BEHAVIORAL-ADJUSTMENT; INFANTILE-AUTISM; CHILDREN BORN; CEREBRAL MRI; RISK-FACTORS; FOLLOW-UP; OUTCOMES; SCHOOL; GROWTH AB Objective: To evaluate the prevalence of psychiatric symptoms and disorders associated with low birth weight. Design/study groups: A population based follow up study of 56 very low birthweight (VLBW: birth weight less than or equal to1500 g), 60 term small for gestational age (SGA: birth weight <10th centile), and 83 term control (birth weight &GE;10th centile) children at 14 years of age. Outcome measures: Schedule for affective disorders and schizophrenia for school aged children, attention deficit/hyperactivity disorder (ADHD) rating scale IV, autism spectrum screening questionnaire, and children's global assessment scale. Results: VLBW adolescents had a higher prevalence of psychiatric symptoms (46%) than controls (13%) (odds ratio (OR) 5.7, 95% confidence interval (CI) 2.5 to 13.0) and more psychiatric disorders (25%) than controls (7%) (OR 4.3, 95% CI 1.5 to 12.0), especially anxiety disorders. Although 25% of the VLBW adolescents had attention problems, ADHD was diagnosed in only 7%.. Four VLBW adolescents had symptoms of Asperger's disorder, and the VLBW group had a higher sum score than controls on the, autism spectrum screening questionnaire. Although more SGA adolescents had psychiatric symptoms than controls (23% v 13%), the difference was not statistically significant. Results remained essentially the same when adolescents with low estimated intelligence quotient were excluded, and persisted after possible psychosocial confounders had been controlled for. Conclusion: VLBW, but not SGA adolescents, have a high risk of developing psychiatric symptoms and disorders by the age of 14, especially attention deficit, anxiety symptoms, and relational problems. C1 Norwegian Univ Sci & Technol, Dept Neurosci, N-7034 Trondheim, Norway. Norwegian Univ Sci & Technol, Dept Community Med & Gen Practice, N-7034 Trondheim, Norway. Reg Ctr Child & Adolescent Psychiat, Oslo, Norway. Norwegian Univ Sci & Technol, Dept Lab Med Childrens & Womens Hlth, N-7034 Trondheim, Norway. 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Dis. Child. PD SEP PY 2004 VL 89 IS 5 SI SI BP F445 EP F450 DI 10.1136/adc.2003.038943 PG 6 WC Pediatrics SC Pediatrics GA 850OF UT WOS:000223621600017 PM 15321968 ER PT J AU Gomes, E Rotta, NT Pedroso, FS Sleifer, P Danesi, MC AF Gomes, E Rotta, NT Pedroso, FS Sleifer, P Danesi, MC TI Auditory hypersensitivity in children and teenagers with autistic spectrum disorder SO ARQUIVOS DE NEURO-PSIQUIATRIA LA English DT Article DE autism; hypersensitivity; sound ID CLINICAL GUIDELINES; CLASSIFICATION; HYPERACUSIS; ABNORMALITIES AB Objective: To verify if the clinical behavior of auditory hypersensitivity, reported in interviews with parents/caregivers and therapists/teachers of 46 children and teenagers suffering from autistic spectrum disorder, correspond to audiological findings. Method: The clinical diagnosis for auditory hypersensitivity was investigated by means of an interview. Subsequently, a test of the acoustic stapedial reflex was conducted, and responses to intense acoustic stimulus in open field were observed. Results: Of the 46 subjects, 11 (23.9%) were clinically diagnosed as oversensitive to sound and only 2 showed discomfort when exposed to intense acoustic stimulus in open field. There was no statistically significant difference for the test of the ipsilateral acoustic stapedial reflex between the groups. Conclusion: Behavioral manifestations to sounds are not associated to hypersensitivity of the auditory pathways, but instead these are associated to difficulties in the upper processing, involving systems that usually are impaired in autistic spectrum patients, such as the limbic system. C1 Rede Metodista IPA, Porto Alegre, RS, Brazil. Univ Fed Rio Grande Sul, Dept Pediat, Postdoctorship Neurol, Porto Alegre, RS, Brazil. Univ Fed Santa Maria, BR-97119900 Santa Maria, RS, Brazil. Univ Fed Rio Grande Sul, Porto Alegre, RS, Brazil. RP Gomes, E (reprint author), Rua Duque Caxias 955-406, BR-90010282 Porto Alegre, RS, Brazil. EM erifono@hotmail.com CR Anari M, 1999, SCAND AUDIOL, V28, P219, DOI 10.1080/010503999424653 Bauman ML, 1996, J AUTISM DEV DISORD, V26, P199, DOI 10.1007/BF02172012 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Bettison S, 1996, J AUTISM DEV DISORD, V26, P361, DOI 10.1007/BF02172480 BINGHAM P, 2001, SEGREDOS PEDIAT, P275 Brandy WT, 1995, AM J AUDIOL, V4, P46 Calderón-González R, 1988, Bol Med Hosp Infant Mex, V45, P79 EDELSON SM, 1984, AM J MENT DEF, V89, P140 Gadia CA, 2003, REV NEUROLOGIA, V36, P166 GORDON A G, 1986, British Journal of Audiology, V20, P95, DOI 10.3109/03005368609079002 GRANDIN G, 1999, COMPANHIA DAS LETRAS GREWE TSD, 1994, INT J PEDIATR OTORHI, V30, P123, DOI 10.1016/0165-5876(94)90195-3 Jastreboff PJ, 2001, OTOL NEUROTOL, V22, P326 Kanner L, 1943, NERV CHILD, V2, P217 KATZ J, 1999, TRATADO AUDIOLOGICA Katzenell U, 2001, OTOL NEUROTOL, V22, P321, DOI 10.1097/00129492-200105000-00009 Kern JK, 2002, MED HYPOTHESES, V59, P255, DOI 10.1016/S0306-9877(02)00212-8 Lonsbury-Martin BL, 2001, PERSPECTIVAS ATUAIS, P163 Lord C, 2001, AM J MED GENET, V105, P36, DOI 10.1002/1096-8628(20010108)105:1<36::AID-AJMG1053>3.0.CO;2-4 NIGAM A, 1994, J LARYNGOL OTOL, V108, P494 ONeill M, 1997, J AUTISM DEV DISORD, V27, P283, DOI 10.1023/A:1025850431170 Phillips D P, 1998, J Am Acad Audiol, V9, P371 Rosenhall U, 1999, J AUTISM DEV DISORD, V29, P349, DOI 10.1023/A:1023022709710 SANCHEZ T, 1999, ARQ FUND OTORRINOL, V3, P184 Tanguay PE, 1998, J AM ACAD CHILD PSY, V37, P271, DOI 10.1097/00004583-199803000-00011 WATHERHOUSE L, 1996, J AUTISM DEV DISORD, V26, P59 WETHERBY A, 2001, AUTISM SPECTRUM DISO, P1 WILBER LA, 2001, PERSPECTIVAS ATUAIS, P1 WILSON R, 2001, PERSPECTIVAS ATUAIS, P127 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 30 TC 11 Z9 11 PU ASSOC ARQUIVOS DE NEURO- PSIQUIATRIA PI SAO PAULO SP PA PR AMADEU AMARAL 47/33, 01327-010 SAO PAULO SP, BRAZIL SN 0004-282X J9 ARQ NEURO-PSIQUIAT JI Arq. Neuro-Psiquiatr. PD SEP PY 2004 VL 62 IS 3B BP 797 EP 801 DI 10.1590/S0004-282X2004000500011 PG 5 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 907EH UT WOS:000227697700011 PM 15476072 ER PT J AU O'Riordan, MA AF O'Riordan, MA TI Superior visual search in adults with autism SO AUTISM LA English DT Article DE autism; developmental profile; visual discrimination; visual search AB Recent studies have suggested that children with autism perform better than matched controls on visual search tasks and that this stems from a superior visual discrimination ability. This study assessed whether these findings generalize from children to adults with autism. Experiments 1 and 2 showed that, like children, adults with autism were superior to controls at searching for targets. Experiment 3 showed that increases in target-distractor similarity slowed the visual search performance of the control group significantly more than that of the autism group, suggesting that the adults with autism have a superior visual discrimination ability. Thus, these experiments replicate in adults previous findings in children with autism. Superior unique item detection in adults with autism, stemming from enhanced discrimination, is discussed in the light of the possible role of stimulus processing disturbances in the disorder in general. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. RP O'Riordan, MA (reprint author), Univ Cambridge, Dept Expt Psychol, Downing St, Cambridge CB2 3EB, England. EM mafo100@cus.cam.ac.uk CR DUNCAN J, 1989, PSYCHOL REV, V96, P433, DOI 10.1037//0033-295X.96.3.433 Kanner L, 1943, NERV CHILD, V2, P217 O'Riordan MA, 2001, J EXP PSYCHOL HUMAN, V27, P719, DOI 10.1037//0096-1523.27.3.719 TREISMAN A, 1988, PSYCHOL REV, V95, P15, DOI 10.1037//0033-295X.95.1.15 WOLFE JM, 1989, J EXP PSYCHOL HUMAN, V15, P419, DOI 10.1037/0096-1523.15.3.419 NR 5 TC 74 Z9 74 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2004 VL 8 IS 3 BP 229 EP 248 DI 10.1177/1362361304045219 PG 20 WC Psychology, Developmental SC Psychology GA 849VI UT WOS:000223568900002 PM 15358868 ER PT J AU Ponnet, KS Roeyers, H Buysse, A De Clercq, A Van der Heyden, E AF Ponnet, KS Roeyers, H Buysse, A De Clercq, A Van der Heyden, E TI Advanced mind-reading in adults with Asperger syndrome SO AUTISM LA English DT Article DE Asperger syndrome; empathic accuracy; perspective taking; social cognition ID AUTISM AB This study investigated the mind-reading abilities of 19 adults with Asperger syndrome and 19 typically developing adults. Two static mind-reading tests and a more naturalistic empathic accuracy task were used. In the empathic accuracy task, participants attempted to infer the thoughts and feelings of target persons, while viewing a videotape of the target persons in a naturally occurring conversation with another person. The results are consistent with earlier findings. The empathic accuracy task indicated significant between-group differences, whereas no such differences were found on the static mindreading tasks. The most innovative finding of the present study is that the inference ability of adults with pervasive developmental disorder (PDD) and controls depends on the focus of the target's thoughts and feelings, and that the empathic accuracy of adults with Asperger syndrome and control adults might be different in terms of quantity and quality. C1 State Univ Ghent, Res Grp Dev Disorders, B-9000 Ghent, Belgium. RP Ponnet, KS (reprint author), State Univ Ghent, Res Grp Dev Disorders, Henri Dunantlaan 2, B-9000 Ghent, Belgium. EM koen.ponnet@UGent.be CR Baron-Cohen S, 2001, J CHILD PSYCHOL PSYC, V42, P241, DOI 10.1017/S0021963001006643 Bowler DM, 2000, J AUTISM DEV DISORD, V30, P295, DOI 10.1023/A:1005575216176 Eisenberg N., 1991, HDB MORAL BEHAVIOR D, V2, P63 Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 Jolliffe T, 1999, J AUTISM DEV DISORD, V29, P395, DOI 10.1023/A:1023082928366 MARANGONI C, 1995, J PERS SOC PSYCHOL, V68, P854, DOI 10.1037//0022-3514.68.5.854 TAGERFLUSBERG H, 1995, APPL PSYCHOLINGUIST, V16, P241, DOI 10.1017/S0142716400007281 NR 7 TC 38 Z9 41 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2004 VL 8 IS 3 BP 249 EP 266 DI 10.1177/1362361304045214 PG 18 WC Psychology, Developmental SC Psychology GA 849VI UT WOS:000223568900003 PM 15358869 ER PT J AU Hoy, JA Hatton, C Hare, D AF Hoy, JA Hatton, C Hare, D TI Weak central coherence: a cross-domain phenomenon specific to autism? SO AUTISM LA English DT Article DE Asperger syndrome; autism; central coherence theory ID INDIVIDUALS; PERFORMANCE; ILLUSIONS AB This study investigated whether evidence for the weak central coherence theory could be specifically associated with a group of children with autism compared with normally developing children (n = 17 per group). Two tasks were employed, one involving visual illusions and the other verbal homophones. Both were based on tasks used in previous central coherence research. Incorporation of tasks involving the use of different domains (verbal versus visual) also enabled the investigation of claims that weak central coherence is a cross-domain processing style or deficit. The autistic group were found to be no different to the control group in performance on the visual illusions task. The autistic group made more errors than the normally developing group on the rare condition of the homophone task. However, analysis suggests this difference is mediated by verbal ability level and not diagnostic status per se. Theoretical implications and alternative explanations are discussed. C1 Blackpool Victoria Hosp, Dept Clin Psychol, Blackpool FY3 8NR, Lancs, England. Univ Lancaster, Lancaster LA1 4YW, England. Wythenshawe Hosp, Manchester M23 9LT, Lancs, England. RP Hoy, JA (reprint author), Blackpool Victoria Hosp, Dept Clin Psychol, E Pk Dr, Blackpool FY3 8NR, Lancs, England. EM jamiehoy@btinternet.com CR Brian JA, 1996, J CHILD PSYCHOL PSYC, V37, P865, DOI 10.1111/j.1469-7610.1996.tb01482.x FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Ropar D, 1999, J CHILD PSYCHOL PSYC, V40, P1283, DOI 10.1017/S0021963099004667 Ropar D, 2001, J CHILD PSYCHOL PSYC, V42, P539, DOI 10.1111/1469-7610.00748 SHAH A, 1983, J CHILD PSYCHOL PSYC, V24, P613, DOI 10.1111/j.1469-7610.1983.tb00137.x NR 5 TC 21 Z9 21 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2004 VL 8 IS 3 BP 267 EP 281 DI 10.1177/1362361304045218 PG 15 WC Psychology, Developmental SC Psychology GA 849VI UT WOS:000223568900004 PM 15358870 ER PT J AU Brent, E Rios, P Happe, F Charman, T AF Brent, E Rios, P Happe, F Charman, T TI Performance of children with autism spectrum disorder on advanced theory of mind tasks SO AUTISM LA English DT Article DE Asperger syndrome; autism; emotion recognition; mentalizing; theory of mind AB Although a number of advanced theory of mind tasks have been developed, there is sparse information on whether performance on different tasks is associated. The study examined the performance of 20 high-functioning 6- to 12-year-old children with autism spectrum disorder and 20 controls on three high-level theory of mind tasks: Strange Stories, Cartoons and the children's version of the Eyes task. The pattern of findings suggests that the three tasks may share differing, non-specific, information-processing requirements in addition to tapping any putative mentalizing ability. They may also indicate a degree of dissociation between social-cognitive and social-perceptual or affective components of the mentalizing system. C1 Inst Child Hlth, Behav & Brain Sci Unit, London WC1N 1EH, England. Brent Child & Family Clin, London, England. Inst Psychiat, London, England. RP Charman, T (reprint author), Inst Child Hlth, Behav & Brain Sci Unit, 30 Guilford St, London WC1N 1EH, England. EM t.charman@ich.ucl.ac.uk RI Happe, Francesca/D-5544-2012; Charman, Tony/A-2085-2014 OI Charman, Tony/0000-0003-1993-6549 CR BARONCOHEN S, 1985, COGNITION, V21, P37, DOI 10.1016/0010-0277(85)90022-8 Frith U., 1994, SOCIAL DEV, V3, P108, DOI DOI 10.1111/J.1467-9507.1994.TB00031.X Gillberg C., 2000, AUTISM, V4, P11, DOI 10.1177/1362361300004001002 Happe F, 1999, COGNITION, V70, P211, DOI 10.1016/S0010-0277(99)00005-0 HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x Jolliffe T, 1999, J AUTISM DEV DISORD, V29, P395, DOI 10.1023/A:1023082928366 Lord C, 1998, MENT RETARD DEV D R, V4, P90, DOI 10.1002/(SICI)1098-2779(1998)4:2<90::AID-MRDD5>3.0.CO;2-0 OZONOFF S, 1991, J CHILD PSYCHOL PSYC, V32, P1081, DOI 10.1111/j.1469-7610.1991.tb00351.x PERNER J, 1987, BRIT J DEV PSYCHOL, V5, P125 NR 9 TC 37 Z9 37 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2004 VL 8 IS 3 BP 283 EP 299 DI 10.1177/1362361304045217 PG 17 WC Psychology, Developmental SC Psychology GA 849VI UT WOS:000223568900005 PM 15358871 ER PT J AU Sofronoff, K Leslie, A Brown, W AF Sofronoff, K Leslie, A Brown, W TI Parent management training and Asperger syndrome - A randomized controlled trial to evaluate a parent based intervention SO AUTISM LA English DT Article DE Asperger syndrome; parent management training; workshop format ID CHILDHOOD ANXIETY; CHILDREN; FAMILY; BEHAVIOR; AUTISM AB This controlled trial of a parent management intervention aimed to increase parental competence in management of problem behaviours associated with Asperger syndrome. The intervention compared two formats, a 1 day workshop and six individual sessions. Measures were taken on three occasions: pre-intervention, at 4 weeks, and at 3 month follow-up. Variables of interest were number and intensity of problem behaviours, and parent evaluation of social interaction skills. Results showed parents reporting fewer and lower intensity of problem behaviours and increased social interactions at 4 weeks and 3 months. Results held across formats and suggest that parent management training can provide an effective intervention for parents of a child with Asperger syndrome. Group differences on outcome measures and in the use of strategies are discussed along with limitations of the study. C1 Univ Queensland, Sch Psychol, St Lucia, Qld 4072, Australia. Univ Queensland, Mater Childrens Hosp, Brisbane, Qld 4101, Australia. RP Sofronoff, K (reprint author), Univ Queensland, Sch Psychol, St Lucia, Qld 4072, Australia. EM kate@psy.uq.edu.au CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ANASTOPOULOS AD, 1998, HDB PARENT TRAINING ATTWOOD A, 1998, ASPERGERS SYNDROME G Attwood T., 2000, AUTISM, V4, P85, DOI DOI 10.1177/1362361300004001006 Barrett PM, 1998, J CLIN CHILD PSYCHOL, V27, P459, DOI 10.1207/s15374424jccp2704_10 Boyd RD, 2001, AUTISM, V5, P430, DOI 10.1177/1362361301005004007 BRASWELL L, 1991, CHILD ADOLESCENT THE, P316 BRIGHTMAN RP, 1982, J BEHAV THER EXP PSY, V13, P113, DOI 10.1016/0005-7916(82)90051-9 Cobham VE, 1998, BEHAV CHANGE, V15, P203 EISEN AR, 1998, HDB PARENT TRAINING EYBERG SM, 1978, J CLIN CHILD PSYCHOL, V7, P113 Eyberg SM, 1998, CLIN PSYCHOL-SCI PR, V5, P544 Frith U, 1991, AUTISM ASPERGER SYND FULLERTON A, 1996, HIGH FUNCTIONING ADO Gray C., 1994, COMIC STRIP CONVERSA Gray C., 1994, NEW SOCIAL STORY BOO GRAY C, 1992, TAMING RECESS JUNGLE Gray C. A., 1993, FOCUS AUTISTIC BEHAV, V8, P1, DOI DOI 10.1177/108835769300800101 Gray C.A., 1998, ASPERGER SYNDROME HI, P167 Howlin P, 1998, CHILDREN AUTISM ASPE JOHNSTON C, 1998, HDB PARENT TRAINING Norris C, 1999, FOCUS AUTISM OTHER D, V14, P180, DOI DOI 10.1177/108835769901400307 Pakenham KI, 2004, RES DEV DISABIL, V25, P245, DOI 10.1016/j.ridd.2003.06.003 PEVSNER R, 1982, J BEHAV THER EXP PSY, V13, P119, DOI 10.1016/0005-7916(82)90052-0 Ruma PR, 1996, BEHAV THER, V27, P159, DOI 10.1016/S0005-7894(96)80012-8 Sanders M. R., 1992, EVERY PARENT POSITIV Sanders M. R., 1996, EARLY INTERVENTION P, P59 Sanders MR, 1993, BEHAV FAMILY INTERVE SCHOPLER E, 1998, ASPERGER SYNDROME HI Schwartz IS, 1998, TOP EARLY CHILD SPEC, V18, P132 Serketich WJ, 1996, BEHAV THER, V27, P171, DOI 10.1016/S0005-7894(96)80013-X Smith MR, 1999, RES DEV DISABIL, V20, P183, DOI 10.1016/S0891-4222(99)00002-5 Sofronoff K. V., 2003, GOOD AUTISM PRACTICE, V4, P2 Solomon P, 1996, SCHIZOPHRENIA BULL, V22, P41 Spence S. H., 1995, SOCIAL SKILLS TRAINI Swaggart B. L., 1995, FOCUS AUTISTIC BEHAV, V10, P1 WING L, 1981, PSYCHOL MED, V11, P115 Wing L, 1998, ASPERGER SYNDROME HI, P11 NR 38 TC 38 Z9 38 PU SAGE PUBLICATIONS LTD PI LONDON PA 1 OLIVERS YARD, 55 CITY ROAD, LONDON EC1Y 1SP, ENGLAND SN 1362-3613 J9 AUTISM JI Autism PD SEP PY 2004 VL 8 IS 3 BP 301 EP 317 DI 10.1177/136261304045215 PG 17 WC Psychology, Developmental SC Psychology GA 849VI UT WOS:000223568900006 PM 15358872 ER PT J AU Bernard-Opitz, V Ing, S Kong, TY AF Bernard-Opitz, V Ing, S Kong, TY TI Comparison of behavioural and natural play interventions for young children with autism SO AUTISM LA English DT Article DE autism; behaviour modification; natural language; play; Singapore ID LANGUAGE; DISORDERS; SPEECH AB The article reports the results of a pilot study comparing traditional behavioural approaches and natural play interventions for young children with autism over a 10 week period. Two matched groups of eight young children with autism participated. Using a crossover design, children in both groups showed positive gains in compliance, attending, play and communication with their therapists and parents. Improvements in attending and compliance were higher following the behavioural condition compared with the natural play condition. Seven participants had reduced autism scores after the intervention. The findings suggest that behavioural and play approaches affect behaviour in different ways and that autistic symptomatology of young children may be amenable to treatment. The discussion focuses on the active ingredients of treatments and the need to base efficacy research on well-planned treatment comparisons. C1 Natl Univ Singapore, Singapore 117548, Singapore. RP Bernard-Opitz, V (reprint author), 7 Fuertes St, Irvine, CA 92612 USA. EM verabernard@cox.net CR Anderson S. R., 1987, ED TREATMENT CHILDRE, V10, P352 BAKER BL, 1976, BEHAV PROBLEMS Barlow D. 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This paper presents a contingency analysis of gaze shift in JA initiation. The analysis describes reinforcer-establishing and evocative effects of antecedent objects or events, discriminative and conditioned reinforcing functions of stimuli generated by adult behavior, and socially mediated reinforcers that may maintain JA behavior. A functional analysis of JA may describe multiple operant classes. The paper concludes with a discussion of JA deficits in children with autism spectrum disorders and suggestions for research and treatment. C1 Univ Massachusetts, Sch Med, Shriver Ctr, Psychol Sci Div, Waltham, MA 02452 USA. RP Dube, WV (reprint author), Univ Massachusetts, Sch Med, Shriver Ctr, Psychol Sci Div, 200 Trapelo Rd, Waltham, MA 02452 USA. EM william.dube@umassmed.edu CR BAKEMAN R, 1984, CHILD DEV, V55, P1278, DOI 10.2307/1129997 BaronCohen S, 1997, CHILD DEV, V68, P48 BARONCOHEN S, 1989, BRIT J DEV PSYCHOL, V7, P113 Bijou S. 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PD FAL PY 2004 VL 27 IS 2 BP 197 EP 207 PG 11 WC Psychology, Clinical SC Psychology GA 879DF UT WOS:000225695900006 PM 22478429 ER PT J AU Bondy, A Tincani, M Frost, L AF Bondy, A Tincani, M Frost, L TI Multiply controlled verbal operants: An analysis and extension to the picture exchange communication system SO BEHAVIOR ANALYST LA English DT Article DE augmentative communication; autism; verbal behavior; picture exchange communication system ID DEVELOPMENTAL-DISABILITIES; STUDENTS AB This paper presents Skinner's (1957) analysis of verbal behavior as a framework for understanding language acquisition in children with autism. We describe Skinner's analysis of pure and impure verbal operants and illustrate how this analysis may be applied to the design of communication training programs. The picture exchange communication system (PECS) is a training program influenced by Skinner's framework. 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PD FAL PY 2004 VL 27 IS 2 BP 247 EP 261 PG 15 WC Psychology, Clinical SC Psychology GA 879DF UT WOS:000225695900010 PM 22478433 ER PT J AU Muller, RA Cauich, C Rubio, MA Mizuno, A Courchesne, E AF Muller, RA Cauich, C Rubio, MA Mizuno, A Courchesne, E TI Abnormal activity patterns in premotor cortex during sequence learning in autistic patients SO BIOLOGICAL PSYCHIATRY LA English DT Article DE autism; frontal cortex; functional MRI; hemispheric asymmetry; motor learning ID PERVASIVE DEVELOPMENTAL DISORDERS; FUNCTIONAL MAGNETIC-RESONANCE; CHILDHOOD AUTISM; EXECUTIVE DYSFUNCTION; FRONTAL-CORTEX; HUMAN BRAIN; MOTOR; MOVEMENT; CHILDREN; FMRI AB Background: Evidence for frontal abnormality in autism has accumulated in recent years. Our own studies have shown abnormal activation in prefrontal cortex during finger tapping and visuomotor coordination. Studies in healthy adults, suggest reduced premotor and increased prefrontal activity during, advanced learning stages. We examined hemodynamic changes during visuomotor learning in autistic patients. Methods: We studied eight high-functioning autistic patients and eight control subjects during learning of an 8-digit sequence over a period of 8 min, using functional magnetic resonance imaging. Results: Autistic patients showed overall less prefrontal activation during late visuomotor learning, however, the main finding was a complementary; one of enhanced activation in right pericentral and premotor cortex. In the autism group Brodmann areas 3 4, and 6 of the right hemisphere became more involved during late learning stages (trials 25-48), compared with early stages (trials 1-24). This effect was not seen in the control group. Conclusions: Our findings suggests that in autistic patients 1) primary sensorimotor and premotor cortex, which is normally predominant in early stages of visuomotor learning, plays an atypical role in later stages, even when learning is evident: and 2) handedness and side of execution interact with asymmetry of visuomotor learning activations, contrary to what is seen in normal adults. C1 San Diego State Univ, Dept Psychol, San Diego, CA 92120 USA. Univ Calif San Diego, Dept Cognit Sci, San Diego, CA 92103 USA. Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA. Univ Calif San Diego, Ctr Autism Res, Childrens Hosp, Res Ctr, San Diego, CA 92103 USA. RP Muller, RA (reprint author), San Diego State Univ, Dept Psychol, 6363 Alvarado Court,225 E-MC1863, San Diego, CA 92120 USA. 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Psychiatry PD SEP 1 PY 2004 VL 56 IS 5 BP 323 EP 332 DI 10.1016/j.biopsych.2004.06.007 PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 849ZJ UT WOS:000223580100004 PM 15336514 ER PT J AU [Anonymous] AF [Anonymous] TI Going against the grain - A look at autism SO CANADIAN JOURNAL OF DIETETIC PRACTICE AND RESEARCH LA English DT Article CR *INT CHILD DEV RES, 2002, OP WIND ESS TRAIN *KIRKM LAB, 2002, KIRKM GUID INT HLTH Lewis Lisa, 1998, SPECIAL DIETS SPECIA SEROUSSI K, 2002, UNRAVELING MYSTERY A NR 4 TC 0 Z9 0 PU DIETITIANS CANADA PI TORONTO PA 480 UNIV AVE, SUITE 604, TORONTO, ONTARIO M5G 1V2, CANADA SN 1486-3847 J9 CAN J DIET PRACT RES JI Can. J. Diet. Pract. Res. PD FAL PY 2004 VL 65 IS 3 BP 1 EP 2 PG 2 WC Nutrition & Dietetics SC Nutrition & Dietetics GA 854FT UT WOS:000223887700008 ER PT J AU Keenan, JM Simon, JA AF Keenan, JM Simon, JA TI Inference deficits in women with Fragile X Syndrome: A problem in working memory SO COGNITIVE NEUROPSYCHOLOGY LA English DT Article ID COGNITIVE PROFILES; FEMALE CARRIERS; FULL MUTATION; MALES; AUTISM; GENE; INVOLVEMENT; LANGUAGE AB Inferential processing and its component processes-working memory and set shifting-were examined in women with Fragile X Syndrome (FXS), in an attempt to understand the language phenotype of FXS and to better understand discourse processing by examining which components are affected by a biological breakdown. Participants read short passages and answered both factual and inference questions, and performance was correlated with neuropsychological measures of working memory and set-shifting. Three groups of nonretarded women were examined: (a) 12 women with FXS who carry the full mutation; (b) 22 women who carry the premutation; and (c) 16 women without the fragile X mutation. The results show that full mutation women do more poorly on both factual and inference questions. They do not appear to have a specific deficit in inferencing, however, because even though they do worse on inference questions than on factual questions, they do no worse, proportionately speaking, than the comparison groups. Analysis of the types of errors indicates that what underlies their poor performance on this discourse task is a specific deficit in working memory; the working memory deficit appears to be due specifically to FXS and not just to lower IQ. The deficits in discourse and working memory are also shown to relate to molecular measures of the syndrome. C1 Univ Denver, Dept Psychol, Denver, CO 80208 USA. Sopris W Educ Serv, Longmont, CO 80504 USA. 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PD SEP PY 2004 VL 21 IS 6 BP 579 EP 596 DI 10.1080/02643290342000294 PG 18 WC Psychology; Psychology, Experimental SC Psychology GA 844GQ UT WOS:000223146400001 PM 21038223 ER PT J AU Gray, KM Mohr, C AF Gray, KM Mohr, C TI Mental health problems in children and adolescents with intellectual disability SO CURRENT OPINION IN PSYCHIATRY LA English DT Article DE adolescents; children; intellectual disability; mental health; psychopathology ID SOCIAL-BEHAVIOR QUESTIONNAIRE; DSM-IV DISORDERS; LEARNING-DISABILITIES; WILLIAMS-SYNDROME; RETARDATION; AUTISM; PSYCHOPATHOLOGY; RISPERIDONE; BORDERLINE; STRESS AB Purpose of review This review examines papers published in the last 12 months in the area of mental health problems in children and adolescents with intellectual disability. The research is organized into the following sections: mental health investigations, specific syndromes, family/carer-related papers, treatment findings and theoretical papers. Recent findings Significant findings are presented on the nature and prevalence of psychopathology in young people with intellectual disability and some specific syndrome groups. Summary Whilst much progress has been made recently in defining the nature of mental health problems in children and adolescents with intellectual disability, further information is needed on the development of psychopathology in this population. It is now essential that more research be undertaken in developing efficacious treatments for these children and their families. C1 Monash Univ, Ctr Dev Psychiat & Psychol, Capital & Coast Dist Hlth Board, Wellington, New Zealand. Monash Univ, Ctr Dev Psychiat & Psychol, Ctr Med, Clayton, Vic 3168, Australia. RP Mohr, C (reprint author), Monash Univ, Ctr Dev Psychiat & Psychol, Capital & Coast Dist Hlth Board, POB 50-233, Wellington, New Zealand. 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Med PD SEP PY 2004 VL 65 IS 9 BP 542 EP 545 PG 4 WC Medicine, General & Internal SC General & Internal Medicine GA 854NP UT WOS:000223910900010 PM 15449491 ER PT J AU Mitchell, P Ropar, D AF Mitchell, P Ropar, D TI Visuo-spatial abilities in autism: A review SO INFANT AND CHILD DEVELOPMENT LA English DT Article DE weak central coherence; prior knowledge; visual illusions; hierarchical stimuli ID ASPERGERS-SYNDROME; VISUAL ILLUSIONS; SHAPE CONSTANCY; PRIOR KNOWLEDGE; CHILDREN; INDIVIDUALS; PERFORMANCE; MEMORY; TASK; INTEGRATION AB Individuals with autism show various signs of heightened abilities in visuo-spatial functioning. First, it is long-established that they excel on embedded figures and block design tests relative to comparison participants. Second, some evidence suggests that processing global features is affected by inappropriate processing of the constituent elements of a stimulus. Third, they are more accurate than comparison participants in judging the shape of a slanted circle in a context in which ambient visual cues are eliminated. This suggests that their perception of the shape is less influenced by prior knowledge. Fourth, they are fast at searching for feature and conjunctive targets in a visual array. Contrary to earlier reports, however, they are susceptible to visual illusions. Also, they do show evidence of utilising prior knowledge when pairing a colour with an atypically coloured target. Accordingly, we conclude that there is something distinctive about autistic visuo-spatial functioning, but not necessarily in ways that are predicted by the 'weak central coherence' hypothesis. Copyright (C) 2004 John Wiley Sons, Ltd. C1 Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Mitchell, P (reprint author), Univ Nottingham, Sch Psychol, Univ Pk, Nottingham NG7 2RD, England. EM plm@psychology.nottingham.ac.uk CR Bailey A, 1996, J CHILD PSYCHOL PSYC, V37, P89, DOI 10.1111/j.1469-7610.1996.tb01381.x Baron-Cohen S, 1995, MINDBLINDNESS Bauman M.L, 1994, NEUROBIOLOGY AUTISM Bowler DM, 2000, J ABNORM PSYCHOL, V109, P663, DOI 10.1037//0021-843X.109.4.663 Brian JA, 1996, J CHILD PSYCHOL PSYC, V37, P865, DOI 10.1111/j.1469-7610.1996.tb01482.x Bruce V., 1996, VISUAL PERCEPTION PH Frith U., 1989, AUTISM EXPLAINING EN Happe F, 1999, TRENDS COGN SCI, V3, P216, DOI 10.1016/S1364-6613(99)01318-2 Happe FGE, 1996, J CHILD PSYCHOL PSYC, V37, P873, DOI 10.1111/j.1469-7610.1996.tb01483.x HUGHES C, 1993, DEV PSYCHOL, V29, P498, DOI 10.1037/0012-1649.29.3.498 Bailey A, 1998, HUM MOL GENET, V7, P571 Jolliffe T, 1997, J CHILD PSYCHOL PSYC, V38, P527, DOI 10.1111/j.1469-7610.1997.tb01539.x Mitchell P, 1999, COGNITION, V70, P167, DOI 10.1016/S0010-0277(99)00011-6 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, 1993, BRAIN COGNITION, V23, P279, DOI 10.1006/brcg.1993.1060 MOTTRON L, 1995, PSYCHOL MED, V25, P639 NAVON D, 1977, COGNITIVE PSYCHOL, V9, P353, DOI 10.1016/0010-0285(77)90012-3 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 Pickles A, 2000, J CHILD PSYCHOL PSYC, V41, P491, DOI 10.1017/S0021963099005557 Plaisted K, 1998, J CHILD PSYCHOL PSYC, V39, P765, DOI 10.1017/S0021963098002601 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 PRING L, 1993, J CHILD PSYCHOL PSYC, V34, P1365, DOI 10.1111/j.1469-7610.1993.tb02096.x Rinehart NJ, 2000, J CHILD PSYCHOL PSYC, V41, P769, DOI 10.1017/S002196309900596X Ropar D, 1999, J CHILD PSYCHOL PSYC, V40, P1283, DOI 10.1017/S0021963099004667 Ropar D, 2001, J CHILD PSYCHOL PSYC, V42, P539, DOI 10.1111/1469-7610.00748 Ropar D, 2002, J CHILD PSYCHOL PSYC, V43, P647, DOI 10.1111/1469-7610.00053 Ropar D, 2003, BRIT J DEV PSYCHOL, V21, P387, DOI 10.1348/026151003322277766 Ropar D, 2001, DEVELOPMENTAL SCI, V4, P433, DOI 10.1111/1467-7687.00185 Russell J., 1998, AUTISM EXECUTIVE DIS 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 Thouless RH, 1931, B J PSYCHOL-GEN SECT, V21, P339 TREISMAN AM, 1980, COGNITIVE PSYCHOL, V12, P97, DOI 10.1016/0010-0285(80)90005-5 WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 NR 37 TC 31 Z9 31 PU JOHN WILEY & SONS LTD PI CHICHESTER PA THE ATRIUM, SOUTHERN GATE, CHICHESTER PO19 8SQ, W SUSSEX, ENGLAND SN 1522-7227 J9 INFANT CHILD DEV JI Infant Child Dev. PD SEP PY 2004 VL 13 IS 3 BP 185 EP 198 DI 10.1002/icd.348 PG 14 WC Psychology, Developmental SC Psychology GA 854VI UT WOS:000223931200001 ER PT J AU Novotny, S Hollander, E Phillips, A Allen, A Wasserman, S Iyengar, R AF Novotny, S Hollander, E Phillips, A Allen, A Wasserman, S Iyengar, R TI Increased repetitive behaviours and prolactin responsivity to oral m-chlorophenylpiperazine in adults with autism spectrum disorders SO INTERNATIONAL JOURNAL OF NEUROPSYCHOPHARMACOLOGY LA English DT Article DE Asperger's disorder; autism; obsessive-compulsive behaviours; oxytocin; peptide ID OBSESSIVE-COMPULSIVE DISORDER; WHOLE-BLOOD SEROTONIN; GROWTH-HORMONE RESPONSE; 1ST-DEGREE RELATIVES; META-CHLOROPHENYLPIPERAZINE; NEUROENDOCRINE RESPONSES; SUMATRIPTAN CHALLENGE; PLATELET SEROTONIN; 5-HT2A RECEPTORS; DOUBLE-BLIND AB Autism is a neurodevelopmental disorder characterized by dysfunction in three primary behavioural domains: repetitive behaviours, social deficits, and language abnormalities. There is evidence that abnormalities exist in the serotonin (5-HT) system in autism spectrum patients. Furthermore, 5-HT is known to play a role in repetitive and social behaviours. This study examined the effect of m-chlorophenylpiperazine (m-CPP) on repetitive behaviours and prolactin response in 11 adults with autism or Asperger's disorder and 8 age- and gender-matched healthy controls via randomized double-blind, m-CPP and placebo challenges. The primary outcome measure was an instrument rating six repetitive behaviours: need to know, repeating, ordering, need to tell/ask, self-injury, and touching. Patients with autism spectrum disorders showed a significant increase in repetitive behaviours at end-point following oral m-CPP in comparison to placebo. Additionally subjects with autism spectrum disorders showed a significantly increased prolactin response to m-CPP compared to normal controls, with neither group responding to placebo. This study provides further evidence for altered 5-HT sensitivity in individuals with autism spectrum disorders, as well as a possible relationship between repetitive behaviours in autism spectrum disorders and abnormalities in the 5-HT system. C1 CUNY Mt Sinai Sch Med, Dept Psychiat, Seaver Autism Res Ctr, New York, NY 10029 USA. RP Hollander, E (reprint author), CUNY Mt Sinai Sch Med, Dept Psychiat, Seaver Autism Res Ctr, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA. EM eric.hollander@mssm.edu CR ABRAMSON RK, 1989, J AUTISM DEV DISORD, V19, P397, DOI 10.1007/BF02212938 ALOI JA, 1984, LIFE SCI, V34, P1325, DOI 10.1016/0024-3205(84)90003-1 American Psychiatric Association (APA), 1994, DIAGN STAT MAN MENT, V4th CHARNEY DS, 1988, ARCH GEN PSYCHIAT, V45, P177 Chugani DC, 1997, ANN NEUROL, V42, P666, DOI 10.1002/ana.410420420 Cook Edwin H. 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J. Neuropsychopharmacol. PD SEP PY 2004 VL 7 IS 3 BP 249 EP 254 DI 10.1017/S146114570400433X PG 6 WC Clinical Neurology; Neurosciences; Pharmacology & Pharmacy; Psychiatry SC Neurosciences & Neurology; Pharmacology & Pharmacy; Psychiatry GA 857FX UT WOS:000224102800002 PM 15132762 ER PT J AU Lazarev, VV Pontes, A Deazevedo, LC AF Lazarev, VV Pontes, A Deazevedo, LC TI Right hemisphere deficit in EEG photic driving reactivity in childhood autism SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Meeting Abstract C1 Oswaldo Cruz Fdn, Rio De Janeiro, Brazil. NR 0 TC 4 Z9 4 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. J. Psychophysiol. PD SEP PY 2004 VL 54 IS 1-2 BP 79 EP 79 PG 1 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 842YF UT WOS:000223039900185 ER PT J AU McDowell, MJ AF McDowell, MJ TI Autism, early narcissistic injury and self-organization: a role for the image of the mother's eyes? SO JOURNAL OF ANALYTICAL PSYCHOLOGY LA English DT Article DE archetypal image; autism; eye contact; narcissistic injury; newborn; primary deficit; self-organization ID CHILDREN; ARCHETYPES; INFANCY; OBJECT; VIEW AB Holland elucidated the new paradigm of self-organization in complex adaptive systems. This paradigm holds for all living systems, including the personality. In conjunction with the theory of archetypes, self-organization suggests two radical hypotheses, one about early development, the other about the origins of autism. Autism is associated with several medical conditions, with genetic markers, and with infant visual deprivation. However none of these factors is either necessary or sufficient to cause autism. It is hypothesized that each of these factors increases the likelihood of a primary psychological deficit: failure to acquire, or retain, the image of the mother's eyes. This hypothesis was initially derived from analytic work with patients who have early narcissistic injury and with patients who have mild autistic traits. Both diagnoses may arise from the same initial disturbance: Symington argued that autism is an extreme form of infantile narcissism. Indirect evidence for the image-of-the-eyes hypotheses comes from the evolution of primates, from infant-mother observations, from observations of infant vision, and from experiments on vision in other vertebrates. Byrd recently confirmed that the incidence of autism is increasing dramatically. The image-of-the-eyes hypotheses suggest that this increase may be linked to increased use of non-maternal childcare for young infants. C1 CG Jung Fdn, New York, NY USA. RP McDowell, MJ (reprint author), 26 W 9th St,9B, New York, NY 10011 USA. EM maxmcdowell@earthlink.net CR Als H, 1980, HIGH RISK INFANTS CH, P181 Baron-Cohen S, 2001, J AUTISM DEV DISORD, V31, P5, DOI 10.1023/A:1005653411471 BaronCohen S, 1997, VIS COGN, V4, P311, DOI 10.1080/713756761 Beebe B., 1997, PSYCHOANALYTIC DIALO, V7, P133 BERGMAN A, 1985, PARENTAL INFLUENCES BION WR, 1962, 7 SERVANTS Brown R, 1997, J CHILD PSYCHOL PSYC, V38, P693, DOI 10.1111/j.1469-7610.1997.tb01696.x BYRD R, 2002, EPIDEMIOLOGY AUTISM California Department of Developmental Services, 1999, CHANG POP PERS AUT P Elrnan J. L., 1998, RETHINKING INNATENES Emery NJ, 2000, NEUROSCI BIOBEHAV R, V24, P581, DOI 10.1016/S0149-7634(00)00025-7 Farroni T, 2002, P NATL ACAD SCI USA, V99, P9602, DOI 10.1073/pnas.152159999 Fordham M., 1976, SELF AUTISM Fraiberg S., 1977, INSIGHTS BLIND COMP FRIEDMAN D, 1964, J CHILD PSYCHOL PSYC, V5, P171 GANS C, 1973, BIOL REPTILES, V4 Gergely G, 1996, INT J PSYCHOANAL, V77, P1181 Gergely G, 2001, B MENNINGER CLIN, V65, P411, DOI 10.1521/bumc.65.3.411.19853 GOMBEROFF MJ, 1990, INT J PSYCHOANAL, V71, P249 Grandin T, 1996, THINKING PICTURES OT GREEN MJ, 1993, CELTIC MYTHS Haaf RA, 1967, CHILD DEV, V38, P892 HAITH MM, 1966, J EXP CHILD PSYCHOL, V3, P235, DOI 10.1016/0022-0965(66)90067-1 Hobson RP, 1999, J AUTISM DEV DISORD, V29, P45 Hogenson GB, 2001, J ANAL PSYCHOL, V46, P591, DOI 10.1111/1465-5922.00269 Holland J.H., 1998, EMERGENCE CHAOS ORDE HUFF R, 2003, REPORT CALIFORNIA DE Jaffe J, 2001, MONOGR SOC RES CHILD, V66, P1, DOI 10.1111/1540-5834.00137 KARMEL BZ, 1974, CHILD DEV, V45, P39, DOI 10.1111/j.1467-8624.1974.tb00556.x Klin A, 2002, ARCH GEN PSYCHIAT, V59, P809, DOI 10.1001/archpsyc.59.9.809 Knox J., 2003, ARCHETYPE ATTACHMENT Knox J, 1999, J ANAL PSYCHOL, V44, P511, DOI 10.1111/1465-5922.00117 Knox JM, 2001, J ANAL PSYCHOL, V46, P613, DOI 10.1111/1465-5922.00270 Kohut H., 1971, ANAL SELF Kohut H., 1984, DOES ANAL CURE KOHUT H, 1978, SEARCH SELF, V1 Maestro S, 2001, PSYCHOPATHOLOGY, V34, P147, DOI 10.1159/000049298 Mahler M., 1975, PSYCHOL BIRTH HUMAN MCDOWELL MJ, 1999, QUADRANT J C G JUNG, V29, P12 MCDOWELL MJ, 2001, IMAGE MOTHERS EYE AU McDowell MJ, 2001, J ANAL PSYCHOL, V46, P637, DOI 10.1111/1465-5922.00271 Michael CR, 1969, SCI AM MAY, P104 Allhusen V, 2003, CHILD DEV, V74, P976 RIDEOUT VJ, 2003, 3378 HJ KAIS FAM FDN Rodier PM, 2000, SCI AM, V282, P56 Rutter ML, 2001, BRIT J PSYCHIAT, V179, P97, DOI 10.1192/bjp.179.2.97 Salapatek P, 1975, INFANT PERCEPTION SE, VI, P144 Samuels Andrew, 1985, FATHER CONT JUNGIAN Saunders P, 2001, J ANAL PSYCHOL, V46, P305, DOI 10.1111/1465-5922.00238 Spitz RA, 1946, GENET PSYCHOL MONOGR, V34, P57 Stern D., 1985, INTERPERSONAL WORLD Stern D. 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PD SEP PY 2004 VL 49 IS 4 BP 495 EP 519 DI 10.1111/j.0021-8774.2004.00481.x PG 25 WC Psychology, Multidisciplinary SC Psychology GA 847CL UT WOS:000223366300003 PM 15317530 ER PT J AU White, N Hastings, RP AF White, N Hastings, RP TI Social and professional support for parents of adolescents with severe intellectual disabilities SO JOURNAL OF APPLIED RESEARCH IN INTELLECTUAL DISABILITIES LA English DT Article DE adolescence; parents; services; severe intellectual disabilities; social support ID DEVELOPMENTALLY DISABLED-CHILDREN; FAMILY-LIFE-STYLES; BEHAVIOR-PROBLEMS; MENTAL-RETARDATION; POSITIVE PERCEPTIONS; HANDICAPPED-CHILD; AUTISTIC-CHILDREN; 2-FACTOR MODEL; DOWNS-SYNDROME; STRESS AB Background Previous research has identified various dimensions of social support that are positively associated with parental well-being. However, most research does not include multiple measures of social support and uses heterogeneous samples in terms of child characteristics such as age and severity of intellectual disability. Method Thirty-three parents of adolescent children with moderate-profound intellectual disabilities completed measures of parental well-being (stress, anxiety and depression, and caregiving satisfaction), social support (informal and formal sources, and practical and emotional support), and child characteristics (adaptive and problem behaviours). Results Correlation analyses showed that parental well-being was associated with the child's adaptive and problem behaviours and with the child's autism diagnosis. Parents' ratings of the helpfulness of informal sources of support (spouse, extended family, friends, etc.) was most reliably associated with parental well-being, and remained so after controlling for child characteristics. Parents' access of service and professional support was not associated with parental well-being, but there was some evidence that it was related to their child's needs. Conclusions The research emphasizes the significance of including multiple measures of social support in research with families of children with an intellectual disability. Furthermore, the possibility that parents, during their child's adolescence, may be especially vulnerable to the disruption of their informal support networks is an important practical consideration. C1 Univ Wales Bangor, Sch Psychol, Bangor LL57 2DG, Gwynedd, Wales. RP Hastings, RP (reprint author), Univ Wales Bangor, Sch Psychol, Bangor LL57 2DG, Gwynedd, Wales. 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Appl. Res. Intellect. Disabil. PD SEP PY 2004 VL 17 IS 3 BP 181 EP 190 DI 10.1111/j.1468-3148.2004.00197.x PG 10 WC Psychology, Educational; Rehabilitation SC Psychology; Rehabilitation GA 847CS UT WOS:000223367200005 ER PT J AU Oner, O Aysev, A Kaplan, I AF Oner, O Aysev, A Kaplan, I TI Possible acute confusional state after risperidone in a pediatric patient SO JOURNAL OF CHILD AND ADOLESCENT PSYCHOPHARMACOLOGY LA English DT Letter ID CHILDREN; AUTISM C1 Ankara Univ, Fac Med, Child Psychiat Dept, TR-06100 Ankara, Turkey. Cumhuriyet Univ, Fac Med, Dept Pediat, Sivas, Turkey. RP Oner, O (reprint author), Ankara Univ, Fac Med, Child Psychiat Dept, TR-06100 Ankara, Turkey. RI aysev, Ayla/B-9696-2013 CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Doig A, 2000, INT J GERIATR PSYCH, V15, P534 Malone RP, 2002, J AM ACAD CHILD PSY, V41, P140, DOI 10.1097/00004583-200202000-00007 Ravona-Springer R, 1998, J CLIN PSYCHOPHARM, V18, P171, DOI 10.1097/00004714-199804000-00011 McCracken JT, 2002, NEW ENGL J MED, V347, P314, DOI 10.1056/NEJMoa013171 NR 5 TC 0 Z9 0 PU MARY ANN LIEBERT INC PI LARCHMONT PA 2 MADISON AVENUE, LARCHMONT, NY 10538 USA SN 1044-5463 J9 J CHILD ADOL PSYCHOP JI J. Child Adolesc. Psychopharmacol. PD FAL PY 2004 VL 14 IS 3 BP 339 EP 341 PG 3 WC Pediatrics; Pharmacology & Pharmacy; Psychiatry SC Pediatrics; Pharmacology & Pharmacy; Psychiatry GA 867JI UT WOS:000224838500006 PM 15650487 ER PT J AU Ridler, K Suckling, J Higgins, N Bolton, P Bullmore, ET AF Ridler, K Suckling, J Higgins, N Bolton, P Bullmore, ET TI Standardized whole brain mapping of tubers and subependymal nodules in tuberous sclerosis complex SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 32nd Annual Meeting of the Child-Neurology-Society CY OCT 01-04, 2003 CL MIAMI BEACH, FL SP Child Neruol Soc ID AUTISM; ABNORMALITIES AB Tuberous sclerosis complex is associated with radiologically visible abnormalities of brain structure, principally tubers and subependymal nodules. We reviewed the literature on neuroimaging of tubers and subependymal nodules and found qualitative evidence of bilateral, predominantly frontal distribution of tubers and bilateral, predominantly subcortical distribution of subependymal nodules in prior studies of pediatric samples. We studied 25 high-functioning adults with tuberous sclerosis complex and normal IQ, acquiring both dual spin-echo and fluid-attenuated inversion recovery magnetic resonance imaging sequences to optimize radiologic diagnosis of tubers and nodules. Individual lesion maps were then coregistered in a standard stereotactic space to facilitate construction of lesion density maps and estimation of lesion density in cortical and subcortical regions reliably defined by a parcellated template image. We found the highest frequency of tubers in frontal lobes and the highest density of tubers in parietal regions. There was significant regional variation in tuber density but no significant lateralization of frequently bilateral tubers. Nodules were located predominantly in the caudate nucleus and were not significantly lateralized. Tuber and nodule volumes were significantly positively correlated. Tuber volume was larger, on average, in patients with a lifetime history of epilepsy, but there was no correlation between IQ and these measures of lesion load. Contemporary image processing tools can be used to enhance quantitative, whole brain analysis of lesion load in patients with tuberous sclerosis complex. C1 Univ Cambridge, Dept Psychiat, Brain Mapping Unit, Addenbrookes Hosp, Cambridge CB2 2QQ, England. Univ Cambridge, Dept Radiol, Addenbrookes Hosp, Cambridge CB2 2QQ, England. Inst Psychiat, Dept Child & Adolescent Psychiat, London, England. RP Ridler, K (reprint author), Univ Cambridge, Dept Psychiat, Brain Mapping Unit, Addenbrookes Hosp, Box 255, Cambridge CB2 2QQ, England. EM kr240@cam.ac.uk RI Bullmore, Edward/C-1706-2012; Bolton, Patrick/E-8501-2010 OI Bullmore, Edward/0000-0002-8955-8283; Bolton, Patrick/0000-0002-5270-6262 CR Asano E, 2000, NEUROLOGY, V54, P1976 Baron Y, 1999, AM J NEURORADIOL, V20, P907 Bolton PF, 2002, BRAIN, V125, P1247, DOI 10.1093/brain/awf124 Bolton PF, 1997, LANCET, V349, P392, DOI 10.1016/S0140-6736(97)80012-8 BRAFFMAN BH, 1992, RADIOLOGY, V183, P227 Brammer MJ, 1997, MAGN RESON IMAGING, V15, P763, DOI 10.1016/S0730-725X(97)00135-5 CUSMAI R, 1990, EPILEPSIA, V31, P747, DOI 10.1111/j.1528-1157.1990.tb05516.x Griffiths PD, 1997, NEUROPEDIATRICS, V28, P244, DOI 10.1055/s-2007-973708 Griffiths PD, 1998, ACTA RADIOL, V39, P482 JAMBAQUE I, 1991, DEV MED CHILD NEUROL, V33, P698 MAEDA M, 1995, J COMPUT ASSIST TOMO, V19, P660, DOI 10.1097/00004728-199507000-00033 Marti-Bonmati L, 2000, AM J NEURORADIOL, V21, P557 PRESS WH, 1992, NUMERIC RECIPES C AR, V2 Ridler K, 2001, PSYCHOL MED, V31, P1437 Roach ES, 1998, J CHILD NEUROL, V13, P624 Seri S, 1999, CLIN NEUROPHYSIOL, V110, P1825, DOI 10.1016/S1388-2457(99)00137-6 SHEPHERD CW, 1995, AM J NEURORADIOL, V16, P149 TAKANASHI J, 1995, AM J NEURORADIOL, V16, P1923 Talairach J., 1988, CO PLANAR STEREOTAXI Tzourio-Mazoyer N, 2002, NEUROIMAGE, V15, P273, DOI 10.1006/nimg.2001.0978 VanTassel P, 1997, AM J NEURORADIOL, V18, P1367 Walz NC, 2002, J CHILD NEUROL, V17, P830, DOI 10.1177/08830738020170111401 WEBB DW, 1991, ARCH DIS CHILD, V66, P1375 Weber AM, 2000, J AUTISM DEV DISORD, V30, P511, DOI 10.1023/A:1005679108529 Wechsler D, 1999, WECHSLER ABBREVIATED NR 25 TC 30 Z9 33 PU SAGE PUBLICATIONS INC PI THOUSAND OAKS PA 2455 TELLER RD, THOUSAND OAKS, CA 91320 USA SN 0883-0738 EI 1708-8283 J9 J CHILD NEUROL JI J. Child Neurol. PD SEP PY 2004 VL 19 IS 9 BP 658 EP 665 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 938GT UT WOS:000229988600005 PM 15563011 ER PT J AU Prather, P de Vries, PJ AF Prather, P de Vries, PJ TI Behavioral and cognitive aspects of tuberous sclerosis complex SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 32nd Annual Meeting of the Child-Neurology-Society CY OCT 01-04, 2003 CL MIAMI BEACH, FL SP Child Neruol Soc ID ATTENTION DEFICITS; EPILEPSY; AUTISM; PREVALENCE; DISORDERS; CHILDREN; TSC1; DISABILITY; SEVERITY; SEIZURES AB Tuberous sclerosis complex is a multisystem genetic disorder. Of all the possible manifestations of this complex disorder, the cognitive and behavioral problems represent the area of greatest concern to parents and caregivers. This review outlines the current evidence regarding global intellectual abilities, behavioral problems, psychiatric diagnoses, learning disorders, and specific neuropsychologic deficits for which individuals with tuberous sclerosis complex are at particularly increased risk, and outlines approaches to intervention. Approximately half of individuals diagnosed with tuberous sclerosis complex present with global intellectual impairment and developmental psychopathologies. Those with normal intellectual abilities are also at high risk of specific neuropsychologic deficits and behavioral, learning, and other psychiatric disorders. There is no evidence for an inevitable decline in cognition or behavior, and any such changes should be investigated. The evolving neurocognitive literature suggests that frontal brain systems might be most consistently disrupted by tuberous sclerosis complex-related neuropathology, thus leading to abnormalities in regulatory and goal-directed behaviors. C1 Massachusetts Gen Hosp, Dept Psychiat, Boston, MA USA. Massachusetts Gen Hosp, Dept Neurol, Boston, MA USA. Harvard Univ, Sch Med, Cambridge, MA 02138 USA. Univ Cambridge, Dev Psychiat Sect, Cambridge, England. RP Prather, P (reprint author), 23 Pleasant St, Newton, MA 02459 USA. 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Child Neurol. PD SEP PY 2004 VL 19 IS 9 BP 666 EP 674 PG 9 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 938GT UT WOS:000229988600006 PM 15563012 ER PT J AU Wiznitzer, M AF Wiznitzer, M TI Autism and tuberous sclerosis SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 32nd Annual Meeting of the Child-Neurology-Society CY OCT 01-04, 2003 CL MIAMI BEACH, FL SP Child Neruol Soc ID SPECTRUM DISORDERS; EPILEPSY SURGERY; ATYPICAL AUTISM; CHILDREN; COMPLEX; ADOLESCENTS; PREVALENCE; BEHAVIOR AB The co-occurrence of autism spectrum disorder and tuberous sclerosis complex has been recognized for decades. The prevalence of tuberous sclerosis complex in the autism spectrum disorder population is 1 to 4%, whereas features of autism spectrum disorder are present in 25 to 50% of individuals with tuberous sclerosis complex. The underlying reason for this association might be a nonspecific disruption of brain function owing to tuberous sclerosis complex, including tuber location, seizures and their effect on brain development, cognitive impainnent, a disturbance in brain development in regions associated with autism spectrum disorder, or, less likely, a linkage between a TSC gene and an autism susceptibility gene. Awareness of the relationship between autism spectrum disorder and tuberous sclerosis complex is important during the evaluation of individuals with either disorder. Better delineation of the association and its causative factors is needed for the development of possible interventions. C1 Rainbow Babies & Childrens Hosp, Cleveland, OH 44106 USA. Case Western Reserve Univ, Sch Med, Cleveland, OH USA. RP Wiznitzer, M (reprint author), Rainbow Babies & Childrens Hosp, 11100 Euclid Ave, Cleveland, OH 44106 USA. 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Child Neurol. PD SEP PY 2004 VL 19 IS 9 BP 675 EP 679 PG 5 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 938GT UT WOS:000229988600007 PM 15563013 ER PT J AU Astrinidis, A Henske, EP AF Astrinidis, A Henske, EP TI Aberrant cellular differentiation and migration in renal and pulmonary tuberous sclerosis complex SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 32nd Annual Meeting of the Child-Neurology-Society CY OCT 01-04, 2003 CL MIAMI BEACH, FL SP Child Neruol Soc ID TUMOR-SUPPRESSOR GENE; LYMPHANGIOLEIOMYOMATOSIS LAM; MUTATIONAL ANALYSIS; SOMATIC MUTATIONS; RHO GTPASES; TSC2; LYMPHANGIOMYOMATOSIS; HETEROZYGOSITY; PROLIFERATION; DROSOPHILA AB This review is focused on pathways and mechanisms that might provide molecular links between the pathogenesis of renal and pulmonary disease in tuberous sclerosis complex and the pathogenesis of the neurologic manifestations of tuberous sclerosis complex. Tuberous sclerosis complex is an autosomal dominant disorder in which the manifestations can include seizures; mental retardation; autism; benign tumors of the brain, retina, skin, and kidneys; and pulmonary lymphan-giomyomatosis. Lymphangiomyomatosis is a life-threatening lung disease affecting almost exclusively young women. Genetic data have demonstrated that the cells giving rise to renal angiomyolipomas, the most frequent tumor type in patients with tuberous sclerosis complex, exhibit differentiation plasticity. Genetic studies have also shown that the benign smooth muscle cells of angiomyolipomas and pulmonary lymphangiomyomatosis have the ability to migrate or metasta-size to other organs. These findings indicate that hamartin and tuberin play functional roles in the regulation of cell migration and differentiation. The biochemical pathways responsible for these effects are not yet fully understood but might involve dysregulation of the small guanosine triphosphatase Rho. Similar pathways might contribute to aberrant neuronal differentiation and migration in tuberous sclerosis complex. C1 Fox Chase Canc Ctr, Dept Med Oncol, Philadelphia, PA 19111 USA. Fox Chase Canc Ctr, Human Genet Working Grp, Philadelphia, PA 19111 USA. RP Henske, EP (reprint author), Fox Chase Canc Ctr, Dept Med Oncol, 333 Cottman Ave, Philadelphia, PA 19111 USA. 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Child Neurol. PD SEP PY 2004 VL 19 IS 9 BP 710 EP 715 PG 6 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 938GT UT WOS:000229988600012 PM 15563018 ER PT J AU Scheidenhelm, DK Gutmann, DH AF Scheidenhelm, DK Gutmann, DH TI Mouse models of tuberous sclerosis complex SO JOURNAL OF CHILD NEUROLOGY LA English DT Article; Proceedings Paper CT 32nd Annual Meeting of the Child-Neurology-Society CY OCT 01-04, 2003 CL MIAMI BEACH, FL SP Child Neruol Soc ID TUMOR-SUPPRESSOR PROTEINS; TSC1 GENE-PRODUCT; CELL-GROWTH; RHEB GTPASE; EMBRYONIC LETHALITY; DIRECT TARGET; GIANT-CELLS; EKER RAT; MTOR; DROSOPHILA AB The most devastating complications of tuberous sclerosis complex affect the central nervous system and include epilepsy, mental retardation, autism, and glial tumors. Mutations in one of two genes, TSC1 and TSC2, result in a similar disease phenotype by disrupting the normal interaction of their protein products, hamartin and tuberin, which form a functional signaling complex. Disruption of these genes in the brain results in abnormal cellular differentiation, migration, and proliferation, giving rise to characteristic brain lesions called cortical tubers. Relevant animal models, including conventional and conditional knockout mice, are valuable tools for studying the normal functions of tuberin and hamartin and how disruption of their expression gives rise to the variety of clinical features that characterize tuberous sclerosis complex. In the future, these animals will be invaluable preclinical models for the development of highly specific and efficacious treatments for children affected with tuberous sclerosis complex. C1 Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA. RP Gutmann, DH (reprint author), Washington Univ, Sch Med, Dept Neurol, Box 8111,660 S Euclid Ave, St Louis, MO 63110 USA. 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Child Neurol. PD SEP PY 2004 VL 19 IS 9 BP 726 EP 733 PG 8 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 938GT UT WOS:000229988600014 PM 15563020 ER PT J AU Peterson, CC AF Peterson, CC TI Theory-of-mind development in oral deaf children with cochlear implants or conventional hearing aids SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE deafness; children; social cognition; theory-of-mind; cochlear implant ID AUTISM; COMMUNICATION; LANGUAGE; STATES AB Background: In the context of the established finding that theory-of-mind (ToM) growth is seriously delayed in late-signing deaf children, and some evidence of equivalent delays in those learning speech with conventional hearing aids, this study's novel contribution was to explore ToM development in deaf children with cochlear implants. Implants can substantially boost auditory acuity and rates of language growth. Despite the implant, there are often problems socialising with hearing peers and some language difficulties, lending special theoretical interest to the present comparative design. Methods: A total of 52 children aged 4 to 12 years took a battery of false belief tests of ToM. There were 26 oral deaf children, half with implants and half with hearing aids, evenly divided between oral-only versus sign-plus-oral schools. Comparison groups of age-matched high-functioning children with autism and younger hearing children were also included. Results: No significant ToM differences emerged between deaf children with implants and those with hearing aids, nor between those in oral-only versus sign-plus-oral schools. Nor did the deaf children perform any better on the ToM tasks than their age peers with autism. Hearing preschoolers scored significantly higher than all other groups. For the deaf and the autistic children, as well as the preschoolers, rate of language development and verbal maturity significantly predicted variability in ToM, over and above chronological age. Conclusions: The finding that deaf children with cochlear implants are as delayed in ToM development as children with autism and their deaf peers with hearing aids or late sign language highlights the likely significance of peer interaction and early fluent communication with peers and family, whether in sign or in speech, in order to optimally facilitate the growth of social cognition and language. C1 Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. RP Peterson, CC (reprint author), Univ Queensland, Sch Psychol, Brisbane, Qld 4072, Australia. 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Psychiatry PD SEP PY 2004 VL 45 IS 6 BP 1096 EP 1106 DI 10.1111/j.1469-7610.2004.t01-1-00302.x PG 11 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 842SO UT WOS:000223024700007 PM 15257666 ER PT J AU Alcantara, JI Weisblatt, EJL Moore, BCJ Bolton, PF AF Alcantara, JI Weisblatt, EJL Moore, BCJ Bolton, PF TI Speech-in-noise perception in high-functioning individuals with autism or Asperger's syndrome SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE autism; Asperger's syndrome; speech perception; dip listening; temporal resolution and integration; frequency selectivity ID AUDITORY FILTER SHAPES; NORMAL-HEARING; GAP DETECTION; RECEPTION THRESHOLD; TEMPORAL DIPS; INTELLIGIBILITY; IDENTIFICATION; COMPREHENSION; BACKGROUNDS; CHILDREN AB Background: High-functioning individuals with autism (HFA) or Asperger's syndrome (AS) commonly report difficulties understanding speech in situations where there is background speech or noise. The objective of this study was threefold: (1) to verify the validity of these reports; (2) to quantify the difficulties experienced; and (3) to propose possible mechanisms to explain the perceptual deficits described. Method: Speech-in-noise perception abilities were measured using speech reception thresholds (SRTs), defined as the speech-to-noise ratio (SNR) at which approximately 50% of the speech is correctly identified. SRTs were measured for 11 individuals with HFA/AS and 9 age/IQ-matched normal-hearing control subjects, using an adaptive procedure, in a non-reverberant sound-attenuating chamber. The speech materials were standardised lists of everyday sentences spoken by a British male speaker. The background sounds were: (1) a single female talker; (2) a steady speech-shaped noise; (3) a speech-shaped noise with temporal dips; (4) a steady speech-shaped noise with regularly spaced spectral dips; and (5) a speech-shaped noise with temporal and spectral dips. Results: SRTs for the HFA/AS group were generally higher (worse) than those for the controls, across the five background sounds. A statistically significant difference in SRTs between the subject groups was found only for those background sounds that contained temporal or spectro-temporal dips. SRTs for the HFA/AS individuals were 2 to 3.5 dB higher than for the controls, equivalent to a substantial decrease in speech recognition. Expressed another way, the HFA/AS individuals required a higher SNR, whenever there were temporal dips in the background sound, to perform at the same level as the controls. Conclusions: The results suggest that the speech-in-noise perception difficulties experienced by individuals with autism may be due, in part, to a reduced ability to integrate information from glimpses present in the temporal dips in the noise. C1 Univ Cambridge, Dept Expt Psychol, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Dev Psychiat Sect, Cambridge, England. 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S., 1986, FREQUENCY SELECTIVIT, P309 World Health Organisation, 1992, ICD 10 CLASS MENT BE NR 42 TC 77 Z9 81 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 PD SEP PY 2004 VL 45 IS 6 BP 1107 EP 1114 DI 10.1111/j.1469-7610.2004.t01-1-00303.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 842SO UT WOS:000223024700008 PM 15257667 ER PT J AU Landry, R Bryson, SE AF Landry, R Bryson, SE TI Impaired disengagement of attention in young children with autism SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE attention; autistic disorder; Down syndrome; pervasive developmental disorder; temperament; visuo-spatial functioning ID NORMAL INFANTS; CEREBELLAR; DEFICITS AB Background: The present study examined the disengage and shift operations of visual attention in young children with autism. Methods: For this purpose, we used a simple visual orienting task that is thought to engage attention automatically. Once attention was first engaged on a central fixation stimulus, a second stimulus was presented on either side, either simultaneously or successively. Latency to begin an eye movement to the peripheral stimulus served as the main dependent measure. The two stimulus conditions (simultaneous and successive) provided independent measures of disengaging and shifting attention, respectively. Performance of children with autism was compared to that of children with Down syndrome and a normal group. Results: The main finding was that relative to both comparison groups, children with autism had marked difficulty in disengaging attention. Indeed, on 20% of trials they remained fixated on the first of two competing stimuli for the entire 8-second trial duration. Evidence is also provided for a more subtle problem in executing rapid shifts of attention. Conclusions: Our findings on disengagement in autism parallel those reported in normal 2-month-olds, in whom attention has been described as 'obligatory'. Discussion focuses on the potential role of general versus domain-specific processes in producing some of the core features of autism. C1 Child & Adolescent Serv, Sydney, NS B1P 1P3, Canada. York Univ, Dept Psychol, Toronto & Brain & Behav Program, Res Inst,Hosp Sick Children, Toronto, ON, Canada. RP Landry, R (reprint author), Child & Adolescent Serv, Cape Breton Reg Healthcare Complex,1482 George St, Sydney, NS B1P 1P3, Canada. 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Child Psychol. Psychiatry PD SEP PY 2004 VL 45 IS 6 BP 1115 EP 1122 DI 10.1111/j.1469-7610.2004.00304.x PG 8 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 842SO UT WOS:000223024700009 PM 15257668 ER PT J AU Rutgers, AH Bakermans-Kranenburg, MJ van Ijzendoorn, MH van Berckelaer-Onnes, IA AF Rutgers, AH Bakermans-Kranenburg, MJ van Ijzendoorn, MH van Berckelaer-Onnes, IA TI Autism and attachment: a meta-analytic review SO JOURNAL OF CHILD PSYCHOLOGY AND PSYCHIATRY LA English DT Article DE attachment; autistic disorder; pervasive developmental disorder; meta-analysis; mental retardation; sensitivity ID PERVASIVE DEVELOPMENTAL DISORDERS; YOUNG-CHILDREN; DISORGANIZED ATTACHMENT; SOCIAL-INTERACTION; STRANGE SITUATION; MOTHER ATTACHMENT; DOWN-SYNDROME; CLASSIFICATION; BEHAVIOR; QUALITY AB Method: Sixteen studies on attachment in children with autism were reviewed, and ten studies with data on observed attachment security (N=287) were included in a quantitative meta-analysis. Results: Despite the impairments of children with autism in reciprocal social interaction, the majority of the studies found evidence for attachment behaviours in these children. In four samples using the Strange Situation procedure the average percentage of secure attachments amounted to 53% (n=72). Meta-analytic results showed that children with autism were significantly less securely attached to their parents than comparison children, and the combined effect size for this difference was moderate (r=.24). Children with autism displayed less attachment security than comparisons without autism, but this difference disappeared in samples with children with higher mental development, and in samples in which autism was mixed with less severe symptoms of autistic spectrum disorders. Conclusions: It is concluded that attachment security is compatible with autism, and can be assessed with Strange Situation type of procedures. The co-morbidity of autism and mental retardation appears to be associated with attachment insecurity. C1 Leiden Univ, Ctr Family & Child Studies, NL-2300 RB Leiden, Netherlands. RP van Berckelaer-Onnes, IA (reprint author), Leiden Univ, Ctr Family & Child Studies, POB 9555, NL-2300 RB Leiden, Netherlands. EM vanijzen@fsw.leidenuniv.nl RI van IJzendoorn, Marinus/I-1379-2012 CR Ainsworth M. 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Psychiatry PD SEP PY 2004 VL 45 IS 6 BP 1123 EP 1134 DI 10.1111/j.1469-7610.2004.t01-1-00305.x PG 12 WC Psychology, Developmental; Psychiatry; Psychology SC Psychology; Psychiatry GA 842SO UT WOS:000223024700010 PM 15257669 ER PT J AU Mayes, SD Calhoun, SL AF Mayes, SD Calhoun, SL TI Influence of IQ and age in childhood autism: Lack of support for DSM-IV Asperger's disorder SO JOURNAL OF DEVELOPMENTAL AND PHYSICAL DISABILITIES LA English DT Article DE autism; Asperger's syndrome; Asperger's disorder; IQ; DSM-IV ID PERVASIVE DEVELOPMENTAL DISORDERS; HIGH-FUNCTIONING AUTISM; SPECTRUM DISORDERS; CLINICAL SYMPTOMS; CLUSTER-ANALYSIS; CHILDREN; SUBTYPES; VALIDITY; CLASSIFICATION; DISABILITIES AB Children with clinical diagnoses of autism or Asperger's disorder who had normal (n = 47) versus below normal (n = 110) intelligence were compared on several variables, including frequency and types of autistic symptoms, discrepancy between nonverbal and verbal IQs, and degree of incoordination, anxiety, and depression. Children with low versus high IQs had more autistic symptoms overall and a greater percentage of social problems. However, when the effects of IQ and age (and, therefore, mental age) were statistically removed, these differences were no longer significant. This finding does not support the DSM-IV's use of normal cognition as one criterion for creating two distinct diagnostic subgroups (Asperger's disorder and autistic disorder) because differences between children with normal versus below normal cognition can be explained simply by differences in IQ and age (as opposed to some intrinsic difference related to autism). C1 Penn State Coll Med, Dept Psychiat, Hershey, PA USA. RP Mayes, SD (reprint author), Penn State Univ, Milton S Hershey Med Ctr, Dept Psychiat, POB 850, Hershey, PA 17033 USA. 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PD SEP PY 2004 VL 16 IS 3 BP 257 EP 272 DI 10.1023/B:JODD.0000032301.07550.0e PG 16 WC Rehabilitation SC Rehabilitation GA 830HU UT WOS:000222113500003 ER PT J AU Schertz, HH Odom, SL AF Schertz, HH Odom, SL TI Joint attention and early intervention with autism: A conceptual framework and promising approaches SO JOURNAL OF EARLY INTERVENTION LA English DT Article ID VISUAL-ATTENTION; YOUNG-CHILDREN; SOCIAL COMMUNICATION; SPECTRUM DISORDERS; LANGUAGE; INFANCY; BEHAVIORS; OBJECTS; SKILLS; DELAY AB This article reviews research on the typical development of joint attention and challenges that infants and toddlers with autism experience in achieving this milestone. We define joint attention as coordinating attention to an event or object with another individual, sharing interest and social engagement, and showing an understanding that the partner is sharing the same focus. 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Early Interv. PD FAL PY 2004 VL 27 IS 1 BP 42 EP 54 DI 10.1177/105381510402700104 PG 13 WC Education, Special; Psychology, Educational; Rehabilitation SC Education & Educational Research; Psychology; Rehabilitation GA 873LY UT WOS:000225283000004 ER PT J AU Gust, DA Gangarosa, P Hibbs, B Pollard, R Wallach, G Chen, RT AF Gust, DA Gangarosa, P Hibbs, B Pollard, R Wallach, G Chen, RT TI National immunization information hotline: Calls concerning adverse events, 1998-2000 SO JOURNAL OF HEALTH COMMUNICATION LA English DT Article ID VACCINE; ASSOCIATION; AUTISM AB Data from the National Immunization Information Hotline (NIIH) concerning vaccine adverse event inquiries were analyzed from 1998 to 2000 (total n = 23,841 [public n = 14,330; health care professionals n = 9,511]). Approximately 20% of calls from the public from 1998 to 2000 concerned vaccine adverse events. These calls increased 199.5% from 1998 (n = 422) to 1999 (n = 1,264), then declined 12.4% from 1999 to 2000 (n = 1,107). A Lexus Nexus search showed that the number of news stories mentioning vaccine safety showed a similar pattern. Women were more likely to call the NIIH concerning vaccine adverse events than men, and persons 40-59 years old and persons 60 years old and over were less likely to call about vaccine adverse events than those 20-39 years. The parallel trends in news stories mentioning vaccine safety and calls to the NIIH concerning adverse events suggests that news stories may stimulate questions about vaccine safety. Understanding that news stories may elicit questions about vaccine adverse events and examining the characteristics of persons who ask vaccine adverse event questions may guide future informational interventions toward those most in need. C1 Ctr Dis Control & Prevent, Epidemiol & Surveillance Div, Natl Immunizat Program, Atlanta, GA 30333 USA. Ctr Dis Control & Prevent, Data Management Div, Natl Immunizat Program, Atlanta, GA USA. Natl Immunizat Informat Hotline, Res Triangle Pk, NC USA. RP Gust, DA (reprint author), Ctr Dis Control & Prevent, Epidemiol & Surveillance Div, Natl Immunizat Program, 1600 Clifton Rd MS E-61, Atlanta, GA 30333 USA. EM dgg6@cdc.gov CR CDC, 1999, MMWR-MORBID MORTAL W, V48, P243 CDC-MMWR, 1999, MMWR-MORBID MORTAL W, V48, P577 Chen RT, 1999, VACCINE, V17, pS41, DOI 10.1016/S0264-410X(99)00292-3 Classen DC, 1997, INFECT DIS CLIN PRAC, V6, P449 Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 Danovaro-Holliday MC, 2002, JAMA-J AM MED ASSOC, V287, P1455, DOI 10.1001/jama.287.11.1455 Davis TC, 2001, PEDIATRICS, V107, DOI 10.1542/peds.107.2.e17 Gout O, 1998, REV NEUROL-FRANCE, V154, P205 Graves PM, 1999, DIABETES CARE, V22, P1694, DOI 10.2337/diacare.22.10.1694 Gust DA, 2004, J HEALTH COMMUN, V9, P371, DOI 10.1080/10810730490468739 Nilsson L, 1998, ARCH PEDIAT ADOL MED, V152, P734 ODENT MR, 1994, JAMA-J AM MED ASSOC, V272, P592 Stryer DB, 2002, HEALTH SERV RES, V37, pXV, DOI 10.1111/1475-6773.00002 Taylor B, 1999, LANCET, V353, P2026, DOI 10.1016/S0140-6736(99)01239-8 Wakefield AJ, 1998, LANCET, V351, P637, DOI 10.1016/S0140-6736(97)11096-0 NR 15 TC 8 Z9 8 PU TAYLOR & FRANCIS INC PI PHILADELPHIA PA 325 CHESTNUT ST, SUITE 800, PHILADELPHIA, PA 19106 USA SN 1081-0730 J9 J HEALTH COMMUN JI J. Health Commun. PD SEP-OCT PY 2004 VL 9 IS 5 BP 387 EP 394 DI 10.1080/10810730490503487 PG 8 WC Communication; Information Science & Library Science SC Communication; Information Science & Library Science GA 861OQ UT WOS:000224426900002 PM 15513788 ER PT J AU Takarae, Y Minshew, NJ Luna, B Sweeney, JA AF Takarae, Y Minshew, NJ Luna, B Sweeney, JA TI Oculomotor abnormalities parallel cerebellar histopathology in autism SO JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY LA English DT Article ID DIAGNOSTIC OBSERVATION SCHEDULE; PURKINJE-CELLS; SACCADIC DYSMETRIA; EYE-MOVEMENTS; VERMIS; LESIONS; MONKEY AB Objective: To investigate cerebellar function in autism by measuring visually guided saccades. Methods: A visually guided saccade task was performed by 46 high-functioning individuals with autism with and without delayed language acquisition, and 104 age and IQ matched healthy individuals. Results: Individuals with autism had increased variability in saccade accuracy, and only those without delayed language development showed a mild saccadic hypometria. Neither autistic group showed a disturbance in peak saccade velocity or latency. Conclusions: The observed saccadic abnormalities suggest a functional disturbance in the cerebellar vermis or its output through the fastigial nuclei, consistent with reported cerebellar histopathology in autism. The pattern of mild hypometria and variable saccade accuracy is consistent with chronic rather than acute effects of cerebellar vermis lesions reported in clinical and non-human primate studies, as might be expected in a neurodevelopmental disorder. The different patterns of oculomotor deficits in individuals with autism with and without delayed language development suggest that pathophysiology at the level of the cerebellum may differ depending on an individual's history of language development. C1 Univ Illinois, Dept Psychiat MC 913, Ctr Cognit Med, Chicago, IL 60612 USA. Univ Pittsburgh, Pittsburgh, PA USA. RP Sweeney, JA (reprint author), Univ Illinois, Dept Psychiat MC 913, Ctr Cognit Med, 912 S Wood St,Suite 235, Chicago, IL 60612 USA. 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The original proposal was based on findings in five children with chronic surgical lesions of the cerebellum and a young adult with a degenerative disorder. The aim of the present study was to repeat Akshoomoff and Courchesne's initial findings in a larger group of children with focal cerebellar lesions. Ten children with cerebellar lesions and 10 age- and sex-matched controls were tested. Neocerebellar areas were affected in all children with cerebellar damage except one based on detailed analysis of MRI scans. Subjects had to perform a focus and a shift attention task. Two visual and two auditory stimuli were presented in a pseudorandom order. An ellipse and a high-pitched tone were presented less frequently than a circle and a low-pitched tone. Rare stimuli were presented at five different time intervals. In the focus tasks, subjects had to react to the same rare stimulus of one of the two modalities. In the shift task, subjects had to switch between the two rare stimuli. Motor deficits based on reaction times were small in cerebellar children compared with controls. The ability of target detection did not significantly differ in the children with cerebellar lesions compared with the control children in both the focus and the shift attention task. In particular, children with cerebellar damage showed no significant impairment in rapid (<2 s) shifts of attention. The present findings indicate that the cerebellum may be less critical in attention related processes than suggested previously. C1 Univ Duisberg Essen, Dept Neurol, D-45122 Essen, Germany. Univ Duisberg Essen, Dept Neurosurg, D-45122 Essen, Germany. Univ Duisberg Essen, Dept Pediat Hematol & Oncol, D-45122 Essen, Germany. Univ Duisberg Essen, Dept Orthoped Surg, D-45122 Essen, Germany. Univ Duisberg Essen, Dept Neuroradiol, D-45122 Essen, Germany. RP Timmann, D (reprint author), Univ Duisberg Essen, Dept Neurol, Hufelandstr 55, D-45122 Essen, Germany. 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PD FAL PY 2004 VL 6 IS 4 BP 195 EP 213 DI 10.1177/10983007040060040201 PG 19 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 857SR UT WOS:000224139100002 ER PT J AU Dauphin, M Kinney, EM Stromer, R AF Dauphin, M Kinney, EM Stromer, R TI Using video-enhanced activity schedules and matrix training to teach sociodramatic play to a child with autism SO JOURNAL OF POSITIVE BEHAVIOR INTERVENTIONS LA English DT Article ID SCRIPT-FADING PROCEDURE; PHOTOGRAPHIC ACTIVITY SCHEDULES; EXCHANGE COMMUNICATION-SYSTEM; SOCIAL-INTERACTION SKILLS; FACILITATE SOCIALIZATION; FUTURE-DIRECTIONS; DISABILITIES; INTERVENTIONS; PRESCHOOLERS; INDIVIDUALS AB We evaluated an intervention package for teaching generative sociodramatic play activities to a young boy with an autism spectrum disorder. In Phase 1, the boy learned computer activity schedules that featured embedded video models of what to say and do. A 3 x 3 instructional matrix defined 9 activities to be performed involving combinations of 3 figurines and 3 actions. In Phase 2, the boy learned to use notebook schedules with pictures cuing sequences of different play activities. Phase 3 clarified and expanded the skills learned so far: Across 3 new instructional matrices, the boy learned 3 of the 9 activities within each matrix using video-enhanced computer schedules. For every activity taught directly, nearly 2 additional activities also occurred. The results recommend video-enhanced activity schedules to teach sociodramatic play and the use of matrix training to program for generative learning outcomes. C1 Univ Massachusetts, Sch Med, Shriver Ctr, Waltham, MA 02452 USA. Nashoba Learning Grp, Westford, MA USA. Bancroft NeuroHlth Presch, Waterville, ME USA. RP Stromer, R (reprint author), Univ Massachusetts, Sch Med, Shriver Ctr, 200 Trapelo Rd, Waltham, MA 02452 USA. 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Posit. Behav. Interv. PD FAL PY 2004 VL 6 IS 4 BP 238 EP 250 DI 10.1177/10983007040060040501 PG 13 WC Psychology, Clinical; Education, Special SC Psychology; Education & Educational Research GA 857SR UT WOS:000224139100005 ER PT J AU Williams, PG Sears, LL Allard, A AF Williams, PG Sears, LL Allard, A TI Sleep problems in children with autism SO JOURNAL OF SLEEP RESEARCH LA English DT Article DE autism; sleep problems ID DISORDER AB Autism is a developmental disability characterized by severe deficits in social interaction and communication, and the presence of repetitive-ritualistic behaviors. Sleep problems are frequently reported by parents of children with autism with prevalence estimates of 44-83% for sleep disorders in this population. To better understand sleep in autism, we surveyed sleep problems in 210 children with autism using a Likert-based questionnaire for parent report. The most frequently reported sleep problems included difficulty in falling asleep, restless sleep, not falling asleep in own bed, and frequent wakenings. Least frequently reported sleep problems were sleep walking, morning headaches, crying during sleep, apnea, and nightmares. When surveys were divided into mental retardation (MR)/not MR categories, no significant differences were identified in frequencies of reported sleep problems except for waking at night which occurred much more frequently in the MR group. There was also no difference in sleep problems related to age of the child other than nocturnal enuresis. An association was noted between certain medical problems and sleep problems. Vision problems, upper respiratory problems, and runny nose were associated with decreased nighttime sleep. Vision problems, poor appetite, and poor growth were associated with increased nighttime waking. Poor appetite and poor growth were associated with decreased willingness to fall asleep. 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The consequences of loss of a transcription factor may be complex, affecting the expression of many proteins, thus limiting understanding of this class of diseases and impeding therapeutic strategies. This is true for RTT. Neither the cell biological mechanism(s) nor the developmental stage affected by MECP2 deficiency is known. In vivo analysis of the olfactory system demonstrates that Mecp2 deficiency leads to a transient delay in the terminal differentiation of olfactory neurons. This delay in maturation disrupts axonal targeting in the olfactory bulb, resulting in abnormal axonal projections, subglomerular disorganization, and a persistent reduction in glomerular size. These results indicate a critical cell biological function for Mecp2 in mediating the final stages of neuronal development. (C) 2004 Elsevier Inc. All rights reserved. C1 Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA. Johns Hopkins Univ, Sch Med, Dept Neurol, Baltimore, MD 21205 USA. 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Cell. Neurosci. PD SEP PY 2004 VL 27 IS 1 BP 44 EP 58 DI 10.1016/j.men.2004.05.005 PG 15 WC Neurosciences SC Neurosciences & Neurology GA 852QA UT WOS:000223770300005 PM 15345242 ER PT J AU Veenstra-VanderWeele, J Cook, EH AF Veenstra-VanderWeele, J Cook, EH TI Molecular genetics of autism spectrum disorder SO MOLECULAR PSYCHIATRY LA English DT Review DE autism; genetic; epigenetic ID SEROTONIN TRANSPORTER GENE; PERVASIVE DEVELOPMENTAL DISORDERS; CPG-BINDING PROTEIN-2; LINKAGE-DISEQUILIBRIUM; ANGELMAN-SYNDROME; SUSCEPTIBILITY GENE; PROMOTER VARIANTS; RETT-SYNDROME; TRANSMISSION DISEQUILIBRIUM; LANGUAGE IMPAIRMENT AB We are on the brink of exciting discoveries into the molecular genetic underpinnings of autism spectrum disorder. Overwhelming evidence of genetic involvement coupled with increased societal attention to the disorder has drawn in more researchers and more research funding. Autism is a strongly genetic yet strikingly complex disorder, in which evidence from different cases supports chromosomal disorders, rare single gene mutations, and multiplicative effects of common gene variants. With more and more interesting yet sometimes divergent findings emerging every year, it is tempting to view these initial molecular studies as so much noise, but the data have also started to coalesce in certain areas. In particular, recent studies in families with autism spectrum disorder have identified uncommon occurrences of a novel genetic syndrome caused by disruptions of the NLGN4 gene on chromosome Xp22. Previous work had identified another uncommon syndrome that is caused by maternal duplications of the chromosome 15q11-13 region. We highlight other converging findings, point toward those areas most likely to yield results, and emphasize the contributions of multiple approaches to identifying the genes of interest. 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Psychiatr. PD SEP PY 2004 VL 9 IS 9 BP 819 EP 832 DI 10.1038/sj.mp.4001505 PG 14 WC Biochemistry & Molecular Biology; Neurosciences; Psychiatry SC Biochemistry & Molecular Biology; Neurosciences & Neurology; Psychiatry GA 850LL UT WOS:000223612800002 PM 15197396 ER PT J AU Hornig, M Chian, D Lipkin, WI AF Hornig, M Chian, D Lipkin, WI TI Neurotoxic effects of postnatal thimerosal are mouse strain dependent SO MOLECULAR PSYCHIATRY LA English DT Article DE autistic disorder; thimerosal; neurotoxicity; autoimmunity; inbred mouse strains ID MERCURY-INDUCED AUTOIMMUNITY; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; PERVASIVE DEVELOPMENTAL DISORDERS; GLUTAMATE TRANSPORTER; RETT-SYNDROME; AUTOANTIBODY PROFILES; MURINE SUSCEPTIBILITY; SYSTEMIC AUTOIMMUNITY; HIPPOCAMPAL-FORMATION; IMMUNE DEPOSITS AB The developing brain is uniquely susceptible to the neurotoxic hazard posed by mercurials. Host differences in maturation, metabolism, nutrition, sex, and autoimmunity influence outcomes. How population-based variability affects the safety of the ethylmercury-containing vaccine preservative, thimerosal, is unknown. Reported increases in the prevalence of autism, a highly heritable neuropsychiatric condition, are intensifying public focus on environmental exposures such as thimerosal. Immune profiles and family history in autism are frequently consistent with autoimmunity. We hypothesized that autoimmune propensity influences outcomes in mice following thimerosal challenges that mimic routine childhood immunizations. Autoimmune disease-sensitive SJL/J mice showed growth delay; reduced locomotion; exaggerated response to novelty; and densely packed, hyperchromic hippocampal neurons with altered glutamate receptors and transporters. Strains resistant to autoimmunity, C57BL/6J and BALB/cJ, were not susceptible. These findings implicate genetic influences and provide a model for investigating thimerosal-related neurotoxicity. 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PD SEP PY 2004 VL 5 IS 9 BP 641 EP 641 DI 10.1038/nrg1438 PG 1 WC Genetics & Heredity SC Genetics & Heredity GA 850PZ UT WOS:000223626200008 ER PT J AU Chung, MK Dalton, KM Alexander, AL Davidson, RJ AF Chung, MK Dalton, KM Alexander, AL Davidson, RJ TI Less white matter concentration in autism: 2D voxel-based morphometry SO NEUROIMAGE LA English DT Article DE autism; voxel; morphometry ID UNIFIED STATISTICAL APPROACH; CORPUS-CALLOSUM SIZE; FALSE DISCOVERY RATE; GROWTH-PATTERNS; MRI; INDIVIDUALS; DEFORMATION; DISORDER; MAPS; GRAY AB Autism is a neurodevelopmental disorder affecting behavioral and social cognition, but there is little understanding about the link between the functional deficit and its underlying neuroanatomy. We applied a 2D version of voxel-based morphometry (VBM) in differentiating the white matter concentration of the corpus callosum for the group of 16 high functioning autistic and 12 normal subjects. Using the white matter density as an index for neural connectivity, autism is shown to exhibit less white matter concentration in the region of the genu, rostrum, and splenium removing the effect of age based on the general linear model (GLM) framework. Further, it is shown that the less white matter concentration in the corpus callosum in autism is due to hypoplasia rather than atrophy. (C) 2004 Elsevier Inc. All rights reserved. C1 Univ Wisconsin, Dept Stat, Madison, WI 53706 USA. Univ Wisconsin, Dept Biostat & Med Informat, Madison, WI 53706 USA. Univ Wisconsin, Keck Lab Funct Brain Imaging & Behav, Madison, WI 53706 USA. Univ Wisconsin, Dept Med Phys, Madison, WI 53706 USA. Univ Wisconsin, Dept Psychiat, Madison, WI 53706 USA. Univ Wisconsin, Dept Psychol, Madison, WI 53706 USA. RP Chung, MK (reprint author), Univ Wisconsin, Dept Stat, 1220 W Dayton St, Madison, WI 53706 USA. 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Few neocortical brain MRI abnormalities have been reported. Using rest functional brain imaging, two independent studies have described localized bilateral temporal hypoperfusion in children with primary autism. In order to search for convergent evidence of anatomical abnormalities in autistic children, we performed an anatomical MRI study using optimized whole-brain voxel-based morphometry (VBM). High-resolution 3-D T1-weighted MRI data sets were acquired in 21 children with primary autism (mean age 9.3+/-2.2 years) and 12 healthy control children (mean age 10.8+/-2.7 years). By comparing autistic children to normal children, we found bilaterally significant decreases of grey matter concentration located in superior temporal sulcus (STS) (P<0.05 corrected, after small volume correction; SVC). Children with autism were also found to have a decrease of white matter concentration located in the right temporal pole and in cerebellum P<0.05 corrected, after small volume correction; SV(P<0.05, corrected) compared to normal children. These results suggest that autism is associated with bilateral anatomical abnormalities localized in the STS and are remarkably consistent with functional hypoperfusion previously reported in children with autism. The multimodal STS areas are involved in highest level of cortical integration of both sensory and limbic information. Moreover, the STS is now recognized as a key cortical area of the "social brain" and is implicated in social perceptual skills that are characteristically impaired in autism. Therefore, the convergent anatomical and functional temporal abnormalities observed in autism may be important in the understanding of brain behavior relationships in this severe developmental disorder. (C) 2004 Elsevier Inc. All rights reserved. C1 Hop Necker Enfants Malad, Dept Pediat Radiol, Serv Radiol Pediat, AP HP, F-75015 Paris, France. CEA, Serv Hosp Frederic Joliot, ERM INSERM 0205, F-91406 Orsay, France. Hop Robert Debre, AP HP, Serv Pedopsychiat, F-75019 Paris, France. UCL, Inst Neurol, Wellcome Dept Imaging Neurosci, London, England. Hop Necker Enfants Malad, AP HP, Serv Neurochirurg, F-75015 Paris, France. CHU Bretonneau, INSERM, U316, F-37044 Tours, France. Grp Hosp Pitie Salpetriere, Serv Urgences Cerebro Vasc, F-75013 Paris, France. RP Boddaert, N (reprint author), Hop Necker Enfants Malad, Dept Pediat Radiol, Serv Radiol Pediat, AP HP, 149 Rue Sevres, F-75015 Paris, France. 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The etiologic contribution of individual cytokines to such psychiatric disorders, however, remains to be evaluated. To estimate the impact of peripheral cytokine challenge on neurobehavioral development, we examined effects of four proinflammatory cytokines on rat neonates and their later behavioral performance. Sublethal doses of interleukin-1alpha, interleukin-2, interleukin-6, or interferon-gamma were subcutaneously administered to rat pups for 9 days. These animals displayed alterations in physical development, including lower weight gain and/or accelerated eyelid opening. In addition, behavioral abnormalities related to fear/anxiety levels and sensorimotor gating emerged at different developmental stages, depending on the cytokine species administered. During juvenile stages, neonatal interleukin-2 treatment increased exploratory locomotor activity, whereas other cytokine treatments did not. At the post-puberty stage, however, the interleukin-2-induced abnormal motor activity became undetectable, whereas interleukin-1alpha-treated rats developed abnormalities in startle response, prepulse inhibition (PPI), and social interaction. Subchronic treatment of an anti-psychotic drug, clozapine, ameliorated the impairment of prepulse inhibition without altering startle responses. These animal experiments illustrate that, during early postnatal development, inflammatory cytokine challenge in the periphery can induce future psychobehavioral and/or cognitive impairments with various latencies, although the pathologic mechanisms underlying these abnormalities remain to be determined. (C) 2004 Elsevier Ireland Ltd and The Japan Neuroscience Society. All rights reserved. C1 Niigata Univ, Inst Brain Res, Div Mol Neurobiol, Niigata 9518585, Japan. Niigata Univ, Inst Brain Res, Brain Resource Ctr, Niigata 9518585, Japan. RP Nawa, H (reprint author), Niigata Univ, Inst Brain Res, Div Mol Neurobiol, Asahimachi Dori 1-757, Niigata 9518585, Japan. 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Res. PD SEP PY 2004 VL 50 IS 1 BP 67 EP 75 DI 10.1016/j.neures.2004.05.010 PG 9 WC Neurosciences SC Neurosciences & Neurology GA 849IH UT WOS:000223531400008 PM 15288500 ER PT J AU Andrews, N Miller, E Grant, A Stowe, J Osborne, V Taylor, B AF Andrews, N Miller, E Grant, A Stowe, J Osborne, V Taylor, B TI Thimerosal exposure in infants and developmental disorders: A retrospective cohort study in the United Kingdom does not support a causal association SO PEDIATRICS LA English DT Article DE cohort study; neurodevelopment; safety; thimerosal; thiomersal; vaccines ID PRACTICE RESEARCH DATABASE; VACCINES; AUTISM; SAFETY AB Objective. After concerns about the possible toxicity of thimerosal-containing vaccines in the United States, this study was designed to investigate whether there is a relationship between the amount of thimerosal that an infant receives via diphtheria-tetanus-whole-cell pertussis (DTP) or diphtheria-tetanus (DT) vaccination at a young age and subsequent neurodevelopmental disorders. Methods. A retrospective cohort study was performed using 109863 children who were born from 1988 to 1997 and were registered in general practices in the United Kingdom that contributed to a research database. The disorders investigated were general developmental disorders, language or speech delay, tics, attention-deficit disorder, autism, unspecified developmental delays, behavior problems, encopresis, and enuresis. Exposure was defined according to the number of DTP/DT doses received by 3 and 4 months of age and also the cumulative age-specific DTP/DT exposure by 6 months. Each DTP/DT dose of vaccine contains 50 mug of thimerosal (25 mug of ethyl mercury). Hazard ratios (HRs) for the disorders were calculated per dose of DTP/DT vaccine or per unit of cumulative DTP/DT exposure. Results. Only in 1 analysis for tics was there some evidence of a higher risk with increasing doses (Cox's HR: 1.50 per dose at 4 months; 95% confidence interval [CI]: 1.02-2.20). Statistically significant negative associations with increasing doses at 4 months were found for general developmental disorders (HR: 0.87; 95% CI: 0.81-0.93), unspecified developmental delay (HR: 0.80; 95% CI: 0.69-0.92), and attention-deficit disorder (HR: 0.79; 95% CI: 0.64-0.98). For the other disorders, there was no evidence of an association with thimerosal exposure. Conclusions. With the possible exception of tics, there was no evidence that thimerosal exposure via DTP/DT vaccines causes neurodevelopmental disorders. C1 Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Hlth Protect Agcy, Immunisat Dept, London NW9 5EQ, England. Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Hlth Protect Agcy, Stat Unit, London NW9 5EQ, England. UCL Royal Free & Univ Coll Med Sch, Ctr Community Child Hlth, London, England. Off Natl Stat, Morbid & Hlth Care Team, London, England. RP Miller, E (reprint author), Publ Hlth Lab Serv, Ctr Communicable Dis Surveillance, Hlth Protect Agcy, Immunisat Dept, 61 Colindale Ave, London NW9 5EQ, England. EM liz.miller@hpa.org.uk CR American Academy of Pediatrics and the Public Health Service, 1999, MMWR-MORBID MORTAL W, V48, P563 Black C, 2002, BRIT MED J, V325, P419, DOI 10.1136/bmj.325.7361.419 Chen RT, 1997, PEDIATRICS, V99, P765, DOI 10.1542/peds.99.6.765 Freed GL, 2002, PEDIATRICS, V109, P1153, DOI 10.1542/peds.109.6.1153 Heron J, 2004, PEDIATRICS, V114, P577, DOI 10.1542/peds.2003-1176-L Hviid A, 2003, JAMA-J AM MED ASSOC, V290, P1763, DOI 10.1001/jama.290.13.1763 Insightful, 2001, S PLUS 6 WIND GUID S, V1 JICK H, 1991, BRIT MED J, V302, P766 Lawson DH, 1998, QJM-MON J ASSOC PHYS, V91, P445, DOI 10.1093/qjmed/91.6.445 Osborn A. F., 1984, SOCIAL LIFE BRITAINS Pichichero ME, 2002, LANCET, V360, P1737, DOI 10.1016/S0140-6736(02)11682-5 vansStaa TP, 1994, PHARMACOEPIDEM DR S, V3, P15, DOI 10.1002/pds.2630030106 Verstraeten T, 2003, PEDIATRICS, V112, P1039 Walley T, 1997, LANCET, V350, P1097, DOI 10.1016/S0140-6736(97)04248-7 WINSHIP KA, 1986, ADVERSE DRUG REACT, V3, P141 2002, WKLY EPIDEMIOL REC, V77, P390 2000, WKLY EPIDEMIOL REC, V75, P12 2001, IMMUNIZATION SAFETY NR 18 TC 93 Z9 103 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD SEP PY 2004 VL 114 IS 3 BP 584 EP 591 DI 10.1542/peds.2003-1177-L PG 8 WC Pediatrics SC Pediatrics GA 851AU UT WOS:000223657600002 PM 15342825 ER PT J AU Parker, SK Schwartz, B Todd, J Pickering, LK AF Parker, SK Schwartz, B Todd, J Pickering, LK TI Thimerosal-containing vaccines and autistic spectrum disorder: A critical review of published original data SO PEDIATRICS LA English DT Review DE thimerosal; thiomersal; mercury; vaccine; methylmercury; ethylmercury; autism; autistic disorder; autistic spectrum disorder; developmental disorder; neurodevelopmental disorder ID PERVASIVE DEVELOPMENTAL DISORDERS; MERCURY CONCENTRATIONS; RUBELLA VACCINATION; POPULATION; CHILDREN; MEASLES; PREVALENCE; SURVEILLANCE; INFANTS; SAFETY AB Objective. The issue of thimerosal-containing vaccines as a possible cause of autistic spectrum disorders (ASD) and neurodevelopmental disorders (NDDs) has been a controversial topic since 1999. Although most practitioners are familiar with the controversy, many are not familiar with the type or quality of evidence in published articles that have addressed this issue. To assess the quality of evidence assessing a potential association between thimerosal-containing vaccines and autism and evaluate whether that evidence suggests accepting or rejecting the hypothesis, we systematically reviewed published articles that report original data pertinent to the potential association between thimerosal-containing vaccines and ASD/NDDs. Methods. Articles for analysis were identified in the National Library of Medicine's Medline database using a PubMed search of the English- language literature for articles published between 1966 and 2004, using keywords thimerosal, thiomersal, mercury, methylmercury, or ethylmercury alone and combined with keywords autistic disorder, autistic spectrum disorder, and neurodevelopment. In addition, we used the "related links" option in PubMed and reviewed the reference sections in the identified articles. All original articles that evaluated an association between thimerosal-containing vaccines and ASD/NDDs or pharmacokinetics of ethylmercury in vaccines were included. Results. Twelve publications that met the selection criteria were identified by the literature search: 10 epidemiologic studies and 2 pharmacokinetic studies of ethylmercury. The design and quality of the studies showed significant variation. The preponderance of epidemiologic evidence does not support an association between thimerosal-containing vaccines and ASD. Epidemiologic studies that support an association are of poor quality and cannot be interpreted. Pharmacokinetic studies suggest that the half-life of ethylmercury is significantly shorter when compared with methylmercury. Conclusions. Studies do not demonstrate a link between thimerosal-containing vaccines and ASD, and the pharmacokinetics of ethylmercury make such an association less likely. Epidemiologic studies that support a link demonstrated significant design flaws that invalidate their conclusions. Evidence does not support a change in the standard of practice with regard to administration of thimerosal-containing vaccines in areas of the world where they are used. C1 Univ Colorado, Hlth Sci Ctr, Sch Med, Dept Microbiol, Denver, CO 80262 USA. Childrens Hosp, Dept Pediat, Denver, CO 80218 USA. 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Spontaneous humorous behavior in everyday life and a humorous performance during assessment situations of children can provide a useful basis for further diagnostic considerations. From a developmental point of view it is important to notice what kinds of humor a child is already capable of understanding and of performing towards others. Whilst the actual readiness for cheerfulness contains information concerning the emotional state, the more general readiness for being cheerful renders insight into basic parameters of temperament. To what extent a child uses humor either supportively or destructively, contains information about psychodynamic connections, motivational aspects and active coping strategies. Concerning the diagnostic approach, reports of parents as well as humor tests or hypothesizing methods (e. g. humorous drawings) can be used. 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Kinderpsychol. Kinderpsychiatr. PD SEP PY 2004 VL 53 IS 7 BP 468 EP 482 PG 15 WC Psychology, Developmental; Psychiatry SC Psychology; Psychiatry GA 860LM UT WOS:000224345100002 PM 15506260 ER PT J AU Bolton, PF Veltman, MWM Weisblatt, E Holmes, JR Thomas, NS Youings, SA Thompson, RJ Roberts, SE Dennis, NR Browne, CE Goodson, S Moore, V Brown, J AF Bolton, PF Veltman, MWM Weisblatt, E Holmes, JR Thomas, NS Youings, SA Thompson, RJ Roberts, SE Dennis, NR Browne, CE Goodson, S Moore, V Brown, J TI Chromosome 15q11-13 abnormalities and other medical conditions in individuals with autism spectrum disorders SO PSYCHIATRIC GENETICS LA English DT Article DE autism; chromosomal abnormalities; genetic; medical disorders ID PERVASIVE DEVELOPMENTAL DISORDERS; PROXIMAL 15Q; INTERSTITIAL DUPLICATIONS; LINKAGE-DISEQUILIBRIUM; TUBEROUS SCLEROSIS; FAMILIES; CHILDREN; GENE; PREVALENCE; POPULATION AB Objectives The frequency of abnormalities of 15q11-q13 and other possibly causal medical disorders including karyotypic abnormalities was investigated in an unselected series of children who were referred to one of two autism assessment centres. Methods Two hundred and twenty-one cases were assessed using the Autism Diagnostic Interview and Observation Schedule and, where appropriate, standardized tests of intelligence and language abilities. Medical histories and notes were reviewed, and molecular and cytogenetic investigations used to detect chromosomal abnormalities. Results One hundred and eighty-one cases were diagnosed according to International Classification of Diseases - version 10 criteria as having an autism spectrum disorder (autistic-like Pervasive Developmental Disorder) and 40 cases as having other disorders. Twenty-one (11.6%) of the children with autism spectrum disorders had a possibly causal condition compared with six (15%) of the children with other diagnoses. One child with an autism spectrum disorder had a paternally inherited familial duplication of 15q11-13. The pattern of genotype-phenotype correlation within the family indicated that this form of abnormality might carry a risk for developmental difficulties, although the risk did not appear to be specific for autism spectrum disorders. Conclusion The overall rate of possibly causal medical and cytogenetic conditions in children with autism spectrum disorders was low and no different from the rate of disorder in children with other developmental/neuropsychiatric disorders that attended the same clinics. Further research is required to determine whether paternal duplication of 15q11-13 gives rise to adverse developmental outcomes. (C) 2004 Lippincott Williams Wilkins. C1 Inst Psychiat, Child Psychiat Dept, London SE5 8AF, England. Inst Psychiat, MRC Ctr Social Genet & Dev Psychiat, London SE5 8AF, England. RP Bolton, PF (reprint author), Inst Psychiat, Child Psychiat Dept, POB 43,De Crespigny Pk, Denmark Hill, London SE5 8AF, England. 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CR Frith U., 2004, AUTISM MIND BRAIN 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 SEP PY 2004 VL 17 IS 9 BP 522 EP 522 PG 1 WC Psychology, Multidisciplinary SC Psychology GA 854OZ UT WOS:000223914500026 ER PT J AU Laviola, G Adriani, W Rea, M Aloe, L Alleva, E AF Laviola, G Adriani, W Rea, M Aloe, L Alleva, E TI Social withdrawal, neophobia, and stereotyped behavior in developing rats exposed to neonatal asphyxia SO PSYCHOPHARMACOLOGY LA English DT Article DE neonatal asphyxia; adolescence; novelty seeking; play behavior; stereotypies; BDNF ID SPATIAL MEMORY DEFICITS; NEUROTROPHIC FACTOR; PERINATAL ASPHYXIA; PREFRONTAL CORTEX; NUCLEUS-ACCUMBENS; NOVELTY-SEEKING; HYPOXIA-ISCHEMIA; POSTNATAL ANOXIA; D-AMPHETAMINE; BRAIN-INJURY AB Perinatal asphyxia is a concern for public health and may promote subtle neuropsychiatric disorders. Anoxic insults to neonatal rats cause long-lasting neurobehavioral deficits. In the present study, we focussed on changes in emotional behaviors as a consequence of neonatal asphyxia in Wistar rats. Newborn pups (24 h after birth) underwent a single 30-min exposure to a 100% N-2 atmosphere (or air). The offspring was tested for a) locomotor and exploratory activity with or without a d-amphetamine challenge (0, 1, or 2 mg/kg) on postnatal day (pnd) 15; b) social interactions and novelty seeking during adolescence; c) levels of the brain-derived neurotrophic factor (BDNF). In the open-field test (pnd 15), N-2-exposed pups injected with the high (2 mg/kg) amphetamine dose exhibited reduced levels of locomotor hyperactivity, and a more marked involvement in stereotyped behaviors. Individual differences emerged in the locomotor response to the novelty-seeking test: two subgroups of rats (separated on the basis of the median value) showed either arousal/attraction or avoidance/inhibition in response to free-choice novelty. The N-2-exposed group showed a more marked novelty-induced avoidance and inhibition. Time devoted to allogrooming and play-soliciting behaviors was reduced, whereas object exploration was increased. Levels of BDNF were reduced in the striatum of N-2-exposed rats, suggesting poorer synaptic performance of dopamine pathways. In conclusion, these findings suggest an increased risk of developing social withdrawal, neophobia and behavioral stereotypies (common symptoms found in schizophrenia and autism) as a consequence of neonatal asphyxia in preterm humans. C1 Ist Super Sanita, Dipartimento Biol Cellulare & Neurosci, Sect Behav Pathopysiol, Lab Fisiopathol OS, I-00161 Rome, Italy. CNR, Inst Neurobiol & Mol Med, Rome, Italy. RP Laviola, G (reprint author), Ist Super Sanita, Dipartimento Biol Cellulare & Neurosci, Sect Behav Pathopysiol, Lab Fisiopathol OS, Viale Regina Elena 299, I-00161 Rome, Italy. 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PD FAL PY 2004 VL 29 IS 3 BP 214 EP 215 DI 10.2511/rpsd.29.3.214 PG 2 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 885ZY UT WOS:000226197100007 ER PT J AU Grindle, CF Remington, B AF Grindle, CF Remington, B TI Teaching children with autism using conditioned cue-value and response-marking procedures: a socially valid procedure SO RESEARCH IN DEVELOPMENTAL DISABILITIES LA English DT Article DE conditioned reinforcement; cue value; response marking; discrete-trial training; autistic children ID DELAYED REINFORCEMENT; TOKEN-ECONOMY; STIMULUS; SCHEDULES; REWARD; CHAINS AB Five children with autism were taught to match printed words to corresponding pictures. Participants' speed of learning was compared across three training conditions, each involving a 5-s delay of reinforcement, using a within-participants alternating treatments design. In the cue-value condition, a verbal phrase of approval (e.g., "good!") was delivered only after correct responses and again after a 5-s delay when a primary reinforcer was delivered; in the response-marking condition, an attention-eliciting verbal cue (e.g., "look!") was delivered after both correct and incorrect responses, but not prior to the primary reinforcer; in the delay only condition, there were no cues during a 5-s delay. Performance in the no-cue control was inferior to both the cue-value and response-marking conditions, but there was little difference between the latter two conditions. The implications of these results for facilitating learning in applied settings are discussed. (C) 2004 Elsevier Ltd. All rights reserved. C1 Univ Southampton, Sch Psychol, Ctr Behav Res Anal & Intervent Dev Disabil, Southampton SO17 1BJ, Hants, England. 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Dev. Disabil. PD SEP-OCT PY 2004 VL 25 IS 5 BP 413 EP 429 DI 10.1016/j.ridd.2003.09.003 PG 17 WC Education, Special; Rehabilitation SC Education & Educational Research; Rehabilitation GA 848ZJ UT WOS:000223506600002 PM 15217671 ER PT J AU Schwartz, IS Sandall, SR McBride, BJ Boulware, GL AF Schwartz, IS Sandall, SR McBride, BJ Boulware, GL TI Project DATA (Developmentally Appropriate Treatment for Autism): An inclusive school-based approach to educating young children with autism SO TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION LA English DT Article ID PHOTOGRAPHIC ACTIVITY SCHEDULES; SOCIAL-INTERACTION; TEACHING-CHILDREN; LANGUAGE INTERVENTION; PRESCHOOL-CHILDREN; BEHAVIOR; SKILLS; DISABILITIES; PLAY; MAINTENANCE AB Providing appropriate educational services to young children with autism may be one of the defining challenges of the 1990s and early 2000s for early childhood special education. The number of children with autism is increasing dramatically, the research literature is rich with evidence-based instructional strategies, and the Internet is even more full of information and advice of unknown quality. Parents and school district personnel, often working together but sometimes at odds, need to develop programs to meet the needs of these children. Project DATA (Development Appropriate Treatment for Autism) started as a federally funded model demonstration project for developing a school-based program for young children with autism that would be effective and acceptable to consumers (e.g., parents, school personnel). Project DATA consists of five components: a high-quality early childhood environment, extended instructional time, social and technical support for families, collaboration and cooperation across services, and transition support. In this article, we provide data demonstrating the effectiveness of this model and discuss the implications of this type of inclusive programming for young children with autism. C1 Univ Washington, Seattle, WA 98195 USA. RP Schwartz, IS (reprint author), Univ Washington, Box 357925, Seattle, WA 98195 USA. 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PD FAL PY 2004 VL 24 IS 3 BP 156 EP 168 DI 10.1177/02711214040240030301 PG 13 WC Education, Special SC Education & Educational Research GA 869GK UT WOS:000224971200003 ER PT J AU Tuisku, K Tani, P Nieminen-von Wendt, T von Wendt, L Holi, MM Porkka-Heiskanen, T Lauerma, H Lindberg, N Appelberg, B Wahlbeck, K AF Tuisku, K Tani, P Nieminen-von Wendt, T von Wendt, L Holi, MM Porkka-Heiskanen, T Lauerma, H Lindberg, N Appelberg, B Wahlbeck, K TI Lower limb motor restlessness in Asperger's disorder, measured using actometry SO PSYCHIATRY RESEARCH LA English DT Article DE actigraphy; Akathisia; autism; Barnes Akathisia Rating Scale; dopamine; motor activity; movement disorders ID NEUROLEPTIC-INDUCED AKATHISIA; DEFICIT HYPERACTIVITY DISORDER; PERIODIC LEG MOVEMENTS; ATTENTION-DEFICIT; TOURETTES DISORDER; RATING-SCALE; AUTISM; CHILDREN; ACTIGRAPHY; COMORBIDITY AB The movement disturbances and brain imaging findings in Asperger's disorder (AD) suggest a dopaminergic deficit in movement regulation. Movement disorders of different etiologies have been quantified and specified with actometry. We compared 10 AD patients with 10 healthy controls, measuring their rest-activities by actometry. The lower limb motor activity was significantly higher in the AD group. They also displayed a rhythmic, periodic movement pattern similar to akathisia. These findings suggest a hypothesis of idiopathic akathisia and a special sensitivity to adverse effects of neuroleptic drugs. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 HUCH, Dept Psychiat, Helsinki 18, Finland. HUCH, Hosp Child & Adolescents, Child Neurol, Helsinki, Finland. Univ Helsinki, Inst Biomed, Helsinki, Finland. Turku Univ, Dept Psychiat, Turku, Finland. RP Tuisku, K (reprint author), HUCH, Dept Psychiat, PL 320, Helsinki 18, Finland. 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PD AUG 30 PY 2004 VL 128 IS 1 BP 63 EP 70 DI 10.1016/j.psychres.2002.06.001 PG 8 WC Psychiatry SC Psychiatry GA 864BZ UT WOS:000224609200007 PM 15450915 ER PT J AU Cardy, JEO Ferrari, P Flagg, EJ Roberts, W Roberts, TPL AF Cardy, JEO Ferrari, P Flagg, EJ Roberts, W Roberts, TPL TI Prominence of M50 auditory evoked response over M100 in childhood and autism SO NEUROREPORT LA English DT Article DE auditory cortex; autism; children; development; M50; M100; magnetoencephalography (MEG) ID LATENCY; CHILDREN; FREQUENCY; INTENSITY; DISORDER AB This study investigated the 50 ms (M50) and 100 ms (M100) components of the auditory evoked field to explore their change during development. Using MEG, neuromagnetic fields elicited by a 1 kHz sinusoidal tone were recorded in adults and two groups of children and adolescents with typical development or autism spectrum disorder. M50 amplitude was larger in children than in adults, suggesting a developmental trajectory with M50 amplitude decreasing and M100 increasing with age. Child M50 and M100 latencies were prolonged relative to adults. Children with autism did not differ from control children with respect to these observations. The M50 in relation to the M100 is a robust index of early auditory system maturation suitable for future developmental investigations. C1 Univ Turin, Dept Med Imaging, Toronto, ON M5S 2E3, Canada. Univ Turin, Dept Paediat, Toronto, ON M5S 2E3, Canada. Hosp Sick Children, Child Dev Ctr, Toronto, ON M5G 1X8, Canada. RP Cardy, JEO (reprint author), Univ Turin, Dept Med Imaging, 150 Coll St, Toronto, ON M5S 2E3, Canada. EM janis.oram@utoronto.ca CR Borgmann C, 2001, HEARING RES, V158, P57, DOI 10.1016/S0378-5955(01)00292-1 Gage NM, 2000, NEUROREPORT, V11, P2723, DOI 10.1097/00001756-200008210-00023 Gage NM, 2003, NEUROREPORT, V14, P2047, DOI 10.1097/01.wnr.0000090030.460874a LINCOLN AJ, 1995, J AUTISM DEV DISORD, V25, P521, DOI 10.1007/BF02178298 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 McGee T, 1996, EAR HEARING, V17, P419, DOI 10.1097/00003446-199610000-00008 PAETAU R, 1995, J CLIN NEUROPHYSIOL, V12, P177, DOI 10.1097/00004691-199503000-00008 PANTEV C, 1995, ELECTROEN CLIN NEURO, V94, P26, DOI 10.1016/0013-4694(94)00209-4 Roberts TPL, 1996, NEUROREPORT, V7, P1138, DOI 10.1097/00001756-199604260-00007 ROBERTS TPL, 2000, J CLIN NEUROPHYSIOL, V17, P144 Rojas DC, 1998, NEUROREPORT, V9, P1543 Semel E., 2003, CLIN EVALUATION LANG, V4th Stufflebeam SM, 1998, NEUROREPORT, V9, P91, DOI 10.1097/00001756-199801050-00018 Weschler D, 2003, WESCHLER INTELLIGENC, V4th Weschler D., 1997, WESCHLER ADULT INTEL Yvert B, 2001, CEREB CORTEX, V11, P411, DOI 10.1093/cercor/11.5.411 NR 17 TC 27 Z9 28 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 EI 1473-558X J9 NEUROREPORT JI Neuroreport PD AUG 26 PY 2004 VL 15 IS 12 BP 1867 EP 1870 PG 4 WC Neurosciences SC Neurosciences & Neurology GA 871NS UT WOS:000225141000006 ER PT J AU Bah, J Quach, H Ebstein, RP Segman, RH Melke, J Jamain, S Rietschel, M Modai, I Kanas, K Karni, O Lerer, B Gourion, D Krebs, MO Etain, B Schurhoff, F Szoke, A Leboyer, M Bourgeron, T AF Bah, J Quach, H Ebstein, RP Segman, RH Melke, J Jamain, S Rietschel, M Modai, I Kanas, K Karni, O Lerer, B Gourion, D Krebs, MO Etain, B Schurhoff, F Szoke, A Leboyer, M Bourgeron, T TI Maternal transmission disequilibrium of the glutamate receptor GRIK2 in schizophrenia SO NEUROREPORT LA English DT Article DE chromosome 6q; glutamate; imprinting; kainate; polymorphism; schizophrenia ID BIPOLAR DISORDER; GENOME SCAN; LINKAGE DISEQUILIBRIUM; SUSCEPTIBILITY LOCUS; CHROMOSOME 6Q; ASSOCIATION; GENE; EXPRESSION; FAMILIES; AUTISM AB Schizophrenia is characterized by thought disorders, hallucinations and delusions. Genetic studies have shown a high linkage at chromosome 6q16-21. Among the genes located in this region is the glutamate receptor ionotropic kainate 2 gene (GRIK2 or GLUR6), a functional candidate for susceptibility to schizophrenia. In this study, transmission of GRIK2 was evaluated in 356 schizophrenic patients from three different clinical centers. Whereas paternal transmission shows equilibrium, we observed maternal transmission disequilibrium of GRIK2 in the largest population (p=0.03), which was still significant when all populations were added (p=0.05). These results are similar to the maternal GRIK2 transmission disequilibrium previously reported for autism, and support the presence of a susceptibility gene for schizophrenia at 6q16. C1 Univ Paris 07, Inst Pasteur, F-75724 Paris 15, France. Herzog Hosp, Jerusalem, Israel. Hadassah Hebrew Univ Med Ctr, Jerusalem, Israel. Univ Bonn, D-5300 Bonn, Germany. Shaar Menashe Mental Hlth Ctr, Hefer, Israel. Hop St Anne, INSERM E 0117 Paris 5, F-75674 Paris, France. Hop Albert Chenevier & Henri Mondor, Creteil, France. Lab INSERM U513, Creteil, France. RP Bourgeron, T (reprint author), Univ Paris 07, Inst Pasteur, 25 Rue Docteur Roux, F-75724 Paris 15, France. EM thomasb@pasteur.fr CR Abecasis GR, 2000, BIOINFORMATICS, V16, P182, DOI 10.1093/bioinformatics/16.2.182 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailer U, 2002, BIOL PSYCHIAT, V52, P40, DOI 10.1016/S0006-3223(02)01320-3 Begni S, 2002, MOL PSYCHIATR, V7, P416, DOI 10.1038/sj/mp/4000987 Cao QH, 1997, GENOMICS, V43, P1, DOI 10.1006/geno.1997.4815 Delorme R, 2004, NEUROREPORT, V15, P699, DOI 10.1097/01.wnr.000011644797607dc Frankle W. 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L., 1977, SCHEDULE AFFECTIVE D SPITZER RL, 1978, ARCH GEN PSYCHIAT, V35, P773 Tashiro A, 2003, NEURON, V38, P773, DOI 10.1016/S0896-6273(03)00299-X Temple IK, 1996, HUM MOL GENET, V5, P1117, DOI 10.1093/hmg/5.8.1117 NR 25 TC 23 Z9 29 PU LIPPINCOTT WILLIAMS & WILKINS PI PHILADELPHIA PA 530 WALNUT ST, PHILADELPHIA, PA 19106-3621 USA SN 0959-4965 J9 NEUROREPORT JI Neuroreport PD AUG 26 PY 2004 VL 15 IS 12 BP 1987 EP 1991 DI 10.1097/00001756-200408260-00031 PG 5 WC Neurosciences SC Neurosciences & Neurology GA 871NS UT WOS:000225141000031 PM 15305151 ER PT J AU Kolevzon, A Smith, CJ Schmeidler, J Buxbaum, JD Silverman, JM AF Kolevzon, A Smith, CJ Schmeidler, J Buxbaum, JD Silverman, JM TI Familial symptom domains in monozygotic siblings with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; monozygotic twins; concordance; genetics; heterogeneity; symptom domains ID PERVASIVE DEVELOPMENTAL DISORDERS; MULTIPLEX FAMILIES; CHROMOSOME 7Q; CHILDREN; LANGUAGE; HISTORY; TWINS; INDIVIDUALS; LINKAGE; PHENOTYPES AB Autism is characterized by a triad of symptom domains (impaired social interaction, communication deficits, and repetitive behaviors) that vary significantly in their clinical presentation across the population. Within families with more than one affected member, however, discrepant findings exist with regard to symptom variability. Reduced intrafamily variance is of particular importance because it supports an underlying model of genetic heterogeneity in the transmission of autism, and the identification of familial clinical subtypes can be used to select more homogeneous samples for linkage analysis in the future. This study examines whether there are specific features of autism that show decreased variance within 16 families with monozygotic siblings concordant for autism. Evidence for familiality was defined as significantly decreased variance of symptom levels within monozygotic siblingships as compared to between siblingships. Using regression analysis, we demonstrated Significant aggregation of symptoms within monozygotic siblingships for two of the three main symptom domains in autism: impairments in communication and social interaction showed significant familiality. Within the repetitive behavior domain, only the categories of circumscribed interests and preoccupation with part-objects showed reduced variance within siblingships. In addition, with the exception of a negative association between the social and behavior domains, partial correlation coefficients did not reveal significant associations between the levels of different symptom domains within families, suggesting that the levels of clinical features seen in autism may be a result of mainly independent genetic traits. Because of presumed genetic heterogeneity and the wide clinical variation seen in autism and other pervasive developmental disorders, selecting probands according to specific features known to show reduced variance within families may provide more homogeneous samples for genetic analysis and strengthen the power to detect the specific genes involved in autism. (C) 2004 Wiley-Liss, Inc. C1 Mt Sinai Sch Med, Dept Psychiat, New York, NY 10029 USA. Bronx Vet Adm Med Ctr, Psychiat Serv, Bronx, NY USA. Mt Sinai Sch Med, Seaver Autism Res Ctr, New York, NY USA. RP Kolevzon, A (reprint author), Mt Sinai Sch Med, Dept Psychiat, Box 1230,1 Gustave L Levy Pl, New York, NY 10029 USA. 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J. Med. Genet. B PD AUG 15 PY 2004 VL 129B IS 1 BP 76 EP 81 DI 10.1002/ajmg.b.30011 PG 6 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 842AW UT WOS:000222975700018 PM 15274045 ER PT J AU Vincent, JB Kolozsvari, D Roberts, WS Bolton, PF Gurling, HMD Scherer, SW AF Vincent, JB Kolozsvari, D Roberts, WS Bolton, PF Gurling, HMD Scherer, SW TI Mutation screening of X-chromosomal neuroligin genes: No mutations in 196 autism probands SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; neuroligin; synaptogenesis; mutation screening; DHPLC AB Autism, a childhood neuropsychiatric disorder with a strong genetic component, is currently the focus of considerable attention within the field of human genetics as well many other medical-related disciplines. A recent study has implicated two X-chromosomal neuroligin genes, NLGN3 and NLGN4, as having an etiological role in autism, having identified a frameshift mutation in one gene and a substitution mutation in the other, segregating in multiplex autism spectrum families (Jamain et al. [2003: Nat Genet 34:27-29]). The function of neuroligin as a trigger for synapse formation would suggest that such mutations would likely result in some form of pathological manifestation. Our own study, screening a larger sample of 196 autism probands, failed to identify any mutations that would affect the coding regions of these genes. Our findings suggest that mutations in these two genes are infrequent in autism. (C) 2004 Wiley-Liss, Inc. C1 Ctr Addict & Mental Hlth, Neurogenet Sect, Toronto, ON M5T 1R8, Canada. Hosp Sick Children, Dept Genet & Genom Biol, Toronto, ON M5G 1X8, Canada. Hosp Sick Children, Child Dev Ctr, Toronto, ON M5G 1X8, Canada. Inst Psychiat, London, England. UCL, Windeyer Inst Med Sci, Dept Psychiat & Behav Sci, Mol Psychiat Lab, London, England. RP Vincent, JB (reprint author), Ctr Addict & Mental Hlth, Neurogenet Sect, 250 Coll St, Toronto, ON M5T 1R8, Canada. EM john_vincent@camh.net RI Howe, Jennifer/I-9013-2012; Scherer, Stephen /B-3785-2013; Gurling, Hugh/A-5029-2010; Bolton, Patrick/E-8501-2010 OI Scherer, Stephen /0000-0002-8326-1999; Bolton, Patrick/0000-0002-5270-6262 CR BOLTON P, 1994, J CHILD PSYCHOL PSYC, V35, P877, DOI 10.1111/j.1469-7610.1994.tb02300.x Dean C, 2003, NAT NEUROSCI, V6, P708, DOI 10.1038/nn1074 Jamain S, 2003, NAT GENET, V34, P27, DOI 10.1038/ng1136 LECOUTEUR A, 1989, J AUTISM DEV DISORD, V19, P363 LORD C, 1989, J AUTISM DEV DISORD, V19, P185, DOI 10.1007/BF02211841 Scheiffele P, 2000, CELL, V101, P657, DOI 10.1016/S0092-8674(00)80877-6 Thomas NS, 1999, HUM GENET, V104, P43, DOI 10.1007/s004390050908 VINCENT JB, 2002, GENOMICS, V80, P245 NR 8 TC 75 Z9 79 PU WILEY-BLACKWELL PI MALDEN PA COMMERCE PLACE, 350 MAIN ST, MALDEN 02148, MA USA SN 1552-4841 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD AUG 15 PY 2004 VL 129B IS 1 BP 82 EP 84 DI 10.1002/ajmg.b.30069 PG 3 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 842AW UT WOS:000222975700019 PM 15274046 ER PT J AU Allen, G Muller, RA Courchesne, E AF Allen, G Muller, RA Courchesne, E TI Cerebellar function-in autism: Functional magnetic resonance image activation during a simple motor task SO BIOLOGICAL PSYCHIATRY LA English DT Review DE autism; brain development; cerebellum; magnetic resonance imaging; motor; pervasive developmental disorders ID ANATOMIC-MR CORRELATION; POSITRON-EMISSION-TOMOGRAPHY; COGNITIVE-AFFECTIVE SYNDROME; POSTERIOR-FOSSA STRUCTURES; CEREBRAL BLOOD-FLOW; INFANTILE-AUTISM; SHIFTING ATTENTION; SOCIAL-BEHAVIOR; SAGITTAL PLANE; WORKING-MEMORY AB Background. The cerebellum is one of the most consistent sites of neuroanatomic abnormality in autism, yet it is still unclear bow such pathology impacts cerebellar function. In normal subjects, we previously demonstrated with functional magnetic resonance imaging (fMRI) a dissociation between cerebellar regions involved in attention and those involved in a simple motor task, with motor activation localized to the anterior cerebellum ipsilateral to the moving band. The purpose of the present investigation was to examine activation in the cerebella of autistic patients and normal control subjects performing this motor task. Methods. We studied eight autistic patients and eight matched normal subjects, using,fMRI. An anatomic region-Of-interest approach was used, allowing a detailed examination of cerebellar function. Results. Autistic individuals showed significantly increased motor activation in the ipsilateral anterior cerebellar hemisphere relative to normal subjects, in addition to atypical activation in contralateral and posterior cerebellar regions. Moreover, increased activation was correlated with the degree of cerebellar structural abnormality. 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Psychiatry PD AUG 15 PY 2004 VL 56 IS 4 BP 269 EP 278 DI 10.1016/j.biophsych.2004.06.005 PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 846PG UT WOS:000223327300009 PM 15312815 ER PT J AU Tay, J Goulet, M Rusche, J Boismenu, R AF Tay, J Goulet, M Rusche, J Boismenu, R TI Age-related and regional differences in secretin and secretin receptor mRNA levels in the rat brain SO NEUROSCIENCE LETTERS LA English DT Article DE development; gene expression; G-protein coupled receptors; peptides; quantitative real-time TaqMan PCR analysis ID GENE-EXPRESSION; MOLECULAR-CLONING; CONTROLLED TRIAL; IN-VITRO; AUTISM; CHILDREN; BINDING; NEURONS; SITES AB In the present study expression levels of secretin and secretin receptor mRNAs in several brain regions of rats ranging in age from postnatal days 7 to 60 were investigated by quantitative real-time PCR. Expression of secretin and secretin receptor was detected in the central amygdala, hippocampus, area postrema, nucleus of the tractus solitary and cerebellum. The cerebellum expressed secretin receptor at significantly higher levels than that found in other brain regions within all the ages examined. In contrast, secretin mRNA was significantly higher in the nucleus of the tractus solitary than in the other four brain regions examined in postnatal day-21, -30 and -60 rats. Within most brain regions, both secretin and secretin receptor mRNAs were more abundant in postnatal day-7 and -14 rats as compared to postnatal day-21 -30 and -60 rats. Thus, secretin and its receptor are widely expressed in rat brain and the expression of both genes is developmentally regulated during the first few weeks following birth. (C) 2004 Elsevier Ireland Ltd. All rights reserved. C1 Repligen Corp, Waltham, MA 02453 USA. RP Boismenu, R (reprint author), Repligen Corp, 41 Seyon St, Waltham, MA 02453 USA. 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Autism is not usually diagnosed until around the age of 3, whereas AS usually is not diagnosed until the child is 6 or 7 years of age. In the present article, using Eshkol-Wachman movement notation, we present evidence that abnormal movement patterns can be detected in AS in infancy. This finding suggests that AS can be diagnosed very early, independent of the presence of language. As shown earlier by us, almost all of the movement disturbances in autism can be interpreted as infantile reflexes "gone astray"; i.e., some reflexes are not inhibited at the appropriate age in development, whereas others fail to appear when they should. This phenomenon appears to apply to AS as well. Based on preliminary results, a simple test using one such reflex is proposed for the early detection of a subgroup of children with AS or autism. C1 Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. Univ Florida, Dept Phys Therapy, Gainesville, FL 32610 USA. Benton Pediat, Gainesville, FL 32653 USA. RP Teitelbaum, O (reprint author), Univ Florida, Dept Psychol, Gainesville, FL 32611 USA. EM ewmn2003@yahoo.com CR ASPERGER H, 1992, AUTISM ASPERGER SYND, P37 Eshkol N, 2001, EWMN 1 Eshkol N., 1958, MOVEMENT NOTATION FAY T, 1955, AM J PSYCHIAT, V111, P644 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 FIORENTINO MR, 1980, NORMAL ABNORMAL DEV FREEDLAND RL, 1994, PSYCHOL SCI, V5, P26, DOI 10.1111/j.1467-9280.1994.tb00609.x FRITH U, 1992, AUTISM ASPERGER SYND, P1 GILLBERG C, 1989, ACTA PAEDIATR SCAND, V78, P314, DOI 10.1111/j.1651-2227.1989.tb11076.x GODDARD S, 1996, TEACHERS WINDOW CHIL GOLDBLATT D, 1986, J CHILD NEUROL, V1, P71, DOI 10.1177/088307388600100114 Klin A., 1997, HDB AUTISM PERVASIVE, P94 MCGRAW MB, 1989, NEUROMUSCULAR MATURA Miller M T, 1998, Trans Am Ophthalmol Soc, V96, P369 PAINE RS, 1964, NEUROLOGY, V14, P1036 PEIPER A, 1963, CEREBRAL FUNCTION IN Teitelbaum P, 2002, J DEV LEARNING DISOR, V6, P15 Teitelbaum P, 1998, P NATL ACAD SCI USA, V95, P13982, DOI 10.1073/pnas.95.23.13982 WING L, 1992, AUTISM ASPERGER SYND, P93 NR 19 TC 64 Z9 67 PU NATL ACAD SCIENCES PI WASHINGTON PA 2101 CONSTITUTION AVE NW, WASHINGTON, DC 20418 USA SN 0027-8424 J9 P NATL ACAD SCI USA JI Proc. Natl. Acad. Sci. U. S. A. PD AUG 10 PY 2004 VL 101 IS 32 BP 11909 EP 11914 DI 10.1073/pnas.0403919101 PG 6 WC Multidisciplinary Sciences SC Science & Technology - Other Topics GA 845WT UT WOS:000223276700068 PM 15282371 ER PT J AU Hultman, CM Sparen, P AF Hultman, CM Sparen, P TI Autism - prenatal insults or an epiphenomenon of a strongly genetic disorder? SO LANCET LA English DT Editorial Material ID PERINATAL RISK-FACTORS; SCHIZOPHRENIA C1 Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden. RP Hultman, CM (reprint author), Karolinska Inst, Dept Med Epidemiol & Biostat, SE-17177 Stockholm, Sweden. EM Christina.Hultman@meb.ki.se CR Cnattingius S, 1999, ARCH GEN PSYCHIAT, V56, P634, DOI 10.1001/archpsyc.56.7.634 Constantino JN, 2004, J CHILD PSYCHOL PSYC, V45, P719, DOI 10.1111/j.1469-7610.2004.00266.x Glasson EJ, 2004, ARCH GEN PSYCHIAT, V61, P618, DOI 10.1001/archpsyc.61.6.618 Hultman CM, 1999, BRIT MED J, V318, P421 Hultman CM, 2002, EPIDEMIOLOGY, V13, P417, DOI 10.1097/01.EDE.0000016968.14007.E6 Muhle R., 2004, PEDIATRICS, V113, P472 Nilsson E, 2002, SCHIZOPHR RES, V58, P221, DOI 10.1016/S0920-9964(01)00370-X RODIER PM, 2004, CLIN MOL TERATOL, V70, P1 NR 8 TC 8 Z9 8 PU LANCET LTD PI LONDON PA 84 THEOBALDS RD, LONDON WC1X 8RR, ENGLAND SN 0140-6736 J9 LANCET JI Lancet PD AUG 7 PY 2004 VL 364 IS 9433 BP 485 EP 487 DI 10.1016/S0140-6736(04)16825-6 PG 3 WC Medicine, General & Internal SC General & Internal Medicine GA 844BS UT WOS:000223132700008 PM 15302177 ER PT J AU Wang, NJ Liu, DH Parokonny, AS Schanen, NC AF Wang, NJ Liu, DH Parokonny, AS Schanen, NC TI High-resolution molecular characterization of 15q11-q13 rearrangements by array comparative genomic hybridization (array CGH) with detection of gene dosage SO AMERICAN JOURNAL OF HUMAN GENETICS LA English DT Article ID SUPERNUMERARY MARKER CHROMOSOMES; PRADER-WILLI-SYNDROME; INV DUP(15); INTERSTITIAL DUPLICATIONS; COMMON BREAKPOINT; ANGELMAN-SYNDROME; PROXIMAL 15Q; DELETION; REGION; MICROARRAY AB Maternally derived duplication of the imprinted region of chromosome 15q11-q14 leads to a complex neurobehavioral phenotype that often includes autism, cognitive deficits, and seizures. Multiple repeat elements within the region mediate a variety of rearrangements, including interstitial duplications, interstitial triplications, and supernumerary isodicentric marker chromosomes, as well as the deletions that cause Prader-Willi and Angelman syndromes. To elucidate the molecular structure of these duplication chromosomes, we designed a high-resolution array comparative genomic hybridization (array CGH) platform. The array contains 79 clones that form a gapped contig across the critical region on chromosome 15q11-q14 and 21 control clones from other autosomes and the sex chromosomes. We used this array to examine a set of 48 samples from patients with segmental aneuploidy of chromosome 15q. Using the array, we were able to determine accurately the dosage, which ranged from 1 to 6 copies, and also to detect atypical and asymmetric rearrangements. In addition, the increased resolution of the array allowed us to position two previously reported breakpoints within the contig. These results indicate that array CGH is a powerful technique to study rearrangements of proximal chromosome 15q. C1 Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90095 USA. Alfred I Dupont Hosp Children, Nemours Childrens Clin, Nemours Biomed Res, Wilmington, DE USA. RP Schanen, NC (reprint author), Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90095 USA. 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J. Hum. Genet. PD AUG PY 2004 VL 75 IS 2 BP 267 EP 281 DI 10.1086/422854 PG 15 WC Genetics & Heredity SC Genetics & Heredity GA 838GR UT WOS:000222702000011 PM 15197683 ER PT J AU Cooper, WO Hickson, GB Fuchs, C Arbogast, PG Ray, WA AF Cooper, WO Hickson, GB Fuchs, C Arbogast, PG Ray, WA TI New users of antipsychotic medications among children enrolled in TennCare SO ARCHIVES OF PEDIATRICS & ADOLESCENT MEDICINE LA English DT Article ID DOUBLE-BLIND; AUTISTIC DISORDER; YOUNG-CHILDREN; MENTAL-HEALTH; RISPERIDONE; ADOLESCENTS; ZIPRASIDONE; TRIAL; DRUG; PHARMACOEPIDEMIOLOGY AB Background: The use of antipsychotic medications in children and adolescents for indications other than psychosis or Tourette syndrome is controversial. Newer atypical antipsychotics with profiles of adverse effects that differ from those of traditional antipsychotics may lead providers to prescribe antipsychotics more frequently than in the past for behavioral indications not strongly supported by clinical study. Objective: To identify population-based new use of antipsychotics among patients aged 2 to 18 years. Design: Retrospective cohort study, January 1, 1996, through December 31, 2001. Setting: Tennessee's managed care program for Medicaid enrollees and the uninsured (TennCare). Main Outcome Measures: New use of antipsychotic medications and indications for use by the child's diagnosis, adjusted for age, sex, race, county of residence, enrollment category, and income. Results: The proportion of TennCare children who were new users of antipsychotics, adjusted for demographic characteristics, nearly doubled from 23/10000 in 1996 to 45/10000 in 2001 (adjusted incidence rate ratio, 1.98; 95% confidence interval, 1.82-2.16). In 1996, 6.8% of new users received an atypical antipsychotic; by 2001, this had increased to 95.9%. New use for attention-deficit/hyperactivity disorder and affective disorders increased 2.5-fold. New use of antipsychotics for schizophrenia, acute psychotic reaction, Tourette syndrome, and mental retardation or autism remained relatively constant. Secular trends of increasing use were most pronounced for those aged 6 to 12 years (93% increase) and 13 to 18 years (116% increase), although use among preschool children increased 61% during the study period. Conclusion: The proportion of TennCare children who became new users of antipsychotics nearly doubled from 1996 to 2001, with a substantial increase in use of antipsychotics for attention-deficit/hyperactivity disorder, conduct disorder, and affective disorders. C1 Vanderbilt Univ, Sch Med, Dept Pediat, Div Gen Pediat, Nashville, TN 37232 USA. Vanderbilt Univ, Div Child & Adolescent Psychiat, Dept Psychiat, Nashville, TN 37232 USA. Vanderbilt Univ, Div Biostat, Dept Prevent Med, Nashville, TN 37232 USA. Vanderbilt Univ, Div Pharmacoepidemiol, Dept Prevent Med, Nashville, TN 37232 USA. RP Cooper, WO (reprint author), Vanderbilt Univ, Sch Med, Dept Pediat, Div Gen Pediat, Suite 5028 MCE, Nashville, TN 37232 USA. 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SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID MOTION; DEFICITS; ORGANIZATION; SENSITIVITY; CHILDREN AB Phillips & Silverstein (P&S, 2003) propose that NMDA-receptor dysfunction may be the fundamental neurobiological mechanism underlying and associating impaired holistic perception and cognitive coordination with schizophrenic psychopathology. We discuss how the P&S hypothesis shares different aspects of the weak central coherence account of autism from both theoretical and experimental perspectives. Specifically, we believe that neither those persons with autism nor those with schizophrenia integrate visuo-perceptual information efficiently, resulting in incongruous internal representations of their external world. However, although NMDA-hypofunction may be responsible for perceptual impairments in schizophrenia and possibly autism, we suggest that it is highly unlikely that NMDA-hypofunction is specifically responsible for the autistic behavioral symptomology, as described by P&S in their target article. C1 Univ Montreal, Ecole Optometrie, Visual Psychophys & Percept Lab, Montreal, PQ H3C 1C1, Canada. Hop Riviere des Prairies, Clin Specialisee Troubles Envahissants Dev, Montreal, PQ H1E 1A4, Canada. RP Bertone, A (reprint author), Univ Montreal, Ecole Optometrie, Visual Psychophys & Percept Lab, Montreal, PQ H3C 1C1, Canada. EM armando.bertone@umontreal.ca; mottronl@istar.ca; jocelyn.faubert@umontreal.ca RI Faubert, Jocelyn/E-2207-2011 CR ARIETI S, 1966, PSYCHOPATHOLOGY SCHI, P37 Bertone A, 2003, J COGNITIVE NEUROSCI, V15, P218, DOI 10.1162/089892903321208150 Blake R, 2003, PSYCHOL SCI, V14, P151, DOI 10.1111/1467-9280.01434 Carlsson ML, 1998, J NEURAL TRANSM, V105, P525, DOI 10.1007/s007020050076 Chen Y, 2003, SCHIZOPHR RES, V61, P215, DOI 10.1016/S0920-9964(02)00222-0 Cornelissen PL, 1998, VISION RES, V38, P2181, DOI 10.1016/S0042-6989(98)00016-9 Frith U., 1989, AUTISM EXPLAINING EN Gepner B, 2002, TRENDS COGN SCI, V6, P455, DOI 10.1016/S1364-6613(02)02004-1 Gerland G., 1997, REAL PERSON LIFE OUT Gilmore G. 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Brain Sci. PD AUG PY 2004 VL 27 IS 4 BP 592 EP + PG 4 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 895KM UT WOS:000226860300071 ER PT J AU Faubert, J Bertone, A AF Faubert, J Bertone, A TI A common link between aging, schizophrenia, and autism? SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID AGED RATS; PERCEPTION; MOTION; MEMORY; LUMINANCE; MONKEYS AB Phillips & Silverstein (P&S, 2003) have proposed that NMDA-receptor hypofunction is the central reason for impaired cognitive coordination and abnormal gestalt-like perceptual processing in schizophrenia. We suggest that this model may also be applicable to non-pathological (or normal) aging given the compelling evidence of NMDA-receptor involvement during the aging process that results in age-related change in higher-level perceptual performance. Given that such deficits are present in other neurological disorders such as autism, an argument for a systematic assessment of perceptual functioning in these conditions may be posited. C1 Univ Montreal, Ecol Optometrie, Visual Psychophys & Percept Lab, Montreal, PQ H3C 1C1, Canada. RP Faubert, J (reprint author), Univ Montreal, Ecol Optometrie, Visual Psychophys & Percept Lab, Montreal, PQ H3C 1C1, Canada. EM jocelyn.faubert@montreal.ca; armando.bertone@umontreal.ca RI Faubert, Jocelyn/E-2207-2011 CR BAXTER MG, 1994, NEUROBIOL AGING, V15, P207, DOI 10.1016/0197-4580(94)90114-7 Bertone A, 2003, VISION RES, V43, P2591, DOI 10.1016/S0042-6989(03)00465-6 BERTONE A, 2005, BEHAV BRAIN SCI, V28 CAVANAGH P, 1989, Spatial Vision, V4, P103, DOI 10.1163/156856889X00077 Chubb C, 2001, J OPT SOC AM A, V18, P2175, DOI 10.1364/JOSAA.18.002175 Faubert J, 2002, CAN J EXP PSYCHOL, V56, P164, DOI 10.1037/h0087394 Faubert J, 2002, VISION RES, V42, P369, DOI 10.1016/S0042-6989(01)00292-9 Gazzaley AH, 1996, P NATL ACAD SCI USA, V93, P3121, DOI 10.1073/pnas.93.7.3121 Habak C, 2000, VISION RES, V40, P943, DOI 10.1016/S0042-6989(99)00235-7 Held K, 2002, PHARMACOPSYCHIATRY, V35, P135, DOI 10.1055/s-2002-33195 Herbert A.M., 2002, J GERONTOL B-PSYCHOL, V57, P241 Nishida S, 1997, VISION RES, V37, P2685, DOI 10.1016/S0042-6989(97)00092-8 Rosenzweig ES, 2003, PROG NEUROBIOL, V69, P143, DOI 10.1016/S0301-0082(02)00126-0 Sara M, 2000, OPHTHAL PHYSL OPT, V20, P314, DOI 10.1046/j.1475-1313.2000.00531.x Segovia G, 2001, MECH AGEING DEV, V122, P1, DOI 10.1016/S0047-6374(00)00225-6 TRICK GL, 1991, NEUROLOGY, V41, P1437 WENK GL, 1991, NEUROBIOL AGING, V12, P93, DOI 10.1016/0197-4580(91)90047-N WILSON HR, 1992, VISUAL NEUROSCI, V9, P79 NR 18 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0140-525X J9 BEHAV BRAIN SCI JI Behav. Brain Sci. PD AUG PY 2004 VL 27 IS 4 BP 593 EP + PG 4 WC Psychology, Biological; Behavioral Sciences; Neurosciences SC Psychology; Behavioral Sciences; Neurosciences & Neurology GA 895KM UT WOS:000226860300072 ER PT J AU Phillips, WA Silverstein, SM AF Phillips, WA Silverstein, SM TI Unity and diversity in disorders of cognitive coordination - Response SO BEHAVIORAL AND BRAIN SCIENCES LA English DT Editorial Material ID PERCEPTUAL ORGANIZATION; SCHIZOPHRENIA; AUTISM; PHARMACOTHERAPY; DYSFUNCTION; PROCESSORS; HYPOTHESIS; LUMINANCE; STIMULI; CONTEXT AB Studies of aging and autism as outlined by Bertone, Mottron, & Faubert (Bertone et A) and by Faubert & Bertone suggest that disorders of cognitive coordination involving impairments of dynamic gestalt grouping and context-sensitivity may be common to several different disorders. We agree that such studies may shed light on these processes and their neuronal bases. However, we also emphasize that dynamic grouping and context-sensitivity can fail in various ways, and that, although the underlying pathophysiology may often involve NMDA-receptor malfunction, many different malfunctions are possible, and each of these may result from any one of a number of different etiologies. C1 Univ Stirling, Dept Psychol, Stirling FK9 4LA, Scotland. Univ Illinois, Ctr Cognit Med, Dept Psychiat, Chicago, IL 60612 USA. RP Phillips, WA (reprint author), Univ Stirling, Dept Psychol, Stirling FK9 4LA, Scotland. 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EM spmamlp@iop.kcl.ac.uk CR Barton JJS, 2004, BRAIN, V127, P1706, DOI 10.1093/brain/awh194 Castelli F, 2002, BRAIN, V125, P1839, DOI 10.1093/brain/awf189 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 Haxby JV, 2000, TRENDS COGN SCI, V4, P223, DOI 10.1016/S1364-6613(00)01482-0 HOBSON RP, 1988, BRIT J PSYCHOL, V79, P441 Howard MA, 2000, NEUROREPORT, V11, P2931, DOI 10.1097/00001756-200009110-00020 Hubl D, 2003, NEUROLOGY, V61, P1232 Phillips ML, 2003, BIOL PSYCHIAT, V54, P504, DOI 10.1016/S0006-3223(03)00168-9 Pierce K, 2001, BRAIN, V124, P2059, DOI 10.1093/brain/124.10.2059 Salmond CH, 2003, PHILOS T ROY SOC B, V358, P405, DOI 10.1098/rstb.2002.1210 NR 10 TC 3 Z9 3 PU OXFORD UNIV PRESS PI OXFORD PA GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND SN 0006-8950 J9 BRAIN JI Brain PD AUG PY 2004 VL 127 BP 1691 EP 1692 DI 10.1093/brain/awh254 PN 8 PG 2 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 845GJ UT WOS:000223228600001 PM 15277305 ER PT J AU Barton, JJS Cherkasova, MV Hefter, R Cox, TA O'Connor, M Manoach, DS AF Barton, JJS Cherkasova, MV Hefter, R Cox, TA O'Connor, M Manoach, DS TI Are patients with social developmental disorders prosopagnosic? Perceptual heterogeneity in the Asperger and socio-emotional processing disorders SO BRAIN LA English DT Article DE Asperger's disorder; autism; face recognition; prosopagnosia ID RIGHT-HEMISPHERE; FACE RECOGNITION; LEARNING-DISABILITIES; AUTISTIC SYNDROME; COVERT RECOGNITION; FACIAL EXPRESSIONS; CHILDHOOD AUTISM; VISUAL AGNOSIA; CHILDREN; DISCRIMINATION AB It has been hypothesized that social developmental disorders (SDD) like autism, Asperger's disorder and the social-emotional processing disorder may be associated with prosopagnosic-like deficits in face recognition. We studied the ability to recognize famous faces in 24 adults with a variety of SDD diagnoses. We also measured their ability to discriminate changes in internal facial configuration, a perceptual function that is important in face recognition, and their imagery for famous faces, an index of their facial memory stores. We contrasted their performance with both healthy subjects and prosopagnosic patients. We also performed a cluster analysis of the SDD patients. One group of eight SDD subjects performed normally on all tests of face perception and recognition. The other 16 subjects were impaired in recognition, though most were better than prosopagnosic patients. One impaired SDD subgroup had poor perception of facial structure but relatively preserved imagery, resembling prosopagnosic patients with medial occipitotemporal lesions. Another subgroup had better perception than imagery, resembling one prosopagnosic with bilateral anterior temporal lesions. Overall, SDD subgroup membership by face recognition did not correlate with a particular SDD diagnosis or subjective ratings of social impairment. We conclude that the social disturbance in SDD does not invariably lead to impaired face recognition. Abnormal face recognition in some SDD subjects is related to impaired perception of facial structure in a manner suggestive of occipitotemporal dysfunction. Heterogeneity in the perceptual processing of faces may imply pathogenetic heterogeneity, with important implications for genetic and rehabilitative studies of SDD. C1 Beth Israel Deaconess Med Ctr, Dept Neurol, Boston, MA 02215 USA. Beth Israel Deaconess Med Ctr, Dept Ophthalmol, Boston, MA 02215 USA. Harvard Univ, Sch Med, Athinoula A Martinos Ctr, Boston, MA USA. Massachusetts Gen Hosp, Dept Psychiat, Boston, MA 02114 USA. Boston Univ, Dept Bioengn, Boston, MA 02215 USA. NEI, NIH, Bethesda, MD 20892 USA. RP Barton, JJS (reprint author), Beth Israel Deaconess Med Ctr, Dept Neurol, KS 452,330 Brookline Ave, Boston, MA 02215 USA. 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There tended to be a higher concentration of serum BDNF found in the autistic group (P < 0.05 by analysis of variance (ANOVA)) and the mental retardation group (P < 0.001 by ANOVA) compared to the control group. Serum NT-4 concentration tended to be increased in the mental retardation group (P < 0.05 by ANOVA). We conclude that measuring the serum concentration of two neurotrophins, BDNF and NT-4, might be helpful to diagnose or classify disorders such as autism or mental retardation. (C) 2003 Elsevier B.V. All rights reserved. C1 Univ Tsukuba, Neurobiol Lab, Inst Basic Med Sci, Tsukuba, Ibaraki 3058575, Japan. Dokkyo Univ, Sch Med, Dept Pediat, Koshigaya Hosp, Saitama 3438555, Japan. RP Narita, M (reprint author), Univ Tsukuba, Neurobiol Lab, Inst Basic Med Sci, 1-1-1 Tennodai, Tsukuba, Ibaraki 3058575, Japan. 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PD AUG PY 2004 VL 26 IS 5 BP 292 EP 295 DI 10.1016/S0387-7604(03)00168-2 PG 4 WC Clinical Neurology SC Neurosciences & Neurology GA 829PW UT WOS:000222063100003 PM 15165668 ER PT J AU Geier, DA Geier, MR AF Geier, DA Geier, MR TI An evaluation of serious neurological disorders following immunization: a comparison of whole-cell pertussis and acellular pertussis vaccines SO BRAIN & DEVELOPMENT LA English DT Article DE acellular; death; encephalopathy; pertussis; vaccine adverse event reporting system; whole-cell ID EVENT REPORTING SYSTEM; VAERS; EPIDEMIOLOGY; VACCINATION; JAPAN AB Serious neurological disorders reported following whole-cell pertussis in comparison to acellular pertussis vaccines were evaluated. The Vaccine Adverse Events Reporting System (VAERS) was analyzed for Emergency Department (ED) visits, life-threatening reactions, hospitalizations, disabilities, deaths, seizures, infantile spasms, encephalitis/encephalopathy, autism, Sudden Infant Death Syndrome (SIDS) and speech disorders reported with an initial onset of symptoms within 3 days following whole-cell pertussis and acellular pertussis vaccines among those residing in the US from 1997 to 1999. Controls were employed to evaluate potential biases in VAERS. Evaluations as to whether whole-cell and acellular vaccines were administered to populations of similar age and sex were undertaken because these factors might influence the study's results. Statistical increases were observed for all events examined following whole-cell pertussis vaccination in comparison to acellular pertussis vaccination, excepting cerebellar ataxia. Reporting biases were minimal in VAERS, and whole-cell and acellular pertussis vaccines were administered to populations of similar age and sex. Biologic mechanisms for the increased reactogenicity of whole-cell pertussis vaccines may stem from the fact that whole-cell per-tussis vaccines contain 3000 different proteins, whereas DTaP contains two to five proteins. Whole-cell pertussis vaccine contains known neurotoxins including: endotoxin, pertussis toxin and adenylate cyclase. Our results, and conclusions by the US Institute of Medicine, suggest an association between serious neurological disorders and whole-cell pertussis immunization. In light of the presence of a safer and at least equally efficacious acellular pertussis vaccine alternative, the Japanese and US switch to using acellular pertussis vaccine seems well justified. Other countries using whole-cell pertussis-containing vaccines should consider following suite in the near future. (C) 2003 Elsevier B.V. All rights reserved. C1 MedCon Inc, Silver Spring, MD 20905 USA. Genet Ctr Amer, Silver Spring, MD 20905 USA. RP Geier, MR (reprint author), 14 Redgate Ct, Silver Spring, MD 20905 USA. EM mgeier@erols.com CR Alderslade R, 1981, WHOOPING COUGH, P79 Braun MM, 2000, PEDIATRICS, V106, part. no., DOI 10.1542/peds.106.4.e51 Donnelly S, 2001, INFECT IMMUN, V69, P4217, DOI 10.1128/IAI.69.7.4217-4223.2001 DuVernoy TS, 2000, PEDIATRICS, V106, part. no., DOI 10.1542/peds.106.4.e52 Geier D, 2002, J HIST MED ALL SCI, V57, P249, DOI 10.1093/jhmas/57.3.249 Geier DA, 2002, ANN PHARMACOTHER, V36, P776 Greco D, 1996, NEW ENGL J MED, V334, P341, DOI 10.1056/NEJM199602083340601 *I MED, 1985, NEW VACC DEV EST PRI *I MED, 1994, DPT VACC CHRON NERV Institute of Medicine, 1991, ADV EFF PERT RUB VAC KIMURA M, 1990, PEDIATR INFECT DIS J, V9, P705, DOI 10.1097/00006454-199010000-00004 KunoSakai H, 1997, DEV BIOL STAND, V89, P331 MILLER D, 1993, BRIT MED J, V307, P1171 Rosenthal S, 1996, ARCH PEDIAT ADOL MED, V150, P457 Singleton JA, 1999, VACCINE, V17, P2908, DOI 10.1016/S0264-410X(99)00132-2 WARDLAW AC, 1982, PHARMACOL THERAPEUT, V19, P1, DOI 10.1016/0163-7258(82)90041-9 NR 16 TC 9 Z9 10 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0387-7604 J9 BRAIN DEV-JPN JI Brain Dev. PD AUG PY 2004 VL 26 IS 5 BP 296 EP 300 DI 10.1016/S0387-7604(03)00169-4 PG 5 WC Clinical Neurology SC Neurosciences & Neurology GA 829PW UT WOS:000222063100004 PM 15165669 ER PT J AU Adachi, T Koeda, T Hirabayashi, S Maeoka, Y Shiota, M Wright, EC Wada, A AF Adachi, T Koeda, T Hirabayashi, S Maeoka, Y Shiota, M Wright, EC Wada, A TI The metaphor and sarcasm scenario test: a new instrument to help differentiate high functioning pervasive developmental disorder from attention deficit/hyperactivity disorder SO BRAIN & DEVELOPMENT LA English DT Article DE high functioning pervasive developmental disorder; attention deficit hyperactivity disorder; social cognition; metaphor; sarcasm ID ASPERGER-SYNDROME; AUTISM; MIND; COMMUNICATION AB It is sometimes difficult to discriminate high functioning pervasive developmental disorders (HFPDD) from attention deficit/hyperactivity disorders (AD/HD) in young children because of the behavioral similarities between the two. For adequate diagnosis, understanding fundamental differences in their social cognitive abilities might become significant. In order to detect the differences in social cognitive abilities between AD/HD and HFPDD, a new test, the Metaphor and Sarcasm Scenario Test (MSST) was developed. One hundred and ninety-nine normal school children (the control group), 29 AD/HD children and 54 HFPDD children were involved. The results showed that the inability to understand a sarcastic situation was specific to children with HFPDD, both children with AD/HD and HFPDD could not equally understand metaphor. The correlation between the comprehension of sarcasm and success in the theory of mind task was remarkably high but not for comprehension of metaphor. In conclusion, the MSST has the potential to discriminate HFPDD from AD/HD in young children. (C) 2003 Elsevier B.V. All rights reserved. C1 Tottori Univ, Dept Human Educ, Fac Educ & Reg Sci, Tottori 6808551, Japan. Tottori Univ, Grad Sch Med, Div Neurobiol, Dept Biomed Sci, Tottori 680, Japan. Matsue Co Med Coll, Dept Speech Pathol, Matsue, Shimane, Japan. Nagano Childrens Hosp, Dept Neurol, Nagano, Japan. Hiroshima Prefectural Coll Hlth Sci, Dept Occupat Therapy, Hiroshima, Japan. Tottori Prefectural Kaike Rehabil Ctr Disabled Ch, Dept Pediat, Tottori, Japan. Tottori Univ, Dept Curriculum & Instruct, Fac Educ & Reg Sci, Tottori 680, Japan. RP Koeda, T (reprint author), Tottori Univ, Dept Human Educ, Fac Educ & Reg Sci, Koyama Cho Minami 4-101, Tottori 6808551, Japan. 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PD AUG PY 2004 VL 26 IS 5 BP 301 EP 306 DI 10.1016/S0387-7604(03)00170-0 PG 6 WC Clinical Neurology SC Neurosciences & Neurology GA 829PW UT WOS:000222063100005 PM 15165670 ER PT J AU Szelag, E Kowalska, J Galkowski, T Poppel, E AF Szelag, E Kowalska, J Galkowski, T Poppel, E TI Temporal processing deficits in high-functioning children with autism SO BRITISH JOURNAL OF PSYCHOLOGY LA English DT Article ID EVENT-RELATED POTENTIALS; INTERNAL CLOCK; DURATION JUDGMENTS; TIME; CEREBELLAR; PERCEPTION; ATTENTION; SEGMENTATION; REPRODUCTION; IMPAIRMENT AB It is well known that complex functions (e.g. perception, attention, memory, emotions, social interactions and language) are usually disturbed in autism. As these functions are characterized by specific temporal patterns, the present study examined whether children with autism show typical temporal processing in the time domain of a few seconds. Using a temporal-reproduction paradigm, we found that they were unable to link their responses to stimulus duration. Independently of stimulus duration, they reproduced auditory or visual stimuli with the same response duration of, on average, 3 s. These results demonstrate important deficits in duration judgment in individuals with autism. As other experiments provide evidence for a temporal processing platform of approximate to 2-3 s in normal individuals, this platform may be preserved in a residual form in autism. C1 M Nencki Inst Expt Biol, Dept Neurophysiol, PL-02093 Warsaw, Poland. Univ Warsaw, Fac Psychol, PL-00325 Warsaw, Poland. Univ Munich, Inst Med Psychol, Munich, Germany. RP Szelag, E (reprint author), M Nencki Inst Expt Biol, Dept Neurophysiol, 3 Pasteur St, PL-02093 Warsaw, Poland. 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We have used a combination of mercury L-III-edge X-ray absorption spectroscopy and density functional theory calculations to investigate the chemistry of interaction of mercuric ions with each of these chelation therapy drugs. We show that neither DMSA nor DMPS forms a true chelate complex with mercuric ions and that these drugs should be considered suboptimal for their clinical task of binding mercuric ions. We discuss the design criteria for a mercuric specific chelator molecule or "custom chelator", which might form the basis for an improved clinical treatment. C1 Univ Saskatchewan, Dept Geol Sci, Saskatoon, SK S7N 5E2, Canada. ExxonMobil Res & Engn Co, Annandale, NJ 08801 USA. Boehringer Ingelheim Austria GMBH, A-1120 Vienna, Austria. Univ Arizona, Dept Chem, Tucson, AZ 85721 USA. Univ Sydney, Sch Chem, Sydney, NSW 2006, Australia. RP George, GN (reprint author), Univ Saskatchewan, Dept Geol Sci, Saskatoon, SK S7N 5E2, Canada. 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Res. Toxicol. PD AUG PY 2004 VL 17 IS 8 BP 999 EP 1006 DI 10.1021/tx049904e PG 8 WC Chemistry, Medicinal; Chemistry, Multidisciplinary; Toxicology SC Pharmacology & Pharmacy; Chemistry; Toxicology GA 847RG UT WOS:000223412000002 PM 15310232 ER PT J AU Baron-Cohen, S AF Baron-Cohen, S TI A guide to Asperger syndrome SO CONTEMPORARY PSYCHOLOGY-APA REVIEW OF BOOKS LA English DT Book Review ID AUTISM C1 Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Cambridge CB2 3EB, England. Univ Cambridge, Dept Psychiat, Autism Res Ctr, Cambridge CB2 3EB, England. RP Baron-Cohen, S (reprint author), Univ Cambridge, Dept Expt Psychol, Autism Res Ctr, Downing St, Cambridge CB2 3EB, England. EM sb205@cam.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Attwood T., 1998, ASPERGERS SYNDROME G Baron-Cohen S., 2003, ESSENTIAL DIFFERENCE Baron-Cohen S, 2002, TRENDS COGN SCI, V6, P248, DOI 10.1016/S1364-6613(02)01904-6 Gillberg C, 2002, GUIDE ASPERGER SYNDR GILLBERG CL, 1992, J CHILD PSYCHOL PSYC, V33, P813, DOI 10.1111/j.1469-7610.1992.tb01959.x NR 6 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 AUG PY 2004 VL 49 IS 4 BP 427 EP 428 PG 2 WC Psychology, Multidisciplinary SC Psychology GA 842VF UT WOS:000223031800017 ER PT J AU Courchesne, E Redcay, E Kennedy, DP AF Courchesne, E Redcay, E Kennedy, DP TI The autistic brain: birth through adulthood SO CURRENT OPINION IN NEUROLOGY LA English DT Article DE autism; brain growth; development; neuroimaging head; circumference; MRI; fMRI; postmortem ID SPECTRUM DISORDER; HEAD CIRCUMFERENCE; INFANTILE-AUTISM; YOUNG-CHILDREN; CEREBELLAR; ABNORMALITIES; VOLUME; MRI; AGE; INFECTION AB Purpose of review We discuss evidence of brain maldevelopment in the first years of life in autism and new neuroanatomical and functional evidence from later ages of development. Recent findings Head circumference, an accurate indicator of brain size in children, was reported to jump from normal or below normal size in the first postnatal months in autistic infants to the 84th percentile by about 1 year of age; this abnormally accelerated growth was concluded by 2 years of age. Infants with extreme head (and therefore brain) growth fell into the severe end of the clinical spectrum and had more extreme neuroanatomical abnormalities. In the frontal and temporal lobes in autism, there have been reports of abnormal increases in gray and white matter at 2 to 4 years; reduced metabolic measures; deviant diffusion tensor imaging results in white matter; underdeveloped cortical minicolumns; and reduced functional activation during socioemotional, cognitive and attention tasks. Cerebellar abnormalities included abnormal volumes, reduced number and size of Purkinje neurons in the vermis and hemispheres, molecular defects, and reduced functional activation in posterior regions. Summary A new neurobiological phenomenon in autism has been described that precedes the onset of clinical behavioral symptoms, and is brief and age-delimited to the first two years of life. The neurobiological defects that precede, trigger, and underlie it may form part of the developmental precursors of some of the anatomical, functional, and behavioral manifestations of autism. Future studies of the first years of life may help elucidate the factors and processes that bring about the unfolding of autistic behavior. C1 Univ Calif San Diego, Dept Neurosci, San Diego, CA 92103 USA. Univ Calif San Diego, Dept Psychol, San Diego, CA 92103 USA. Childrens Hosp, Res Ctr, Ctr Autism Res, San Diego, CA USA. RP Courchesne, E (reprint author), Ctr Autism Res, 8110 La Jolla Shores Dr,Suite 201, La Jolla, CA 92037 USA. 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Opin. Neurol. PD AUG PY 2004 VL 17 IS 4 BP 489 EP 496 DI 10.1097/01.wco.0000137542.14610.b4 PG 8 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 849FW UT WOS:000223525100015 PM 15247547 ER PT J AU Morris, SA Bernstein, HH AF Morris, SA Bernstein, HH TI Immunizations, neonatal jaundice, and animal-induced injuries SO CURRENT OPINION IN PEDIATRICS LA English DT Review DE immunization; vaccine; hyperbilirubinemia; animal bite ID PNEUMOCOCCAL CONJUGATE VACCINE; INFLUENZA-VIRUS VACCINE; POSTTRAUMATIC-STRESS-DISORDER; DIPHTHERIA-TETANUS-PERTUSSIS; VARICELLA VACCINE; RUBELLA VACCINATION; HEALTHY-CHILDREN; CARBON-MONOXIDE; SERUM BILIRUBIN; YOUNG-CHILDREN AB Purpose of review Published studies during the past year about three topics important to the pediatric clinician-immunizations, neonatal jaundice, and animal-induced injuries-are concisely reviewed. Recent findings Recent updates regarding vaccines including the questionable link with autism, implementation of universal influenza vaccination for young children, the efficacy of pneumococcal vaccine against invasive disease, and new information on pertussis, varicella, hepatitis A, hepatitis B, measles, and rotavirus vaccination are discussed. No association between measles/mumps/rubella vaccine or thimerosal-containing pertussis vaccine and autism is evident. Universal influenza vaccination for children 6 to 23 months of age will be recommended for the 2004-2005 flu season, and this implementation should reduce significant school absenteeism as well as complications seen last year including encephalopathy, seizures, respiratory failure, and pneumonia. Pneumococcal vaccine significantly reduces rates of invasive pneumococcal vaccine in healthy and HIV-infected children, although it does not appear to greatly affect otitis media rates. A reduction in post-vaccine febrile seizures appears to be present since the introduction of acellular pertussis vaccine. Multiple outbreaks in varicella have been reported since the introduction of the varicella vaccine, and a booster vaccination may be necessary in the future. Methods for detecting and preventing severe neonatal hyperbilirubinemia are reviewed, as well as anticipated recommendations from the American Academy of Pediatrics for the detection and management of hyperbilirubinemia. High bilirubin levels in preterm infants may result in hearing dysfunction and developmental impairment. The American Academy of Pediatrics has recommended a higher level of monitoring for newborn jaundice and treatment of hyperbilirubinemia in an effort to prevent kernicterus and sequelae from elevated bilirubin levels, including post-discharge follow-up appointment by day 3 to 5 of age. Dog bites in children with resultant post-traumatic stress disorder, rabies, and salmonellosis from pet reptiles in the home are also addressed. Clinicians need to be aware of the risk for rabies bites, need to recognize that dog bites in children appear to cause post-traumatic stress disorder in more than half of cases, and need to know how to educate patients on how to prevent salmonellosis from pet reptiles and amphibians. Summary Progress has been made in immunizations, especially immunization for influenza, pneumonia, and pertussis. It is recommended that monitoring for neonatal hyperbilirubinemia be more thorough to prevent the consequences of this condition. Rabies, post-traumatic stress disorder from dog bites, and salmonellosis associated with pet reptiles constitute an important area for patient education. C1 Childrens Hosp, Boston, MA 02115 USA. Harvard Univ, Sch Med, Dept Med, Boston, MA USA. 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F., 1947, TXB MENTAL DEFICIENC VAILLANT GE, 1962, AM J PSYCHIAT, V119, P376 VANKREVELEN DA, 1963, ACTA PAEDOPSYCHIATR, V30, P303 Whitaker P, 2002, AUTISM, V6, P411, DOI 10.1177/1362361302006004007 WILLEY LH, 1999, PRETENDING NORMAL LI Wing J. K., 1976, EARLY CHILDHOOD AUTI, P3 Wing L., 1997, AUTISM, V1, P13, DOI 10.1177/1362361397011004 WING L, 1971, AUTISTIC CHILDREN GU WING L, 1979, J AUTISM DEV DISORD, V9, P11, DOI 10.1007/BF01531288 WING L, 1981, PSYCHOL MED, V11, P115 WOLFF S, 1980, PSYCHOL MED, V10, P85 Wolff S, 1996, EUR CHILD ADOLES PSY, V5, P119 Wolff S., 1995, LONERS LIFE PATH UNU WOLFF S, 1988, J CHILD PSYCHOL PSYC, V29, P143, DOI 10.1111/j.1469-7610.1988.tb00699.x NR 86 TC 24 Z9 24 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD AUG PY 2004 VL 13 IS 4 BP 201 EP 208 DI 10.1007/s00787-004-0363-5 PG 8 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 857DB UT WOS:000224095300001 PM 15365889 ER PT J AU Hrdlicka, M Komarek, V Propper, L Kulisek, R Zumrova, A Faladova, L Havlovicova, M Sedlacek, Z Blatny, M Urbanek, T AF Hrdlicka, M Komarek, V Propper, L Kulisek, R Zumrova, A Faladova, L Havlovicova, M Sedlacek, Z Blatny, M Urbanek, T TI Not EEG abnormalities but epilepsy is associated with autistic regression and mental functioning in childhood autism SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE childhood autism; epilepsy; EEG; autistic regression; mental retardation ID PERVASIVE DEVELOPMENTAL DISORDERS; INFANTILE-AUTISM; DISINTEGRATIVE PSYCHOSIS; DYSPHASIC CHILDREN; SPEECH LOSS; FOLLOW-UP; PATTERNS AB The aim of the study was to investigate the potential association of epilepsy and EEG abnormalities with autistic regression and mental retardation. We examined a group of 77 autistic children (61 boys, 16 girls) with an average age of 9.1 +/- 5.3 years. Clinical interview, neurological examination focused on the evaluation of epilepsy, IQ testing, and 21-channel EEG (including night sleep EEG recording) were performed. Normal EEGs were observed in 44.4% of the patients, non-epileptiform abnormal EEGs in 17.5%, and abnormal EEGs with epileptiform discharges in 38.1% of the patients. Epilepsy was found in 22.1% of the subjects. A history of regression was reported in 25.8% of the patients, 54.8% of the sample had abnormal development during the first year of life, and 79.7% of the patients were mentally retarded. Autistic regression was significantly more frequent in patients with epilepsy than in non-epileptic patients (p = 0.003). Abnormal development during the first year of life was significantly associated with epileptiform EEG abnormalities (p = 0.014). Epilepsy correlated significantly with mental retardation (p = 0.001). Although the biological basis and possible causal relationships of these associations remain to be explained, they may point to different subgroups of patients with autistic spectrum disorders. C1 Charles Univ, Sch Med 2, Dept Child Psychiat, Prague 15006, Czech Republic. Charles Univ, Sch Med 2, Dept Child Neurol, Prague 15006, Czech Republic. Charles Univ, Sch Med 2, Inst Biol & Med Genet, Prague 15006, Czech Republic. Acad Sci Czech Republ, Inst Psychol, Brno 60200, Czech Republic. RP Hrdlicka, M (reprint author), Charles Univ, Sch Med 2, Dept Child Psychiat, 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 BAILEY A, 1995, PSYCHOL MED, V25, P63 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 Cohen D. 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R., 1998, AUTISM PERVASIVE DEV VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 NR 33 TC 38 Z9 39 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD AUG PY 2004 VL 13 IS 4 BP 209 EP 213 DI 10.1007/s00787-004-0353-7 PG 5 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 857DB UT WOS:000224095300002 PM 15365890 ER PT J AU Steinhausen, HC Metzke, CW AF Steinhausen, HC Metzke, CW TI Differentiating the behavioural profile in autism and mental retardation and testing of a screener SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE behavioural profile; autism; mental retardation ID DIAGNOSTIC OBSERVATION SCHEDULE; FETAL ALCOHOL SYNDROME; INTELLECTUAL DISABILITY; POPULATION PREVALENCE; SOCIAL-BEHAVIOR; ADOLESCENTS; CHILDREN; PSYCHOPATHOLOGY; INTERVIEW; CHECKLIST AB In order to differentiate the behavioural profiles in autism and mental retardation and to cross-validate a behavioural autism screen, 84 subjects with autism (64 males and 20 females) with a mean age of 10 years selected from a Swiss national survey were compared to a control group of 84 subjects matched by age and gender with mental retardation, but without autistic features. The behavioural profile was assessed using the Developmental Behaviour Checklist (DBC). The behavioural profile in autism, in contrast to mental retardation, was marked by higher scores in the domains of disruptive, self-absorbed, communication disturbed, anxious and autistic behaviour, and a higher total DBC score. Furthermore, a higher vulnerability for behavioural abnormalities became evident for females with autism. A recently proposed DBC-Autism Screen was cross-validated, and a slight extension of the screen led to even higher correct classification rates. It was concluded that the DBC is a suitable instrument for the assessment of the behavioural. profile and for screening in autism. C1 Univ Zurich, Dept Child & Adolescent Psychiat, CH-8032 Zurich, Switzerland. RP Steinhausen, HC (reprint author), Univ Zurich, Dept Child & Adolescent Psychiat, Neumunsteralle 9, CH-8032 Zurich, Switzerland. EM steinh@kjpd.unizh.ch CR BARONCOHEN S, 1992, BRIT J PSYCHIAT, V161, P839, DOI 10.1192/bjp.161.6.839 Brereton AV, 2002, J AM ACAD CHILD PSY, V41, P1369, DOI 10.1097/01.CHI.0000024838.94814.A5 DILAVORE PC, 1995, J AUTISM DEV DISORD, V25, P355, DOI 10.1007/BF02179373 Einfeld S., 1992, MANUAL DEV BEHAV CHE EINFELD S, 1996, COMMUNICATION Einfeld S. L., 2002, MANUAL DEV BEHAV CHE Einfeld SL, 1996, J INTELL DISABIL RES, V40, P99, DOI 10.1111/j.1365-2788.1996.tb00611.x EINFELD SL, 1995, J AUTISM DEV DISORD, V25, P81, DOI 10.1007/BF02178498 Einfeld SL, 1996, J INTELL DISABIL RES, V40, P91, DOI 10.1111/j.1365-2788.1996.tb00610.x Howlin P, 1997, AUTISM, V1, P135, DOI DOI 10.1177/1362361397012003 KAZAKBERUMENT S, 1999, BRIT J PSYCHIAT, V175, P444 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 Luteijn E, 2000, J AUTISM DEV DISORD, V30, P317, DOI 10.1023/A:1005527300247 Steinhausen HC, 2003, DEV MED CHILD NEUROL, V45, P179, DOI 10.1017/S0012162203000343 STEINHAUSEN HC, 2004, LEBEN AUTISMUS LIVIN Steinhausen HC, 2002, AM J MED GENET, V111, P381, DOI 10.1002/ajmg.10627 Wing L, 2002, J CHILD PSYCHOL PSYC, V43, P307, DOI 10.1111/1469-7610.00023 WING L, 1981, PSYCHIAT RES, V5, P129, DOI 10.1016/0165-1781(81)90043-3 NR 19 TC 20 Z9 20 PU DR DIETRICH STEINKOPFF VERLAG PI DARMSTADT PA PO BOX 10 04 62, D-64204 DARMSTADT, GERMANY SN 1018-8827 J9 EUR CHILD ADOLES PSY JI Eur. Child Adolesc. Psych. PD AUG PY 2004 VL 13 IS 4 BP 214 EP 220 DI 10.1007/s00787-004-0400-4 PG 7 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 857DB UT WOS:000224095300003 PM 15365891 ER PT J AU Kurita, H Koyama, T Setoya, Y Shimizu, K Osada, H AF Kurita, H Koyama, T Setoya, Y Shimizu, K Osada, H TI Validity of childhood disintegrative disorder apart from autistic disorder with speech loss SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autistic disorder; childhood disintegrative disorder; disintegrative psychosis; pervasive developmental disorder; speech loss ID PERVASIVE DEVELOPMENTAL DISORDERS; FOLLOW-UP; INFANTILE-AUTISM; RATING-SCALE; DSM-IV; PSYCHOSIS; CHILDREN; REGRESSION; ABILITY; ONSET AB In order to test clinical validity of DSM-IV childhood disintegrative disorder (CDD), 10 CDD children (mean age = 8.2 years, SD = 3.8; 7 male and 3 female) and 30 age- and gender-matched children with DSM-IV autistic disorder (AD) with speech loss (SL) (ADSL) were compared on 24 variables not directly related to CDD criteria. Compared with the ADSL children, the CDD children showed fearfulness significantly more frequently during the period of SL; displayed epilepsy significantly more frequently and stereotypy significantly more prominently at first visit on average about 6 years after SL; and had significantly less uneven intellectual profile at first visit to support the validity of CDD to a certain extent. No significant difference in the retardation level at first visit between the two groups suggested no worse short-term outcome in CDD than ADSL, although a long-term prospective study to compare them from infancy is needed. C1 Univ Tokyo, Grad Sch Med, Dept Mental Hlth, Bunkyo Ku, Tokyo 1130033, Japan. Shinshu Univ, Grad Sch Med, Dept Psychiat, Matsumoto, Nagano 390, Japan. Univ Senshu, Fac Law, Tokyo, Japan. RP Kurita, H (reprint author), Univ Tokyo, Grad Sch Med, Dept Mental Hlth, Bunkyo Ku, 7-3-1 Hongo, Tokyo 1130033, Japan. 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Child Adolesc. Psych. PD AUG PY 2004 VL 13 IS 4 BP 221 EP 226 DI 10.1007/s00787-004-0397-8 PG 6 WC Psychology, Developmental; Pediatrics; Psychiatry SC Psychology; Pediatrics; Psychiatry GA 857DB UT WOS:000224095300004 PM 15365892 ER PT J AU Robel, L Ennouri, K Piana, HN Vaivre-Douret, L Perier, A Flament, MF Mouren-Simoni, MC AF Robel, L Ennouri, K Piana, HN Vaivre-Douret, L Perier, A Flament, MF Mouren-Simoni, MC TI Discrimination of face identities and expressions in children with autism: Same or different? SO EUROPEAN CHILD & ADOLESCENT PSYCHIATRY LA English DT Article DE autism; pervasive development disorder; face discrimination; expression discrimination; MNTAP ID PERVASIVE DEVELOPMENTAL DISORDERS; RECOGNITION; EMOTION; MIND; INDIVIDUALS; INFORMATION; PERCEPTION; APPRAISAL; DELAY AB Autism is a pervasive developmental disorder (PDD) characterized by the association of communication and socialization impairments, and by repetitive stereotyped behaviours. The Minnesota Test of Affective Processing (MNTAP) was used to investigate the discrimination of face identities and face expressions by autistic children. Young children in the 6- to 10-year-old age range suffering from PDD were compared to paired normal children. When the expressions on faces remained neutral, autistic patients had more difficulty in distinguishing different faces than in matching the same facial identities in face pairs: they perceived different faces as being identical. However, recognition errors disappeared when expressions were changed together with face identity. When autistic children were asked to distinguish expressions, they discriminated better identity than difference, just as normal children do. Analysis of face and expression discrimination in terms of identity and difference is a novel approach for the understanding of the clinical features of autism. Autistic children seek sameness and use an atypical strategy to analyse human faces and expressions. C1 Hop Necker Enfants Malad, Serv Pedopsychiat Pr B Golse, F-75015 Paris, France. Hop Necker Enfants Malad, INSERM, U483, Equipe Dev Unite, F-75015 Paris, France. Hop Robert Debre, Serv Psychopathol Enfant & Adolescent, F-75019 Paris, France. Univ Ottawa, Dept Psychiat, Ottawa, ON K1N 6N5, Canada. RP Robel, L (reprint author), Hop Necker Enfants Malad, Serv Pedopsychiat Pr B Golse, 149-161 Rue Sevres, F-75015 Paris, France. 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Rett syndrome is a monogenic X-linked dominant condition due to de novo mutations in the MECP2 gene, whereas autism is a neurodevelopmental and behavioral disorder with complex genetic basis. Maternally inherited duplications on 15q11-q13 are found in a fraction of autistic children suggesting that an abnormal dosage of gene(s) within this region might cause susceptibility to autism. Now we show that three Rett patients are carriers of both a MECP2 mutation and a 15q11-q13 rearrangement, suggesting that there might be a relationship between autism-related genes and the MECP2 gene. European Journal of Human Genetics (2004). C1 Univ Sacred Heart, Fac Med, Ist Genet Med, I-00168 Rome, Italy. Univ Siena, I-53100 Siena, Italy. Azienda Osped Senese, Siena, Italy. RP Gurrieri, F (reprint author), Univ Sacred Heart, Fac Med, Ist Genet Med, Lgo F Vito 1, I-00168 Rome, Italy. 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J. Hum. Genet. PD AUG PY 2004 VL 12 IS 8 BP 682 EP 685 DI 10.1038/sj.ejhg.5201198 PG 4 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 839WG UT WOS:000222815000015 PM 15069458 ER PT J AU Kumandas, S Akcakus, M Coskun, A Gumus, H AF Kumandas, S Akcakus, M Coskun, A Gumus, H TI Joubert syndrome: review and report of seven new cases SO EUROPEAN JOURNAL OF NEUROLOGY LA English DT Review DE abnormal eye movements; abnormal respiratory pattern; cerebellar hypoplasia; Joubert syndrome; hypotonia ID ABNORMAL EYE-MOVEMENTS; EPISODIC HYPERPNEA; CEREBELLAR VERMIS; MALFORMATIONS; RETARDATION; FAMILIES; FEATURES; ATAXIA; LOCUS AB Joubert syndrome (JS) is an autosomal-recessive disorder, characterized by hypotonia, ataxia, global developmental delay and molar tooth sign on magnetic resonance imaging. A variety of other abnormalities have been described in children with JS, including abnormal breathing, abnormal eye movements, a characteristic facial appearance, delayed language, hypersensitivity to noise, autism, ocular and oculomotor abnormalities, meningoencephaloceles, microcephaly, low-set ears, polydactyly, retinal dysplasia, kidney abnormalities (renal cysts), soft tissue tumor of the tongue, liver disease and duodenal atresia. Even within siblings the phenotype may vary, making it difficult to establish the exact clinical diagnostic boundaries of JS. We review the clinical characteristics of seven cases that fulfill the criteria of JS. C1 Erciyes Univ, Dept Pediat, Sch Med, TR-38039 Kayseri, Turkey. Erciyes Univ, Dept Radiol, Sch Med, TR-38039 Kayseri, Turkey. RP Akcakus, M (reprint author), Erciyes Univ, Dept Pediat, Sch Med, TR-38039 Kayseri, Turkey. 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J. Neurol. PD AUG PY 2004 VL 11 IS 8 BP 505 EP 510 DI 10.1111/j.1468-1331.2004.00819.x PG 6 WC Clinical Neurology; Neurosciences SC Neurosciences & Neurology GA 845MS UT WOS:000223249100001 PM 15272893 ER PT J AU Monji, A Maekawa, T Yanagimoto, K Yoshida, I Hashioka, S AF Monji, A Maekawa, T Yanagimoto, K Yoshida, I Hashioka, S TI Carbamazepine may trigger new-onset epileptic seizures in an individual with autism spectrum disorders: a case report SO EUROPEAN PSYCHIATRY LA English DT Article DE autism spectrum disorders; carbamazepine; new-onset epileptic seizures ID ANTIEPILEPTIC DRUGS; CHILDREN AB We herein report a case of new-onset epileptic seizures induced by carbamazepine in an individual with autism spectrum disorders (ASD). We clinicians should bear in mind the possibility that epileptic seizures may possibly be either precipitated or exacerbated by carbamazepine especially in individuals with ASD. (C) 2004 Elsevier SAS. All rights reserved. C1 Kyushu Univ, Grad Sch Med Sci, Dept Neuropsychiat, Fukuoka 8128582, Japan. RP Monji, A (reprint author), Kyushu Univ, Grad Sch Med Sci, Dept Neuropsychiat, Fukuoka 8128582, Japan. EM amonji@hf.rim.or.jp CR Guerrini R, 1998, EPILEPSIA, V39, pS2, DOI 10.1111/j.1528-1157.1998.tb05118.x Hollander E, 2001, J CLIN PSYCHIAT, V62, P530 Loiseau P, 1998, EPILEPSIA, V39, P2, DOI 10.1111/j.1528-1157.1998.tb01267.x MARTINO AD, 2001, PEDIATR NEUROL, V25, P199 Perucca E, 1998, EPILEPSIA, V39, P5, DOI 10.1111/j.1528-1157.1998.tb01268.x TUCHMAN RF, 1991, PEDIATRICS, V88, P1219 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 Yang MT, 2003, BRAIN DEV-JPN, V25, P51, DOI 10.1016/S0387-7604(02)00120-1 NR 8 TC 4 Z9 4 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0924-9338 J9 EUR PSYCHIAT JI Eur. Psychiat. PD AUG PY 2004 VL 19 IS 5 BP 322 EP 323 DI 10.1016/j.eurpsy.2004.06.001 PG 2 WC Psychiatry SC Psychiatry GA 848QC UT WOS:000223481200016 PM 15276670 ER PT J AU Bomba, MD Pang, EW AF Bomba, MD Pang, EW TI Cortical auditory evoked potentials in autism: a review SO INTERNATIONAL JOURNAL OF PSYCHOPHYSIOLOGY LA English DT Review DE auditory; autism; cortical evoked potentials; event-related potentials (ERP); N1; mismatch negativity (MMN); P3; review ID EVENT-RELATED POTENTIALS; DEVELOPMENTAL LANGUAGE DISORDER; MISMATCH NEGATIVITY MMN; BRAIN-STEM RESPONSES; N1 WAVE; STIMULUS DEVIANCE; MAGNETIC-FIELDS; ACOUSTIC CHANGE; EARLY-CHILDHOOD; SPEECH STIMULI AB The question of etiology in autism remains elusive primarily due to the fact that autism does not result from a single dysfunction but is multi-faceted in nature. Investigations into etiology have ranged from identifying abnormalities in the genome to describing structural/functional brain abnormalities. Bearing in mind the risk of over-simplification, there is still utility in isolating a specific deficit to examine its etiologic contribution. It is known that individuals with autism have difficulty processing auditory information at the cortical level but this is not consistently seen subcortically. In recent years, cortical auditory processing has been extensively researched using event-related potentials (ERPs); however, these results in relation to autism have not been reviewed. This paper will examine this literature and discuss implications for future research. (C) 2004 Elsevier B.V. All rights reserved. C1 Hosp Sick Children, Div Neurol, Toronto, ON M5G 1X8, Canada. Univ Toronto, Toronto, ON, Canada. RP Pang, EW (reprint author), Hosp Sick Children, Div Neurol, 555 Univ Ave, Toronto, ON M5G 1X8, Canada. 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P194, DOI 10.1080/080352500750028825 NR 96 TC 38 Z9 38 PU ELSEVIER SCIENCE BV PI AMSTERDAM PA PO BOX 211, 1000 AE AMSTERDAM, NETHERLANDS SN 0167-8760 J9 INT J PSYCHOPHYSIOL JI Int. 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PD AUG PY 2004 VL 53 IS 3 BP 161 EP 169 DI 10.1016/j.ijpsycho.2004.04.001 PG 9 WC Psychology, Biological; Neurosciences; Physiology; Psychology; Psychology, Experimental SC Psychology; Neurosciences & Neurology; Physiology GA 841LX UT WOS:000222932700001 PM 15246670 ER PT J AU Eaves, LC Ho, HH AF Eaves, LC Ho, HH TI The very early identification of autism: Outcome to age 41/2-5 SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE early identification; autism; pervasive developmental disorders; preschoolers with autism; stability of early diagnosis ID PERVASIVE DEVELOPMENTAL DISORDERS; INTENSIVE BEHAVIORAL TREATMENT; 6-YEAR FOLLOW-UP; YOUNG-CHILDREN; PRESCHOOL-CHILDREN; DIAGNOSTIC INTERVIEW; SPECTRUM DISORDERS; ADI-R; INTERVENTION; PREDICTORS AB Forty-nine 2 years olds with social and language characteristics suggestive of autism were identified by community professionals and screening tools, then given a diagnostic assessment and reexamined at age 4 1/2. Agreement between autism clinic and screenings was high, with 88% receiving a diagnosis on the autism spectrum. The children were lower functioning relative to the autism population, thus more likely to be identified early. Reliability of diagnoses from 2 1/2 to 4 1/2 was high with 79% staying in the same diagnostic category, but more so for clear autism than for PDDNOS. About a third improved over 20 IQ points and similar number similarly declined. Changes were not related to amount or type of intervention but were related to the children's characteristics. Higher functioning children with milder autism were the most improved. C1 Sunny Hill Hlth Ctr Children, Dept Psychol, Vancouver, BC V5M 3E8, Canada. RP Eaves, LC (reprint author), Sunny Hill Hlth Ctr Children, Dept Psychol, 3644 Slocan St, Vancouver, BC V5M 3E8, Canada. EM leaves@cw.bc.ca CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Baird G, 2000, J AM ACAD CHILD PSY, V39, P694, DOI 10.1097/00004583-200006000-00007 Baird G, 2001, ARCH DIS CHILD, V84, P468, DOI 10.1136/adc.84.6.468 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 Bayley N, 1993, BAYLEY SCALES INFANT Bondy AS, 1995, LEARNING COGNITION A, P311 Boyd RD, 2001, AUTISM, V5, P430, DOI 10.1177/1362361301005004007 Chakrabarti S, 2001, JAMA-J AM MED ASSOC, V285, P3093, DOI 10.1001/jama.285.24.3093 Charman T, 2002, J CHILD PSYCHOL PSYC, V43, P289, DOI 10.1111/1469-7610.00022 Cox A, 1999, J CHILD PSYCHOL PSYC, V40, P719, DOI 10.1111/1469-7610.00488 Filipek PA, 1999, J AUTISM DEV DISORD, V29, P439, DOI 10.1023/A:1021943802493 FISCH GS, 2000, J AUTISM DEV DISORDE Gabriels RL, 2001, AUTISM, V5, P407, DOI 10.1177/1362361301005004006 GILLBERG C, 1990, J CHILD PSYCHOL PSYC, V31, P921, DOI 10.1111/j.1469-7610.1990.tb00834.x Grunau RE, 2000, J DEV BEHAV PEDIATR, V21, P401, DOI 10.1097/00004703-200012000-00001 Guralnick M, 2001, INFANT YOUNG CHILD, V14, P1 Harris SL, 2000, J AUTISM DEV DISORD, V30, P137, DOI 10.1023/A:1005459606120 Leiter R. 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S., 1996, PSYCHOSOCIAL TREATME, P573, DOI 10.1037/10196-022 STRAIN PS, 1985, J DIVISION EARLY SPR, P105 Thorndike RL, 1986, STANFORD BINET INTEL Wechsler D., 1989, WECHSLER PRESCHOOL P Wing L, 1988, DIAGNOSIS ASSESSMENT NR 48 TC 80 Z9 83 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2004 VL 34 IS 4 BP 367 EP 378 DI 10.1023/B:JADD.0000037414.33270.a8 PG 12 WC Psychology, Developmental SC Psychology GA 844ZN UT WOS:000223205500001 PM 15449513 ER PT J AU Gadow, KD DeVincent, CJ Pomeroy, J Azizian, A AF Gadow, KD DeVincent, CJ Pomeroy, J Azizian, A TI Psychiatric symptoms in preschool children with PDD and clinic and comparison samples SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Asperger syndrome; PDDNOS; pervasive developmental disorder; attention-defficit/hyperactivity disorder; oppositional defiant disorder; conduct disorder; prevalence; community survey ID PERVASIVE DEVELOPMENTAL DISORDER; RECEPTIVE LANGUAGE DISORDER; CONTROL FAMILY-HISTORY; EARLY ADULT LIFE; AUTISTIC DISORDER; DSM-IV; FOLLOW-UP; ASPERGER-SYNDROME; TOURETTE-SYNDROME; FIELD TRIAL AB Objective: This study describes and compares the severity of DSM-IV symptoms in preschool children with diagnosed pervasive developmental disorder (PDD), clinic controls, and two community-based samples. Method: Parents (/and teachers) completed the early child inventory-4 (ECI-4), a DSM-IV-referenced rating scale for four samples: PDD (n=172/160) and nonPDD psychiatric clinic referrals (n=135/101) and youngsters in regular (n=507/407) and special (n=64/140) early childhood programs. Children ranged in age from 3 to 5 years old. Results: With the exception of conduct problems, the PDD group generally received higher symptom severity ratings than the regular early childhood group, but the pattern of differences compared with the other two groups often varied by type of symptom and informant. Teachers rated the PDD and nonPDD clinic groups as having equally severe ADHD and oppositional defiant disorder symptoms. Teachers rated the PDD group as having more severe anxiety and depression symptoms than parents. The Asperger group was rated by both informants as more oppositional than the autism and PDDNOS subgroups. Teachers rated males in the regular early childhood sample as having more severe ADHD and aggressive symptoms than females, but this was not the case for the PDD sample. Conclusion: Preschoolers with PDD exhibit more severe DSM-IV psychiatric symptoms than children in regular and special early childhood programs, and to some extent nonPDD psychiatric referrals. The concept of comorbidity warrants further exploration, as does informant-specific syndromes as validators of diagnostic constructs. C1 SUNY Stony Brook, Dept Psychiat & Behav Sci, Stony Brook, NY 11794 USA. SUNY Stony Brook, Dept Pediat, Stony Brook, NY 11794 USA. SUNY Stony Brook, Dept Psychol, Stony Brook, NY 11794 USA. RP Gadow, KD (reprint author), SUNY Stony Brook, Dept Psychiat & Behav Sci, Putnam Hall,South Campus, Stony Brook, NY 11794 USA. 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Autism Dev. Disord. PD AUG PY 2004 VL 34 IS 4 BP 379 EP 393 DI 10.1023/B:JADD.0000037415.21458.93 PG 15 WC Psychology, Developmental SC Psychology GA 844ZN UT WOS:000223205500002 PM 15449514 ER PT J AU Ganz, JB Simpson, RL AF Ganz, JB Simpson, RL TI Effects on communicative requesting and speech development of the picture exchange communication system in children with characteristics of autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; augmentative and alternative communication; developmental diabilities; speech; communication; Picture Exchange Communication System (PECS) ID SIGN LANGUAGE; ACQUISITION; BOY; DISABILITIES; ECHOLALIA; DISORDERS; STUDENTS; MODES AB Few studies on augmentative and alternative communication (AAC) systems have addressed the potential for such systems to impact word utterances in children with autism spectrum disorders (ASD). The Picture Exchange Communication System (PECS) is an AAC system designed specifically to minimize difficulties with communication skills experienced by individuals with ASD. The current study examined the role of PECS in improving the number of words spoken, increasing the complexity and length of phrases, and decreasing the nonword vocalizations of three young children with ASD and developmental delays ( DD) with related characteristics. Participants were taught Phases 1 - 4 of PECS (i.e., picture exchange, increased distance, picture discrimination, and sentence construction). The results indicated that PECS was mastered rapidly by the participants and word utterances increased in number of words and complexity of grammar. C1 Univ Texas, Coll Educ Human Dev, Dept Interdisciplinary Studies & Curriculum & Ins, San Antonio, TX 78249 USA. Univ Kansas, Dept Special Educ, Lawrence, KS 66045 USA. 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PD AUG PY 2004 VL 34 IS 4 BP 395 EP 409 DI 10.1023/B:JADD.0000037416.59095.d7 PG 15 WC Psychology, Developmental SC Psychology GA 844ZN UT WOS:000223205500003 PM 15449515 ER PT J AU Sigafoos, J Drasgow, E Halle, JW O'Reilly, M Seely-York, S Edrisinha, C Andrews, A AF Sigafoos, J Drasgow, E Halle, JW O'Reilly, M Seely-York, S Edrisinha, C Andrews, A TI Teaching VOCA use as a communicative repair strategy SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE augmentative and alternative communication; behavior indication; communicative repair; prelinguistic behavior; requesting; voice-output communication aid ID PROFOUND MENTAL-RETARDATION; VOICE OUTPUT COMMUNICATION; DISABILITIES; BEHAVIORS; INDIVIDUALS; ACQUISITION; STUDENTS; CHILDREN; AUTISM AB Students with developmental disabilities often rely on prelinguistic behavior ( e. g., reaching, leading) to communicate. When listeners fail to attend to prelinguistic behaviors, students may benefit from responding with an alternative form of communication to repair the breakdown. In the present study, we taught two students with developmental disabilities to repair communicative breakdowns by using a voice-output communication aid ( VOCA). Intervention occurred at morning snack time when the students had the opportunity to access preferred items through prelinguistic behavior ( e. g., reaching, guiding). Breakdowns occurred when the listener failed to attend to the student's initial request. Effects of the intervention were evaluated in a multiple-baseline design across subjects. Both students learned to use the VOCA to repair communicative breakdowns. As VOCA use was acquired as a repair strategy, the students also began to use the device to initiate requests when there had been no breakdown in communication. The intervention appeared to be an effective approach for supplementing prelinguistic behaviors with an additional option for communicating a request. C1 Univ Texas, Dept Special Educ, Austin, TX 78712 USA. Univ S Carolina, Columbia, SC 29208 USA. Univ Illinois, Urbana, IL 61801 USA. Autism Treatment Ctr, San Antonio, TX USA. RP Sigafoos, J (reprint author), Univ Texas, Dept Special Educ, 1 Univ Stn,D5300, Austin, TX 78712 USA. EM j.sigafoos@mail.utexas.edu CR American Association on Mental Retardation, 1992, MENT RET DEF CLASS S American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Beukelman D. R., 1998, AUGMENTATIVE ALTERNA Blischak DM, 2001, FOCUS AUTISM OTHER D, V16, P170, DOI 10.1177/108835760101600305 Bondy A, 2001, BEHAV MODIF, V25, P725, DOI 10.1177/0145445501255004 Brady N. C., 2002, EXEMPLARY PRACTICES, P323 BRADY NC, 1995, J SPEECH HEAR RES, V38, P1334 CARR EG, 1983, J APPL BEHAV ANAL, V16, P297, DOI 10.1901/jaba.1983.16-297 CARR EG, 1989, J AUTISM DEV DISORD, V19, P561, DOI 10.1007/BF02212858 Drasgow E., 1999, AUSTRALASIAN J SPECI, V23, P47, DOI 10.1080/1030011990230105 DUKER P, 1994, J INTELL DISABIL RES, V38, P177 DUKER PC, 1993, RES DEV DISABIL, V14, P39, DOI 10.1016/0891-4222(93)90004-4 GOLINKOFF RM, 1986, J CHILD LANG, V13, P455 Harding JW, 2001, J APPL BEHAV ANAL, V34, P61, DOI 10.1901/jaba.2001.34-61 HORNER RH, 1991, J APPL BEHAV ANAL, V24, P719, DOI 10.1901/jaba.1991.24-719 HOUGHTON J, 1987, J ASSOC PERS SEVERE, V12, P18 Iacono T., 1998, AUGMENTATIVE ALTERNA, V14, P102, DOI DOI 10.1080/07434619812331278246 Mayer-Johnson Co, 1994, PICT COMM SYMB COMB Michael J, 2000, J APPL BEHAV ANAL, V33, P401, DOI 10.1901/jaba.2000.33-401 Mirenda P, 2003, LANG SPEECH HEAR SER, V34, P203, DOI 10.1044/0161-1461(2003/017) OGLETREE BT, 1992, AM J MENT RETARD, V97, P186 Reeve C. E., 2000, J POSIT BEHAV INTERV, V2, P144, DOI 10.1177/109830070000200303 REICHLE J, 1986, J ASSOC PERS SEVERE, V11, P68 Schepis MM, 1996, BEHAV MODIF, V20, P451, DOI 10.1177/01454455960204005 Siegel E., 2002, EXEMPLARY PRACTICES, P25 Sigafoos J, 2003, AUGMENTATIVE ALTERNA, V19, P37, DOI 10.1080/0743461032000056487 Sigafoos J., 2002, EXEMPLARY PRACTICES, P123 Skinner B. F., 1957, VERBAL BEHAV Wetherby A. M., 1989, SEMINARS SPEECH LANG, V10, P77, DOI 10.1055/s-0028-1082491 Wetherby A. M., 1998, TRANSITIONS PRELINGU, P135 NR 30 TC 28 Z9 30 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2004 VL 34 IS 4 BP 411 EP 422 DI 10.1023/B:JADD.0000037417.04356.9c PG 12 WC Psychology, Developmental SC Psychology GA 844ZN UT WOS:000223205500004 PM 15449516 ER PT J AU Schilling, DL Schwartz, IS AF Schilling, DL Schwartz, IS TI Alternative seating for young children with autism spectrum disorder: Effects on classroom behavior SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; sensory strategies; school based interventions; classroom behavior; dynamic seating; early childhood ID SENSORY PROFILE AB A single subject, withdrawal design was used to investigate the effects of therapy balls as seating on engagement and in-seat behavior of young children with Autism Spectrum Disorder (ASD). In addition, social validity was assessed to evaluate teachers' opinions regarding the intervention. During baseline and withdrawal ( A phases) participants used their typical classroom seating device ( chair, bench or carpet square). During the intervention ( B phases) participants sat on therapy balls. Results indicated substantial improvements in engagement and in-seat behavior when participants were seated on therapy balls. Social validity findings indicated that the teachers' preferred the therapy balls. This study suggests therapy balls as classroom seating may facilitate engagement and in-seat behavior and create opportunities to provide effective instruction. C1 Univ Washington, Seattle, WA 98195 USA. RP Schilling, DL (reprint author), Silverman Hall,750 E Adams St, Syracuse, NY 13210 USA. EM PT@upstate.edu CR Ayres A. J., 1972, SENSORY INTEGRATION BARANEK G, 1998, SENSORY INTEGRATION, V21, P1 Baranek GT, 1997, AM J OCCUP THER, V51, P91 Bertrand J, 2001, PEDIATRICS, V108, P1155, DOI 10.1542/peds.108.5.1155 Cooper J., 1987, APPL BEHAV ANAL Dawson G, 2000, J AUTISM DEV DISORD, V30, P415, DOI 10.1023/A:1005547422749 DUNN W, 2000, OCCUPATIONAL THERAPY, V20, P6 Dunn W, 2001, AM J OCCUP THER, V55, P608 Elliot C., 1990, DIFFERENTIAL ABILITI Greenspan S. I., 1997, J DEV LEARNING DISOR, V1, P87 Greenstein S, 1997, IEEE MICRO, V17, P5, DOI 10.1109/40.592323 Huebner R.A., 2001, AUTISM SENSORIMOTOR ILLI U, 1994, SWISS J PHYS ED JUN Johnson-Ecker CL, 2000, AM J OCCUP THER, V54, P494, DOI 10.5014/ajot.54.5.494 Kazdin A. E., 1982, SINGLE CASE RES DESI Kientz MA, 1997, AM J OCCUP THER, V51, P530 Kimball J., 1999, FRAMES REFERENCE PED, P169 Koomar J. A., 1991, SENSORY INTEGRATION, P251 LEAR C, 1994, PHYS THERAPY FORUM, V24, P3 Lovaas O. I., 1987, J APPL BEHAV ANAL, V20, P45 MCBRIDE J, 1993, MEDFORD MAIL TRIBUNE, pA1 MCBRIDE J, 1993, MEDFORD MAIL TRIBUNE, pA4 Mulligan Shelley, 2001, Physical and Occupational Therapy in Pediatrics, V20, P25, DOI 10.1300/J006v20n04_03 National Research Council, 2001, ED CHILDR AUT Quill K. A., 2000, DO WATCH LISTEN SAY RICHARDS SB, 1999, SINGLE SUBJECT RES A Rogers SJ, 1998, J CLIN CHILD PSYCHOL, V27, P168, DOI 10.1207/s15374424jccp2702_4 Royeen C., 1991, SENSORY INTEGRATION Schilling DL, 2003, AM J OCCUP THER, V57, P534 SCHRODER T, 1997, TELEGRAFF SPAULDING A, 1999, KIDS BALL SUGAI G, 1984, EDUC TRAIN MENT RET, V19, P23 TROTT MC, 1993, SENSE ABILITIES UNDE WATLING R, 1999, AM J OCCUPATIONAL TH, V53, P489 Watling RL, 2001, AM J OCCUP THER, V55, P416 Wieder S, 1996, INFANT YOUNG CHILD, V8, P24 WILLIAMS M, 1994, SENSORY INTEGRATION, V17, P1 WILLIAMS M, 1996, DOES YOUR ENG RUN Willinger R, 1997, RES LEG MED, V17, P29 Witt D, 1998, ADV PHYSICAL THERAPI, P27 NR 40 TC 26 Z9 26 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2004 VL 34 IS 4 BP 423 EP 432 DI 10.1023/B:JADD.0000037418.48587.f4 PG 10 WC Psychology, Developmental SC Psychology GA 844ZN UT WOS:000223205500005 PM 15449517 ER PT J AU Schreck, KA Williams, K Smith, AF AF Schreck, KA Williams, K Smith, AF TI A comparison of eating Behaviors between children with and without autism SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; food refusal; food selectivity; pediatric feeding ID BOY AB Although clinicians typically assume that feeding problems co-exist with a diagnosis of autism, no previous research has compared the eating behavior of children with autism to typically developing children. This study compared caregiver report of eating problems of children with and without autism on a standardized questionnaire. The questionnaire included items pertaining to food refusal and acceptance patterns as well as food presentation requirements. Caregivers were also asked to complete a food inventory that indicated the number of foods eaten within each food group for both the child and the family. Results indicated children with autism have significantly more feeding problems and eat a significantly narrower range of foods than children without autism. C1 Penn State Harrisburg, Harrisburg, PA USA. Milton S Hershey Med Ctr, Hershey, PA USA. RP Schreck, KA (reprint author), 777 W Harrisburg Pike,W157 Olmsted Bldg, Middletown, PA 17047 USA. EM kas24@psu.edu CR Ahearn WH, 2001, J AUTISM DEV DISORD, V31, P505, DOI 10.1023/A:1012221026124 American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th ARCHER LA, 1991, J PEDIATR PSYCHOL, V16, P629, DOI 10.1093/jpepsy/16.5.629 ARCHER LA, 1990, CAN J PSYCHIAT, V35, P501 *AUT SOC AM, 1994, ADV NEWSL AUT SOC AM, V26 CLARK JH, 1993, JPEN-PARENTER ENTER, V17, P284, DOI 10.1177/0148607193017003284 COFFEY K, 1971, FREEDING HANDICAPPED DEMYER MK, 1968, ARCH GEN PSYCHIAT, V18, P584 Gilliam J. E., 1995, GILLIAM AUTISM RATIN JONES TW, 1982, LIFE THREATENING BEH, P3 Kanner L, 1943, NERV CHILD, V2, P217 KINNEL HG, 1983, NURS TIMES, P52 LOPREIATO JO, 1992, J DEV BEHAV PEDIATR, V13, P281 MINSHEW NJ, 1988, CURRENT PROBLEMS PED, V18, P619 NAGAI Y, 1983, JAPANESE J CHILD ADO, V24, P260 Palmer S., 1978, PEDIAT NUTR DEV DISO, P107 PERSKE R, 1977, MEALTIMES SEVERELY P RAITEN DJ, 1986, J AUTISM DEV DISORD, V16, P133, DOI 10.1007/BF01531725 *SPSS INC, 2000, STAT PACK SOC SCI RE Stone W. L., 1995, HDB PEDIAT PSYCHOL, P655 Teplin SW, 1999, DEV BEHAV PEDIAT, P589 NR 21 TC 128 Z9 131 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2004 VL 34 IS 4 BP 433 EP 438 DI 10.1023/B:JADD.0000037419.78531.86 PG 6 WC Psychology, Developmental SC Psychology GA 844ZN UT WOS:000223205500006 PM 15449518 ER PT J AU Bieberich, AA Morgan, SB AF Bieberich, AA Morgan, SB TI Self-regulation and affective expression during play in children with autism or Down syndrome: A short-term longitudinal study SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE autism; Down syndrome; affective expression; self-regulation ID ATTENTION; STABILITY AB Our study examined stability of self-regulation and affective expression in children with autism or Down syndrome over a 2 year period. A behaviorally-anchored rating scale was used to assess a self-regulation factor ( attention, adaptability, object orientation, and persistence), negative affect factor ( hostility, irritability, and compliance), and positive affect factor ( positive affect, affective sharing, and dull affect) from videotapes of play sessions involving each child and his or her mother. The patterns of ratings within each group were similar from time 1 to time 2, with the autism group showing more deviant ratings on measures of self-regulation and affective sharing. From time 1 to time 2, children with autism showed relatively high stability for the self-regulation factor, but less stability than children with Down syndrome for all three factors. C1 Univ Memphis, Dept Psychol, Memphis, TN 38152 USA. RP Morgan, SB (reprint author), Univ Memphis, Dept Psychol, Memphis, TN 38152 USA. EM sam-morgan@mail.psyc.memphis.edu CR ADRIEN JL, 1995, J AUTISM DEV DISORD, V25, P249, DOI 10.1007/BF02179287 Bieberich AA, 1998, J AUTISM DEV DISORD, V28, P333, DOI 10.1023/A:1026016804357 CAPPS L, 1993, J CONSULT CLIN PSYCH, V61, P475, DOI 10.1037/0022-006X.61.3.475 COURCHESNE E, 1995, INT PEDIAT, V10, P141 DAVISON ML, 1988, PSYCHOL BULL, V104, P137, DOI 10.1037//0033-2909.104.1.137 DAWSON G, 1990, J ABNORM CHILD PSYCH, V18, P335, DOI 10.1007/BF00916569 Dissanayake C, 1996, J CHILD PSYCHOL PSYC, V37, P461, DOI 10.1111/j.1469-7610.1996.tb01427.x Dunn L. M., 1981, PEABODY PICTURE VOCA Goldstein G, 2001, J AUTISM DEV DISORD, V31, P433, DOI 10.1023/A:1010620820786 HOLLINGSHEAD AB, 1975, UNPUB 4 FACTOR INDEX KASARI C, 1990, J AUTISM DEV DISORD, V20, P87, DOI 10.1007/BF02206859 KASARI C, 1993, DEV PSYCHOPATHOL, V5, P403, DOI 10.1017/S0954579400004491 Libby S, 1998, J AUTISM DEV DISORD, V28, P487, DOI 10.1023/A:1026095910558 LOVAAS OI, 1971, J ABNORM PSYCHOL, V77, P211, DOI 10.1037/h0031015 MCPHEE JT, 1993, REVISED MANUAL MINNE MORGAN S, 1988, J PSYCHOEDUCATIONAL, V6, P139, DOI 10.1177/073428298800600205 Ozonoff S., 1997, HDB AUTISM PERVASIVE, P868 OZONOFF S, 1994, DEV PSYCHOPATHOL, V6, P415, DOI 10.1017/S0954579400006027 PEDLOW R, 1993, DEV PSYCHOL, V29, P998, DOI 10.1037/0012-1649.29.6.998 PRUESS JB, 1986, J DIVISION EARLY CHI, V10, P65 Schopler E., 1988, CHILDHOOD AUTISM RAT SHAPIRO EG, 1994, J PEDIATR PSYCHOL, V19, P325, DOI 10.1093/jpepsy/19.3.325 SIGMAN M, 1986, J CHILD PSYCHOL PSYC, V27, P647, DOI 10.1111/j.1469-7610.1986.tb00189.x SIGMAN M, 1997, HDB AUTISM PERVASIVE, P248 SNOW ME, 1987, J AM ACAD CHILD PSY, V26, P836, DOI 10.1097/00004583-198726060-00006 WILHELM H, 1976, AM J MENT DEFIC, V81, P20 NR 26 TC 23 Z9 23 PU KLUWER ACADEMIC/PLENUM PUBL PI NEW YORK PA 233 SPRING ST, NEW YORK, NY 10013 USA SN 0162-3257 J9 J AUTISM DEV DISORD JI J. Autism Dev. Disord. PD AUG PY 2004 VL 34 IS 4 BP 439 EP 448 DI 10.1023/B:JADD.0000037420.16169.28 PG 10 WC Psychology, Developmental SC Psychology GA 844ZN UT WOS:000223205500007 PM 15449519 ER PT J AU Parsons, S Mitchell, P Leonard, A AF Parsons, S Mitchell, P Leonard, A TI The use and understanding of virtual environments by adolescents with autistic spectrum disorders SO JOURNAL OF AUTISM AND DEVELOPMENTAL DISORDERS LA English DT Article DE virtual environments; social skills; adolescents; autistic spectrum disorder; executive function ID ASPERGER-SYNDROME; ADAPTIVE-BEHAVIOR; VERBAL-ABILITY; CHILDREN; REALITY; PEOPLE; MIND; REHABILITATION; INSTRUCTION; CLUMSINESS AB The potential of virtual environments for teaching people with autism has been positively promoted in recent years. The present study aimed to systematically investigate this potential with 12 participants with autistic spectrum disorders (ASDs), each individually matched with comparison participants according to either verbal IQ or performance IQ, as well as gender and chronological age. Participants practised using a desktop 'training' virtual environment, before completing a number of tasks in a virtual cafe. We examined time spent completing tasks, errors made, basic understanding of the representational quality of virtual environments and the social appropriateness of performance. The use of the environments by the participants with ASDs was on a par with their PIQ-matched counterparts, and the majority of the group seemed to have a basic understanding of the virtual environment as a representation of reality. However, some participants in the ASD group were significantly more likely to be judged as bumping into, or walking between, other people in the virtual scene, compared to their paired matches. This tendency could not be explained by executive dysfunction or a general motor difficulty. This might be a sign that understanding personal space is impaired in autism. Virtual environments might offer a useful tool for social skills training, and this would be a valuable topic for future research. C1 Univ Nottingham, Sch Psychol, Nottingham NG7 2RD, England. RP Parsons, S (reprint author), Univ Birmingham, Sch Educ, Birmingham B15 2TT, W Midlands, England. EM s.j.parsons@bham.ac.uk CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th BERGER HJC, 1993, J AUTISM DEV DISORD, V23, P341, DOI 10.1007/BF01046224 Bernard-Opitz V, 2001, J AUTISM DEV DISORD, V31, P377, DOI 10.1023/A:1010660502130 BLADE RA, 2001, HDB VIRTUAL ENV DESI, P15 Brown D., 1999, International Journal of Virtual Reality, V4 CHARMAN T, 1992, J CHILD PSYCHOL PSYC, V33, P1105, DOI 10.1111/j.1469-7610.1992.tb00929.x CHEN SHA, 1993, MENT RETARD, V31, P368 CLANCY H, 1996, COMPUTER RESELLER NE, V698, P76 Cobb SVG, 1999, PRESENCE-TELEOP VIRT, V8, P169, DOI 10.1162/105474699566152 Cromby JJ, 1996, J INTELL DISABIL RES, V40, P489, DOI 10.1111/j.1365-2788.1996.tb00659.x EYNON A, 1997, COMMUNICATION SUM, P18 FOMBONNE E, 1994, EUR CHILD ADOLES PSY, V3, P176 Freeman BJ, 1999, J AUTISM DEV DISORD, V29, P379, DOI 10.1023/A:1023078827457 Frith U., 1994, SOCIAL DEV, V3, P108, DOI DOI 10.1111/J.1467-9507.1994.TB00031.X GHAZIUDDIN M, 1994, J INTELL DISABIL RES, V38, P519 Ghaziuddin M, 1998, J INTELL DISABIL RES, V42, P43, DOI 10.1046/j.1365-2788.1998.00065.x HAPPE FGE, 1995, CHILD DEV, V66, P843, DOI 10.1111/j.1467-8624.1995.tb00909.x HEIMANN M, 1995, J AUTISM DEV DISORD, V25, P459, DOI 10.1007/BF02178294 Hobson R. 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Autism Dev. Disord. PD AUG PY 2004 VL 34 IS 4 BP 449 EP 466 DI 10.1023/B:JADD.0000037421.98517.8d PG 18 WC Psychology, Developmental SC Psychology GA 844ZN UT WOS:000223205500008 PM 15449520 ER PT J AU Dixon-Salazar, TJ Keeler, LC Trauner, DA Gleeson, JG AF Dixon-Salazar, TJ Keeler, LC Trauner, DA Gleeson, JG TI Autism in several members of a family with generalized epilepsy with febrile seizures plus SO JOURNAL OF CHILD NEUROLOGY LA English DT Article ID SEVERE MYOCLONIC EPILEPSY; SODIUM-CHANNEL; LINKAGE ANALYSIS; CHILDHOOD; MUTATION; GENE; DISORDER; GAMMA-2-SUBUNIT; DYSFUNCTION; CHILDREN AB The neurobiologic basis for autism is not well understood. In contrast, there have been several recent discoveries into the genetics of generalized epilepsy with febrile seizures plus, a group of epilepsy syndromes characterized by multiple seizure phenotypes. Here we describe a family with generalized epilepsy with febrile seizures plus and variably expressed autism spectrum disorder that does not show linkage to any of the four known generalized epilepsy with febrile seizures plus loci. A relationship between these two disorders has not previously been described. C1 Univ Calif San Diego, Div Pediat Neurol, Dept Neurosci, La Jolla, CA 92093 USA. Univ Calif San Diego, Div Biol Sci, Dept Neurosci, La Jolla, CA 92093 USA. RP Gleeson, JG (reprint author), Univ Calif San Diego, Div Pediat Neurol, Dept Neurosci, 9500 Gilman Dr, La Jolla, CA 92093 USA. 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Child Neurol. PD AUG PY 2004 VL 19 IS 8 BP 597 EP 603 PG 7 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 920RK UT WOS:000228707600006 PM 15605469 ER PT J AU Schlosser, RW Blischak, DM AF Schlosser, RW Blischak, DM TI Effects of speech and print feedback on spelling by children with autism SO JOURNAL OF SPEECH LANGUAGE AND HEARING RESEARCH LA English DT Article DE assistive technology; augmentative and alternative communication; autism; feedback; intervention; literacy; speech-generating device; spelling; synthetic speech ID BEHAVIOR ANALYSIS; COMMUNICATION; ACHIEVEMENT; TECHNOLOGY; STRATEGIES; VARIABLES; LANGUAGE; VALIDITY; STUDENTS; WORD AB In this systematic replication of a previous study (R. W Schlosser, D. M. Blischak, P. J. Belfiore, C. Bartley, & N. Barnett, 1998), the effects of speech and print feedback on spelling performance were evaluated. Four children with autism and no functional speech were taught to spell words with a speech-generating device under 3 feedback conditions. In the auditory-visual condition, children received both speech and print feedback, whereas in the auditory and visual conditions, only 1 type of feedback was provided. An adapted alternating treatments design was used. All A children reached criterion across conditions. Although 3 children reached criterion first with print or speech-print feedback, 1 child was most efficient with speeck-print followed by speech feedback. Based on the findings of both studies, 2 distinct profiles of feedback efficiency are proposed. Children that exemplify the primarily visual profile spell words most efficiently when feedback involves print. Children that fit the auditory profile spell words most efficiently when feedback involves speech. The implications for understanding the learning characteristics of children with autism, as well as those for practice and further research are derived. C1 Northeastern Univ, Dept Speech Language Pathol & Audiol, Boston, MA 02115 USA. Univ Florida, Gainesville, FL USA. RP Schlosser, RW (reprint author), Northeastern Univ, Dept Speech Language Pathol & Audiol, 151B Forsyth, Boston, MA 02115 USA. 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PD AUG PY 2004 VL 47 IS 4 BP 848 EP 862 DI 10.1044/1092-4388(2004/063) PG 15 WC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation SC Audiology & Speech-Language Pathology; Linguistics; Rehabilitation GA 970DO UT WOS:000232285600009 PM 15324290 ER PT J AU Gervais, H Belin, P Boddaert, N Leboyer, M Coez, A Sfaello I Barthelemy, C Brunelle, F Samson, Y Zilbovicius, M AF Gervais, H Belin, P Boddaert, N Leboyer, M Coez, A Sfaello, I Barthelemy, C Brunelle, F Samson, Y Zilbovicius, M TI Abnormal cortical voice processing in autism SO NATURE NEUROSCIENCE LA English DT Article ID ASPERGER-SYNDROME; AUDITORY-CORTEX; INDIVIDUALS; CHILDREN; SPEECH; MIND AB Impairments in social interaction are a key feature of autism and are associated with atypical social information processing. Here we report functional magnetic resonance imaging (fMRI) results showing that individuals with autism failed to activate superior temporal sulcus (STS) voice-selective regions in response to vocal sounds, whereas they showed a normal activation pattern in response to nonvocal sounds. These findings suggest abnormal cortical processing of socially relevant auditory information in autism. C1 CEA, Serv Hosp Frederic Joliot, ERM 0205,INSERM, DRM,DSV, F-91406 Orsay, France. Univ Montreal, Ctr Rech Neuropsychol & Cognit, Montreal, PQ, Canada. Univ Montreal, Ctr Rech, Inst Univ Geriatrie Montreal, Montreal, PQ, Canada. AP HP, Serv Radiol Pediat, F-75015 Paris, France. Hop Henri Mondor, Psychiat Serv, AP HP, F-94000 Creteil, France. CHU Bretonneau, INSERM, Unite 619, F-37000 Tours, France. Grp Hosp Pitie Salpetriere, Serv Urgences Cerevrovasc, AP HP, F-75013 Paris, France. RP Zilbovicius, M (reprint author), CEA, Serv Hosp Frederic Joliot, ERM 0205,INSERM, DRM,DSV, 4 Pl Gen Leclerc, F-91406 Orsay, France. EM zilbo@shfj.cea.fr RI Belin, Pascal/C-6247-2009; samson, yves/C-5647-2013 OI Belin, Pascal/0000-0002-7578-6365; CR Allison T, 2000, TRENDS COGN SCI, V4, P267, DOI 10.1016/S1364-6613(00)01501-1 American Psychiatric Association, 2000, DIAGN STAT MAN, V4th Belin P, 2000, NATURE, V403, P309, DOI 10.1038/35002078 Belin P, 1999, NEUROIMAGE, V10, P417, DOI 10.1006/nimg.1999.0480 Bonnel A, 2003, J COGNITIVE NEUROSCI, V15, P226, DOI 10.1162/089892903321208169 BOUCHER J, 1992, J CHILD PSYCHOL PSYC, V33, P843, DOI 10.1111/j.1469-7610.1992.tb01960.x Castelli F, 2002, BRAIN, V125, P1839, DOI 10.1093/brain/awf189 Ceponiene R, 2003, P NATL ACAD SCI USA, V100, P5567, DOI 10.1073/pnas.0835631100 Critchley HD, 2000, BRAIN, V123, P2203, DOI 10.1093/brain/123.11.2203 FRITH U, 1994, COGNITION, V50, P115, DOI 10.1016/0010-0277(94)90024-8 Kanner L, 1943, NERV CHILD, V2, P217 KLIN A, 1991, J AUTISM DEV DISORD, V21, P29, DOI 10.1007/BF02206995 Pierce K, 2001, BRAIN, V124, P2059, DOI 10.1093/brain/124.10.2059 Rutherford MD, 2002, J AUTISM DEV DISORD, V32, P189, DOI 10.1023/A:1015497629971 Schultz RT, 2000, ARCH GEN PSYCHIAT, V57, P331, DOI 10.1001/archpsyc.57.4.331 NR 15 TC 204 Z9 207 PU NATURE PUBLISHING GROUP PI NEW YORK PA 75 VARICK ST, 9TH FLR, NEW YORK, NY 10013-1917 USA SN 1097-6256 J9 NAT NEUROSCI JI Nat. Neurosci. PD AUG PY 2004 VL 7 IS 8 BP 801 EP 802 DI 10.1038/nn1291 PG 2 WC Neurosciences SC Neurosciences & Neurology GA 841LH UT WOS:000222930800008 PM 15258587 ER PT J AU Pavone, P Incorpora, G Flumara, A Parano, E Trifiletti, RR Ruggieri, M AF Pavone, P Incorpora, G Flumara, A Parano, E Trifiletti, RR Ruggieri, M TI Epilepsy is not a prominent feature of primary autism SO NEUROPEDIATRICS LA English DT Article DE seizures; childhood; autistic behaviour; double syndrome; mental retardation ID CHILDREN; DISORDERS; SEIZURES AB The authors report on a series of 72 patients (57 male, 15 female; aged from 4 to 21 years) affected by autism with the aim of evaluate their experience regarding the prevalence of seizure and/or epilepsy. Patients were divided into two groups: the first includes individuals (n = 54) affected by so-called idiopathic or primary autism which was further subdivided according to the grade of mental retardation (MR) and the second (n = 18) in which a known pathological event was associated to the autism (secondary autism). According to these results in the first group 12% of autistic patients with moderate MR (i.e., IQ > 55) suffered from seizures but in three patients (9%) they were occasional and only in one recurrent (i.e., epileptic) (3%). Autistic patients with severe MR (i.e., IQ < 55) suffered from seizures in 20% of the cases: in three the episodes were recurrent (15%) and in one occasional (5%). In the second group in which autism was associated to other morbidities 61% (n = 11/18) had seizures, being recurrent in 10 (55%). According to this series, in autism the risk of epilepsy is higher compared to the general population but it does not seem to be correlated to the autism itself, but rather to the associated co-morbidities and underlying brain dysfunction (overall prevalence of epilepsy in primary autism [4/54 or 7.4%] vs. secondary autism [10/18 or 55%]). C1 CNR, ISN, I-95125 Catania, Italy. Catania Univ, Dept Paediat, Catania, Italy. NYU, Coll Med, Dept Neurol & Paediat, St Vincent Hosp, New York, NY USA. RP Ruggieri, M (reprint author), CNR, ISN, Viale R Margherita 6, I-95125 Catania, Italy. EM m.ruggieri@isn.cnr.it RI Fiumara, Agata/F-7200-2012 CR Aicardi J., 1998, DIS NERVOUS SYSTEM C BEAUMANOIR A, 1995, CONTINUOUS SPIKE WAV Browne T.R., 2000, HDB EPILEPSY Carod F J, 1995, Rev Neurol, V23, P1203 Curatolo P, 2003, TUBEROUS SCLEROSIS C ELIA M, 1995, AM J MENT RETARD, V100, P6 ELIA M, 2002, BIOL BASES CLIN PERS GILLBERG C, 1987, J AUTISM DEV DISORD, V17, P213 Gillberg C., 2000, BIOL AUTISTIC SYNDRO Herder Gyro Aas, 1993, Tidsskrift for den Norske Laegeforening, V113, P2247 Kanner L, 1943, NERV CHILD, V2, P217 KANNER L, 1971, J AUTISM CHILD SCHIZ, V1, P119, DOI 10.1007/BF01537953 Rapin I, 1997, NEW ENGL J MED, V337, P97, DOI 10.1056/NEJM199707103370206 ROSSI PG, 1995, BRAIN DEV-JPN, V17, P169, DOI 10.1016/0387-7604(95)00019-8 RUTTER M, 1970, SEMIN PSYCHIAT, V2, P435 SO NK, 1993, CLEV CLIN J MED, V60, P439 STEFFENBURG U, 1995, ACTA PAEDIATR, V84, P1147, DOI 10.1111/j.1651-2227.1995.tb13515.x Tuchman R, 2002, LANCET NEUROL, V1, P352, DOI 10.1016/S1474-4422(02)00160-6 TUCHMAN RF, 1991, EPILEPSY PEDIAT, V88, P1212 Tuchman RF, 1997, PEDIATRICS, V99, P560, DOI 10.1542/peds.99.4.560 VOLKMAR FR, 1990, J AM ACAD CHILD PSY, V29, P127, DOI 10.1097/00004583-199001000-00020 NR 21 TC 29 Z9 29 PU GEORG THIEME VERLAG KG PI STUTTGART PA RUDIGERSTR 14, D-70469 STUTTGART, GERMANY SN 0174-304X J9 NEUROPEDIATRICS JI Neuropediatrics PD AUG PY 2004 VL 35 IS 4 BP 207 EP 210 DI 10.1055/s-2004-821079 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 851YI UT WOS:000223722000001 PM 15328558 ER PT J AU Wong, V Hui, LHS Lee, WC Leung, LSJ Ho, PKP Lau, WLC Fung, CW Chung, B AF Wong, V Hui, LHS Lee, WC Leung, LSJ Ho, PKP Lau, WLC Fung, CW Chung, B TI A modified screening tool for autism (Checklist for Autism in Toddlers [CHAT-23]) for Chinese children SO PEDIATRICS LA English DT Article; Proceedings Paper CT Child Neurology Symposium CY JAN 17, 2004 CL Macau, PORTUGAL DE CHAT; M-CHAT; CHAT-23; autistic spectrum disorder; autism pervasive developmental disorder; children; Chinese; screening; sensitivity; specificity ID PERVASIVE DEVELOPMENTAL DISORDERS; SPECTRUM DISORDERS; PREVALENCE; POPULATION; DIAGNOSIS AB Background. There is a recent trend of a worldwide increase in the incidence of autistic spectrum disorder. Early identification and intervention have proved to be beneficial. The original version of the Checklist for Autism in Toddlers ( CHAT) was a simple screening tool for identification of autistic children at 18 months of age in the United Kingdom. Children with an absence of joint attention (including protodeclarative pointing and gaze monitoring) and pretend play at 18 months were at high risk of autism. Section A of the CHAT was a self-administered questionnaire for parents, with 9 yes/no questions addressing the following areas of child development: rough and tumble play, social interest, motor development, social play, pretend play, protoimperative pointing ( pointing to ask for something), protodeclarative pointing, functional play, and showing. Section B of the CHAT consisted of 5 items, which were recorded with observation of the children by general practitioners or health visitors. The 5 items addressed the child's eye contact, ability to follow a point ( gaze monitoring), pretend ( pretend play), produce a point ( protodeclarative pointing), and make a tower of blocks. A 6-year follow-up study of >16 000 children screened with the CHAT at 18 months in the United Kingdom showed a sensitivity of only 0.40 and a specificity of 0.98, with a positive predictive value (PPV) of 0.26. Rescreening using the same instrument at 19 months for those who failed the 18-month screening yielded a higher PPV of 0.75. Therefore, children were likely to have autism if they failed the CHAT at 18 months and failed again at 19 months. It was estimated that consistent failure in 3 key questions (ie, protodeclarative pointing, gaze monitoring, and pretend play) at 18 months indicated an 83.3% risk of having autism. Because of the poor sensitivity of the original CHAT for autism, a Modified Checklist for Autism in Toddlers (MCHAT), consisting of 23 questions, with 9 questions from the original CHAT and an additional 14 questions addressing core symptoms present among young autistic children, was designed in the United States. The original observational part ( ie, section B) was omitted. The M-CHAT was designed as a simple, self-administered, parental questionnaire for use during regular pediatric visits. The more questions children failed, the higher their risk of having autism. Two criteria were used to measure the sensitivity and specificity of M-CHAT. Criterion 1 used any 3 of the 23 questions, and criterion 2 used 2 of the 6 best questions that could be used to discriminate autism from other groups. The sensitivity and specificity for criterion 1 were 0.97 and 0.95 and those for criterion 2 were 0.95 and 0.99, respectively. M-CHAT had a better sensitivity than the original CHAT, because children up to 24 months of age were screened, with the aim of identifying those who might regress between 18 and 24 months. The 6 best questions of the M-CHAT addressed areas of social relatedness ( interest in other children and imitation), joint attention (protodeclarative pointing and gaze monitoring), bringing objects to show parents, and responses to calling. Joint attention was addressed in the original CHAT, whereas the other areas were addressed only in the M-CHAT. To date, there has been no study of the application of either the original CHAT or the M-CHAT for Chinese populations. Objectives. CHAT-23 is a new checklist translated into Chinese, combining the M-CHAT ( 23 questions) with graded scores and section B (observational section) of the CHAT. We aimed to determine whether CHAT-23 could discriminate autism at mental ages of 18 to 24 months for Chinese children and to determine the best combination of questions to identify autism. Methods. A cross-sectional cohort study was performed with 212 children with mental ages of 18 to 24 months. The children were categorized into 2 groups, ie, group 1 (N = 87) (autistic disorder: N = 53; pervasive developmental disorder: N = 33) and group 2 (N = 125) (nonautistic). The checklist included self-administered questionnaires with 23 questions ( part A) and direct observations of 5 items by trained investigators ( part B). We performed discriminant function analysis to determine the key questions that could best discriminate autism from nonautism. The sensitivity and specificity of CHAT-23 were calculated. Results. We found that 7 key questions, addressing areas of joint attention, pretend play, social relatedness, and social referencing, were identified as discriminative for autism. For part A, failing any 2 of 7 key questions, ie, question 13 (does your child imitate you? [eg, you make a face; will your child imitate it?]), question 5 ( does your child ever pretend, for example, to talk on the phone or take care of dolls, or pretend other things?), question 7 ( does your child ever use his/her index finger to point, to indicate interest in something?), question 23 ( does your child look at your face to check your reaction when faced with something unfamiliar?), question 9 ( does your child ever bring objects over to you [ parent] to show you something?), question 15 ( if you point at a toy across the room, does your child look at it?), and question 2 ( does your child take an interest in other children?), yielded sensitivity of 0.931 and specificity of 0.768. Failing any 6 of all 23 questions produced sensitivity of 0.839 and specificity of 0.848. For part B, failing any 2 of 4 items produced sensitivity of 0.736, specificity of 0.912, and PPV of 0.853. The 4 observational items were as follows: item B1: during the appointment, has the child made eye contact with you? item B2: does the child look across to see what you are pointing at? item B3: does the child pretend to pour out tea, drink it, etc?; item B4: does the child point with his/her index finger at the light? Conclusion. We found that integrating the screening questions of the M-CHAT ( from the United States) and observational section B of the original CHAT ( from the United Kingdom) yielded high sensitivity and specificity in discriminating autism at 18 to 24 months of age for our Chinese cohort. This new screening instrument (CHAT23) is simple to administer. We found that a 2-stage screening program for autism can offer a cost-effective method for early detection of autism at 18 to 24 months. For CHAT-23, use of both the parental questionnaire and direct observation and use of the criterion of failing any 2 of 7 key questions yielded the highest sensitivity but a relatively lower specificity, whereas use of part B yielded the highest specificity but a lower sensitivity. We recommend identifying the possible positive cases with part A ( parental questionnaire) and then proceeding to part B (observation) with trained assessors. The proposed algorithm for screening for autism is as follows. 1) The parents or chief caretakers complete a 23-item questionnaire when their children are 18 to 24 months of age. 2) The parents mail, fax, or hand this 23-item questionnaire to the local child health agency. 3) Clerical staff members check for and score failure, with the criteria of failing any 2 of 7 key questions or failing any 6 of 23 questions; if either criterion is met, then the staff members highlight the medical records of the suspicious cases. 4) Trained child health care professionals observe the children who failed any 2 of 7 key questions or any 6 of 23 questions. These identified patients are observed for 5 minutes for part B of the CHAT-23. 5) Any child who fails any 2 of 4 items requires direct referral to a comprehensive autism evaluation team, for early diagnostic evaluation and early intervention. The high sensitivity and specificity of the criteria observed in our study suggested that CHAT-23 might be used to differentiate children with autism. Additional international collaboration with the use of the CHAT, M-CHAT, and CHAT-23 could provide more prospective epidemiologic data, to establish whether there is a genuine increase in the worldwide incidence of autism. C1 Univ Hong Kong, Dept Paediat & Adolescent Med, Div Neurodev Paediat, Hong Kong, Hong Kong, Peoples R China. RP Wong, V (reprint author), Univ Hong Kong, Dept Paediat & Adolescent Med, Div Neurodev Paediat, Hong Kong, Hong Kong, Peoples R China. 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G., INTERPRETING DIAGNOS Wing L, 2002, MENT RETARD DEV D R, V8, P151, DOI 10.1002/mrdd.10029 WONG V, 2002, BRAIN DEV, V24, P331 WONG V, 2002, BRAIN DEV, V24, P335 NR 26 TC 30 Z9 32 PU AMER ACAD PEDIATRICS PI ELK GROVE VILLAGE PA 141 NORTH-WEST POINT BLVD,, ELK GROVE VILLAGE, IL 60007-1098 USA SN 0031-4005 J9 PEDIATRICS JI Pediatrics PD AUG PY 2004 VL 114 IS 2 BP 166 EP 176 PG 11 WC Pediatrics SC Pediatrics GA 842YG UT WOS:000223040000048 ER PT J AU Manning, MA Cassidy, SB Clericuzio, C Cherry, AM Schwartz, S Hudgins, L Enns, GM Hoyme, HE AF Manning, MA Cassidy, SB Clericuzio, C Cherry, AM Schwartz, S Hudgins, L Enns, GM Hoyme, HE TI Terminal 22q deletion syndrome: A newly recognized cause of speech and language disability in the autism spectrum SO PEDIATRICS LA English DT Article DE 22q deletion syndrome; autism; speech and language disability; fluorescence in situ hybridization ID IDIOPATHIC MENTAL-RETARDATION; PARTIAL MONOSOMY; CHROMOSOMAL REARRANGEMENTS; MOLECULAR CHARACTERIZATION; FISH; 22Q13.3; CHILDREN; BANDS AB Objective. Cryptic subtelomeric chromosome rearrangements account for 6% to 10% of idiopathic mental retardation. As cytogenetic and molecular techniques have become more sophisticated, the number of genetic syndromes attributed to these microdeletions has increased. To date, 64 patients have been described in the literature with a more recently recognized microdeletion syndrome, del 22q13.3. The purpose of this study is to present 11 new cases of this recently described syndrome to delineate further the phenotype and to alert the clinician to another genetic condition that should be considered in the differential diagnosis of early hypotonia, delayed speech acquisition, and autistic behavior. Methods. Eleven patients were evaluated in 3 academic institutions. Clinical features and results of cytogenetic testing were recorded and tabulated. Reasons for referral for genetic evaluation included developmental delay, severe expressive speech and language delay, and dysmorphic features. Results. Age of presentation ranged from 5 months to 46 years. There were 10 female patients and 1 male patient. All of the patients exhibited delayed motor development, some degree of hypotonia, and severe expressive speech and language delay. Dysmorphic facial features included epicanthal folds, large cupped ears, underdeveloped philtrum, loss of cupid's bow, and full supraorbital ridges. Six patients exhibited autistic-like behaviors. Microscopically visible chromosome deletions were observed in 6 patients. In the remainder, the deletion was detected with the use of fluorescence in situ hybridization. Conclusions. Hypotonia and developmental delay are nonspecific findings observed in many malformation and genetic syndromes. However, in association with severe speech and language delay and autistic-like behavior, this phenotype may be a significant indication to consider the 22q13 deletion syndrome as a potential cause. C1 Stanford Univ, Sch Med, Dept Pediat, Div Med Genet, Stanford, CA 94305 USA. Univ Calif Irvine, Sch Med, Dept Pediat, Div Human Genet, Irvine, CA 92717 USA. Univ New Mexico, Sch Med, Dept Pediat, Div Clin Genet Dysmorphol, Albuquerque, NM 87131 USA. Stanford Univ, Sch Med, Dept Pathol, Stanford, CA 94305 USA. Case Western Reserve Univ, Sch Med, Ctr Human Genet, Cleveland, OH USA. RP Manning, MA (reprint author), Stanford Univ, Sch Med, Dept Pediat, Div Med Genet, H-315, Stanford, CA 94305 USA. 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Without denying the existence of this so-called much greater thanmindblindnessmuch less than, it can be doubted from the psychoanalytic point of view whether this phenomenon is as isolated as cognitive theorists claim. Donald Meltzer relates autism to the failure of projective identification: since the autistic child has never felt persecuted, there can be no further differentiation of the relationship to the other through entering into the depressive position. This means that the prerequisite for the achievements which are the object of the tests used by cognitive psychologists is lacking. An attempt is made to establish a link between Kleiman theory (projective identification as the result of the expulsion of an inner corpus alienum) and deconstructivism (affirmation of a heterogenous factor inherent to any auto-affection). RP Turnheim, M (reprint author), 9 Rue Sentier, F-75002 Paris, France. 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Psychoanal. Ihre Anwendungen PD AUG PY 2004 VL 58 IS 8 BP 707 EP 735 PG 33 WC Psychology, Psychoanalysis SC Psychology GA 843ZP UT WOS:000223126900002 ER PT J AU Kano, Y Ohta, M Nagai, Y Pauls, DL Leckman, JF AF Kano, Y Ohta, M Nagai, Y Pauls, DL Leckman, JF TI Obsessive-compulsive symptoms in parents of Tourette syndrome probands and autism spectrum disorder probands SO PSYCHIATRY AND CLINICAL NEUROSCIENCES LA English DT Article DE autism spectrum disorders; genetics; obsessive-compulsive symptoms; Tourette syndrome ID FAMILY; CHILDREN; SCALE AB Obsessive-compulsive symptoms (OCS) frequently occur in patients with Tourette syndrome (TS) and autism spectrum disorders (ASD). It has been suggested that genetic factors play a role in the transmission of both TS and ASD and that obsessive-compulsive disorder (OCD) may have some genetic relationship with these disorders. The objective of this study was to explore whether the OCS associated with TS and ASD were found in the parents of TS and ASD probands by comparing them with normal controls. The subjects were parents of 13 TS and 16 ASD probands. All parents underwent an examination for tic symptoms and OCD, and completed the Maudsley Obsessional Compulsive Inventory (MOCI) and State-Trait Anxiety Inventory (STAI). No significant differences were observed in the MOCI and STAI scores among all three groups. However, the MOCI total score was higher in fathers of ASD probands than in male normal controls with a marginal significance. There was a significant tendency for the mean cleaning score of MOCI in fathers of ASD probands to be higher than that in male normal controls, and the mean checking score in fathers of ASD probands was fourfold higher than that in male normal controls, although there was no significant difference. No significant relationship was observed between OCS in TS or ASD probands and OCS of their parents. Further studies on OCD and OCS including a dimensional approach within ASD families are needed. C1 Kitasato Univ, Grad Sch Med Sci, Sagamihara, Kanagawa 2288555, Japan. Tokyo Gakugei Univ, Res Inst Educ Except Children, Tokyo, Japan. Univ Shizuoka, Sch Nursing, Shizuoka, Japan. Harvard Univ, Sch Med, Massachusetts Gen Hosp, Psychiat & Neurodev Genet Unit, Charlestown, MA USA. Yale Univ, Sch Med, Yale Child Study Ctr, New Haven, CT USA. RP Kano, Y (reprint author), Kitasato Univ, Grad Sch Med Sci, 1-15-1 Kitasato, Sagamihara, Kanagawa 2288555, Japan. EM yukiko-k@kitasato-u.ac.jp CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Bailey A, 1998, J AUTISM DEV DISORD, V28, P369, DOI 10.1023/A:1026048320785 Baron-Cohen S, 1999, BRIT J PSYCHIAT, V175, P484, DOI 10.1192/bjp.175.5.484 BARONCOHEN S, 1989, BRIT J CLIN PSYCHOL, V28, P193 BLACK DW, 1992, ARCH GEN PSYCHIAT, V49, P362 Bolton PF, 1998, PSYCHOL MED, V28, P385, DOI 10.1017/S0033291797006004 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1012 GOODMAN WK, 1989, ARCH GEN PSYCHIAT, V46, P1006 HODGSON RJ, 1977, BEHAV RES THER, V15, P389, DOI 10.1016/0005-7967(77)90042-0 HOLLANDER E, 1998, BR J PSYCHIAT S, V35, P7 HOLZER JC, 1994, BRIT J PSYCHIAT, V164, P469, DOI 10.1192/bjp.164.4.469 KANO Y, 1998, KOKORO NO RINSYO C S, V17, P281 Leckman JF, 2003, AM J MED GENET B, V116B, P60, DOI 10.1002/ajmg.b.10001 MCDOUGLE CJ, 1995, AM J PSYCHIAT, V152, P772 Miguel E C, 2001, Adv Neurol, V85, P43 MIZUGUCHI K, 1991, JAPANESE STATE TRAIT PAULS DL, 1991, AM J HUM GENET, V48, P154 PAULS DL, 1999, TOURETTES SYNDROME T, P194 Shapiro A.K., 1988, GILLES TOURETTE SYND Spielberger CD, 1970, STAI MANUAL Starr E, 2001, J AUTISM DEV DISORD, V31, P89, DOI 10.1023/A:1005669915105 YOSHIDA M, 1995, SEISHIN IGAKU, V37, P291 NR 22 TC 8 Z9 8 PU BLACKWELL PUBLISHING ASIA PI CARLTON PA 54 UNIVERSITY ST, P O BOX 378, CARLTON, VICTORIA 3053, AUSTRALIA SN 1323-1316 J9 PSYCHIAT CLIN NEUROS JI Psychiatry Clin. Neurosci. PD AUG PY 2004 VL 58 IS 4 BP 348 EP 352 DI 10.1111/j.1440-1819.2004.01266.x PG 5 WC Clinical Neurology; Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 842DE UT WOS:000222982400002 PM 15298645 ER PT J AU Dolan, M Fullam, R AF Dolan, M Fullam, R TI Theory of mind and mentalizing ability in antisocial personality disorders with and without psychopathy SO PSYCHOLOGICAL MEDICINE LA English DT Article ID FACIAL EXPRESSIONS; ASPERGER-SYNDROME; HUMAN AMYGDALA; NORMAL ADULTS; EMPATHY; BEHAVIOR; EMOTION; AUTISM; EYES; DISSOCIATION AB Background. The literature on Theory of Mind (ToM) in antisocial samples is limited despite evidence that the neural substrates of theory of mind task involve the same circuits implicated in the pathogenesis of antisocial behaviour. Method. Eighty-nine male DSM-IV Antisocial Personality Disordered subjects (ASPDs) and 20 controls (matched for age and IQ) completed a battery of ToM tasks. The ASPD group was categorized into psychopathic and non-psychopathic groups based on a cut-off score of 18 on the Psychopathy Checklist: Screening Version. Results. There were no significant group (control v. psychopath v. non-psychopathic ASPD) differences on basic tests of ToM but both psychopathic and non-psychopathic ASPDs performed worse on subtle tests of mentalizing ability (faux pas tasks). ASPDs can detect and understand faux pas, but show an indifference to the impact of faux pas. On the face/eye task non-psychopathic ASPDs showed impairments in the recognition of basic emotions compared with controls and psychopathic ASPDs. For complex emotions, no significant group differences were detected largely due to task difficulty. Conclusions. The deficits in mentalizing ability in ASPD are subtle. For the majority of criminals with ASPD and psychopathy ToM abilities are relatively intact and may have an adaptive function in maintaining a criminal lifestyle. 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Med. PD AUG PY 2004 VL 34 IS 6 BP 1093 EP 1102 DI 10.1017/S0033291704002028 PG 10 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 857GL UT WOS:000224104300013 PM 15554579 ER PT J AU Scott, FJ AF Scott, FJ TI Autism - Explaining the enigma, 2nd ed SO PSYCHOLOGICAL MEDICINE LA English DT Book Review CR FRITH U, 2003, AUTISM EXPLANING ENI NR 1 TC 0 Z9 0 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0033-2917 J9 PSYCHOL MED JI Psychol. Med. PD AUG PY 2004 VL 34 IS 6 BP 1140 EP 1141 DI 10.1017/S0033291704243203 PG 2 WC Psychology, Clinical; Psychiatry; Psychology SC Psychology; Psychiatry GA 857GL UT WOS:000224104300020 ER PT J AU Friedman, O Leslie, AM AF Friedman, O Leslie, AM TI Mechanisms of belief-desire reasoning - Inhibition and bias SO PSYCHOLOGICAL SCIENCE LA English DT Article ID FALSE BELIEF; MIND; AUTISM; REPRESENTATION; DECEPTION; TASK AB Biases in reasoning can provide insight into underlying processing mechanisms. We demonstrate a new bias in children's belief-desire reasoning. Children between 4 and 8 years of age were told a story in which a character was mistaken about which of three boxes contained some object. The character wanted to go to one of the boxes, but only if it did not contain the object. In this scenario, the character would be expected to avoid the box where she falsely believed the object to be, but might go to either of the remaining boxes. Though the character was equally likely to go to either box, children were biased to predict that the character would go to the box that contained the object. In a control task, the character had the same desire but did not have a false belief; in this case, children showed no bias, choosing the two correct answers equally often. The observed pattern of bias was predicted by a developmental model of belief-desire reasoning. Competent belief-desire reasoning depends on a process of selection by inhibition in which the best belief content emerges from a set of candidates. C1 Rutgers State Univ, Ctr Cognit Sci, Piscataway, NJ 08854 USA. Rutgers State Univ, Dept Psychol, Piscataway, NJ 08854 USA. RP Leslie, AM (reprint author), Rutgers State Univ, Ctr Cognit Sci, 152 Frelinghuysen Rd, Piscataway, NJ 08854 USA. 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Nevertheless, R.J. has developed normal, consensually accurate knowledge of his own personality traits (Klein, Chan, & Loftus, 1999). Moreover, his self-ratings show that he sees his own personality as distinct from the personalities of others. But R.J.'s facility in learning about his own personality does nottranslate into a facility in learning about the personality traits of others: He fails to differentiate between the personalities of his various family members, and his ratings of them appear to be less nuanced and less situationally specific than his ratings of his own personality. This pattern is radically at variance from that shown by cognitively normal individuals. Because R.J.'s dissociation is developmental in origin, it can illuminate the nature of the learning mechanisms by which knowledge of personality traits is acquired. 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It has been suggested that individuals with autism have difficulty in holistic processing, however the extent to which this difficulty may be moderated by attentional cues is uncertain. The present study included a condition that cued participants to the relevant face feature for matching. In the comparison group, the cue did not moderate the whole-face matching advantage. In the participants with autism, cueing generated a whole-face advantage, while uncued stimuli showed no difference between whole face and feature matching. This suggests that a lack of holistic processing in face processing, which is associated with individuals with autism, can be moderated with cueing. The implications for weak central coherence theory are discussed. C1 York St John Coll, Sch Sports Sci & Psychol, York YO31 7EX, N Yorkshire, England. Univ Southampton, Ctr Visual Cognit, Southampton SO9 5NH, Hants, England. Univ Southampton, Dept Psychol, Ctr Res Psychol Dev, Southampton SO9 5NH, Hants, England. 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C1 Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA. Univ Illinois, Beckman Inst Adv Sci & Technol, NeuroTech Grp, Urbana, IL 61801 USA. Univ Illinois, Neurosci Program, Urbana, IL 61801 USA. Univ Illinois, Med Scholars Program, Urbana, IL 61801 USA. RP Li, YQ (reprint author), Univ Illinois, Dept Mol & Integrat Physiol, Urbana, IL 61801 USA. 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We found that tuberin expression increases p42/44 MAPK phosphorylation and B-Raf kinase activity. Short interfering RNA down-regulation of tuberin decreased the p42/44 MAPK phosphorylation and B-Raf activity. Expression of Rheb, the target of the GTPase-activating domain of tuberin, inhibited wildtype B-Raf kinase but not activated forms of B-Raf. The interaction of endogenous Rheb with B-Raf was enhanced by serum and by Ras overexpression. A farnesylation-defective mutant of Rheb co-immunoprecipitated with and inhibited B-Raf but did not activate ribosomal protein S6 kinase, indicating that farnesylation is not required for B-Raf inhibition by Rheb and that B-Raf inhibition and S6 kinase activation are separable activities of Rheb. Consistent with this, inhibition of B-Raf and p42/44 MAPK by Rheb was resistant to rapamycin in contrast to Rheb activation of S6 kinase, which is rapamycin-sensitive. Taken together these data demonstrate that inhibition of B-Raf kinase via Rheb is an mTOR-independent function of tuberin. C1 Fox Chase Canc Ctr, Philadelphia, PA 19111 USA. Penn State Coll Med, Dept Pharmacol, Hershey, PA 17033 USA. RP Henske, EP (reprint author), Fox Chase Canc Ctr, 333 Cottman Ave, Philadelphia, PA 19111 USA. 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AS is characterized by severe mental retardation, ataxia, and a defined behavioral pattern characterized mainly by happy/sociable disposition. This study used the Bayley Scales of Infant Development and the Vineland Adaptive Behavior Scales to examine the cognitive abilities and adaptive behavior of children (n = 20) with the four known molecular classes of AS, including patterns of strengths and weaknesses across adaptive behavior domains, and the relationship between adaptive behavior and overall cognitive abilities. Cognitive skills fell within the severe to profound range of mental deficiency. Differences in cognitive skills according to genetic subtype only partially supported previous research and suggest that there is overlap in abilities across genetic subtypes of AS. Adaptive behavior skills were also significantly delayed, with participants demonstrating a significant strength in socialization, and a weakness in motor skills. 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PD JUL 15 PY 2004 VL 13 IS 14 BP 1471 EP 1477 DI 10.1093/hmg/ddh158 PG 7 WC Biochemistry & Molecular Biology; Genetics & Heredity SC Biochemistry & Molecular Biology; Genetics & Heredity GA 834GU UT WOS:000222400400007 PM 15150161 ER PT J AU Schumann, CM Hamstra, J Goodlin-Jones, BL Lotspeich, LJ Kwon, H Buonocore, MH Lammers, CR Reiss, AL Amaral, DG AF Schumann, CM Hamstra, J Goodlin-Jones, BL Lotspeich, LJ Kwon, H Buonocore, MH Lammers, CR Reiss, AL Amaral, DG TI The amygdala is enlarged in children but not adolescents with autism; The hippocampus is enlarged at all ages SO JOURNAL OF NEUROSCIENCE LA English DT Article DE Asperger; amygdaloid complex; development; mental retardation; MRI; neuroanatomy ID PERVASIVE DEVELOPMENTAL DISORDERS; DIAGNOSTIC OBSERVATION SCHEDULE; IMPAIRED MEMORY FUNCTIONS; ASPERGER-SYNDROME; NEURAL SYSTEMS; RECOGNITION MEMORY; INFANTILE-AUTISM; BRAIN; FEAR; INDIVIDUALS AB Autism is a neurodevelopmental disorder characterized by impairments in reciprocal social interaction, deficits in verbal and nonverbal communication, and a restricted repertoire of activities or interests. We performed a magnetic resonance imaging study to better define the neuropathology of autistic spectrum disorders. Here we report findings on the amygdala and the hippocampal formation. Borders of the amygdala, hippocampus, and cerebrum were defined, and their volumes were measured in male children (7.5 - 18.5 years of age) in four diagnostic groups: autism with mental retardation, autism without mental retardation, Asperger syndrome, and age-matched typically developing controls. Although there were no differences between groups in terms of total cerebral volume, children with autism ( 7.5 - 12.5 years of age) had larger right and left amygdala volumes than control children. There were no differences in amygdala volume between the adolescent groups (12.75 - 18.5 years of age). Interestingly, the amygdala in typically developing children increases substantially in volume from 7.5 to 18.5 years of age. Thus, the amygdala in children with autism is initially larger, but does not undergo the age-related increase observed in typically developing children. Children with autism, with and without mental retardation, also had a larger right hippocampal volume than typically developing controls, even after controlling for total cerebral volume. Children with autism but without mental retardation also had a larger left hippocampal volume relative to controls. These cross-sectional findings indicate an abnormal program of early amygdala development in autism and an abnormal pattern of hippocampal development that persists through adolescence. The cause of amygdala and hippocampal abnormalities in autism is currently unknown. C1 Univ Calif Davis, MIND Inst, Sacramento, CA 95817 USA. Univ Calif Davis, Dept Psychiat & Behav Sci, Ctr Neurosci, Sacramento, CA 95817 USA. Stanford Univ, Sch Med, Dept Psychiat & Behav Sci, Stanford Psychiat Neuroimaging Lab, Stanford, CA 94305 USA. 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Neurosci. PD JUL 14 PY 2004 VL 24 IS 28 BP 6392 EP 6401 DI 10.1523/JNEUROSCI.1297-04.2004 PG 10 WC Neurosciences SC Neurosciences & Neurology GA 837QI UT WOS:000222650000018 PM 15254095 ER PT J AU Altable, CR Pastor, CM Antoranz, AV AF Altable, CR Pastor, CM Antoranz, AV TI Schizophrenia and subjectivity SO ACTAS ESPANOLAS DE PSIQUIATRIA LA Spanish DT Review DE subjectivity; depersonalization; mental automatism; disorders of the self autism; psychopathology ID DEPERSONALIZATION; EXPERIENCES; PSYCHOPATHOLOGY; DISORDERS; CONSCIOUSNESS; AUTISM; SELF AB Recently, the group of symptoms known as much less thansubjective experiencesmuch greater than of schizophrenia has raised a growing interest. These phenomena have been shaped through concepts like depersonalization-derealization, mental automatism, disorders of the self and autism. 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PD JUL-AUG PY 2004 VL 32 IS 4 BP 249 EP 258 PG 10 WC Neurosciences; Psychiatry SC Neurosciences & Neurology; Psychiatry GA 845US UT WOS:000223271400008 ER PT J AU Shibayama, A Cook, EH Feng, JN Glanzmann, C Yan, J Craddock, N Jones, IR Goldman, D Heston, LL Sommer, SS AF Shibayama, A Cook, EH Feng, JN Glanzmann, C Yan, J Craddock, N Jones, IR Goldman, D Heston, LL Sommer, SS TI MECP2 structural and 3 '-UTR variants in schizophrenia, autism and other psychiatric diseases: A possible association with autism SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE MECP2; 3 '-UTR; schizophrenia; autism; psychiatric diseases; mutation detection ID CPG-BINDING PROTEIN-2; RETT-SYNDROME; HISTONE DEACETYLASE; GENE MECP2; DOVAM-S; MUTATIONS; SEQUENCE; DISORDER; RECEPTOR; COMPLEX AB Mutations in the gene coding for methyl-CpG-binding protein 2 (MECP2) cause Rett syndrome (RTT) and have also been reported in a number of X-linked mental retardation syndromes. Furthermore, putative mutations recently have been described in a few autistic patients and a boy with language disorder and schizophrenia. In this study, DNA samples from individuals with schizophrenia and other psychiatric diseases were scanned in order to explore whether the phenotypic spectrum of mutations in the MECP2 gene can extend beyond the traditional diagnoses of RTT in females and severe neonatal encephalopathy in males. The coding regions, adjacent splicing junctions, and highly conserved segments of the T-untranslated region (3'-UTR) were examined in 214 patients, including 106 with schizophrenia, 24 with autism, and 84 patients with other psychiatric diseases by detection of virtually all mutations-single strand conformation polymorphism (SSCP) (DOVAM-S). To our knowledge, this is the first analysis of variants in conserved regions of the 3'-UTR of this gene. A total of 5.2 kb per haploid gene was analyzed (1.5 Mb for 214 patients). A higher frequency of missense and 3'-UTR variants was found in autism. One missense and two 3'-UTR variants were found in 24 patients with autism versus one patient with a missense change in 144 ethnically similar individuals without autism (P = 0.009). These mutations suggest that a possible association between MECP2 mutations and autism may warrant further study. (C) 2004 Wiley-Liss, Inc. C1 City Hope Natl Med Ctr, Dept Mol Genet, Duarte, CA 91010 USA. Univ Chicago, Dept Psychiat, Chicago, IL 60637 USA. Univ Birmingham, Queen Elizabeth Psychiat Hosp, Div Neurosci, Birmingham, W Midlands, England. NIAAA, Dept Psychiat, NIH, Bethesda, MD USA. Univ Washington, Dept Psychiat, Seattle, WA 98195 USA. RP Sommer, SS (reprint author), City Hope Natl Med Ctr, Dept Mol Genet & Mol Diag, 1500 E Duarte Rd, Duarte, CA 91010 USA. EM sommerlab@coh.org RI Jones, Ian/B-4925-2009; Goldman, David/F-9772-2010 CR Amir RE, 1999, NAT GENET, V23, P185 Amir RE, 2000, AM J MED GENET, V97, P147, DOI 10.1002/1096-8628(200022)97:2<147::AID-AJMG6>3.0.CO;2-O Beyer KS, 2002, HUM GENET, V111, P305, DOI 10.1007/s00439-002-0786-3 Buzin CH, 2000, BIOTECHNIQUES, V28, P746 Carney RM, 2003, PEDIATR NEUROL, V28, P205, DOI 10.1016/S0887-8994(02)00624-0 Cohen D, 2002, AM J PSYCHIAT, V159, P148, DOI 10.1176/appi.ajp.159.1.148-a Couvert P, 2001, HUM MOL GENET, V10, P941, DOI 10.1093/hmg/10.9.941 Coy JF, 1999, HUM MOL GENET, V8, P1253, DOI 10.1093/hmg/8.7.1253 Feng J, 2001, MOL PSYCHIATR, V6, P168, DOI 10.1038/sj.mp.4000817 Feng JN, 1998, AM J MED GENET, V81, P172 Jones PL, 1998, NAT GENET, V19, P187, DOI 10.1038/561 Lam C W, 2000, J Med Genet, V37, pE41, DOI 10.1136/jmg.37.12.e41 Liu Q, 1999, BIOTECHNIQUES, V26, P932 Lobo-Menendez F, 2003, AM J MED GENET B, V117B, P97, DOI 10.1002/ajmg.b.10016 Nan XS, 1997, CELL, V88, P471, DOI 10.1016/S0092-8674(00)81887-5 Nan XS, 1998, NATURE, V393, P386 SCRIVER CR, 1995, METBOLIC MOL BASIS I van Karnebeek CDM, 2002, J MED GENET, V39, P205, DOI 10.1136/jmg.39.3.205 Vourc'h P, 2001, EUR J HUM GENET, V9, P556, DOI 10.1038/sj.ejhg.5200660 Zappella M, 2003, AM J MED GENET B, V119B, P102, DOI 10.1002/ajmg.b.10070 NR 20 TC 69 Z9 70 PU WILEY-LISS PI HOBOKEN PA DIV JOHN WILEY & SONS INC, 111 RIVER ST, HOBOKEN, NJ 07030 USA SN 0148-7299 J9 AM J MED GENET B JI Am. J. Med. Genet. B PD JUL 1 PY 2004 VL 128B IS 1 BP 50 EP 53 DI 10.1002/ajmg.b.30016 PG 4 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 834PT UT WOS:000222423700012 PM 15211631 ER PT J AU Bishop, DVM Maybery, M Wong, D Maley, A Hill, W Hallmayer, J AF Bishop, DVM Maybery, M Wong, D Maley, A Hill, W Hallmayer, J TI Are phonological processing deficits part of the broad autism phenotype? SO AMERICAN JOURNAL OF MEDICAL GENETICS PART B-NEUROPSYCHIATRIC GENETICS LA English DT Article DE autism; specific language impairment; phonological processing; family; broad phenotype ID LANGUAGE IMPAIRMENT; FAMILIAL AGGREGATION; SUSCEPTIBILITY GENE; CHROMOSOME 7Q; CHILDREN; PARENTS; INDIVIDUALS; RELATIVES; DISORDER; SIBLINGS AB Two tests of phonological processing, nonword repetition, and nonsense passage reading, were administered to 80 probands with autistic disorder or PDDNOS (index cases) and 59 typically developing controls, together with their parents and siblings. In addition, parents completed a questionnaire about history of language and literacy problems, and all participants were given tests of verbal (VIQ) and performance IQ (PIQ). Parents also completed the Autism-Spectrum Quotient, which was used to index the broad autism phenotype. Index probands scored well below control probands on the two phonological tests. However, on neither phonological measure did index relatives differ from control relatives. Within the index group, there was no relationship between the proband's level of VIQ, or age at achieving phrase speech, and phonological score of relatives. VIQ was the only measure to show any familiality within the index group. Reported history of language and literacy problems did not differentiate index parents from control parents overall, but those who were categorized as cases of the broad phenotype reported more history of language and literacy problems than did other index parents. However, they did not have poorer scores on the phonological measures. It is concluded that phonological processing deficits are not part of the broad autism phenotype. (C) 2004 Wiley-Liss, Inc. C1 Univ Oxford, Dept Expt Psychol, Oxford Study Childrens Commun Impairments, Oxford OX1 3UD, England. Univ Western Australia, Dept Psychiat, Crawley, WA 6009, Australia. Stanford Univ, Stanford, CA 94305 USA. RP Bishop, DVM (reprint author), Univ Oxford, Dept Expt Psychol, Oxford Study Childrens Commun Impairments, S Parks Rd, Oxford OX1 3UD, England. 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J. Med. Genet. B PD JUL 1 PY 2004 VL 128B IS 1 BP 54 EP 60 DI 10.1002/ajmg.b.30039 PG 7 WC Genetics & Heredity; Psychiatry SC Genetics & Heredity; Psychiatry GA 834PT UT WOS:000222423700013 PM 15211632 ER PT J AU Muller, RA AF Muller, RA TI Abnormal variability and distribution of functional maps in autism: An fMRI study of visuomotor learning (vol 160, pg 1847, 2003) SO AMERICAN JOURNAL OF PSYCHIATRY LA English DT Correction CR Muller RA, 2003, AM J PSYCHIAT, V160, P1847, DOI 10.1176/appi.ajp.160.10.1847 NR 1 TC 0 Z9 0 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 JUL PY 2004 VL 161 IS 7 BP 1320 EP 1320 PG 1 WC Psychiatry SC Psychiatry GA 835EG UT WOS:000222462700051 ER PT J AU Verri, A Maraschio, P Devriendt, K Uggetti, C Spadoni, E Haeusler, E Federico, A AF Verri, A Maraschio, P Devriendt, K Uggetti, C Spadoni, E Haeusler, E Federico, A TI Chromosome 10p deletion in a patient with hypoparathyroidism, severe mental retardation, autism and basal ganglia calcifications SO ANNALES DE GENETIQUE LA English DT Article DE 10p deletion; HDR; mental retardation; autism ID RENAL DYSPLASIA SYNDROME; PARTIAL MONOSOMY 10P; DIGEORGE-SYNDROME; SENSORINEURAL DEAFNESS; HDR SYNDROME; PHENOTYPIC SPECTRUM; BEHAVIOR CHECKLIST; GATA3; REGION; DISORDERS AB Chromosome 10p terminal deletions have been associated with a DiGeorge like phenotype. Haploinsufficiency of the region 10p14-pter, results in hypoparathyroidism, sensorineural deafness, renal anomaly, that is the triad that features the HDR syndrome. Van Esch (2000) identified in a HDR patient, within a 200 kb critical region, the GATA3 gene, a transcription factor involved in the embryonic development of the parathyroids, auditory system and kidneys. We describe a new male patient, 33-year-old, with 10p partial deletion affected by hypocalcemia, basal ganglia calcifications and a severe autistic syndrome associated with mental retardation. Neurologically he presented severe impairment of language, hypotonia, clumsiness and a postural dystonic attitude. A peripheral involvement of auditory pathways was documented by auditory evoked potentials alterations. CT scan documented basal ganglia calcifications. Hyperintensity of the lentiform nuclei was evident at the MRI examination. Renal ultrasound scan was normal. Haploinsufficiency for GATA3 gene was documented with FISH analysis using cosmid clone 1.2. Phenotypic spectrum observed in del (10p) is more severe than the classical DGS spectrum. GATA3 has been found to regulate the development of serotoninergic neurons. A serotoninergic dysfunction may be linked with autism in this patient. (C) 2004 Elsevier SAS. All rights reserved. C1 Neurol Inst C Mondino Fdn, I-27100 Pavia, Italy. Univ Pavia, Inst Biol & Med Genet, Pavia, Italy. Univ Leuven, Ctr Human Genet, Louvain, Belgium. IRCCS, Policlin S Matteo, Milan, Italy. Univ Siena, Policlin Le Scotte, Res Ctr Diag Therapy & Prevent Neurohandicap, Siena, Italy. RP Verri, A (reprint author), Neurol Inst C Mondino Fdn, Via Ferrata 6, I-27100 Pavia, Italy. EM annapia.verri@mondino.it CR AMAN MG, 1985, AM J MENT DEF, V89, P492 Baghdadli A, 2002, ENCEPHALE, V28, P248 BILEOUS RW, 1992, NEW ENGL J MED, V357, P1069 Cook Edwin H. 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Genet. PD JUL-SEP PY 2004 VL 47 IS 3 BP 281 EP 287 DI 10.1016/j.anngen.2004.03.001 PG 7 WC Genetics & Heredity SC Genetics & Heredity GA 857FY UT WOS:000224102900010 PM 15337474 ER PT J AU Lespinasse, J Rethore, MO North, MO Bovier-Lapierre, M Lundsteen, C Fert-Ferrer, S Bugge, M Kirchoff, M AF Lespinasse, J Rethore, MO North, MO Bovier-Lapierre, M Lundsteen, C Fert-Ferrer, S Bugge, M Kirchoff, M TI Balanced complex chromosomal rearrangements (BCCR) with at least three chromosomes and three or more breakpoints: report of three new cases SO ANNALES DE GENETIQUE LA English DT Article DE balanced complex chromosomal rearrangement (BCCR); mental retardation; infertility; recurrent spontaneous abortion; infantile autism; chromosomes 1, 4-11, 14, and 22; comparative genomic hybridization (CGH) ID PRENATAL-DIAGNOSIS AB Balanced complex chromosomal rearrangements (BCCR) encompass a heterogeneous group of rare chromosomal aberrations. In this paper, we report three cases of BCCRs. In two the probands were referred for either genetic counseling or prenatal management. One case was ascertained after chromosome analysis performed because of psychiatric manifestations; this was an isolated finding. We also outline the molecular cytogenctic techniques, which were essential in confirming and precisely delineating the BCCRs identified in these patients. In addition the various aspects of genetic counseling for this type of chromosomal rearrangement, highlighting the details particular to each individual case are discussed. We discuss the classification for this type of chromosomal mutation. (C) 2004 Published by Elsevier SAS. C1 Gen Hosp, Cytogenet Lab, F-73011 Chambery, France. Jerome Lejeune Med Ctr, F-75016 Paris, France. Hop St Vincent de Paul, Cytogenet Lab, F-75014 Paris, France. Gen Hosp, Div Pediat, F-73011 Chambery, France. Rigshosp, Dept Clin Genet, Cytogenet Lab, Copenhagen, Denmark. Univ Copenhagen, Wilhelm Johannsen Ctr Funct Genome Res, Dept Med Genet, DK-2200 Copenhagen N, Denmark. RP Lespinasse, J (reprint author), Gen Hosp, Cytogenet Lab, BP 1125, F-73011 Chambery, France. EM james.lespinasse@ch-chambery.rss.fr CR Batanian JR, 1998, AM J MED GENET, V78, P44, DOI 10.1002/(SICI)1096-8628(19980616)78:1<44::AID-AJMG9>3.0.CO;2-L BATISTA DA, 1993, HUM GENET, P117 BATISTA DAS, 1994, AM J MED GENET, V53, P255, DOI 10.1002/ajmg.1320530311 BOWSERRILEY SM, 1988, J MED GENET, V25, P226 DUTRILLAUX B, 1981, HUM GENET, V57, P93 FARRELL SA, 1994, AM J MED GENET, V52, P360, DOI 10.1002/ajmg.1320520322 FUKUSHIMA Y, 1986, AM J MED GENET, V25, P313, DOI 10.1002/ajmg.1320250217 GARDNER RJ, 1989, CHROMOSOME ABNORMALI, P182 GORSKI JL, 1988, AM J MED GENET, V29, P247, DOI 10.1002/ajmg.1320290202 JOHANNISSON R, 1988, CYTOGENET CELL GENET, V47, P160, DOI 10.1159/000132537 Kirchhoff M, 2000, EUR J HUM GENET, V8, P661, DOI 10.1038/sj.ejhg.5200512 LESPINASSE J, 2004, IN PRESS AM J MED GE LOPREIATO JO, 1992, J DEV BEHAV PEDIATR, V13, P281 LURIE IW, 1994, CLIN GENET, V46, P244 PAI GS, 1980, CLIN GENET, V18, P436 RODRIGUEZ MT, 1985, J MED GENET, V22, P66, DOI 10.1136/jmg.22.1.66 SAADALLAH N, 1985, HUM GENET, V71, P312, DOI 10.1007/BF00388456 SIKKEMARADDATZ B, 1995, PRENATAL DIAG, V15, P467, DOI 10.1002/pd.1970150510 WARBURTON D, 1991, AM J HUM GENET, V49, P995 NR 19 TC 12 Z9 14 PU EDITIONS SCIENTIFIQUES MEDICALES ELSEVIER PI PARIS PA 23 RUE LINOIS, 75724 PARIS, FRANCE SN 0003-3995 J9 ANN GENET-PARIS JI Ann. Genet. PD JUL-SEP PY 2004 VL 47 IS 3 BP 315 EP 324 DI 10.1016/j.anngen.2004.05.002 PG 10 WC Genetics & Heredity SC Genetics & Heredity GA 857FY UT WOS:000224102900014 PM 15337478 ER PT J AU Klein, KC Diehl, EB AF Klein, KC Diehl, EB TI Relationship between MMR vaccine and autism SO ANNALS OF PHARMACOTHERAPY LA English DT Article DE autism; MMR vaccine ID MUMPS-RUBELLA VACCINATION; CAUSAL ASSOCIATION; NO EVIDENCE; MEASLES; POPULATION; CHILDREN AB OBJECTIVE: To evaluate the proposed link between the administration of the measles, mumps, and rubella (MMR) vaccine and the development of autism. DATA SOURCES: A literature search utilizing MEDLINE (1966-November 2003), with the key terms measles, mumps, rubella, and autism, was conducted. Review of the references listed in the articles identified was also performed. DATA SYNTHESIS: Ten articles that specifically evaluated the possible relationship between the MMR vaccine and autism were identified. Review articles, commentaries, and evaluations of a link between gastrointestinal symptoms in autistic children and MMR immunization were excluded. CONCLUSIONS: Based upon the current literature, it appears that there is no relationship between MMR vaccination and the development of autism. C1 Univ Michigan, Hlth Syst, Coll Pharm, Dept Clin Sci, Ann Arbor, MI 48109 USA. Univ Michigan, Hlth Syst, Serv Pharm, Ann Arbor, MI 48109 USA. Univ Missouri, Sch Pharm, Kansas City, KS USA. RP Klein, KC (reprint author), Univ Michigan, Hlth Syst, Coll Pharm, Dept Clin Sci, MCHC F2758,Box 0221,1500 E Med Ctr Dr, Ann Arbor, MI 48109 USA. EM kriklein@umich.edu CR Dales L, 2001, JAMA-J AM MED ASSOC, V285, P1183, DOI 10.1001/jama.285.9.1183 DeStefano F, 2002, MOL PSYCHIATR, V7, pS51, DOI 10.1038/sj.mp.4001181 Fombonne E, 2001, PEDIATRICS, V108, part. no., DOI 10.1542/peds.108.4.e58 *I MED, 2001, IMM SAF REV MEAS MUM Kaye JA, 2001, BRIT MED J, V322, P460, DOI 10.1136/bmj.322.7284.460 Madsen KM, 2002, NEW ENGL J MED, V347, P1477, DOI 10.1056/NEJMoa021134 Makela A, 2002, PEDIATRICS, V110, P957, DOI 10.1542/peds.110.5.957 Patja A, 2000, PEDIATR INFECT DIS J, V19, P1127, DOI 10.1097/00006454-200012000-00002 Peltola H, 1998, LANCET, V351, P1327, DOI 10.1016/S0140-6736(98)24018-9 ROSS E, CHILDHOOD VACCINE AU 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 2002, EPIDEMIOLOGY PREVENT 2001, REUTERS MED NEW 0806 NR 15 TC 5 Z9 5 PU HARVEY WHITNEY BOOKS CO PI CINCINNATI PA PO BOX 42696, CINCINNATI, OH 45242 USA SN 1060-0280 J9 ANN PHARMACOTHER JI Ann. Pharmacother. PD JUL-AUG PY 2004 VL 38 IS 7-8 BP 1297 EP 1300 DI 10.1345/aph.1D293 PG 4 WC Pharmacology & Pharmacy SC Pharmacology & Pharmacy GA 831IT UT WOS:000222188800035 PM 15173555 ER PT J AU Roberts, JA Rice, ML Tager-Flusberg, H AF Roberts, JA Rice, ML Tager-Flusberg, H TI Tense marking in children with autism SO APPLIED PSYCHOLINGUISTICS LA English DT Article ID PERVASIVE DEVELOPMENTAL DISORDERS; MENTALLY-RETARDED SUBJECTS; LANGUAGE IMPAIRMENT; PSYCHOLINGUISTIC MARKERS; PRAGMATIC DIFFICULTIES; GRAMMATICAL MORPHEMES; DOWNS-SYNDROME; ACQUISITION; DEFICITS; SLI AB A recent large-scale study identified a subgroup of children with autism who had a language profile similar to that found among children with specific language impairment (SLI). including difficulties with nonsense word repetition, an ability that has been implicated as one clinical marker for SLI. A second clinical marker for English-speaking children with SLI is high rates of omission of grammatical morphemes that mark tense in obligatory contexts. This study used experimental probes designed to elicit third person and past tense morphology with a large heterogeneous sample of children with autism. The subgroup of children with autism who were language impaired showed high rates of omission of tense marking on the experimental tasks. in addition, some of the children with autism made performance errors that were specific to the autistic population, such as echolalia. These findings further refine the characteristics of language impairment found in a subgroup of children with autism. C1 Boston Univ, Sch Med, Dept Anat & Neurobiol, Lab Dev Cognit Neurosci, Boston, MA 02118 USA. Temple Univ, Philadelphia, PA 19122 USA. Univ Kansas, Lawrence, KS 66045 USA. 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PD JUL PY 2004 VL 25 IS 3 BP 429 EP 448 DI 10.1017/S0142716404001201 PG 20 WC Linguistics; Psychology, Experimental SC Linguistics; Psychology GA 835FK UT WOS:000222466200006 ER PT J AU Shaw, P Lawrence, EJ Radbourne, C Bramham, J Polkey, CE David, AS AF Shaw, P Lawrence, EJ Radbourne, C Bramham, J Polkey, CE David, AS TI The impact of early and late damage to the human amygdala on 'theory of mind' reasoning SO BRAIN LA English DT Article DE amygdala; theory of mind; autism; executive function ID DYSEMBRYOPLASTIC NEUROEPITHELIAL TUMOR; TEMPORAL-LOBE EPILEPSY; FRONTOTEMPORAL DEMENTIA; TUBEROUS SCLEROSIS; ASPERGER-SYNDROME; WILLIAMS-SYNDROME; SOCIAL COGNITION; ACQUIRED THEORY; AUTISM; LESIONS AB There is a burgeoning interest in the neural basis of the ability to attribute mental states to others; a capacity referred to as 'theory of mind' (ToM). We examined the effects of lesions of the amygdala which arise at different stages of development on this key aspect of social cognition. Tests of ToM, executive and general neuropsychological function were given to subjects with lesions of the amygdala arising congenitally or in early childhood ('early damage', n = 15), subjects who acquired damage to the amygdala in adulthood ('late damage' n = 11) and matched clinical (n = 14) and healthy comparison groups (n = 38). Subjects with early damage to the amygdala, particularly if the lesion was associated with childhood onset of seizures, were impaired relative to all other groups on more advanced tests of ToM reasoning, such as detecting tactless or ironic comments or interpreting non-literal utterances. These deficits held for subjects with either left or right early amygdala damage and encompassed the understanding of both the beliefs and emotional states of others. 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Aim: To describe parents' beliefs about the MMR vaccination and to explore the best predictors of uptake by the age of 2 years. Design of study: Prospective questionnaire study. Setting: Brighton and Hove area of East Sussex. Method: Five hundred and eleven parents (response rate 56.9%) completed a baseline questionnaire regarding their profile characteristics, beliefs about MMR and previous vaccination history prior to receiving a letter to attend for their child's vaccination. Attendance data was collected at follow-up by the age of 2 years. Results: The majority of parents believed that measles, mumps and rubella were serious illnesses and stated that they would feel guilty about any adverse consequences of their decision about vaccination. Many responders were ambivalent about the benefit of vaccinations and were unsure whether to trust either the medical profession or the media. Uptake of MMR vaccination at follow-up was related to previous uptake for vaccination, increased faith in the medical profession, increased faith in the media, and a lower belief that vaccination is unhealthy and can harm the immune system. Conclusion: Many parents hold mixed beliefs about the MMR vaccination and the doctors who administer it. Uptake relates to past vaccination and more positive beliefs. C1 Guys Kings & St Thomas Sch Med, Dept Gen Practice, London SE11 6SP, England. Ardingly Court Surg, Brighton, E Sussex, England. RP Ogden, J (reprint author), Guys Kings & St Thomas Sch Med, Dept Gen Practice, 5 Lambeth Walk, London SE11 6SP, England. 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PD JUL PY 2004 VL 49 IS 7 BP 500 EP 500 PG 1 WC Psychiatry SC Psychiatry GA 003UO UT WOS:000234707300023 PM 15362263 ER PT J AU Adamson, LB Bakeman, R Deckner, DF AF Adamson, LB Bakeman, R Deckner, DF TI The development of symbol-infused joint engagement SO CHILD DEVELOPMENT LA English DT Article ID MOTHER-INFANT; DOWN-SYNDROME; 2ND YEAR; ATTENTION; CHILDREN; AUTISM; LANGUAGE; CONTINUITY; BEHAVIOR; CONTEXT AB Fifty-six children were observed longitudinally from 18 to 30 months of age interacting with their mothers during a Communication Play that contained 8 scenes designed to encourage interacting, requesting, commenting, and narrating. Of primary concern was how often symbols infused the child's states of engagement with people and objects and how experience in such symbol-infused states related to language acquisition. 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PD JUL-AUG PY 2004 VL 75 IS 4 BP 1171 EP 1187 DI 10.1111/j.1467-8624.2004.00732.x PG 17 WC Psychology, Educational; Psychology, Developmental SC Psychology GA 843FQ UT WOS:000223064300013 PM 15260871 ER PT J AU Sturm, H Fernell, E Gillberg, C AF Sturm, H Fernell, E Gillberg, C TI Autism spectrum disorders in children with normal intellectual levels: associated impairments and subgroup SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID DEVELOPMENTAL DISORDER; ONSET SCHIZOPHRENIA; ASPERGER-SYNDROME; ATTENTION; ADHD AB In order to define potential subgroups pertaining to the spectrum of 'high-functioning' pervasive developmental disorders (PDDs) the medical and psychiatric records of 101 children with PDD were reviewed. Ninety-one children had a diagnosis of Asperger syndrome, nine had a PDD not otherwise specified, and one had 'high-functioning' autism. Mean age of the children (71 males, 30 females) was 9 years 8 months (age range 5 to 12 years). Apart from the core dysfunctions of the PDD, i.e. deficient social interaction, communication and repertoires, and restricted interests, 95% had attentional problems, 75% had motor difficulties, 86% had problems with regulation of activity level, and 50% had impulsiveness. About three-quarters had symptoms compatible with mild or severe attention-deficit-hyperactivity disorder (ADHD) or had deficits in attention, motor control, and perception (DAMP), indicating a considerable overlap between these disorders and high-functioning PDD in children of normal or near-normal intelligence. A combination of affective dysregulation, thought disturbance, and severely restricted social interaction, referred to as a multiple complex developmental disorder (MCDD; a condition possibly related to schizoaffective disorder), was recorded in about 8% of the children. Seventeen percent had another major medical diagnosis or medical syndrome, which highlights the importance of completing a neurological assessment of all children with PDDs. C1 Astrid Lindgren Childrens Hosp, Neuropsychiat Unit, S-17176 Stockholm, Sweden. Univ Gothenburg, Dept Child & Adolescent Psychiat, Gothenburg, Sweden. RP Sturm, H (reprint author), Astrid Lindgren Childrens Hosp, Neuropsychiat Unit, S-17176 Stockholm, Sweden. EM harald.sturm@bup.sll.se CR American Psychiatric Association, 1994, DIAGN STAT MAN MENT, V4th Asarnow RF, 1999, EUR CHILD ADOLESC S1, V8, P15 Asperger H, 1944, ARCH PSYCHIAT NERVEN, V117, P76, DOI 10.1007/BF01837709 Barkley RA, 1997, PSYCHOL BULL, V121, P65, DOI 10.1037//0033-2909.121.1.65 Buitelaar JK, 1998, J CHILD PSYCHOL PSYC, V39, P911, DOI 10.1017/S0021963098002820 Buitelaar JK, 1999, J AUTISM DEV DISORD, V29, P33, DOI 10.1023/A:1025966532041 COHEN DJ, 1996, DIAGNOSIS CLASSIFICA, P5 Eggers C, 1999, EUR CHILD ADOLES PSY, V8, P1 EHLERS S, 1993, J CHILD PSYCHOL PSYC, V34, P1327, DOI 10.1111/j.1469-7610.1993.tb02094.x GILLBERG C, 1983, J CHILD PSYCHOL PSYC, V24, P377, DOI 10.1111/j.1469-7610.1983.tb00116.x KOPP S, 1999, EUR CHILD ADOLES PSY, V1, P89 NORDSTROM A, 2001, FAKTA BARN UNGDOM, P12 Nyden A, 2001, DEV MED CHILD NEUROL, V43, P165, DOI 10.1017/S0012162201000329 Ozonoff S, 2001, J AUTISM DEV DISORD, V31, P257, DOI 10.1023/A:1010794902139 Taylor E, 1999, DEV PSYCHOPATHOL, V11, P607, DOI 10.1017/S0954579499002230 WATKINS JM, 1988, J CHILD PSYCHOL PSYC, V29, P865, DOI 10.1111/j.1469-7610.1988.tb00759.x Wechsler D., 1999, WECHSLER INTELLIGENC WECHSLER D, 1977, WECHSLER INTELLIGEN WHO, 1993, ICD 10 CLASS MENT BE World Health Organisation, 2001, INT CLASS FUNCT DIS NR 20 TC 80 Z9 85 PU CAMBRIDGE UNIV PRESS PI NEW YORK PA 40 WEST 20TH ST, NEW YORK, NY 10011-4211 USA SN 0012-1622 J9 DEV MED CHILD NEUROL JI Dev. Med. Child Neurol. PD JUL PY 2004 VL 46 IS 7 BP 444 EP 447 DI 10.1017/S0012162204000738 PG 4 WC Clinical Neurology; Pediatrics SC Neurosciences & Neurology; Pediatrics GA 835MH UT WOS:000222487000003 PM 15230456 ER PT J AU Nyden, A Carlsson, M Carlsson, A Gillberg, C AF Nyden, A Carlsson, M Carlsson, A Gillberg, C TI Interhemispheric transfer in high-functioning children and adolescents with autism spectrum disorders: a controlled pilot study SO DEVELOPMENTAL MEDICINE AND CHILD NEUROLOGY LA English DT Article ID CORPUS-CALLOSUM; INFANTILE-AUTISM; ASPERGER-SYNDROME; CHILDHOOD AUTISM; HAND PREFERENCE; LEFT-HANDEDNESS; COMMISSUROTOMY; AGENESIS; BRAIN AB Autism is a neurodevelopmental disorder with strong genetic influences. Clinical experience and limited empirical evidence support the view that autism may be associated with aberrant interhemispheric information transfer. This empirical controlled study examined whether, at neuropsychological testing, children with autism showed problems with interhemispheric information transfer. The study included auditory, visual, and motor measures covering information transfer within, as well as across, modalities. Thirty children (24 males, 6 females; mean age 12 years 8 months, SD 2 years 8 months; range 9 years 5 months to 17 years 5 months) without learning disability* but with autism spectrum disorders were compared with 30 children from a mainstream school matched for age, sex, and IQ>75. Children with autism spectrum disorder performed significantly worse than the comparison group on most of the tests (p=0.02 for auditory perception and attention, p=0.005 for visual perception, p=0.0001 for motor control,p=0.04 for tactile perception). Results support the notion that aberrant interhemispheric transfer may be involved in the pathogenesis or clinical course of autism. The findings were not accounted for by lower IQ in the group with autism. C1 Univ Gothenburg, Dept Child & Adolescent Psychiat, SE-41119 Gothenburg, Sweden. Univ Gothenburg, Inst Clin Neurosci, Neuropsychiat Res Unit, SE-41119 Gothenburg, Sweden. A Carlsson Res, Gothenburg, Sweden. Univ London St Georges Hosp, Sch Med, London SW17 0RE, England. RP Nyden, A (reprint author), Univ Gothenburg, Dept Child & Adolescent Psychiat, Kungsgatan 12, SE-41119 Gothenburg, Sweden. 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